2022 Book FootAndAnkleDisorders

Foot and Ankle
Disorders
A Comprehensive Approach
in Pediatric and Adult
Populations
Emilio Wagner Hitschfeld
Pablo Wagner Hitschfeld
Editors
123
Foot and Ankle Disorders
Emilio Wagner Hitschfeld
Pablo Wagner Hitschfeld
Editors
Foot and Ankle Disorders

A Comprehensive Approach in Pediatric
and Adult Populations
Editors
Emilio Wagner Hitschfeld Pablo Wagner Hitschfeld
Orthopedic Surgery Department Orthopedic Surgery Department
Clínica Alemana de Santiago - Universidad Clínica Alemana de Santiago - Universidad
del Desarrollo del Desarrollo, Hospital Militar de
Santiago, RM - Santiago, Chile Santiago – Universidad de los Andes
Santiago, RM - Santiago, Chile
ISBN 978-3-030-95737-7 ISBN 978-3-030-95738-4 (eBook)

https://doi.org/10.1007/978-3-030-95738-4
© The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature
Switzerland AG 2022
This work is subject to copyright. All rights are solely and exclusively licensed by the Publisher, whether
the whole or part of the material is concerned, specifically the rights of reprinting, reuse of illustrations,
recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or
information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar
methodology now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication
does not imply, even in the absence of a specific statement, that such names are exempt from the relevant
protective laws and regulations and therefore free for general use.
The publisher, the authors and the editors are safe to assume that the advice and information in this book
are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the
editors give a warranty, expressed or implied, with respect to the material contained herein or for any
errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional
claims in published maps and institutional affiliations.
This Springer imprint is published by the registered company Springer Nature Switzerland AG
The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
This book is gratefully dedicated to our mom
and dad, Sonia and Rodolfo, for their life
guidance, support, unconditional love,
patience, and continuous teachings. Parents
are the unsung heroes of every life. Thank
you for everything.
Emilio and Pablo
Foreword
On so many levels, it is an extraordinary pleasure to review this book. Foot and

ankle surgeons globally have benefited from the incredible insight, creativity, and
innovation of Emilio and Pablo Wagner, and I now have the privilege to review work
not only of good friends but also surgeons who I admire very much.
All textbooks carry a unique message which conveys the philosophy not only of
the editors but also of the carefully selected contributors, and this is clearly evident
here. The contributors are all world renowned in our field, giving this book tremen-
dous credibility. There is a preponderance of contributors from Latin America which
makes this book very appealing. While we may strive for global standardization of
approaches to treatment of foot and ankle deformities, this is unrealistic. Treatments
are determined by our training and experiences, the cultural and regional context in
which patients are examined, as well as materials and availability of implants. The
inclusion of regional experts each with a very different focus of foot and ankle treat-
ment presents the reader with an excellent overview of the most important
pathologies.
The book has been organized into different important sections including princi-
ples of foot and ankle evaluation, pediatric conditions, adult deformities, and
trauma. The inclusion of a very comprehensive section on pediatric foot and ankle
deformities is outstanding. These chapters cover all the essentials and are an out-
standing additional contribution to our understanding of childhood deformities. All
too often, foot and ankle surgery textbooks focus on the adult, ignoring the patho-
genesis, principles, and evolution of deformity. A good example and a wonderful
chapter to read is on the clubfoot by Dalia Sepúlveda. It is extraordinarily thorough,
extremely well illustrated, and not only focuses on the Ponseti method of treatment
but also provides a very good overview of the kinematics of the subtalar joint and
principles of treatment. The chapter by another world leader, Vince Mosca, is a must
read for any surgeon interested in foot and ankle with a focus on principles of evalu-
ation and treatment, so well-stated “techniques change, but principles are forever.”
When I read the book in preparation for writing this preface, I was obviously
drawn to those topics in which I myself have a specific interest, and the chapter by
Emilio and Pablo Wagner on localized osteoarthritis of the ankle is a great example.
vii
viii Foreword
It is incredibly well illustrated, and the thoughtful approach to supramalleolar oste-

otomies is one of the best overviews of this subject that I have ever read. The inclu-
sion of three chapters on the management of ankle arthritis is a good reflection of
the editors’ interest in this topic, and each one thoughtfully presented by great
authorities on this subject.
This textbook is a wonderful compilation of topics which are germane to our
practice, written by global leaders in the field, and will be an excellent resource for
all of us.
Mark S. Myerson
University of Colorado
Boulder, CO, USA
Steps2Walk
Greenwood Village, CO, USA
Preface
Foot and ankle orthopedics and traumatology is a fascinating subspecialty within gen-
eral orthopedics which has been receiving increased attention in the world in the last
20 years. Enormous development in understanding its complex biomechanics, joint
pathology, soft tissue stress pathology, and trauma has pushed this subspecialty to
unknown levels of interest worldwide. More orthopedic centers around the world now
focus their attention on foot and ankle lesions, training orthopedic surgeons in this area,
forming fellowship training groups, and generating basic and clinical science studies.
As our general understanding in foot and ankle trauma and orthopedics in adult
population has improved, simultaneous interest and development has been seen in
pediatric literature, where a unique approach is currently followed with significant
differences from adult approach. As any medical specialty with an ever-expanding
field of basic science, diagnosis, and treatment options, it is difficult to find a com-
mon place for a focused approach to foot and ankle pathology in adult and pediatric
population. This difficulty is seen in residency and fellowship programs where our
residents and fellows need a text to base their knowledge.
This book tries to fill the gap of information and interconnection between adult
and pediatric foot and ankle lesions, describing, analyzing, and offering treatment
alternatives for the most common topics in both groups of patients. Written by rec-
ognized experts in their respective fields from 14 different countries, this book pro-
vides information about foot and ankle biomechanics, soft tissue lesions, trauma
and sports lesions, orthopedic deformities, and systemic disorders. Every chapter is
written with a focused approach, allowing the reader to fully understand from the
basics up to the most current surgical or conservative treatment for each problem.
Lower limb reconstruction concepts are also included, such as tibial posttraumatic
deformities, tibial osteomyelitis, and tibial bone defects reconstruction techniques.
We are sure that this book will serve as a guide for orthopedic surgeons, foot and
ankle fellowship programs, and any orthopedic surgeon who wants to know more
about this incredible subspecialty.
Santiago, RM - Santiago, Chile Emilio Wagner Hitschfeld

Santiago, RM - Santiago, Chile Pablo Wagner Hitschfeld
ix
Acknowledgment
We would like to acknowledge the extraordinary work of all authors present in this
book. They all did an outstanding work with their respective chapters, giving the
reader updated information.
We would as well like to recognize and thank our mentors, John Gould, Mark
Myerson, John Herzenberg, and Beat Hintermann. Without their influence in our
lives, neither this book nor our current practice would exist.
xi
Contents
Part I Basic Science and General Considerations

Foot and Ankle Biomechanics Gait Analysis �� 3
Manuel Monteagudo and Pilar Martínez de Albornoz

Imaging in Ankle and Foot�� 25
Nicolas Zilleruelo V.

Open vs Minimally Invasive Surgery: Advantages and Disadvantages�� 43
Mariano De Prado, Manuel Cuervas-Mons, and Virginia De Prado

Tumors of the Foot and Ankle�� 71
Eduardo Botello and Tomas Zamora

Care and Management of Surgical Wounds, Wounds Dehiscence,
and Scars�� 89
Leonardo Parada and Günther Mangelsdorff
Part II Pediatric Orthopaedics and Traumatology

Biomechanics, Assessment, and Management Principles
for Pediatric Foot Deformities�� 115
Vincent S. Mosca
Clubfoot�� 133
Dalia Sepúlveda Arriagada and Nicolas Valdivia Rojo

Pediatric Metatarsus Adductus and Cavovarus Foot �� 157
Maryse Bouchard

Pediatric Flexible and Rigid Flatfoot �� 179
Kyle M. Natsuhara and Jacob R. Zide
Foot Osteochondrosis�� 197
Pablo J. Echenique Díaz and Pablo Schaufele Muñoz
xiii
xiv Contents

Fibular Hemimelia: Principles and Techniques of Management�� 213
Philip K. McClure and John E. Herzenberg

Brachymetatarsia: Surgical Management with Internal
and External Fixation�� 273
Noman A. Siddiqui
Lesser Toe Deformities�� 291
Carlos Pargas and Pablo Wagner Hitschfeld
Neurologic Foot�� 313
Gino Martínez and Gonzalo Chorbadjian

Pediatric Diaphyseal Tibia and Distal Tibia Fractures�� 335
Cristian Olmedo Gárate and Cristian Artigas Preller
Ankle Transitional Fractures�� 351
Matias Sepulveda and Estefania Birrer
Part III Adult Orthopaedics: Forefoot

Hallux Valgus�� 371
Pablo Wagner Hitschfeld and Emilio Wagner Hitschfeld

Hallux Rigidus: A Comprehensive Review�� 409
Gaston Slullitel and Valeria Lopez
Sesamoiditis�� 427
Florencia Pacheco Martinez and Eduardo Fuentes Morales
Metatarsalgia�� 443
Pilar Martinez de Albornoz and Manuel Monteagudo

Deformity of the Lesser Toes�� 467
Pablo Sotelano and Daniel Sebastián Villena
Morton’s Neuroma�� 493
Rodrigo Melo Grollmus and Cristián Ortiz Mateluna
Bunionette�� 517
Manuel Resende Sousa, Daniel Ribeiro Mendes, and João Vide
Part IV Adult Orthopaedics: Midfoot, Rearfoot and Ankle

Progressive Collapsing Foot Deformity – Flatfoot�� 537
Jaeyoung Kim and Jonathan T. Deland

Latest Trends in Flatfoot Management: Contributions
of the Spring Ligament Complex and the Deltoid Ligament�� 555
Brian T. Sleasman and Anish R. Kadakia
Contents xv
Cavus Foot�� 567

Mark S. Myerson and Shuyuan Li

“Management of Severe Untreated and Recurrent Clubfoot
Deformity in the Child and Adult”�� 593
Muller Weiss Disease �� 615
Manuel Monteagudo and Ernesto Maceira

Surgical Techniques for Peritalar Osteoarthrosis:
Talonavicular, Subtalar, Calcaneocuboid, and Midfoot �� 637
José Antônio Veiga Sanhudo and Marco Túlio Costa

Forefoot-Driven Hindfoot Deformity: Coupled Deformity�� 669
Norman Espinosa and Georg Klammer

Localized Osteoarthritis of the Ankle�� 691
Emilio Wagner Hitschfeld and Pablo Wagner Hitschfeld
Diffuse Ankle Osteoarthritis �� 723
Markus Knupp
Part V Adult Orthopaedics: Tibial Reconstruction

Tibial Post-traumatic Deformity�� 745
Arnd F. Viehöfer and Stephan H. Wirth
Septic Ankle Arthritis and Tibial Osteomyelitis�� 759
Pablo Mery and Joaquín Palma

Tibial Bone Defect Reconstruction Techniques�� 801
Gonzalo F. Bastías and Gregorio Verschae
Below-Knee Amputations�� 817
Roberto Muñoz Molina and Octavio Polanco Torres
Part VI Adult Orthopaedics: Tendinopathy, Soft Tissue Pathology

and Systemic Diseases
Insertional Achilles Tendinopathy: Diagnosis and Treatment �� 841
Giovanni Carcuro and Manuel J. Pellegrini P.
Non-insertional Achilles Tendinopathy�� 855
Rocco Aicale and Nicola Maffulli
Achilles Lengthening �� 869
xvi Contents
Plantar Fasciitis�� 885

Mario Abarca and Jorge Filippi

Foot and Ankle Tendon Transfers: Surgical Techniques�� 901
Jose Carlos Cohen
Diabetic Foot�� 941
Alexandre Leme Godoy-Santos and Rafael Barban Sposeto
Rheumatoid Foot�� 955
Sergio Fernandez C. and Hugo Henriquez
Charcot Neuroarthropathy �� 985
Rafael Barban Sposeto and Alexandre Leme Godoy-Santos

Nerve Entrapment Syndromes of the Lower Limbs�� 1005
Marcelo Pires Prado and Guilherme Honda Saito
Part VII Adult Sports Lesions and Traumatology

Peroneal Tendon Tears: Evaluation and Treatment�� 1023
James W. Brodsky and Daniel D. Bohl

Anterior Ankle Impingement and Ankle Instability�� 1045
Jordi Vega and Miki Dalmau-Pastor

Diagnosis and Treatment of Talus Osteochondral Lesions:
Current Concepts�� 1065
Caio Nery and Marcelo Pires Prado
Posterior Ankle Impingement �� 1107
Daniel Baumfeld and Tiago Baumfeld

Common Stress Fractures Around the Foot and Ankle�� 1119
Roberto Zambelli and Nacime Salomão Barbachan Mansur
Achilles Tendon Ruptures �� 1137
Diego Zanolli and Rubén Radkievich
Ankle Fractures�� 1165
Guillermo Arrondo and Florencio Pablo Segura
Tibial Pilon Fracture �� 1207
Christian Bastias and Leonardo Lagos
Calcaneus Fractures�� 1225
Stefan Rammelt and Christine Marx
Talus Fracture�� 1253
Florencio Pablo Segura and Guillermo Arrondo
Contents xvii
Midfoot Injuries �� 1281

Leandro Casola and German Joannas

Diaphyseal and Distal Tibia Fractures�� 1315
Rodrigo Pesántez and Eduardo José Burgos
Metatarsal Fractures �� 1329
Gabriel Khazen

Compartment Syndrome of the Leg and Foot�� 1361
Omar Ituriel Vela Goñi and Luis Felipe Hermida Galindo
Index�� 1385
Contributors
Mario Abarca Hospital Sótero del Río, Santiago, Chile

Rocco Aicale Department of Musculoskeletal Disorders, Faculty of Medicine and
Surgery, University of Salerno, Baronissi, Italy
Clinica Ortopedica, Ospedale San Giovanni di Dio e Ruggi D’Aragona, Salerno, Italy
Gonzalo Chorbadjian Clínica Alemana – Universidad del Desarrollo,
Santiago, Chile
Hospital Clínico San Borja Arriarán, Santiago, Chile
Dalia Sepúlveda Arriagada Private Practice, COTI Chile, Santiago, Chile
Guillermo Arrondo Instituto Dupuytren, Ciudad Autónoma de Buenos Aires,
Argentina
Department of Leg, Ankle and Foot, Dupuytren Institute, Ciudad Autónoma de
Buenos Aires, Argentina
Christian Bastias Hospital Mutual de Seguridad C. Ch. C., Clínica Santa Maria,
Santiago, Chile
Gonzalo F. Bastías Clínica las Condes, Santiago, Chile
Hospital del trabajador de Santiago, Santiago, Chile
Daniel Baumfeld Federal University of Minas Gerais, Felicio Rocho Hospital,
Belo Horizonte, MG, Brazil
Tiago Baumfeld Felicio Rocho Hospital, Belo Horizonte, MG, Brazil
Estefania Birrer Universidad Austral de Chile, Valdivia, Chile
Hospital Base de Valdivia, Valdivia, Chile
Daniel D. Bohl Baylor University Medical Center, Dallas, TX, USA
Eduardo Botello Orthopaedic Oncology and Lower Limb Reconstructive Surgery,
Orthopaedic Surgery Department, Pontificia Universidad Católica de Chile, ,
Santiago, Chile
xix
xx Contributors
Maryse Bouchard The Hospital for Sick Children, Division of Orthopaedic

Surgery, University of Toronto, Toronto, ON, Canada
James W. Brodsky Baylor University Medical Center, Dallas, TX, USA
Eduardo José Burgos Hospital Universitario Fundación Santa Fé, Bogotá,
Colombia
Giovanni Carcuro University of the Andes Clinic, Las Condes, Chile
Leandro Casola Foot and Ankle Division, Dupuytren Institute, Ciudad Autónoma
de Buenos Aires (CABA), Argentina
Jose Carlos Cohen Foot and Ankle Surgery, Federal University Hospital of Rio
De Janeiro/Brazil (UFRJ/ HUCFF), Rio De Janeiro, Brazil
Marco Túlio Costa Hospital Santa Casa de Misericórdia de São Paulo, São
Paulo, Brazil
Manuel Cuervas-Mons Orthopedic Surgery and Traumatology Service, Hospital
General Universitario Greogrio Marañon, Madrid, Madrid, Spain
Miki Dalmau-Pastor Laboratory of Arthroscopic and Surgical Anatomy,
Department of Pathology and Experimental Therapeutics (Human Anatomy Unit),
University of Barcelona, Barcelona, Spain
MIFAS by GRECMIP, Merignac, France
Martinez de Albornoz Pilar Quiron salud University Hospital Madrid,
Madrid, Spain
Pilar Martínez de Albornoz Orthopaedic Foot and Ankle Unit, Orthopaedic and
Trauma Department, Hospital Universitario Quirónsalud Madrid, Madrid, Spain
Jonathan T. Deland Hospital for Special Surgery, New York, NY, USA
Mariano De Prado Service of Orthopedic Surgery and Traumatology, Hospital
Quironsalud Murcia, Murcia, Spain
Virginia De Prado Podiatry Service, Hospital Quironsalud Murcia, Murcia, Spain
Pablo J. Echenique Díaz Universidad Austral de Chile, Valdivia, Chile
Hospital Base Valdivia, Los Ríos, Chile
Norman Espinosa Institute for Foot and Ankle Reconstruction Zurich, FussInstitut
Zurich, Zurich, Switzerland
Sergio Fernandez C. Clínica Santa María, Servicio de Ortopedia y Traumatología,
Equipo de Pie y Tobillo, Santiago, Chile
Jorge Filippi Clínica Las Condes, Santiago, Chile
Hospital del Trabajador, Santiago, Chile
Contributors xxi
Luis Felipe Hermida Galindo ABC Medical Center, Santa Fe Campus, Ciudad de
México, México
Cristian Olmedo Gárate Clinica Alemana de Santiago, Santiago, Chile
Hospital Padre Hurtado, Santiago, Chile
Alexandre Leme Godoy-Santos University of São Paulo/Hospital Israelita Albert
Einstein, São Paulo, Brazil
Omar Ituriel Vela Goñi Orthopaedics and Traumatology Institute at Zambrano
Hellion Hospital, San Pedro Garza García, Nuevo León, México
Rodrigo Melo Grollmus Department of Orthopedic Surgery, Foot and Ankle Unit,
Clinica Las Condes, Santiago, Chile
Department of Orthopedic Surgery, Foot and Ankle Unit, Hospital Militar de
Santiago, Santiago, Chile
Hugo Henriquez Clínica Santa María, Servicio de Ortopedia y Traumatología,
Equipo de Pie y Tobillo, Santiago, Chile
Instituto Traumatológico de Santiago, Equipo de Pie y Tobillo, Santiago, Chile
John E. Herzenberg International Center for Limb Lengthening, Rubin Institute
for Advanced Orthopedics, Sinai Hospital of Baltimore, Baltimore, MD, USA
German Joannas Foot and Ankle Division “CEPP”, Dupuytren Institute, Ciudad
Autónoma de Buenos Aires (CABA), Argentina
Foot and Ankle Division, Centro Artroscópico Jorge Batista SA, Ciudad Autónoma
de Buenos Aires (CABA), Argentina
Foot and Ankle Division, Barrancas Institute, Buenos Aires, Argentina
Anish R. Kadakia Northwestern University – Feinberg School of Medicine,
Northwestern Memorial Hospital, Department of Orthopedic Surgery,
Chicago, IL, USA
Gabriel Khazen Hospital de Clinicas Caracas, Caracas, Venezuela
Jaeyoung Kim Hospital for Special Surgery, New York, NY, USA
Georg Klammer Institute for Foot and Ankle Reconstruction Zurich, FussInstitut
Zurich, Zurich, Switzerland
Markus Knupp University of Basel, Mein Fusszentum Basel, Basel, Switzerland
Leonardo Lagos Hospital Mutual de Seguridad C. Ch. C., Clínica Santa Maria,
Santiago, Chile
Shuyuan Li, MD, PhD Department of Orthopaedics, University of Colorado
Anschutz Medical Campus, Aurora, CO, USA
Steps2Walk, Greenwood Village, CO, USA
xxii Contributors
Valeria Lopez Instituto de Ortopedia y Traumatología Dr. Jaime Slullitel, Rosario,

Santa Fe, Argentina
Ernesto Maceira Orthopaedic Foot and Ankle Unit, Complejo Hospitalario La
Mancha Centro, Alcázar de San Juan, Ciudad Real, Spain
Nicola Maffulli Department of Musculoskeletal Disorders, Faculty of Medicine
and Surgery, University of Salerno, Baronissi, Italy
Queen Mary University of London, Barts and the London School of Medicine and
Dentistry, Centre for Sports and Exercise Medicine, Mile End Hospital, London, UK
Keele University, Faculty of Medicine, School of Pharmacy and Bioengineering,
Guy Hilton Research Centre, Hartshill, Stoke-on-Trent, UK
Günther Mangelsdorff Department of Plastic Surgery and Burns, Hospital del
Trabajador, Santiago, Chile
Department of Plastic Surgery, Clínica Santa Maria, Santiago, Chile
Nacime Salomão Barbachan Mansur Grupo de Medicina e Cirurgia do Pé e
Tornozelo, Departamento de Ortopedia e Traumatologia, Escola Paulista de
Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brazil
Florencia Pacheco Martinez Instituto de Seguridad del Trabajo Viña del Mar,
Clínica Ciudad del Mar, Viña del Mar, Chile
Christine Marx University Center for Orthopaedics, Trauma and Plastic Surgery,
University Hospital Carl Gustav Carus at TU Dresden, Dresden, Germany
Cristián Ortiz Mateluna Department of Orthopedic Surgery, Foot and Ankle
Unit, Clinica Universidad de los Andes, Santiago, Chile
Philip K. McClure International Center for Limb Lengthening, Rubin Institute for
Advanced Orthopedics, Sinai Hospital of Baltimore, Baltimore, MD, USA
Daniel Ribeiro Mendes Foot and Ankle Unit at Hospital Cuf Tejo, Lisbon, Portugal
Pablo Mery Pontificia Universidad Católica de Chile, Santiago, Chile
Roberto Muñoz Molina Clínica Bupa Antofagasta, Universidad de Antofagasta,
Antofagasta, Chile
Manuel Monteagudo Quironsalud University Hospital Madrid, Madrid, Spain
Eduardo Fuentes Morales Instituto de Seguridad del Trabajo Viña del Mar,
Clínica Ciudad del Mar, Viña del Mar, Chile
Vincent S. Mosca Orthopedics, University of Washington School of Medicine,
Seattle, WA, USA
Pediatric Orthopedic Surgeon, Seattle Children’s Hospital, Seattle, WA, USA
Contributors xxiii
Pablo Schaufele Muñoz Universidad de Concepción, Concepción, Chile

Hospital Clínico Regional de Concepción Dr. Guillermo Grant Benavente,
Biobío, Chile
Mark S. Myerson, MD Department of Orthopaedics, U
niversity of Colorado
Anschutz Medical Campus, Aurora, CO, USA
Kyle M. Natsuhara Department of Orthopaedic Surgery, Baylor University
Medical Center, Dallas, TX, USA
Caio Nery Hospital Israelita Albert Einstein, São Paulo, Brasil
Joaquín Palma Pontificia Universidad Católica de Chile, Complejo Asistencial
Dr. Sótero del Río, Santiago, Chile
Leonardo Parada Department of Plastic Surgery and Burns, Hospital del
Trabajador, Santiago, Chile
Department of Plastic Surgery, Clínica Las Condes, Santiago, Chile
Carlos Pargas Sinai Hospital of Baltimore, Baltimore, MD, USA
Manuel J. Pellegrini P. University of the Andes Clinic, Las Condes, Chile
Clinical Hospital of the University of Chile, Santiago, Chile
Rodrigo Pesántez Hospital Universitario Fundación Santa Fé, Universidad de Los
Andes, Bogota, Colombia
Marcelo Pires Prado Department of Orthopaedics, Hospital Israelita Albert
Einstein, Sao Paulo, SP, Brazil
Hospital Israelita Albert Einstein, Foot and Ankle Department, Sao Paulo, SP, Brazil
Cristian Artigas Preller Universidad de Chile, Santiago, Chile
Hospital de Niños Roberto del Río, Santiago, Chile
Rubén Radkievich Clínica Alemana, Santiago, Chile
Hospital DIPRECA, Santiago, Chile
Stefan Rammelt University Center for Orthopaedics, Trauma and Plastic Surgery,
University Hospital Carl Gustav Carus at TU Dresden, Dresden, Germany
Nicolas Valdivia Rojo Servicio de Salud Bio bio, Concepción, Chile
Hospital Base Los Angeles, Concepción, Chile
Sanatorio Alemán, Concepción, Chile
Guilherme Honda Saito Department of Orthopaedics, Hospital Sírio Libanês,
Sao Paulo, SP, Brazil
José Antônio Veiga Sanhudo Hospital Moinhos de Vento de Porto Alegre, Porto
Alegre, RS, Brazil
xxiv Contributors
Florencio Pablo Segura Universidad Nacional de Córdoba, Nuevo Hospital San

Roque, Ciudad de Córdoba, Argentina
Centro Privado de Ortopedia y Traumatología, Ciudad de Córdoba, Argentina
O. Matías Sepúlveda Universidad Austral de Chile, Valdivia, Chile
AO Foundation, PAEG Expert Group, Davos, Switzerland
Noman A. Siddiqui International Center for Limb Lengthening/Rubin Institute
for Advanced Orthopedics, Sinai Hospital of Baltimore, Baltimore, MD, USA
Brian T. Sleasman Northwestern University – Feinberg School of Medicine,
Northwestern Memorial Hospital, Department of Orthopedic Surgery,
Chicago, IL, USA
Gaston Slullitel Instituto de Ortopedia y Traumatología Dr. Jaime Slullitel,
Rosario, Santa Fe, Argentina
Pablo Sotelano Hospital Italiano de Buenos Aires, Buenos Aires, Argentina
Gino Martínez Clínica Universidad de Los Andes, Santiago, Chile
Instituto Teletón, Santiago, Chile
Manuel Resende Sousa Foot and Ankle Unit at Hospital da Luz, Lisbon, Portugal
Department of Youth Football at Sport Lisboa e Benfica, Lisbon, Portugal
Rafael Barban Sposeto University of São Paulo, São Paulo, Brazil
Octavio Polanco Torres Hospital Regional Talca, Universidad Católica del Maule,
Talca, Chile
Jordi Vega Laboratory of Arthroscopic and Surgical Anatomy, Department of
Pathology and Experimental Therapeutics (Human Anatomy Unit), University of
Barcelona, Barcelona, Spain
Foot and Ankle Unit, iMove Traumatology-Clinica Tres Torres, and Hospital Quirón
Foot and Ankle Consultant, Clinique Montchoisi, Lausanne, Switzerland
Gregorio Verschae Clinica Redsalud, Santiago, Chile
João Vide Foot and Ankle Surgeon at Hospital da Luz, Lisbon, Portugal
Foot and Ankle Surgeon at Hospital Particular do Algarve, Faro, Portugal
Arnd F. Viehöfer University Hospital Balgrist, Zurich, Switzerland
Daniel Sebastián Villena Hospital Italiano de Buenos Aires, Buenos Aires,
Argentina
Emilio Wagner Hitschfeld Orthopedic Surgery Department, Clínica Alemana de
Santiago - Universidad del Desarrollo, Santiago, RM - Santiago, Chile
Contributors xxv
Pablo Wagner Hitschfeld Orthopedic Surgery Department, Clínica Alemana de

Santiago - Universidad del Desarrollo, Hospital Militar de Santiago – Universidad
de los Andes, Santiago, RM - Santiago, Chile
Stephan H. Wirth University Hospital Balgrist, Zurich, Switzerland
Roberto Zambelli Serviço de Ortopedia da Rede Mater Dei de Saúde, Belo
Horizonte, MG, Brazil
Faculdade de Ciências Médicas de Minas Gerais, Belo Horizonte, MG, Brazil
Tomas Zamora Orthopaedic Oncology and Lower Limb Reconstructive Surgery,
Orthopaedic Surgery Department, Pontificia Universidad Católica de Chile,
Santiago, Chile
Diego Zanolli Clínica Alemana, Santiago, Chile
Hospital Militar, Santiago, Chile
Jacob R. Zide Department of Orthopaedic Surgery, Baylor University Medical
Center, Dallas, TX, USA
Department of Orthopaedic Surgery, UT Southwestern Medical School,
Dallas, TX, USA
Department of Surgery, Texas A&M Health Science Center College of Medicine,
Dallas, TX, USA
Nicolas Zilleruelo V. Musculoskeletal Radiologist, Clinica Alemana de Santiago,
Santiago, Chile
Part I
Basic Science and General Considerations
Foot and Ankle Biomechanics Gait
Analysis
Manuel Monteagudo and Pilar Martínez de Albornoz
1 Introduction and History
Biomechanics is the study of mechanical engineering, specifically Newton’s laws,

applied to the musculoskeletal system. Understanding the biomechanics of the foot
and ankle allows us to appreciate the intrinsic and extrinsic function of the compo-
nents of the system, their mutual relationships, and helps us to understand the
pathology, to propose an orthopedic (mechanical) treatment and also a surgical indi-
cation. The potential impact of a surgery can be intuited after a biomechanical study
of a pathology, and the outcome can be evaluated postoperatively with quantitative
and qualitative means. Although the focus of this chapter and this book is the foot
and ankle, these body segments cannot be considered as isolated elements but as a
kinetic chain that can function in an open and closed manner. The biomechanics of
the foot and ankle are intimately related to the knee, hip, and spine.
Gait analysis is the systematic study of the human gait. Since gait is a mechanical
process within a biological system, gait analysis allows us to put the knowledge of
foot and ankle biomechanics to practical use. We cannot understand or interpret gait
without knowing its mechanics. In recent years, gait analysis has gained popularity
for its applications in footwear and insole design.
The observation of human gait dates back to the very origin of man. Aristotle,
around 340 BC, is credited with the first comments on human gait [1]. However, it
was not until the Renaissance that the first systematic studies appeared. Giovanni
M. Monteagudo (*)
Quironsalud University Hospital Madrid, Madrid, Spain
P. Martínez de Albornoz
Orthopaedic Foot and Ankle Unit, Orthopaedic and Trauma Department, Hospital
Universitario Quirónsalud Madrid, Madrid, Spain
© The Author(s), under exclusive license to Springer Nature 3

Switzerland AG 2022
E. Wagner Hitschfeld, P. Wagner Hitschfeld (eds.), Foot and Ankle Disorders,
https://doi.org/10.1007/978-3-030-95738-4_1
4 M. Monteagudo and P. Martínez de Albornoz
Alfonso Borelli was a physicist and mathematician who made notable contributions
to medicine as a pioneer in the school of iatromechanics [2]. Iatrophysics or iatro-
mechanics was a current in the medical sciences that developed in the seventeenth
century and sought the application of physics to provide an answer to the questions
of human physiology and pathology. The explanation of biological phenomena was
based on the assumption that living beings functioned as if they were machines. In
his work De Motu Animalium, published in 1680, Borelli measured the center of
gravity of the human body and described how we maintain our balance during walk-
ing with the constant forward movement of the support zone provided by the feet.
Other Renaissance classics such as Leonardo da Vinci, Galileo, and Newton also
gave us useful descriptions of human gait [1]. In 1836, the Weber brothers in
Germany gave us the first clear description of gait and made precise measurements
of the gait times and pendulum swing of a cadaver leg [1].
Two pioneers of kinematic gait measurements worked in the 1870s, far apart
geographically. In Paris, Marey published a study of human limb movements in
1873 and plotted the body’s center of gravity and the pressures recorded in the feet
[3]. In 1878, Muybridge made a name for himself in California by demonstrating
that, when a horse trotted, there were times when all four legs were in the air.
Measurements were made using 24 cameras that were triggered in rapid succession
as the horse touched fine threads placed on the race track. Muybridge also con-
ducted studies of naked human bodies walking, running, and performing other kinds
of amazing activities [3].
In 1895, Braune and Fischer’s knowledge of three-dimensional trajectories,
velocities, and accelerations of different body segments were incorporated in the
book Der Gang des Menschen [4]. In the 1930s, Bernstein studied in Moscow the
center of gravity of each segment of the lower limbs and of the whole body [1].
Amar in 1924 and Elftman in 1938 developed the first gait platforms that contributed
significantly to the scientific study of gait [1]. In the 1940s, Scherb in Switzerland
studied the musculature and its activation during gait with the use of electromyogra-
phy [2]. In the 1950s, a group of researchers at the University of California led by
Inman and Eberhart integrated many of the existing studies and eventually published
Human Walking, one of the universal reference books in the study of gait [5].
Sutherland and Perry pioneered the clinical applications of gait analysis in America
and Rose and Baumann in Europe [6, 7]. Gage developed in recent decades the study
of gait in neurological diseases, with modern imaging techniques in his laboratory
[8, 9]. Kirtley wrote one of the reference works – Clinical Gait Analysis – for under-
standing the latest advances in gait analysis and has developed numerous Internet
resources for the study of gait mechanics [3]. The development of computer engi-
neering with modern computers has universalized gait studies in recent years.
2 Human Gait
Human gait is a form of bipedal locomotion, with alternating activity of the lower
limbs and maintenance of dynamic balance [10]. The phasic action of the lower
Foot and Ankle Biomechanics Gait Analysis 5
limbs is described in terms of a series of events that occur repeatedly, constituting

the so-called gait cycle [6]. In an arbitrary manner (an easily recorded event), the
start of the gait cycle is taken as the contact of a limb with the ground, so that the
end of the cycle is reached when the same limb contacts the ground again [6].
During this time interval, a series of events will allow the cycle to be divided into
distinct phases and periods (Fig. 1). The first consideration in understanding these
divisions is whether or not the limb contacts the ground. The phases of stance (60%)
and swing (40%) are thus defined. The activity of the opposite limb in normal gait
is similar to that of the reference limb but offset by half a cycle as the stance period
is longer than the swing period. There will thus be two subphases of simultaneous
support of the two limbs: the initial double support (braking double support) and the
final double support (thrusting double support), each of which will account for
around 10% of the cycle and determine the loading response and pre-swing periods,
respectively [11]. From the above it can be deduced that during gait there is always
contact of at least one foot with the ground. However, in other forms of locomotion
such as running, there are periods of flight in which none of the lower limbs contact
the ground. Running is a succession of jumps [12]. In race walking, disqualification
from sport occurs when the participant moves forward without maintaining contact
with the ground [13].
Under normal conditions, the initial contact with the ground is made with the
heel, and the rest of the foot descends progressively to a plantigrade position. This
position is reached approximately when the opposite limb lifts off the ground. During
this interval, which coincides with the initial double stance, the lower supporting
limb takes the heel as a fulcrum. When the foot is plantigrade, and until the heel
separates from the ground, the ankle becomes the pivot fulcrum, which defines the
intermediate stance period (midstance) that occupies between 10% and 30% of the
gait cycle. As soon as the heel is no longer in contact with the ground, the forefoot
becomes the fulcrum on which the supporting limb progresses. The interval during
which the only contact of the body with the ground is the forefoot of the reference
limb is known as the terminal stance period (30–50% of the cycle) and ends when the
Gait cycle
Stance phase Swing phase
Double Double Single Double

stance stance stance stance
Fig. 1 The gait cycle with its different phases of stance (60%), swing (40%), and rockers
double push-off begins, i.e., when the opposite foot contacts the ground. From this
moment on, although from a descriptive point of view the limb under study contin-
ues to be in stance phase with the forefoot as fulcrum, preparing for the next flight
when it is freed from the support of the body weight. The opposite limb progres-
sively assumes this load, which is why the interval between the contact of the oppo-
site foot and the take-off of the homolateral foot (final double support or push-off) is
also known as the pre-balance period (50–60%) [14].
In gait analysis terminology, the periods of stance during which the anterograde
rotation of the tibia occurs on each of these three fulcrums are known as rockers [6].
Each of these rockers requires active muscular control to effectively ensure the
coexistence of two phenomena that are in principle difficult to reconcile: the
achievement of a stable stance and the maintenance of progression. From a mechan-
ical point of view, the rockers are responsible for controlling the point of application
of the ground reaction force vector (GRF) which, under normal conditions, progres-
sively advances from the heel towards the forefoot on the first ray. The representa-
tion of each of the ground reaction force vectors throughout the stance period gives
rise to a diagram that has been compared to the wings of a butterfly. Each of these
vectors is applied more distally each time than the previous one and points towards
the instantaneous position of the body center of mass. This is with the exception of
the first recordings, in which the first vectors do not point towards the center of mass
at the initial contact, but in a vertical direction, revealing the character of the free
fall experienced after the swing. Jacqueline Perry divided the gait cycle into three
rockers to explain the different leg-foot-floor interactions [6].
First rocker: The control of the first rocker is due to the ankle dorsiflexor muscles
(L5 root) which work in eccentric action (during their contraction their points of
origin and insertion move away). Our muscles are more effective when working in
eccentric action than when working in concentric action and resist isometric action
very well. The main ankle dorsiflexor is the tibialis anterior, assisted by the extensor
digitorum longus and modulated by the extensor hallucis longus and peroneus ter-
tius (Fig. 2). Functional failure of the extensor digitorum longus leads to persistent
Fig. 2 First rocker (“heel

rocker”). Photograph at
slow shutter speed showing
the descent of the foot and
heel contact. The extensor
digitorum longus, along
with the peroneus tertius,
modulates the Achilles
tendon and extensor
hallucis longus during
swing and initial contact
abnormal foot roll in inversion, especially if the peroneal tertius is missing, which
occurs in about 10% of the normal population [15]. Global failure of the dorsiflex-
ors, whether primary (flaccid paralysis of the dorsiflexors) or secondary (spastic
triceps paralysis or passive block to ankle dorsiflexion), will produce an abnormal
first rocker, which may be shortened in time (abrupt and uncontrolled descent of the
sole of the foot) producing an “audible clap” as the foot slumps to the ground, or
even not present at all. The absence of the first rocker obviously occurs when the
initial contact is made with the forefoot (severe equinus) or with the entire sole
(moderate equinus) (Fig. 3). There is another form of mild or subclinical equinus in
which the initial contact is made with the heel but the relative duration of the first
rocker is reduced; its clinical importance lies in the tendency of the subtalar joint to
compensate for the lack of ankle dorsiflexion with persistent eversion to achieve a
“pseudodorsiflexion” of the foot, which can end up producing a plano-valgus defor-
mity and/or metatarsalgia of the central rays due to insufficiency of the first when
the plantar aponeurosis and the peroneus longus are unable to stabilize the first
metatarsal against the ground.
Second rocker: The second roll, known as the ankle rocker, occurs while the foot
under study adopts a plantigrade stance (Fig. 4). The rotation of the lower limb that
allows the progression of the body’s center of mass is performed by taking the
Fig. 3 Neurological
equinus. Absence of
conventional first rocker.
The first rocker is over the
forefoot
Fig. 4 Second rocker

(“ankle rocker”). The foot
under study adopts a
plantigrade support under
the control of the soleus
“supra-ankle” joint as the fulcrum. Its control is due to the soleus (S1 root), the
monoarticular element of the triceps suralis, which brakes the advancement of the
tibia over the talus. The muscle undergoes a remarkable electromyographic activa-
tion, just as soon as the center of mass moves forward with respect to the vertical to
the fulcrum. This reference makes it possible to subdivide the intermediate stance
period into an initial subphase and a final subphase. In the latter, the tibia is tilted
forward with respect to the vertical to the ankle axis, and the activation of the soleus
brakes its advance in eccentric action. In classical anatomy, it is stated that a muscle
acts on the joints it crosses. However, the eccentric action of the soleus in closed
kinetic chain produces a whipping effect on the knee so that, by braking the tibia,
the simultaneous and maintained advance of the body center of mass (due to its
inertial properties) induces an extension of the knee during the intermediate stance
without the quadriceps showing electrical activity.
This association of plantar flexion of the ankle (made impossible by the ground
in a closed kinetic chain) with knee extension is known as the ankle-flexion/knee-
extension couple [6, 8] and has its pathological expression in the knee recurvatum
that appears as a consequence of rigid equinus deformities of the foot and ankle. The
quadriceps actively participates just before the initial contact, to collaborate with the
inertia in the knee extension at the end of the swing. Should the quadriceps not do
this action, the step would be shorter. The extension of the knee during the swing is
fundamentally due to the inertia of the leg-foot segments that produces the active
flexion of the hip during the swing (fundamentally by the action of the psoas). The
involvement of the quadriceps in knee extension is a matter of velocity: the inertial
forces extend the knee, but not fast enough for the knee to be extended at the moment
of initial contact. The quadriceps is also still active during the initial contact, being
then the shock absorber of the first peak of knee flexion. But the quadriceps is inac-
tive when, during the second rocker, the knee is extended to functionally lengthen
the supporting limb.
Fig. 5 Third rocker

(“forefoot rocker”). The
generation of power at the
ankle pushes up the body’s
center of mass and allows
the foot to take off
Third rocker: The third rocker, or forefoot rocker, comprises 30% of the total
cycle (30–60%) and 50% of the stance period. Maintenance of gait progression is
executed with a roll over the metatarsophalangeal “break point” (Fig. 5). The
knee, which during the intermediate period had been extended, initiates its second
peak of flexion when the opposite limb contacts the ground. The control of the
third rocker is no longer due only to the soleus but to the entire triceps suralis
including its biarticular component, the gastrocnemius. During the initial two
thirds of the third rocker (30–50% of the cycle: period of final support or terminal
stance), contact with the ground is exclusive to the homolateral limb, with the
greatest degree of muscular activity being registered in the calf, with a peak of
power generation in the ankle (concentric action). When the opposite limb con-
tacts the ground (50% of the cycle), the homolateral limb begins to unload, prepar-
ing for the swing (pre-swing), and knee flexion accelerates, reaching its peak in
the swing. This can be seen in the curve of the kinematic record of the knee in the
sagittal plane. The double hump of a camel corresponds to the first peak of flexion
as a damping mechanism (resisted by the monoarticular components of the quad-
riceps in eccentric action) and to the second which ensures the advancement of the
limb and the clearance of the foot from the ground. The active flexion of the hip
by the psoas is determinant for the achievement of the second peak of knee flex-
ion. This situation is possible by making use of the inertial properties of a body
segment, in this case, the leg. This led authors as relevant in the study of gait
analysis as J Perry, to consider the end of stance phase as a pull-off rather than a
push-off (Fig. 6) [1]. The power generation peak at the ankle is a true push-off that
raises the body center of mass at final stance, increasing its potential energy to the
detriment of its kinetic component. But the hip drag component during pre-swing
is also indisputable [8].
Normal gait has five attributes that must be considered and kept in mind in order
to judge whether it is pathological or not: [9]
1. Stability during stance.
2. Clearance of the foot from the ground during the swing.
3. Proper stride length.
4. Correct prepositioning of the foot for initial contact.
5. Conservation of energy.
Fig. 6 Posterior view of a

normal foot in third rocker,
already in pre-balance
phase. Note the inversion
of the heel and the correct
functioning of the windlass
mechanism. At this point,
the length of the
metatarsals (especially
relative among them) is
important as a factor in
generating overload
3 Mechanical Functioning of the Ankle and Foot

During Gait
It is very important for the clinician to be aware of the relative foot-floor position –
the contact pattern – during each of the three rockers and to understand what the
mission of the foot is during each of these three periods of gait.
The first rocker involves heel contact with the ground, and its primary function is
to cushion impact. The entire lower limb, together with the axial skeleton, partici-
pates in this cushioning effect. The trunk erector muscles, the hip flexors, the exten-
sor apparatus of the knee, and the viscoelastic properties of the plantar fibroadipose
tissue contribute to the cushioning of the initial contact. In the foot there is a very
peculiar shock absorption mechanism, which uses the phenomenon of the variable
configuration of the plantar vault. This mechanism provided by the tarsal joints in
response to load is due to tarsal pronation. Pronation is passive, and occurs because
the point of contact of the heel with the ground is slightly outside the projection of
the axis of the leg. If it coincided exactly with it, no movement would be produced
in the subtalar joint at the moment of initial contact. If the heel is too far inside the
projection of the leg, the foot will tend to twist into supination. This occurs in severe
varus feet, in which the peroneals (especially the shortened peroneals) end up being
victims of the effort in eversion required from them and for which they are not pre-
pared (Fig. 7). When heel and leg are coaxial, a significant part of the cushioning is
simply lost after the initial contact, which will end up being paid for by the upper
segments in the form of overload injuries. This situation occurs in the mildest forms
of varus foot. If, on the other hand, the heel is too far outward with respect to the
projection of the leg, the external (passive) pronator moment that the foot will have
to withstand after initial contact will be of such magnitude that the inverters will
eventually be overwhelmed, giving way. The passive soft tissues, which together
with the skeletal architecture are the main maintainers of the plantar vault, will
become distended by the cumulative tensile damage, and the foot will eventually
claudicate in a progressive pronation. The invertors (muscles), primarily the tibialis
posterior, do not directly oppose to the flattening of the vault, but rather their func-
tion is to position the tarsal skeleton in such a way as to avoid joint overload posi-
tions. The tibialis posterior, in particular, rotates the leg externally, which induces a
supination in the foot that causes the lax foot that had served to cushion to transform
(along the second rocker) into a stiff foot, an effective propellant for the third rocker.
A shock absorber can be ineffective by being excessively hard or excessively soft.
When it is hard, the upper segments pay for it, and when it is soft, the lower and
distal segments pay for it.
The second rocker corresponds to the period of monopodal support. The contact
pattern with the ground is plantigrade, which will determine the lesional morphol-
ogy of the plantar soft tissues. The stance foot during this phase is responsible for
supporting the entire body weight, for which it has the most stable contact pattern.
The limb must be stretched to its greatest possible length, so that the opposite foot,
which is flying, does not collide with the ground. The tarsus, which started from a
Fig. 7 If the heel is inside

the axis of leg projection,
the foot is twisted in
supination. In this case, a
patient with cavovarus feet
who consulted for chronic
peroneal pain and ankle
instability
pronated position at the beginning of the second rocker, has to move into a supi-
nated position, as mentioned above. The leg has to move from the talus-driven inter-
nal rotation due to pronation to an external rotation that places the head of the talus
over the anterior process of the calcaneus. The passive pronation of the foot is trans-
mitted by the talus to the leg in the form of internal rotation, and the active external
rotation of the leg is transmitted to the foot in the form of supination, by means of
the external rotation of the talus. The second rocker is controlled exclusively by the
soleus. The calves are electrically silent during this rocker under normal conditions,
so as not to produce a flexor moment in the knee, which would be undesirable
because of the need to maintain as long a leg as possible. But there may be cases of
relative retraction of the inactive elastic component of the calf, which could gener-
ate overloads at different levels of the foot, as long as the knee remains extended.
Some authors see in these forms of equinism the evolutionary vestiges of the adap-
tation of the foot from a quadruped and equinized foot to a bipodal plantigrade foot,
in which the heel has descended to the ground. The unanswered question is how
much is equinus? Most of the population will probably barely, if at all, reach neutral
ankle position when the inverted foot is brought into passive dorsiflexion and the
knee remains extended. Equinism can be defined as the inability to achieve adequate
heel to ground contact in static stance with the knee fully extended, without having
to resort to pronation of the foot to provide additional intrinsic midtarsal dorsiflex-
ion [16].
The function of the third rocker is to provide the necessary propulsion to allow
elevation of the body center of mass. It should always be noted that here only the
forefoot contacts the ground through the digit-plantar eminence and that the meta-
tarsal is vertical to the ground. The load is passed from the external rays, protago-
nists during the second rocker, to the talar foot, protagonist of propulsion. The first
three metatarsals are verticalized and – through three intermediate pieces, the cunei-
forms – hold the navicular to the talus, so that it acts as a saddle: the “navicular
stool”. If the inner leg of this stool fails, the stool can tilt towards it and cause the
talus to slip into adduction. If the alignment of the stool is correct, and the talus sits
properly aligned on it at the third rocker, the calcaneus will behave like a wheelbar-
row lifted by the triceps suralis and balanced by the other plantar flexors. But these
plantar flexors, inverters or eversors, must act on a well-aligned skeleton. If proper
osteoarticular alignment is not achieved, triceps and ground reaction forces can
worsen skeletal malalignment when the capacity of the active and passive stabilizers
is exceeded. What the foot has to do during this third rocker is to form (with the leg)
a firm lever that slightly elevates the body center of mass, which advances by its
moment of inertia. The transition from the second to the third rocker is a critical
moment for many reasons, comparable to the moment when the pole vaulter drives
his pole into the ground.
It involves a large concentric, acceleration, and power flow activity at the ankle
joint. It also involves the application of a net force on the ground greater than body
weight, as occurred after initial contact. With regard to the clinical applications of
the mechanical study of gait, injuries that occur in this transition exhibit characteris-
tics of both rockers, as will be seen later, which can make their identification and the
establishment of the pathogenesis in a particular case difficult. On the other hand,

not a few patients present disorders that produce undesirable effects during the sec-
ond rocker and simultaneously others that do so during the third. External rotational
forces can overcome rotational frictional forces, allowing many subjects to make a
true external rotation of the foot on the ground during the third rocker. The final third
of this rocker is no longer propulsive but prepares the limb for swing. The plantar
flexors are activated sequentially but cease to act as the opposing limb is loaded. The
third rocker requires adequate passive dorsiflexion of the toes. When the first radius
loses the ability to dorsiflex while supporting body weight (functional hallux limi-
tus), the foot can no longer rocker on the first metatarsophalangeal joint, but does so
on the interphalangeal joint of the big toe, forcing the foot to supinate, with the
consequent overloading of the distal end of the most lateral rays. This model explains
the frequent association between functional hallux limitus and neuropathic pain of
the third interdigital space, eventually leading to the development of a neuroma.
4 Gait Study
Gait analysis is the systematic study of human gait using the eyes and brain of expe-
rienced observers, supplemented by tools to measure body movements, body
mechanics, and muscle activity [17]. In people with walking problems, gait analysis
can be used to make a diagnosis and plan appropriate treatment.
Gait analysis can be approached from two points of view: qualitative and quan-
titative. In the first case, essential for any clinician, the aim is to describe the move-
ment of the different body segments during gait based on visual inspection. It is
necessary to have a sufficiently large open space for the subject to reach his normal
cadence, something complicated in most of our (small) offices. The use of video
recordings is very convenient, not only because of the possibility of repeating the
inspection as many times as necessary but also because the human eye is incapable
of recording beyond the equivalent of about 12–14 frames per second. The key to
qualitative gait analysis lies in following a systematic, personal approach for each
observer, so that the events seen in each of the body segments and in each of the
planes of space are described in an orderly fashion, keeping in mind the five attri-
butes of normal gait [18, 19]. A good visual gait analysis should be the beginning of
any examination of a patient who consults us for a foot or ankle problem.
Biomechanical gait analysis is based on the quantification of the movement of
body segments (kinematics), the forces produced as a consequence of the move-
ment (kinetics), and complementary parameters such as muscle electrical activity
and energy consumption [14, 20]. Lord Kelvin said that when one succeeded in
converting a problem into a number, it ceased to be a problem [3]. Quantitative
analysis requires the use of expensive equipment and highly specialized medical,
engineering, and technical personnel. Its fundamental clinical application is the
study of gait in infantile cerebral palsy, both to plan the appropriate treatment and to
assess its results from a mechanical point of view [8]. Prosthetic fitting in amputees,
the assessment of joint replacements, and the study of other neuro-orthopedic inju-
ries are clinical fields in which quantitative gait analysis has, and will have impor-
tant applications [21].
In one of the gait quantification systems (Vicon, Oxford Metrics), kinematic
recording is based on stereophotogrammetry, a procedure by which the position of
a series of markers in space is determined in real time. Once the position and orien-
tation of two cameras in space with respect to a given theoretical center of coordi-
nates are known, the pairs of coordinates (2D) with which each camera records a
point (marker) can be integrated to determine the 3D coordinates of that point with
respect to the Cartesian system. In this case the markers are passive, reflecting the
infrared light emitted by the cameras themselves via a stroboscopic flash, and are
fixed at specific anatomical locations on the subject to define the body segments
pelvis, thigh, leg, and foot [18]. When using the standard Vicon Conventional Gait
Model (CGM) program for the generation of kinematic and/or kinetic registration
plots (Helen Hayes marker set), each body segment is actually a plane and is defined
by three points, except in the case of the foot, which is an actual segment defined by
only two points (which prevents inversion-eversion from being assessed) [22].
The kinetic recording of ground reaction forces is carried out with force plat-
forms (AMTI) [6]. These record the components of the GRF vector in the three axes
of space (vertical, transverse, and longitudinal). A computer system integrates the
kinematic data with the ground reaction force vector (GRF) and by a calculation
procedure known as inverse dynamics it deduces the internal forces necessary to
generate the recorded movement [17]. To do this, it is also necessary to provide the
computer with some anthropometric parameters of the subject, such as weight,
height, ankle and knee width, etc., with which it can estimate the theoretical joint
centers and inertial properties of each body segment. This whole study, which can
nowadays be carried out in a few minutes thanks to data capture and processing
systems, was developed by Braune and Fischer and presented in their book Der
Gang des Menschen at the end of the nineteenth century, and it took them 9 years
(1895–1904) to complete: three-dimensional mechanical gait analysis [4].
Finally, dynamic electromyography provides insight into the phasic electrical
activity of a muscle (needle electrodes) or muscle group (surface electrodes). It can-
not record the muscle force generated; it only detects whether there is electrical
activity or not [3]. By knowing the joint kinematics, it can be determined whether
the muscle is working in concentric or eccentric action. Much of the muscle activity
in general during gait is braking, in eccentric action, with the corresponding absorp-
tion of power. The fifth attribute of normal gait refers precisely to the conservation
of energy, through its transfer from one body segment to another, and to the trans-
formation of kinetic energy to potential and vice versa of the center of mass. The
kinetic component is maximum in the periods of double support and minimum in
those of monopodal support, occurring inversely with the potential component. The
processing of the data obtained allows the elaboration of graphs that represent the
angular movement, the moments, and the generation or absorption of power (prod-
uct of the other two curves) in each joint and in each of the three planes of space
(Fig. 8).
Fig. 8 Patient with

post-polio sequelae. The
right lower limb is the least
affected but presents a
rigid equinus of the ankle
that has produced a
recurvatum of the knee by
the “ankle-flexion-knee-
extension” mechanism.
The position of the tibia
would correspond to an
early stage of the second
rocker (early period of
intermediate stance), but
the body center of mass is
markedly advanced. Note
the anterior pelvic tilt; this
is usually due to hip flexor
retraction, but in this case,
it is due to gluteus
maximus weakness
Gait is a learned process [10]. It is one of the most difficult movement patterns to
acquire but, once learned, it is performed almost subconsciously [11]. Each indi-
vidual’s gait is so peculiar that we can identify someone without seeing them, just
by the sound of their footsteps [3]. (Kirtley) We each have a peculiar way of walk-
ing, precisely because gait is a learned process. However, if we graphically repre-
sent the movement of each joint (kinematics) or the forces involved in that movement
(kinetics), we can consider that there are patterns of normality, similar curves among
healthy individuals, which are altered in pathological conditions.
The quantification of any natural phenomenon is an essential achievement to be
able to study it from a scientific point of view. The current technological develop-
ment offers different motion capture systems, thanks to which we can quantify and
graphically represent what happens in each of the major joints during gait. Since the
progression takes place in the sagittal plane, it is in this plane that the largest ampli-
tude joint movements are recorded, both in the hip and in the knee and ankle. On the
other hand, we also have devices that record the ground reaction forces in the three
planes of space. We know from Newton’s third law that the same forces will be act-
ing along our lower extremities in magnitude and direction but in the opposite direc-
tion: the recording, in real time, of joint movements and ground reaction forces
allows, by the inverse dynamics method and knowing the inertial parameters of the
various body segments (mass and its distribution), the location of the joint centers
of rotation and the disposition of the muscles with respect to the joints, to determine
which motor actions were necessary to produce the recorded movement. Dynamic
electromyography and the estimation of energy consumption, mainly through the
exchange of O2 and CO2, complete the current quantitative analysis of human gait,
whose most important clinical applications at the beginning of this millennium are
the study of various forms of paralysis and the adaptation of orthoprosthetic ele-
ments, but its potential field of application is impressive with much more profitable
applications such as the world of video games.
5 Kinematic and Kinetic Recordings of the Hip, Knee,

and Ankle During Gait
The hip joint in the sagittal plane makes initial contact in flexion (Fig. 9). This flex-
ion is about 40° with respect to the anatomical axis of the pelvis, which is equivalent
to about 30° with respect to the vertical axis of the laboratory, since the anterior tilt
of the pelvic ring is about 10°. Its maximum flexion is reached shortly after the
initial contact. From that point it will progressively extend until it reaches a peak
which is determined by the tension of the soft tissues ventral to the instantaneous
center of rotation (mainly the Y ligament of Bertin), which occurs at about 50% of
the total cycle. The total amplitude of the arc of motion is about 40°. At the end of
the cycle, shortly before the next initial contact, it must be flexed, for which it relies
on the action of the psoas and the inertial properties of the distal segments of the
limb, since their combined mass is considerable. On the coronal plane, its kinetic
behavior is very important; during the stance phase, the body weight generates an
adductor moment which tends to lower the opposite hemipelvis. The abductors as a
whole, captained by the gluteus medius, must generate an important action, initially
eccentric, to oppose with a shorter moment arm, the weight of the passenger seg-
ment (HAT segment: head, arms, trunk) and that of the opposite motor segment,
which have a greater moment arm with respect to the instantaneous center of rota-
tion of the hip in support [6]. On the transverse plane, the rotation of the pelvis
Fig. 9 Kinematics of the

hip joint in the sagittal flex
plane
30
hip
0
-10
ext
% cycle
determines the movement of the hip. Initial contact is made with the ipsilateral
hemipelvis maximally forward (hip external rotation) and during stance is lagging
behind the contralateral hemipelvis (hip internal rotation). The internal moment
generation requirements of the hip joint in the transverse plane explain the predomi-
nance of the external rotator musculature over the internal rotators. Internal rotation
is largely passive, generated by an external moment due to the inertia of the opposite
limb, while external rotation, which must occur during swing, is active [3].
The kinematic registration curve of the knee in the sagittal plane reproduces a
double hump silhouette, with the first one having a smaller amplitude (Fig. 10).
There is a first flexion peak that occurs during stance, the purpose of which is to
cushion the impact of the initial contact. The first flexion peak may be absent in
healthy subjects, sometimes because they perform the stance with the knee in recur-
vatum (“recurvatum gait”) and sometimes because they walk at low speed, which
decreases the damping needs. The upward ramp of damping flexion is controlled by
the quadriceps in eccentric action, except for the anterior rectus, which would unde-
sirably flex the hip during this period. After the flexion peak, which reaches approx-
imately 15°, knee extension occurs during intermediate stance, the mission of which
is to lengthen the effective length of the stance limb to facilitate the clearance of the
opposing limb which is in swing. During this extension peak, the quadriceps remains
inactive, a fact that can be seen on dynamic electromyography. Knee extension dur-
ing intermediate stance is controlled by the soleus. Although in classical anatomy it
is said that a muscle acts on the joints it crosses, the soleus is the only portion of the
triceps suralis that does not cross the knee. The explanation lies in the fact that, dur-
ing stance, the limb works in a closed kinetic chain (the fixed point of the muscles
is the distal one). The inertia of the HAT or passenger segment due to the progres-
sion of the body center of mass, together with the brake to the anterograde rotation
that the tibia would tend to perform on the ankle (for which the monoarticular por-
tion of the triceps suralis is responsible) during the intermediate stance period, gen-
erates a net extensor moment in the knee. It is not desirable for the knee to
hyperextend. In this position, the joint geometry forces locking (locking position or
maximum stability) which is achieved and maintained passively by the screwing in
of the femur and is very useful during static standing but requires an active
Fig. 10 Knee joint

kinematics in the sagittal flex
plane 60
Knee
20
0
ext
% cycle
mechanism, the action of the popliteus muscle/tendon, for unlocking. If during

walking we were to require an additional muscular action to unlock the knee, it
would be energetically more costly and less efficient. The second flexion peak, or
swing flexion, is greater than the first (around 60°), and its mission is to enable the
ipsilateral limb to clear by shortening its effective length. By clearance, we mean
the establishment of sufficient space between the limb and the ground to avoid con-
tact between the two during swing. The upward slope of this second hump is greater,
indicating a higher swing speed in flexion. The final extension of the knee is largely
due to the inertia of the leg-foot segments, under the thigh segment being braked by
the gluteus maximus. But as a matter of timing (speed), the inertial action must be
completed by the action of the quadriceps; otherwise, simply with the participation
of the inertial extensor moment, the knee would not reach an adequate extension at
the initial contact, and the step would be shorter (which would also decrease the
efficiency of gait). To modulate that active extension produced by the quadriceps as
a whole (including the rectus anterior), hamstring involvement is necessary, so that
just prior to initial contact, both knee flexors and extensors are active.
From a kinematic point of view in the sagittal plane, the ankle joint is repre-
sented by a more complex curve than those of the hip and knee, with two peaks of
plantar flexion and two peaks of dorsiflexion (Fig. 11). The initial contact is made
with the heel, the ankle joint being in neutral position. Immediately there is a pas-
sive plantar flexion of low amplitude (about 5°) as the tibia rotates forward almost
as much as the sole of the foot descends. The period between initial contact and
contact of the forefoot with the ground corresponds to the first rocker. During this
interval, the anterograde rotation of the tibia takes the heel as its fulcrum, which is
why it is also known as the heel rocker. In the kinematic recording graph, the first
rocker is represented by the descending portion of a “scoop,” whose peak of plantar
flexion is reached at 10% of the cycle according to most authors, although it prob-
ably represents a somewhat shorter duration. Once the forefoot contacts the ground,
the anterograde rotation of the tibia ceases to occur on the heel and takes as its
fulcrum the geometric center of the talar trochlea. The direction of rotation is
Fig. 11 Kinematics of the

ankle joint in the sagittal df
plane
10
0 ankle
-20
fp
% cycle
inverted towards (passive) dorsal flexion. The slope of the curve is greater in the
first part of the dorsiflexion to reduce later. The second rocker, or ankle rocker, lasts
until the heel comes off the ground, which is about 30% of the cycle. This is the
intermediate stance period and is characterized by the plantigrade nature of the
contact of the foot with the ground. From 30% of the cycle until a little over 60%
at the end of the stance phase, the contact of the foot with the ground is made exclu-
sively on the forefoot; this period corresponds to the third rocker or forefoot rocker.
The continuous anterograde rotation of the tibia will then take place taking as ful-
crum the metatarsophalangeal break point, which is actually a parabolic line. In the
kinematic record, the first peak of dorsiflexion is reached, which is around 10–15
degrees according to different researchers [1, 3, 6]. Then, at high speed (steep
slope), plantar flexion is performed at the ankle until a second maximum peak of
about 10–20° is reached; the total amplitude of the ankle flexion-extension arch in
the sagittal plane during normal gait is approximately 30–35°. Interestingly, most
American studies attribute, of the total ankle flexion-extension motion, a greater
amplitude to plantar flexion than to dorsal flexion from neutral [6], whereas our
records consistently show (coinciding, e.g., with Korean studies) a predominance
of dorsal over plantar flexion [16]. During the swing phase, the ankle must contrib-
ute to foot clearance by returning to dorsiflexion, although it is the functional short-
ening of the limb, provided by the knee, that is the most important component in
avoiding toe-off during flight. The critical moment of foot-ground clearance occurs
when both feet are adjacent; at that instant the separation between the foot and the
ground is about 10–15 mm, which gives an idea of how easy it would be to stumble
when one of the clearing mechanisms fails. In some healthy individuals, the second
peak of dorsiflexion is missing; the clearance provided by the knee is sufficient, and
they do not require additional ankle dorsiflexion to avoid toe strike with the ground
during swing. If we study the generation of internal plantar flexor moments (assign-
ing the + sign to plantar flexion) at the ankle during the cycle, we will see an initial
negative dipper (the active muscle action would oppose plantar flexion; it would be
dorsiflexive), followed by a progressive, and therefore positive, plantar flexion
action. The plantar flexor moment reaches its peak in the propulsive phase, just
before the pre-swing, which is determined by the support of the opposite limb, and
then drops sharply and remains practically nil during the swing. From the kinetic
point of view in the sagittal plane, the control of the landing of the sole of the fore-
foot during the first rocker is performed by the dorsiflexors as a whole, captained
by the tibialis anterior and modulated by the common extensor digitorum and the
third peroneus when present. Failure of these muscles, primarily the tibialis ante-
rior, will shorten (or even obliterate) the first rocker, and an audible slap is often
produced when the forefoot contacts the ground in an uncontrolled manner. L5 root
lesions typically result in this phenomenon, which clinically may be evidenced by
the inability to heel walk. If the tibialis anterior is functioning, but the common
extensor and peroneus tertius are not, the foot will contact the ground in inversion,
so the prepositioning of the foot for initial contact will be inadequate and will pro-
mote instability. The protagonism of the second rocker is carried by the soleus that,
in eccentric action, stops the inertial advance of the tibia and extends the knee
during the intermediate support. Plantar flexion of the ankle during stance (closed
kinetic chain) is associated with knee extension, known as the “ankle plantarflex-
ion-knee extension couple.” [6, 8] In its pathological form, equinization of the foot
is compensated by a recurvatum of the knee (Fig. 12). The soleus is the only portion
of the triceps suralis active during intermediate stance (second rocker). If the gas-
trocnemius muscles were also activated during this period, undesirable knee flexion
would occur. Well into the third rocker, the soleus is joined by the gastrocnemius.
In concentric action, they will produce a plantar flexion whose mechanical objec-
tive is to raise the body’s center of mass (provide potential energy) and then release
it in the next free fall, the next step. Human gait is a succession of potentially cata-
strophic free fall situations. During most of the cycle, muscular activity is directed
towards the control or braking (eccentric action) of this succession of free falls.
Only during the propulsive phase, there is a net generation of power (power +) at
the level of the ankle, which involves acceleration. When a child swings, he gives
himself momentum by rising on the ropes in the upward leg of his swing, in order
to initiate the next swing from a greater height, which will subsequently give him
more kinetic energy, more speed. In the inverted pendulum model, the generation
of potential energy at the end of the support is also obtained by the elevation of the
Fig. 12 Patient under

study with surface EMG
recording equipment
(Motion Lab.) and
reflective markers. In the
foreground, one of the
force platforms (AMTI)
can be seen and in the
background one of the
cameras with infrared light
stroboscopic flash
center of masses. It is the potential energy that will be transformed into kinetic
energy at the end of the next swing and must be absorbed after the initial contact
and so on and so forth.
6 Practical Applications
In recent years, we have made progress in the indications and treatment of foot and
ankle disorders thanks to a better understanding of the underlying mechanical
problem. The human body is capable of compensating to unsuspected limits for a
constitutional (“factory-fitted”) mechanical problem. Sometimes compensations
hide or make it very difficult to detect or diagnose a problem [16]. Diagnosis in our
specialty is a science, but it is also an art in order to know which part of the prob-
lem is due to the primary problem and which part is due to compensation. For
example, a valgus flatfoot that is evident on a visual gait analysis in consultation
may be completely “normal” on weightbearing x-rays if the patient still keeps his
compensatory mechanisms active and functional (“the minute of glory of a weight-
bearing x-ray”) [23]. Even if there is no obvious abduction on the x-ray, it does
exist in real life, so it would be a mistake to plan potential surgery on the x-ray and
not on the patient’s gait pattern in consultation. The knowledge of the “sagittal
plane” has made us change the concepts of conservative and surgical treatment of
disorders affecting the Achilles-calcaneal-plantar system and its understanding of
its pathogenesis [24]. The knowledge of the pathomechanics of amputations has
greatly improved the functional prognosis of diabetic foot and orthopedic aids
[20, 21].
Industry has developed a multitude of its products in an attempt to complement
the attributes of human gait. Rocker-soled shoes are an example of this and allow
for a considerable decrease in the mechanical requirements of patients who have a
problem in the transition between the first and third rockers of gait (e.g., hallux
rigidus, ankle osteoarthritis) [25]. The world of artificial prostheses for amputees is
an example of integration between mechanical knowledge, gait analysis, and bioen-
gineering and industrial development.
7 Resources
Resources for the study of gait are currently available on the internet at sites such as
http://www.clinicalgaitanalysis.com/, run by Kirtley, which is a fantastic gateway to
this exciting world. The ESMAC (European Society for Movement Analysis in
Adults and Children) has its website at https://esmac.org/, the ISB (International
Society of Biomechanics) at https://isbweb.org/, and the International Foot and
Ankle Biomechanics Community at http://www.i-fab.org/.
8 Conclusions
Throughout this work, in its different chapters, you will find continuous references
to the mechanics of the foot and ankle and also to the correlation between visual gait
analysis and diagnoses and treatment indications. It is essential to understand why
things happen in order to know what to do with them, in health and in disease. The
knowledge of foot and ankle mechanics and human gait analysis will allow us to
have a comprehensive view of our specialty and put us in a privileged position to
understand what happens to a patient, explain the why and how of their problem,
and offer an appropriate orthopedic or surgical solution based on the mechanical
resolution of their problem. We know from our experience that the restoration of an
adequate mechanical environment with conservative or surgical treatment usually
provides a good and lasting result.
References
1. Levine D, Richards J, Whittle MW. Whittle’s gait analysis. 5th ed. Edinburgh: Churchill
Livingstone; 2012.
2. Vera P, et al. Biomecánica de la Marcha Humana Normal y Patológica. Valencia: Publicaciones
del Instituto de Biomecánica de; 1999.
3. Kirtley C. Clinical gait analysis: theory and practice. Edinburgh: Churchill Livingstone; 2005.
4. Fischer O. Der Gang des Menschen. Wentworth Press; 2018.
5. Inman VT, Ralston H, Todd F. Human walking. Edwin Mellen Press Ltd; Williams&Wilkins,
Baltimore MD; 1981.
6. Perry J, Burnfield JM. Gait analysis: normal and pathological function. Thorofare: Slack
Inc; 2010.
7. Rose J, Gamble J. Human walking. Philadelphia: Lippincott Williams & Wilkins; 2006.
8. Gage JR. Gait analysis in cerebral palsy. New York: (McKeith Press) Oxford Blackwell Sci.
Pub. Cambridge University Press; 1991.
9. Gage JR, Schwartz MH, Koop SE, Novacheck TF. The identification and treatment of gait
problems in cerebral palsy. London: Mac Keith Press; 2009.
10. Viladot VA. Estudio de la marcha humana. In: Lecciones Básicas de Biomecánica del Aparato
Locomotor. Barcelona: Springer-Verlag Ibérica; 2001.
11. Winter DA. The biomechanics and motor control of human gait: normal, elderly and patho-
logical. 2nd ed. Waterloo: Waterloo Biomechanics; 1991.
12. Hollander K, Zech A, Rahlf AL, Orendurff MS, Stebbins J, Heidt C. The relationship between
static and dynamic foot posture and running biomechanics: a systematic review and meta-
analysis. Gait Posture. 2019;72:109–22.
13. Balius X, Turró C, et al. Marcha humana vs. marcha atlética. Rev Med Cir Pie. 1995;IX(1):27–36.
14. Medved V. Measurement of human locomotion. Boca Ratón: CRC Press; 2001.
15. Sarrafian SK. Anatomy of the foot and ankle: descriptive, topographic, functional. 2nd ed.
Philadelphia: JB Lippincott Company; 1993.
16. Maceira E. Análisis cinemático y cinético de la marcha humana. Rev Pie Tobillo.
2003;17(1):29–37.
17. Robertson GE. Introduction to biomechanics for human motion analysis. Waterloo: Waterloo
Biomechanics; 1997.
18. Siebel A, et al. Gait Analysis Course (ESMAC). Stiftung Orthopaedische Klinik. Heidelberg:
Univ; 1999.
19. Linskell JR, Gibb S, et al. The Dundee Gait Lab: Gait Analysis Course (ESMAC). Dundee:
Tayside Orthopaedic Rehabilitation Technology Centre. Ninewells Hospital; 2000.
20. Winter DA, Patla AE. Signal processing and linear systems for the movement sciences.
Waterloo: Waterloo Biomechanics; 1997.
21. Green C, Plyler D, Masadeh S, Bibbo C. Reconstructive amputations of the foot. Clin Podiatr
Med Surg. 2021;38(1):17–29.
22. Wren TAL, Tucker CA, Rethlefsen SA, Gorton GE 3rd, Õunpuu S. Clinical efficacy of instru-
mented gait analysis: systematic review 2020 update. Gait Posture. 2020;80:274–9.
23. Sutter R, Pfirrmann CW, Espinosa N, Buck FM. Three-dimensional hindfoot alignment mea-
surements based on biplanar radiographs: comparison with standard radiographic measure-
ments. Skelet Radiol. 2013;42(4):493–80, 274–9.
24. Amis J. The split second effect: the mechanism of how equinus can damage the human foot
and ankle. Front Surg. 2016;3:38. https://doi.org/10.3389/fsurg.2016.00038.
25. Taniguchi M, Tateuchi H, Takeoka T, Ichihashi N. Kinematic and kinetic characteristics of
Masai Barefoot Technology footwear. Gait Posture. 2012;35(4):567–72.
Imaging in Ankle and Foot
Nicolas Zilleruelo V.
1 Introduction
The ankle and foot have a special place in musculoskeletal imaging. Due to their
complex anatomy and complex clinical diagnosis, it is necessary to understand in an
adequate way the use of the different imaging techniques as well as a close clinical-
radiological correlation to reach an accurate diagnosis and thus provide the best
treatment to each patient.
The imaging evaluation of ankle and foot pathology has led to the writing of
many books on the subject. In this chapter I will try to summarize the main utilities
of the different imaging techniques in order to help clinicians decide when to order
each image and thus achieve the greatest utility of the studies for the benefit of their
patients.
2 Radiography
The initial evaluation of many musculoskeletal injuries of the ankle and foot is
through plain radiographs. These are performed through variations in the absorption
of ionizing radiation by the different tissues of the body, highlighting its good spa-
tial resolution between soft tissue and bone.
Normally two projections of a body part are taken, conventionally in the antero-
posterior (AP) and lateral planes. Due to the complex anatomy of the ankle and foot,
this is often modified, depending on clinical suspicion. For example, in the ankle,
N. Zilleruelo V. (*)
Musculoskeletal Radiologist, Clinica Alemana de Santiago, Santiago, Chile
e-mail: [email protected]

Switzerland AG 2022
26 N. Zilleruelo V.
Fig. 1 Comparative ankle weight-bearing radiographs in AP and lateral projections
Fig. 2 Plain X-ray and MRI in T2 sequence showing an unstable osteochondral lesion of the tibial
plateau (white arrow)
the use of loaded projections can make a difference in the assessment of joint spaces,
revealing subtle but important changes in alignment (Fig. 1).
A modified AP projection with 15 to 20 degrees of internal rotation, the mortise
projection, has demonstrated great utility, providing unobstructed evaluation of the
talar dome and tibial plafond, allowing evaluation of lesions that may be hidden in
standard AP projections, and is used routinely by many clinicians (Fig. 2).
In the foot, due to the overlap and orientation of the tarsal bones, oblique images
can provide valuable complementary views but do not replace the standard in radio-
logic evaluation [1, 2].
In the foot, the use of loaded projections can also represent a great difference in
the diagnosis of traumatic pathologies, for example, in Lisfranc complex injuries,
where the greater amplitude of the articular space and the associated small bone
fragments can be demonstrated in a comparative manner [3] (Fig. 3).
Imaging in Ankle and Foot 27
Fig. 3 Weight-bearing
radiograph of feet
demonstrating subtle loss
of congruence of the
medial aspect of the base
of the second metatarsal to
the medial aspect of the
medial cuneiform (white
arrow), typical of a
ligamentary lesion of the
Lisfranc complex
One of the main advantages of radiographic studies today is that they are widely
available and relatively inexpensive. The diagnosis of bone lesions on plain radio-
graphs is particularly useful in the acute traumatic area, although they also play a
role in the evaluation of chronic ankle or foot pain. On the other hand, the demon-
stration of joint effusion or soft tissue enlargement becomes relevant to follow up
the study of radiologically occult lesions (Fig. 4).
A relative disadvantage is that the acquisition of plain radiographs involves the
use of ionizing radiation, and although the dose to the extremity is minimal, the
potential dangers of radiation should not be ignored. Another disadvantage is that it
fails to differentiate the various soft tissues from each other, due to the narrow range
of attenuation values between them.
3 Additional Projections
Stress projection: These can be active or passive, demonstrating indirect evidence of

ligamentous injury, resulting in widening of the joint space.
Gravity stress view projections: It is used in patients in which the diagnostic
suspicion of medial ligament injuries is high or in which bone and ligament injuries
coexist, in a patient where the projections with usual load or stress cannot be per-
formed due to excessive pain or there is any suspicion that these were not performed
in an adequate manner. The patient must only withstand the force of gravity, often
enough to demonstrate some degree of altered alignment [4–6] (Fig. 5).
Fluoroscopic techniques are typically used in orthopedics to guide orthopedic
and surgical fracture reduction procedures. This modality uses an X-ray source
28 N. Zilleruelo V.
Fig. 4 Comparative weight-bearing radiograph of both ankles. Dysfunctional osteopenia.

Displaced oblique fracture of the right fibula (white arrow). Displaced marginal fracture of the
right medial malleolus (white arrow head). Asymmetry of the medial clear space (tibiotalar), high-
lighting a deltoid lesion
a b
Fig. 5 (a) Weight-bearing ankle radiographs in AP, mortise, and lateral projections of the ankle
showing a good relationship of the articular surface. (b) Same ankle under a gravity stress view,
showing an abnormally increased medial clear space of the tibiotalar joint. Small interposed bony
fragment is appreciated
but produces dynamic images in real time and allows dynamic evaluation of
the joint.
Tomosynthesis is a conventional radiographic technique modified to acquire
numerous low-dose images of specific bodies in a selected axis at different focal
depths. The radiation dose is higher than conventional radiography but lower than
computed tomography (CT). It plays a role in the possibility of evaluating occult
bone lesions in any area where the anatomy is complex, such as the ankle and foot
[7] (Fig. 6).
a b c
Fig. 6 Tomosynthesis of the ankle. (a) Ankle image in mortise projection. (b and c) Selected
images of the tomosynthesis of the ankle where it is possible to differentiate structures in different
planes in each image. As an example the cortices of the posterior colliculus of the medial malleolus
in image b and the posterior colliculus of the medial malleolus in image c can be seen without
any overlap
Ankle and foot radiographs should always be requested for the acute traumatic
study as an initial study and should be attempted with weight bearing if tolerated by
the patient. In the non-traumatic environment, it is very useful in the initial evalua-
tion of chronic ankle and foot pain where different pathologies such as osteochon-
dral lesions of the talus, bone coalitions, bone tumors, evaluation of the plantar arch,
bone changes secondary to overload, and enthesopathic changes, among others,
could be evaluated (Fig. 7).
4 Ultrasound (US)
Ultrasound plays a key role in the diagnosis and management of musculoskeletal

pathology at the ankle and foot level. A high-frequency transducer is necessary, ide-
ally greater than 14 MHz allowing for greater spatial resolution but limiting its
depth penetration. Most of the structures to be evaluated in these areas are relatively
superficial so US is an extremely useful tool in the hands of a competent operator.
Compared to other modalities, US offers the unique advantage of real-time pas-
sive and active dynamic evaluation of soft tissue, especially tendons and ligaments.
It is a relatively fast, high-resolution examination that can be focused on the exact
site of clinical symptoms and does not involve the use of ionizing radiation [8].
30 N. Zilleruelo V.
a b
Fig. 7 (a) PA radiograph of the right foot. Discrete periosteal reaction of the distal diaphyseal
region of the fourth metatarsal on its medial aspect (white circle). (b) Ultrasound of the right foot
of the same patient showing the periosteal reaction (white arrow) with hypoechogenic area sur-
rounding it secondary to edema and increased vascularization in color Doppler mode, typical of an
overload (stress) fracture
As an example, dynamic ultrasound can elucidate peroneal subluxation not evi-

dent on static imaging [9] (Fig. 8).
It is also possible to perform maneuvers where stress is generated in ligaments in
a specific and dynamic way for an adequate characterization of them, evaluating
their continuity, thickness, reparative phenomena, and regional sequelae calcifica-
tions in a practical and simple way (Fig. 9).
The evaluation of the bone is not complete with US, but the evaluation of perios-
teal alterations in stress fractures can be key for the early diagnosis of these, even
prior to their visualization in plain radiography or computed tomography (Fig. 7).
Power Doppler evaluation is a valuable tool mainly used in the evaluation of the
vascularization of the synovium of the joints to determine active inflammation of
them. It can also be used in tendons to evaluate neovascularization and also in the
evaluation of the type of vascularization of a regional soft tissue lesion (Fig. 10).
Because of the superficial location of the tendons of the ankle and foot, US is an
ideal modality to evaluate these structures. It also plays an important role in the
a b B
L
B
Fib Fib
L
B
B
Fib
Fig. 8 (a) Ankle ultrasound of the long (L) and short (b) peroneal tendons at the site of the supe-
rior peroneal retinaculum (SPR, blue dashed line). (a) Shows properly positioned peroneal tendons
adjacent to the fibula (Fib) and under the SPR. (b) Shows longitudinal rupture of the peroneus
brevis and disinsertion of the SPR from the fibula. In (c) (same patient), dislocation of the peroneus
longus over the fibula and under the disinserted SPR occurs with ankle flexion. The regional
meniscus (blue circle) does not present displacement
a c
b d
Fig. 9 Ultrasound of the ankle with ultrasound pattern of the main ankle ligaments. (a) Anterior
inferior tibiofibular ligament of the syndesmosis. (b) Anterior talofibular ligament. (c)
Fibulocalcaneal ligament, under the peroneal tendons. (d) Deep component of the medial deltoid
ligament complex
32 N. Zilleruelo V.
a b
DER CAB MTT HALL
DER CAB MTT HALL
Fig. 10 Patient with rheumatoid arthritis. (a) AP foot radiography suggestive of erosions (white
arrows) in the medial aspect of the F1 bases of both hallux and in the medial region of the first
metatarsal heads, with increased volume of the soft tissues. (b) Ultrasound of the medial aspect of
the head of the right first metatarsal, showing bone erosion and synovitis, with increased vascular-
ization in power Doppler mode
Fig. 11 Morton’s neuroma

of the third intermetatarsal
space of the left foot, with
clearly defined continuity
with the regional
interdigital nerve (white
arrow)
evaluation of small neurovascular bundles at the level of the ankle and foot, achieving
targeted evaluations of, for example, interdigital nerves for Morton’s neuromas, plan-
tar plate lesions, and small superficial ligaments. Due to its high spatial resolution, it
is able to evaluate small structures with similar resolution compared to MRI (Fig. 11).
US is also widely used as a guide for musculoskeletal procedures, allowing
excellent visualization of the needle throughout the procedure (Fig. 12).
The main limitation of US is that it is an operator-dependent technique. Its results
are dependent on the operator’s degree of knowledge of the pathology and experi-
ence in the technique. Additionally, US has a series of specific artifacts that can
Fig. 12 Fine needle

infiltration of the right
ankle joint through the
anterolateral recess,
highlighting the adequate
distance between the
needle and the
neurovascular bundle
(white star)
Fig. 13 Panoramic view

of the Achilles tendon
under ultrasound
influence the quality of the image, the most frequent is anisotropy, which is when
the normal tendon loses its hyperechoic fibrillar characteristic just because of the
modification of the obliquity of the sound beam. This finding is easily recognized
by a competent operator.
Also, the US gives us the possibility to perform panoramic images of long ten-
dons such as the Achilles tendon or lesions that are larger than the length of the
transducer, giving a continuous evaluation of the lesion, being very useful to give an
adequate vision to the relevant finding for the medical referent (Fig. 13).
US elastography is an add-on that can be performed only on equipment with
special software and is based on morphological changes to indicate underlying
pathology. It provides a measure of tissue stiffness by gentle manual compression,
for example, as part of the evaluation of Achilles tendinopathy [10].
In summary, ultrasound is a very useful tool at the level of the ankle and foot in
the hands of a competent operator. Due to the superficial location of the tendons
and most ligaments of the ankle and foot, US is an ideal initial modality to evalu-
ate these structures, as well as the small regional neurovascular bundles. Its
dynamic evaluation advantage is key in the diagnosis of many tendon and liga-
ment pathologies, making a big difference when compared to all other static
techniques.
34 N. Zilleruelo V.
5 Computed Tomography (CT)
Computed tomography is accomplished by multiple parallel images through an

X-ray array and multiple detectors that move circumferentially around a patient as
the patient passes through the CT scanner.
The high spatial resolution of CT makes it an ideal modality for evaluating bone
and soft tissue calcifications.
As image volumes are acquired, they can be reconstructed in different planes,
usually axial, coronal, and sagittal, with associated 3D reconstruction, useful for
better evaluation of the overall findings and for future surgical planning if necessary.
If one wishes to make any changes regarding the obliquity of the planes, this can be
done thanks to the volumes acquired with isotropic voxels, which means that all
sides have the same dimension, with uniform resolution in all directions (Fig. 14).
Intravenous iodinated contrast can be used to evaluate peripheral vascularization,
for example, in trauma with suspected vascular involvement or for better character-
ization of a soft tissue tumor.
A great advantage of CT is that the acquisition process takes only a few seconds
and is well tolerated by most patients. In the preoperative planning of fractures,
particularly complex intra-articular fractures, CT offers a more detailed assessment
of the fracture, degree of complexity, and articular bodies than other imaging
modalities (Fig. 15).
As a disadvantage, CT involves the use of ionizing radiation in higher doses than
conventional radiography. Multiple techniques have been developed to reduce the
dose without compromising the diagnostic capacity of the study.
CT presents a limited evaluation of the soft tissues without being able to easily
delimit the normal soft tissues from the adjacent abnormal ones. It is also not a
study that is performed in a conventional way with load, which is why many times
the study is complemented with conventional radiographs with load to evaluate
bone or joint alignments.
When we face metallic materials such as osteosynthesis or prosthesis materials,
a beam hardening artifact is generated that limits the study. Multiple teams have
a b
Fig. 14 AP and lateral ankle radiographs (a) together with computed tomography (CT) VRT bone
reconstructions (b) of a trimalleolar ankle fracture
Fig. 15 Computed tomography with VRT cinematic rendering reconstructions of a trimalleolar

ankle fracture
Fig. 16 Computed tomography with optimized protocol for osteosynthesis materials, highlighting
the lower amount of beam artifacts in the axial and coronal images of this patient and the high
quality of visualization in VRT reconstructions of the osteosynthesis materials
developed techniques and software that manage to reduce these artifacts in a remark-
able way for the evaluation of pathology in relation to these metallic components
[11] (Fig. 16).
Also, some equipment has the ability to acquire images with dual-energy tech-
niques, where there are two X-ray tubes of different kilovoltage (Kv) that acquire
the information simultaneously, obtaining a set of data that, by comparing the
behavior of tissues with different attenuation values in the two acquisitions, can dif-
ferentiate between different types of deposited crystals, for example, to differentiate
the deposit of uric acid from calcium pyrophosphate deposit [12] (Fig. 17).
CT with dual energy also has the potential for the evaluation of traumatic tra-
becular bone lesions with the recognition of medullary bone edema, being more
sensitive in the recognition of lesions not visible in a usual CT.
In recent years, technological evolution has led to smaller CT scan designs,
allowing the modification of equipment that can image loaded ankles and feet
36 N. Zilleruelo V.
Fig. 17 Dual-energy
computed tomography of a
patient with gout, where it
is possible to identify and
calculate the load of urate
crystals deposited (green
dots) in the soft tissues
adjacent to the medial
malleolus and the medial
region of the hallux
(weight-bearing CT scans). This modality better demonstrates the true orientation

of the bones and joints during axial loading of the patient. It is especially useful in
investigating the alignment of multiple regional pathologies such as adult-acquired
flatfoot deformity, various ankle impingements, and hallux valgus, among others. In
clinical practice it is increasingly used as orthopedic surgeons strive for better out-
comes in the treatment of ankle and foot disorders [13].
In summary, CT is very useful for the characterization of complex fractures, with
the ability to perform 3D reconstructions for surgical planning. It also has better
sensitivity to small fractures than conventional radiography. Its acquisition is fast,
and currently there is easy access in most institutions. Special equipment and soft-
ware have been developed to eliminate metallic artifacts, reduce ionizing radiation
doses, and study crystal differentiation.
6 SPECT-CT (Single Photon Emission Computed

Tomography-Computed Tomography)
SPECT is based on the detection of gamma rays emitted by a radiopharmaceutical

usually technetium 99 (radiotracer) injected into the patient’s bloodstream, accumu-
lating and marking the regions of greater bone turnover due to greater vasculariza-
tion and osteoblastic presence. This associated to its combination with a
high-resolution CT generates hybrid fused images, reflecting functional informa-
tion associated to an adequate anatomical localization of the lesions [14, 15].
The use of SPECT-CT on the foot and ankle is an emerging modality, and its
benefit is increasingly recognized in the localization of degenerative foci and
Fig. 18 SPEC-CT of the ankle with increased radiotracer uptake in the left navicular secondary to
regional degenerative lesions
also in infections. Historically, the contribution of bone scintigraphy to the diag-

nosis of diseases of the ankle and foot has been restricted by limited resolution
and low specificity. However, fused hybrid SPECT-CT imaging has significantly
improved the diagnostic value in this anatomical region. Current applications of
SPECT-CT in ankle and foot pathology often include patients with chronic pain
symptoms that are not sufficiently explained by clinical findings and conven-
tional imaging. These include localization of active sites of osteoarthritis, coali-
tions, osteoid osteomas, occult stress fractures, tendonitis, plantar fasciitis, and
impingement syndromes. Assessment of response to therapy after surgical inter-
ventions such as evaluation of arthrodesis is a promising application of this tech-
nique (Fig. 18).
The main disadvantage is that both ionizing radiation and the use of radiophar-
maceuticals that emit gamma rays that are distributed throughout the body are used.
They also require instrumentation and image reconstruction methods that differ
from those used in other medical imaging modalities.
7 Magnetic Resonance Imaging (MRI)
Magnetic resonance imaging has revolutionized musculoskeletal imaging, offering

excellent spatial and contrast resolution in both superficial and deep structures. The
MRI image is produced by the effect of a strong homogeneous magnetic field on the
hydrogen nuclei of the different tissues of the body, achieving their differentiation.
MRI does not use ionizing radiation.
Part of the complexity of MRI is centered on the wide variety of sequences avail-
able, being indispensable to have clear and directed protocols for the evaluation of
the main pathologies of the study area.
38 N. Zilleruelo V.
MRI sequences can be simplified into three main groups. T1-weighted sequences
show hyperintense fat (high signal) and hypointense fluid signal (low signal). This
is a particularly useful sequence for evaluation of anatomy. T2-weighted sequences
are sensitive to fluids showing them hyperintense. Fat is also hyperintense on T2.
The fat signal can be suppressed (Fat Sat) and thus increase the visibility of fluids
and bone or soft tissue edema. Another alternative of fat saturation is achieved
through another sequence acquisition process, which is the STIR sequence (short
tau inversion recovery), a sequence that has a very important characteristic in the
evaluation of bone edema, since it is less sensitive to the inhomogeneities of the
magnetic field.
Proton density (PD) sequences are intermediate sequences, optimized for the
evaluation of hyaline cartilage; they are also sensitive to fluids, often combined with
fat suppression.
MRI provides excellent spatial and contrast resolution of the major structures of
the ankle and foot. MRI is widely used in the evaluation of bone, tendon, and liga-
ment pathology, as well as detailed evaluation of cartilage and joints. Multiple new
sequences have been developed as well as multiple software that have increased the
diagnostic capacity of MRI [16] (Fig. 19).
Although MRI is very sensitive, it is not always specific, and the findings of the
study must be interpreted in the context of the patient’s clinical condition. As an
example, it is common to find bone marrow signal alterations in sports patients,
which are mistaken for bone edema in areas where the patient does not report
regional symptoms [17]. There are also alterations of the bone marrow signal in
active children under 15 years of age, which are confused with bone edema being
manifestations of marrow reconversion, without pathological significance and
asymptomatic [18]. Another example is ankle impingement, where images can help
to better define the etiology of the clinical problem, and in other opportunities, inci-
dental findings that are not clinically relevant are visualized. It is also very easy to
a b
Fig. 19 3 Tesla MRI of the ankle in PD Fat Sat (a) and T2 (b) sequences with visualization of the
cartilages with high contrast definition in the tibiotalar joint
determine the existence of bone edema, but it is difficult to differentiate the etiology
with images alone (Fig. 20).
MRI has the disadvantage of being a study that is not fast; it requires at least
30 minutes to achieve the necessary sequences. It requires adequate equipment with
a high Tesla and special coils for the ankle and foot. Due to the strong magnetic
field, many pacemakers are contraindicated for use because they become misconfig-
ured or lose battery charges. Currently most of the new pacemakers come with
systems compatible with MRI use, which is done under the approval and supervi-
sion of your treating cardiologist.
Fig. 20 Anterolateral
ankle impingement. MRI
a
axial T2-weighted (a) and
sagittal PD Fat Sat (b)
sections. It is visualized a
thickening of the anterior
talofibular ligament,
associated with mild
tibiotalar joint effusion in
anterolateral recess of the
ankle where a regional
meniscoid lesion is
observed (white arrow)
b
40 N. Zilleruelo V.
Many times, claustrophobic patients are not able to perform these studies. Low
magnetic field resonators have been developed that are better tolerated by claustro-
phobic patients but in which the spatial and contrast resolution is suboptimal for the
diagnosis of multiple key structures in the foot and ankle joints.
When osteosynthesis or prosthetic materials are present, the study should be
performed in a resonator with a lower magnetic field and use sequences with certain
special technical modifications to reduce the degree of magnetic susceptibility arti-
facts that occur, improving diagnostic sensitivity.
MR arthrography (arthro MRI) is usually performed with intraarticular (direct)
contrast injection, with the benefit of joint distension with better appreciation of the
intraarticular structures. However, it has potential risks as it is an invasive procedure
such as the potential risk of infection. Its intention is to achieve a better character-
ization of ligament pathologies, impingement syndromes, chondral lesions, and
synovial pathologies [19]. But with the advances of 3 Tesla resonators and special
coils for these joints, they are not as widely used today.
Studies directed to articular cartilage can be performed for the characteriza-
tion of acute and chronic lesions, as well as to evaluate them over time, recogniz-
ing the differentiation of hyaline cartilage from reparative fibrocartilage and the
evaluation of operated chondral lesions. Sequences have been developed to eval-
uate the biochemical alterations of cartilage, such as the structural evaluation of
collagen in lesions (T2 map) or the evaluation of the proteoglycan matrix
(dGEMRIC), among others, findings that precede the arthroscopically visible
lesions [20].
MRI is the technique of choice for the global evaluation of superficial and deep
soft tissues, with a great information of the bone marrow signal and a very good
evaluation of the intraarticular structures. Its acquisition takes quite a long time, and
it is not as accessible as the rest of the images, especially the fact that resonators
with a high tessellation (1.5 to 3 Tesla) with special coils for the joints are needed to
achieve high-quality images in order to reach the diagnosis with greater precision
(Fig. 21).
In summary, knowing the different imaging techniques and their variants is fun-
damental for the evaluation of the multiple pathologies of the ankle and foot, and at
the same time, it is essential that they are performed in an adequate and orderly
manner, ensuring that they have the minimum quality for the diagnosis. Especially
dynamic techniques such as US should be performed by radiologists trained in the
area because it is necessary to know the pathology and look for it in a targeted man-
ner, passively and dynamically, achieving accurate diagnoses and in turn a better
final treatment for each patient.
a c
b d
Fig. 21 Magnetic resonance imaging (MRI) of the ankle. Coronal PD Fat Sat (a) coronal T1 (b),
sagittal PD Fat Sat (c), and axial T2 (d). There is a tibiotalar joint effusion where an intra-articular
nodular image is observed with low signal in T2, corresponding to a focal villonodular synovitis
42 N. Zilleruelo V.
References
1. Clark TW, Janzen DL, Ho K, Grunfeld A, Connell DG. Detection of radiographically occult
ankle fractures following acute trauma: positive predictive value of an ankle effusion. Am J
Roentgenol. 1995;164:1185e9.
2. Fonseca LLD, et al. Reproducibility of the Lauge-Hansen, Danis-weber, and AO classifica-
tions for ankle fractures. Rev Bras Ortop. 2018;53:101–6.
3. Kennelly H, Klaassen K, Heitman D, Youngberg R, Platt SR. Utility of weight-bearing radio-
graphs compared to computed tomography scan for the diagnosis of subtle Lisfranc injuries in
the emergency setting. Emerg Med Australas. 2019;31:741–4.
4. Gill JB, Risko T, Raducan V, Grimes JS, Schutt RC Jr. Comparison of manual and gravity
stress radiographs for the evaluation of supination-external rotation fibular fractures. J Bone
Joint Surg Am. 2007;89(5):994–9.
5. Michelson JD, Varner KE, Checcone M. Diagnosing deltoid injury in ankle fractures: the grav-
ity stress view. Clin Orthop Rel Res. 2001;387:178–82.
6. Schock HJ, Pinzur M, Manion L, Stover M. The use of gravity or manual-stress radiographs
in the assessment of supination-external rotation fractures of the ankle. J Bone Joint Surg Br.
2007;89(8):1055–9.
7. Dobbins JT 3rd. Tomosynthesis imaging: at a translational crossroads. Med Phys.
2009;36:1956e67.
8. Bianchi S, Martinoli C, Gaignot C, De Gautard R, Meyer JM. Ultrasound of the ankle: anat-
omy of the tendons, bursae, and ligaments. Semin Musculoskelet Radiol. 2005;9:243–59.
9. Neustadter J, Raikin SM, Nazarian LN. Dynamic sonographic evaluation of peroneal tendon
subluxation. AJR Am J Roentgenol. 2004;183:985–8.
10. Ooi CC, Schneider ME, Malliaras P, Chadwick M, Connell DA. Diagnostic performance
of axial-strain sonoelastography in confirming clinically diagnosed Achilles tendinopathy:
comparison with B-mode ultrasound and color Doppler imaging. Ultrasound Med Biol.
2015;41(1):15–25.
11. Olsen RV, Munk PL, Lee MJ, et al. Metal artifact reduction sequence: early clinical applica-
tions. Radiographics. 2000;20:699e712.
12. Desai MA, Peterson JJ, Garner HW, et al. Clinical utility of dual-energy CT for evaluation of
tophaceous gout. Radiographics. 2011;31:1365–75; discussion 1376–1367.
13. Barg A, Bailey T, Richter M, Netto CDC, Lintz F, Burssens A, Phisitkul P, Hanrahan CJ,
Saltzman CL. Weightbearing Computed Tomography of the Foot and Ankle: Emerging tech-
nology topical review. Foot & Ankle International. 2018;39(3):376–86.
14. Pagenstert GI, Barg A, Leumann AG, Tasch H. Mu¨ ller-brand J, Hintermann B, et al.
SPECT-CT imaging in degenerative joint disease of the foot and ankle. J Bone Joint Surg Br.
2009;91(9):1191–6.
15. Knupp M, Pagenstert GI, Barg A, Bolliger L, Easley ME, Hintermann B. SPECT-CT compared
with conventional imaging modalities for the assessment of the varus and valgus malaligned
hindfoot. J Orthop Res. 2009;27(11):1461–6.
16. Rosenberg ZS, Beltran J, Bencardino JT. From the RSNA refresher courses. Radiological Society
of North America. MR imaging of the ankle and foot. Radiographics. 2000;20(Suppl):153–79.
17. Lohman M, Kivisaari A, Vehmas T, Kallio P, Malmivaara A, Kivisaari L. MRI abnormalities of
foot and ankle in asymptomatic, physically active individuals. Skelet Radiol. 2001;30:61–6.
18. Shabshin N, Schweitzer ME, Morrison WB, Carrino JA, Keller MS, Grissom LE. High-signal
T2 changes of the bone marrow of the foot and ankle in children: red marrow or traumatic
changes? Pediatr Radiol. 2006;36:670–6.
19. Cerezal L, Abascal F, Garcia-Valtuille R, et al. Ankle MR arthrography: how, why, when.
Radiol Clin N Am. 2005;43(4):693–707.
20. Li X, Majumdar S. Quantitative MRI of articular cartilage and its clinical applications. J Magn
Reson Imaging. 2013;38:991e1008.
Open vs Minimally Invasive Surgery:
Advantages and Disadvantages
Mariano De Prado, Manuel Cuervas-Mons, and Virginia De Prado
1 Introduction
Minimally invasive techniques are becoming increasingly popular in modern ortho-

pedic surgery. Their aim is to solve or minimize some of the problems encountered
with open surgery, decreasing possible complications and speeding up the post-
surgical recovery process. Decades ago, arthroscopy represented the spearhead, and
subsequently different minimally invasive surgeries were developed, which today
encompass a heterogeneous group of surgical techniques applicable to upper limb,
lower limb, and spine surgery. These techniques are a point of reference towards
which there is a tendency to converge and are currently the most widely used in
numerous pathologies.
Percutaneous foot surgery, also known as minimally invasive surgery or MIS
(minimal invasive surgery), is a surgical method that allows us to perform interven-
tions on the foot through minimal incisions, without direct exposure of the surgical
plane and under fluoroscopic control (Fig. 1), which results in a reduction of injuries
to the surrounding tissues. In order to be able to offer our patients the most appropri-
ate treatment in each case, it is necessary to know the differences and similarities
between percutaneous and open surgery.
M. De Prado (*)
Service of Orthopedic Surgery and Traumatology, Hospital Quironsalud Murcia,
Murcia, Spain
M. Cuervas-Mons
Orthopedic Surgery and Traumatology Service, Hospital General Universitario Greogrio
Marañon, Madrid, Madrid, Spain
V. De Prado
Podiatry Service, Hospital Quironsalud Murcia, Murcia, Spain

Switzerland AG 2022
44 M. De Prado et al.
Fig. 1 Image during the performance of minimally invasive surgery of the foot
Fig. 2 Approach routes

for hallux valgus with open
surgery
2 Fundamentals
Surgical treatment of foot deformities aims to achieve a painless and biomechani-

cally functional foot. If we want to correct all the pathological elements of the dis-
ease, sometimes it will be necessary to perform multiple surgical gestures.
Using the postulates of open surgery, this translates into wide approach routes
(Fig. 2); however, minimally invasive surgery allows us to perform the same acts, in
a precise manner, through small incisions (Fig. 3).
The surgical indications are the same regardless of the surgical technique to be
used, but in order to be able to perform minimally invasive surgical procedures, it is
essential to have specific instruments. Surgical instruments used in open surgery
Open vs Minimally Invasive Surgery: Advantages and Disadvantages 45
Fig. 3 Approach routes

for hallux valgus with
percutaneous surgery
should not be adapted, as this could favor the appearance of associated

complications.
We can divide the necessary material for percutaneous foot surgery into three
sections: basic, motorized, and radiological control instruments.
2.1 Basic Instruments
The basic instruments include the scalpel, scrapers, and elevators (Fig. 4). Beaver
64 and Beaver 64MIS scalpels are used, allowing us to make minimal incisions
(generally less than 5 mm) with a direct cut to access the desired surgical field. The
scrapers and elevators, with different widths and shapes, allow us to detach and
extract the bony debris through the incisions made.
In addition to these basic instruments, we must have surgical material such as
needle holders and scissors, necessary for suturing surgical wounds, and hemostatic
mosquito forceps, useful for resolving possible intraoperative incidences such as
excessive bleeding or breakage of drills.
2.2 Motorized Instruments
Motorized instruments include the motor, a handpiece, and a complete set of drills
(Fig. 5).
Fig. 4 Basic instruments
Fig. 5 Motorized instrumentation
There is a wide variety of motors that can be used in percutaneous foot surgery,
both electric and compressed air, with common characteristics. The motor must
have a central unit with a speed control knob to achieve the desired revolutions per
minute for each surgical procedure. If we use speeds higher than 10,000 revolutions
per minute, injuries and bone necrosis may occur. The ideal speed to be able to work
will be the minimum speed that allows us to perform the desired gesture without
blocking the drills in the bone, which can also be avoided by making slight back-
and-forth movements in the direction of the cut we want to make. On the other hand,
the lower the speed, the greater the control and tactile sensation of the desired surgi-
cal gesture, without performing osteotomies or bone resections greater than desired.
The ideal speed for this type of surgery will be between 1000 and 8000 revolutions
per minute, since it gives us a better control of the cut and at the same time a preci-
sion in the surgical gestures, all this without producing thermal injuries.
The handpiece must have a small size (similar to a pencil) in order to be handled
with ease and precision. The handpiece is attached to the burs, and rotary move-
ments are performed, not allowing circular movements of the burr or oscillating
movements of the saws. The handpiece must be sterilized in order to be used freely
in the surgical field.
The complete set of drills includes different drills of various shapes and lengths,
in order to perform different surgical procedures (osteotomy, exostectomy-
bunionectomy, wedge extraction, etc.). The most commonly used are as follows:
A. Lateral cutting drills. They are used to perform osteotomies on the metatarsals
or phalanges, as well as to reduce minor bone exostoses.
B. Fine shaving drills. They are used to remove bone from the most important
exostoses. They cause minimal trauma to the soft tissues; they are also used to
mark the size of bone wedges as they are cone-shaped and can also be used as
lateral cutting drills.
C. Coarse reaming drills. They produce a great lifting of the bone and are used,
above all, to extract hallux valgus exostoses because they are very voluminous
and have a powerful articular capsule that protects the rest of the soft parts from
being injured, since this drill is very aggressive.
2.3 Radiological Control Instruments
It is necessary to control the exact point where osteotomies or surgical procedures

on the bone are performed. For this purpose, conventional X-ray systems, such as
image intensifiers, or systems such as fluoroscopes can be used. The fluoroscope is
not equipped with a traditional intensifier but with an X-ray cassette that requires
less radiation for its operation than traditional intensifiers, and, in addition, its
design presents a mini-arch that can be rotated 360° in the three planes (Fig. 6), giv-
ing great versatility and functionality to the surgical act.
3 Relevant Anatomy
Knowing the relationships between the different anatomical structures is of vital

importance for a successful surgical treatment. The objective of surgery is to correct
the deformities causing the pathology while avoiding iatrogenic injuries during the
intervention. Preoperative planning is necessary to know the different anatomical
structures at risk (vessels, nerves, tendons, etc.) in order to choose a specific
approach and protect the structures involved. In open surgery, we can visualize and
protect these structures during the intervention, but in percutaneous foot surgery,
Fig. 6 Radiological control instruments
our intraoperative guide is fluoroscopy, where these structures are not visualized, in
addition to losing the three-dimensional vision by relying on 2D images.
For this reason, in percutaneous surgery, it is of vital importance that the surgeon
accustomed to open surgery undergoes a period of adaptation before starting the
practice of MIS surgery, developing a new anatomical perspective, as we had to do
when we started with arthroscopy, getting used to planning the skin incision, the
angle of incidence on the surface to be treated (approach angle), and the distance
from the incision to the point of surgical action (approach path), since we work with
instruments that we introduce into the skin far away from the performance of the
surgical gesture. We must also adapt to the use of motorized cutting instruments
with burs, which are performed with a rotary movement, quite different from that
described by the cutting saws with an oscillating movement. Finally, we must also
adapt to the loss of the three-dimensional perception of the anatomical structures
that we perceive in open surgery and that we must intuit in MIS, both in the normal
anatomy and in the anatomical alterations produced by the pathology to be treated.
3.1 Incision
The skin incision should be made at an anatomical point that does not produce iat-
rogenic lesions, taking into account the anatomy to avoid vascular, nerve, ligamen-
tous, tendon, etc. structures. Incisions should be made following Langer’s skin
lines, with 90° incidence of the scalpel (Fig. 7), regardless of the posterior direction
Fig. 7 Correct incision

incidence
towards the surgical site. Incisions should not be made in areas of pressure with the
footwear, since this would favor the appearance of hypertrophic or keloid scars and
post-surgical pain at this point. The size should be small but large enough to be able
to introduce the surgical instruments freely and allow the exit of the bone detritus.
If an excessively small incision is made and the edges are injured, it can favor the
appearance of a hypertrophic scar, perilesional calcifications due to accumulation of
bone detritus, or maintenance of prolonged post-surgical inflammatory signs.
3.2 Approach Angle
The direction from the incision to the point of surgical action must allow the sur-
geon’s hand to be free on the outside of the skin, with total freedom of movement
for the use of the surgical instruments. The angle of approach from the incision
should not be perpendicular to the articular surfaces (Fig. 8) on which we are going
to act, except in arthrodesis, in order to avoid cartilage injury, and if, for example,
we must remove an exostosis, we must bring the motorized instruments parallel to
the bone surface to be removed.
3.3 Approach Path
The incision is placed at a specific distance from the point of surgical action, long
enough so that the instruments (motorized or dragging) are covered by the skin and
soft tissues over the whole of their cutting surface, so as not to injure the skin during
their action.
The path from the incision to the surgical point of action must be unique and
not multiple, one incision for each surgical procedure. No vascular, nervous, or
tendon structures should be found in the path. If necessary, an extension of the
trajectory can be made from the point of entry into the skin to the operative area,
with a maximum angle of 60°, performing a detachment from the pivot point (skin
incision) to the operative area (Fig. 9). The extension should be performed with a
Fig. 8 Incision location
Fig. 9 Approach path
scalpel if we are within an anatomical safety zone or with blunt instruments (rasp,
periosteal elevator, etc.) if there are anatomical structures in the trajectory that can
be injured.
The approach path should favor, by its direction and width, the exit of bone
debris after skin pressure on the surgical site.
Once the intervention is completed, the bone and blood debris are removed from
the approach path, the skin incision is closed, and a light compressive bandage is
applied, thus promoting subcutaneous healing. The objective is to achieve a restitu-
tio ad integrum, provided that the subcutaneous structures have been respected.
4 Differences Between Open and Minimally

Invasive Surgery
Open and minimally invasive surgery is a set of techniques with the same objective:
to achieve a painless and biomechanically functional foot. The surgical indications
do not vary, the main difference being in their planning and execution.
4.1 Preoperative Planning
It is necessary to have specific instruments. Under no circumstances should percu-

taneous techniques be performed by adapting instruments (motorized or not) similar
to those specifically designed for this technique, since major complications can
arise if the appropriate instrument is not used.
Similarly, radiological control is necessary during the intervention. The control
allows us to see the exact position of the surgical instruments before performing the
gestures, as well as the result of the same. This control avoids the logical complica-
tions that could occur as a consequence of the lack of direct vision of the surgical field.
4.2 Intraoperative Preparation
4.2.1 Anesthesia
The type of anesthesia is different in the two groups of surgical techniques. In open
surgery, an anesthetic block of the sciatic nerve at the popliteal level is performed in
most patients, while percutaneous surgery is performed with a peripheral block of
the ankle “in sock” (Fig. 10). The type of anesthesia will condition discharge, with
outpatient surgery being performed with early discharge with percutaneous surgery,
since the patient has no blockage of the extrinsic musculature of the foot and can
walk at the end of the intervention without the risk of falling.
4.2.2 Preparation of the Surgical Field
The correct preparation of the patient and the sterility measures of the surgical field
are identical in both techniques (Fig. 11).
Fig. 10 Loco-regional
anesthesia in percutaneous
surgery
Fig. 11 Image of the prepared surgical field
One of the main differences with open surgery is that minimally invasive tech-
niques are performed without an ischemia cuff. Intraoperative bleeding does not
affect the surgery, since it is performed without direct vision and, on the other hand,
blood circulation has a cooling effect on the increase in temperature produced by
the motorized cutting instruments. In the same way, the bleeding favors the cleaning
of the bony debris by dragging it from the surgical site to the skin entrance.
4.3 Types of Surgical Techniques
Although the surgical indications are identical in open and percutaneous surgery,
not all foot surgery techniques can be performed by minimally invasive or percuta-
neous surgery.
The indications are precise and must be adhered to in order to obtain good results.
Percutaneous surgery is a method in the surgeon’s hands, not an end in itself. The
techniques we practice through minimal incisions are divided into three sections:
soft tissue surgery, bone surgery (osteotomies, exostectomies), and arthrodesis.
4.3.1 Soft Tissue Surgery
The indications for this type of surgery are limited. There are techniques frequently
performed in foot surgery that cannot be performed, such as tendon transpositions,
tendon or muscle suturing and repair, or certain tendon lengthening procedures.
On the other hand, capsulotomies and tenotomies, especially of the flexor
(Fig. 12) and extensor tendons, either as a single procedure or as a procedure
associated with other surgeries, are perfectly feasible by minimal incision sur-
gery, with great efficiency and minimal aggression. Percutaneous plantar fasci-
otomy (Fig. 13) will be an excellent indication in the treatment of fasciitis and
heel spurs.
Fig. 12 Tenotomy of the

flexor tendons
Fig. 13 Percutaneous plantar fasciotomy
Fig. 14 Subungual exostosectomy
4.3.2 Bone Surgery
The elimination of small exostoses, especially subungual (Fig. 14), was the origin of
this type of technique. It is therefore not surprising that the performance of osteoto-
mies and exostectomy are the indications with the greatest scope of action in percu-
taneous surgery. The sophistication that has been reached with motorized instruments
and radiological control allows us today to perform all types of osteotomies (distal,
diaphyseal, and proximal) at the level of the metatarsals (Fig. 15) and phalanges.
Fig. 15 DMMO distal

metatarsal osteotomy
Fig. 16 Percutaneous
ankle arthrodesis
4.3.3 Arthrodesis
Although the indications are limited, articular arthrodesis can be performed (Fig. 16)
by removing the articular cartilage with motorized drills, thus promoting fusion of
the articular bony ends.
4.4 Advantages and Disadvantages
Percutaneous foot surgery is a very useful method for the treatment of most foot
deformities, but it must be performed by experienced surgeons. With these tech-
niques very satisfactory results are obtained, equivalent to those of traditional sur-
gery, with minimal surgical damage, which allows a rapid incorporation of the
patient to his social and working life, and a lower incidence of complications.
The main advantages of minimally invasive surgery over open surgery are:
• Surgery under loco-regional anesthesia and without the need for ischemia.
• Smaller incisions: less damage to soft tissues and improved esthetic factors.
• No use of osteosynthesis material.
• Less soft tissue trauma: reduction of postoperative pain.
• Reduction of surgical time: reduction of waiting list.
• Outpatient surgery: reduction of hospital costs and reduction of hospital
infections.
• It can allow less complex revision surgery in certain cases.
The main disadvantages of minimally invasive surgery compared to open sur-
gery are:
• Longer learning curve.
• Lack of precise control of the position and shortening of the osteotomies.
• Less control of osteotomy stabilization.
• Difficulty in the control of bleeding and localization of deep structures.
• Difficulty in spatial perception: loss of depth sensation.
5 Surgery for the Beginner in MIS
There are currently more than 200 techniques described for the treatment of fore-
foot pathology, but none of them alone is capable of solving all the deformities
present. Therefore, nowadays, it does not seem correct to speak of a specific tech-
nique but of the specific combination for each case of different surgical gestures that
can give a definitive and effective solution to the specific deformities of the patient
to be treated.
There are five levels of difficulty according to the surgical techniques that we can
perform in minimally invasive surgery, ranging from level 1, which expresses the
minimum difficulty, to the maximum level 5. Similarly, we classify the surgeon’s
level of experience in four grades (beginner, initiated, advanced, and expert). It is
important to start the learning curve with surgical techniques of level I or II and to
increase the indications to other pathologies as the surgeon’s experience in mini-
mally invasive surgery progresses.
In the first level of experience, beginners, level I surgery should be performed,
such as digital deformities or tailor’s bunion, quintus varus. In the next level of
experience, beginners, level II and III surgeries can be performed, reserving level IV
surgeries for an advanced level of experience and level V surgeries only for experts.
5.1 Difficulty Pathology
I. Tailor’s bunion, digital deformities

II. Achilles tendinopathy, calcaneoplasty
III. Metatarsalgia, mild-moderate hallux valgus.
IV. Severe hallux valgus, calcaneal osteotomy, subtalar arthrodesis
V. Salvage surgery
5.2 Percutaneous Surgical Technique Recommended

for Beginners
In our opinion, the most recommended surgical technique for the beginning of the
learning curve is the treatment of the quintus varus or tailor’s bunion, based on the
lower complexity with respect to other techniques and on the good surgical results
we obtain with this technique.
5.3 Surgical Planning
• Patient in supine decubitus with the foot outside the limit of the operating table.
• Anesthetic block at ankle level. For this technique it is not necessary to block the
saphenous nerve or the deep peroneal nerve.
• Without ischemia cuff.
• Instruments for minimally invasive foot surgery.
• Basic instrumentation (Beaver-type scalpel, rasps).
• Motorized instrumentation (motor and drills).
• Radiological control instruments (fluoroscopic system).
5.4 Surgical Technique
5.4.1 Exostectomy
A 5 mm skin incision is performed, located in front of the external condyle of the

fifth metatarsal. The skin is incised perpendicularly, and immediately we move
towards the capsule, which is crossed towards the metatarsophalangeal joint of the
Fig. 17 Tailor’s bunion approach
Fig. 18 Dorsolateral
exostectomy
fifth toe (Fig. 17). With a dorsal and plantar movement, the entire capsule is detached
from its superior and external aspect of the lateral condyle of the fifth metatarsal,
creating a space between it and the bone where it can be “worked”; a rasp is intro-
duced to check the space created between the condyle and the capsule, which will
protect the soft tissue from injury. The small triangular reamer is introduced, and,
with a slow speed of 2000–6000 rpm and a dorsal and plantar oscillating motion, the
dorsal and lateral exostosis is removed exactly to the desired level, which will be
checked under fluoroscopic control (Fig. 18). This process is interrupted on two or
three occasions, pressing the capsule on the head of the fifth metatarsal in the direc-
tion of the skin incision, to remove the bone paste produced, as well as to introduce
the scraper, in order to remove the fine bony debris and those adhering to the deep
side of the capsule (Fig. 19). With the repetition of these gestures, a complete exos-
tectomy and adequate cleaning is achieved.
Fig. 19 Removal of the bony detritus of the exostosis
Fig. 20 Metatarsophalangeal capsulotomy
5.5 Metatarsophalangeal Capsulotomy
A new 5 mm incision is made at the level of the dorsal and lateral aspect of the
metatarsophalangeal joint of the fifth toe (Fig. 20). Through the incision, the scalpel
is introduced inside the joint, turning it 90° and leaving the cut surface facing later-
ally, the finger is taken with the left hand, and a valgus movement is performed, thus
tightening the medial capsule, which is incised over its entire surface, a gesture that
the surgeon can appreciate perfectly by noticing how the resistance gives way in the
valgus movement of the fifth finger.
5.6 Distal Metatarsal Osteotomy
A new 5 mm incision is made behind the head of the fifth metatarsal at the level of
the 4th–fifth intermetatarsal space, which must be deepened down to the bone at
the neck of the fifth metatarsal (Fig. 21); a long Shannon 44 reamer is then inserted,
following an oblique 45° direction from distal dorsal to proximal plantar, with the
upper limit at the end of the neck when it reaches the cartilage (Fig. 21). We then
introduce a long Shannon 44 reamer, following an oblique direction of 45° from
distal dorsal to plantar proximal, with the upper limit at the final portion of the
neck upon reaching the articular cartilage (Fig. 22); we perform a medial wedge
osteotomy, respecting the external cortex; subsequently, pressing the head of the
fifth metatarsal medially, we produce an osteoclasty that completes the osteotomy.
Fig. 21 Approach for distal metatarsal osteotomy
Fig. 22 Distal metatarsal osteotomy

Fig. 23 Osteotomy of the base of the proximal phalanx of the fifth toe
5.7 Osteotomy of the Base of the Proximal Phalanx

of the Fifth Toe
An incision is made with the Beaver blade on the plantar skin immediately behind
the digitoplantar skin fold, at the mid-height of the fifth toe; a rasp is introduced and
slid from the base of the phalanx through the lateral periosteum of the phalanx,
displacing it; the short Shannon 44 reamer (Fig. 23) is inserted and rests on the lat-
eral aspect of the base of the proximal phalanx, thus performing an osteotomy,
which may be total or incomplete wedge osteotomy, according to the indication
considered appropriate.
5.7.1 Bandaging
Post-surgical dressing plays a vitally important part in the treatment to maintain the
correction obtained, since osteosynthesis is not performed. A slightly compressive
bandage is applied, maintaining a moderate hypercorrection in order to close the
osteotomies performed (Fig. 24).
A check-up is performed after 7 days for removal of the stitches. Subsequently,
a simpler dressing is applied, the technique of which is explained to the patient so
that he/she can change it daily after the toilet. The bandage consists of the place-
ment of some plasters that maintain the correction and a metatarsal strap with a
self-adhesive elastic bandage (Fig. 25). This bandage should be maintained
24 hours a day for 3 or 4 weeks after surgery, and the patient should walk with a
post-surgical shoe with a rigid sole, to help maintain the stability of the
osteosynthesis.
Fig. 24 Post-surgical dressing
Fig. 25 Bandage after the

first revision
6 Complications
The poor results obtained by minimally invasive foot surgery in its beginnings,
30 years ago, were the consequence of a combination of incorrect indication, use of
nonspecific instruments, and lack of technical preparation. The rate of complica-
tions can be significantly reduced by attending specific training courses that allow
us to become accustomed to the use of the new instruments, as well as to clarify the
surgical indications.
6.1 Soft Tissues
6.1.1 Cutaneous
It is possible to find inflammation, edema, and superficial infection as a conse-

quence of laceration or burn of the soft parts (Fig. 26). These complications are
linked to the learning curve, produced by the inadequate and repeated use of drills
Fig. 26 Burn after

and other cutting instruments or extraction of bone detritus (rasps). They are gener-
ally caused by using the cutting drills with a speed higher than 10,000 RPM or by
the pressure exerted by the drill on the skin when changing the direction of the
motor during the performance of an osteotomy or exostectomy.
Occasionally, inflammation and slight exudate production can occur through the
approach route, which can be mistaken for an infectious condition. This condition
is caused by insufficient elimination of bone debris (detritus) produced during sur-
gery by the action of the drills and sometimes appears as minimal bone chips
through the incision after a few days.
6.1.2 Tendinous
Tendon injuries are exceptional. Contrary to what it may seem, it is not easy to sec-
tion a tendon with the action of a drill, since, to section it, it is necessary for the
cutting drill to be in direct contact with the tendon and to act on it while it is in
contact with the bone or in the position of maximum tension.
6.1.3 Neurovascular
No vascular lesions have been described (Fig. 27) that produce ischemia of the
structures distal to the surgical site, and iatrogenic neurological lesions are excep-
tional if we respect the access routes described for each of the different surgical
techniques.
Fig. 27 Bleeding after

Dysesthesias may appear in up to 12% of patients, caused by inflammation or

contusion of the tissues surrounding the peripheral nerves. They disappear within 2
or 3 months, persisting in time in only 0.5% of cases.
6.1.4 Edema
Persistent edema in the forefoot, especially in those cases operated of osteotomies

of the lesser metatarsals, is frequent. It can be considered part of the normal evolu-
tion of this type of technique, being present up to 3 or 4 months after surgery. In
some patients it requires symptomatic treatment.
6.1.5 Joint Stiffness
Joint stiffness is a relatively frequent complication, both in open surgery and in

minimally invasive surgery.
In hallux valgus surgery, a limitation of 20% of the global mobility of the meta-
tarsophalangeal joint can occur in between 1.5% and 6.8% of patients. This compli-
cation can be minimized by complete removal of bone debris, control of the action
of the drills, and early mobilization of the joint (usually at 3 weeks, when there is
sufficient fibrous callus to prevent displacement of the osteotomies).
In metatarsalgia surgery, joint stiffness, in the case of distal lateral metatarsal
osteotomies, is exceptional, being absent or without clinical repercussions in most
series, unlike in open Weil-type techniques where joint stiffness is the main
complication.
6.1.6 Others
Deep infection and deep vein thrombosis occur exceptionally in minimally invasive
foot surgery, with an incidence of less than 0.8% and 1.8%, respectively.
6.2 Bone
6.2.1 Secondary Displacement of Osteotomies
In osteotomies of the first radius, there is a possibility of displacement due to the

absence of osteosynthesis material (Fig. 28). Technical errors in the direction of
Fig. 28 Displacement
after osteotomy of the first
metatarsal
Fig. 29 Displaced DMMO and subsequent adequate consolidation
osteotomy tracing are the main cause of these secondary displacements, and early
treatment should be performed. Modification of the dressing or repositioning to the
correct position and the use of a percutaneous Kirchner wire synthesis may be suf-
ficient to resolve it. If displacement is detected late after vicious consolidation of the
osteotomy, surgical treatment will be necessary.
In distal lateral metatarsal osteotomies, the presence of displacement between the
ends of the osteotomies, even when significant, should not be considered a complica-
tion, since it is the intended effect after surgery (Fig. 29). After these osteotomies
have been performed, immediate loading is authorized so that the free metatarsal
head can find its ideal functional position by receiving the weight of the body during
walking. It is important to avoid dorsal rotation movements of the metatarsal head, for
which it is recommended that during walking, in the first postoperative month, the use
of a stiff-soled shoe without a heel, which allows loading along the sole of the foot
and avoids dorsal flexion of the metatarsophalangeal joints, is recommended.
6.2.2 Healing Disorders
Delays in healing of the osteotomies of the first metatarsal are frequent, reaching
consolidation after 6 months. They are well tolerated despite persistent inflamma-
tion (Fig. 30).
Fig. 30 Delayed
consolidation after
multiple osteotomies
The healing time of lateral metatarsal osteotomies is very variable, ranging from
6 weeks to more than 12 months in some cases, most of which are asymptomatic.
Due to the time of evolution, the presence of pseudarthrosis should not be consid-
ered until 18 months of evolution.
Pseudarthrosis and avascular necrosis of the metatarsal head are exceptional and
without any clinical repercussions in most published cases.
7 Summary
The time when the complications of minimally invasive foot surgery seriously con-
ditioned the results obtained is over. These techniques occupy an important place in
our therapeutic arsenal, but not all interventions performed on the foot can or should
be performed by minimally invasive techniques. Their indications are very precise,

and it is necessary to adhere to them if good results are to be obtained, since mini-
mally invasive surgery is just another method in the surgeon’s hands and not an end
in itself and will be reserved for surgeons with experience in both traditional and
minimally invasive surgery.
To get started in these techniques, a sometimes slow and laborious learning curve
will be necessary, in which we must follow a process of adaptation to the loss of
direct and three-dimensional vision of the surgical field, as well as perfecting our
anatomical knowledge, not only of the access route but also of the path that the
instruments used follow to the place of the designed surgical gesture.
In conclusion, we can say that minimally invasive foot surgery is a surgical
method that allows us to perform some interventions through minimal incisions,
which in order to be performed, with respect to the anatomy, percentage of compli-
cations, and precision equivalent to open surgery, these four conditions will be
necessary:
1. To limit the use of minimally invasive techniques to their indications.
2. To have an exact knowledge of the anatomical relationships of the foot, in order
to be able to use adequate approach routes free of risk of injuring anatomical
structures that must be respected, without producing iatrogenic lesions.
3. To have the specific instruments and to use them in the appropriate manner.
Under no circumstances should these techniques be performed by adapting
instruments, motorized or not, more or less similar to those designed for this
surgery.
4. Use a radiological control method during the intervention not only to check the
result but also to control its development under radiological vision. In this way
we will avoid the complications derived from the lack of direct vision of the
surgical field.
Suggested Readings
1. Addante JB. The metatarsal osteotomy, as a surgical approach to the elimination of plantar
keratosis. J Foot Surg. 1969;8:3.
2. Bauer T, De Lavigne C, Biau D, De Prado M, Isham S, Laffenêtre O. GRECMIP: percutaneous
hallux valgus surgery: a prospective multicenter study of 189 cases. Orthop Clin North Am.
2009;40:505–14.
3. Bauer T, Biau D, Lortat-Jacob A, Hardy P. Percutaneous hallux valgus correction using the
Reverdin-Isham osteotomy. Orthop Traumatol Surg Res. 2010;96(4):407–16.
4. Bösch P, Markowski H, Rannicher V. Technik und erste Ergebnisse der subkutanen distalen
Metatarsale-I-Osteotomie. Orthop Prax. 1990;26:51–6.
5. De Prado M. Minimally invasive foot surgery: a paradigma shift. In: Maffulli N, Easley M,
editors. Minimally invasive surgery of the foot and ankle. Springer: London; 2011. p. 3–11.
6. De Prado M. Complications in minimally invasive foot surgery. FuB and Sprunggelenk.
2013;11:83–94.
7. De Prado M, Cuervas-Mons M, De Prado V, Golanó P, Vaquero J. Does the minimally invasive
complete plantar fasciotomy result in deformity of the Plantar arch? A prospective study. Foot
Ankle Surg. 2020;26(3):347–53.
8. De Prado M, Ripoll PL, Golanó P. Minimally invasive foot surgery. Barcelona: AYH; 2009.
9. De Prado M, Ripoll PL, Golanó P. Cirugía percutánea del pie. Barcelona: Elsevier (mas-
son); 2003.
10. De Prado M, Ripoll PL, Vaquero J, Golanó P. Tratamiento quirúrgico percutáneo del Hallux
Valgus mediante osteotomías múltiples. Rev Ortop Traumatol. 2003;47:406–16.
11. Dhukaram V, Chapman AP, Upadhyay PK. Minimally invasive forefoot surgery: a cadaveric
study. Foot Ankle Int. 2012;33(12):1139–44.
12. García-Fernández D, Larrainzar-Garijo R, Llanos-Alcázar LF. Estudio comparativo de la oste-
otomía de Weil abierta: ¿es necesaria siempre la fijación? Rev Ortop Traumatol. 2006;50:292–7.
13. Giannini S, Ceccarelli R, Bevoni R, Vannini F. Hallux valgus surgery: the minimally
InvasiveBunion Correction (SERI). Tech Foot Ankle Surg. 2003;2(1):11–20.
14. Henry J, Besse JL, Fessy MH. Distal osteotomy of the lateral metatarsals: a series of 72 cases
comparing the Weil osteotomy and the DMMO percutaneous osteotomy. Orthop Traumatol
Surg Res. 2011;97(6 Suppl):S57–65.
15. Isham S. The Reverdin-Isham procedure for the correction of hallux abductus valgus. A distal
metatarsal osteotomy procedure. Clin Podiatr Med Surg. 1991;8:81–94.
16. Maffulli N. Minimally invasive surgery in orthopedic surgery. Orthop Clin North Am.
2009;4(40):491.
17. Magnan B, Pezze L, Rossi N, Bartolozzi P. Percutaneous distal metatarsal osteotomy for cor-
rection of hallux valgus. J Bone Joint Surg. 2005;87-A:1191–9.
18. Stiglitz Y, Cazeau C. Minimally invasive surgery and percutaneous surgery of the hindfoot and
midfoot. Eur J Orthop Surg Traumatol. 2018;28(5):839–47.
Tumors of the Foot and Ankle
Eduardo Botello and Tomas Zamora
1 Introduction
Musculoskeletal tumors in the foot and ankle region are relatively uncommon enti-
ties, and they represent up to 5–8% of all musculoskeletal tumors [1, 2]. Moreover,
sarcomas, malignant neoplasms of mesenchymal origin, arise in this region in only
2% of all sarcoma cases [3]. This being said, the implications of an error in diagno-
sis of a neoplasm in the foot and ankle can be frequent and can lead to significant
morbidity and severe consequences in case of a malignant tumor [4], emphasizing
the importance for any specialist involved to be familiar with the evaluation and
diagnosis of musculoskeletal tumors in this area.
This chapter will focus on the main clinical aspects of bone and soft tissue tumors
of the foot and ankle, including clinical presentation, imaging, and initial manage-
ment. Common subtypes and relevant histologies will also be described.
2 Epidemiology
As previously stated, tumors of the foot and ankle are considered to be relatively
infrequent. A retrospective analysis from a tumor institute in Germany described a
5.5% incidence from a total of 7487 musculoskeletal tumors treated in almost
20 years [2]. Almost two-thirds were bone tumors, and 18% were malignant tumors
of bone and soft tissue. The most common benign bone tumors were simple bone
cysts, enchondroma, osteochondromas, aneurysmal bone cysts, and intraosseous
E. Botello (*) · T. Zamora

Orthopaedic Oncology and Lower Limb Reconstructive Surgery, Orthopaedic Surgery
Department, Pontificia Universidad Católica de Chile, Santiago, Chile
e-mail: [email protected]; [email protected]

Switzerland AG 2022
72 E. Botello and T. Zamora
lipomas. From the malignant bone tumors (8%), 46% were chondrosarcomas. The
most frequent benign soft tissue tumors treated in this cohort were hemangioma,
followed by tenosynovial giant cell tumor (or pigmented villonodular synovitis),
superficial fibromatosis, neurinoma, and schwannoma. Moreover, the most com-
mon malignant soft tissue tumors were synovial sarcoma and myxofibrosarcoma.
Similarly, a North-American series reported a 5.7% rate of tumors in the foot and
ankle [5]. The most common bone tumors were giant cell tumor of bone, osteosar-
coma, and chondrosarcoma, while frequent soft tissue tumors were tenosynovial
giant cell tumor, hemangioma, and synovial sarcoma.
3 Anatomy
The foot and ankle anatomy is unique, given the proximity of different bone and soft
tissue structures such as tendons, muscle, ligaments, nerves, and vessels. Similarly,
the lack of well-defined fascial planes and complex bony anatomy can make a surgi-
cal resection complying with oncological principles and preservation of the extrem-
ity challenging.
Given the size of bony structures, especially in the foot, tumors can erode corti-
ces relatively early during their progression, reaching the soft tissues around them.
In the same way, soft tissue tumors can be diagnosed at a smaller size, compared to
other anatomic sites such as the pelvis, where tumors can be extremely large before
being noticed. Similarly, they can penetrate bone cortices easily, leading to more
extensive surgical resections when margins are a critical consideration.
On the other hand, the distal tibia’s subcutaneous location can make soft tissue
coverage difficult in case of an extraosseous extension of a malignant bone tumor.
Finally, the arterial supply to the distal lower extremity is given by the anterior and
posterior tibial arteries, which communicate extensively through distal anastomosis
around the foot, ensuring adequate blood supply in most cases. In the same way,
neurological structures should be preserved when possible, especially the medial
and lateral plantar divisions of the tibial nerve, which gives the sensorial innervation
of the plantar weight-bearing surface of the foot.
4 Clinical Presentation
Tumors around the foot and ankle can appear at any age and are overall similarly
distributed within males and females, but variations may arise depending on specific
histologies.
As with musculoskeletal neoplasms in other locations, pain and a palpable lump
are the most common presentations of tumors in the foot and ankle [6, 7]. Symptoms
such as night or non-mechanical pain should be considered as a red flag for further
investigations, as well as inflammation or swelling during examination. A soft
Tumors of the Foot and Ankle 73
tissue mass with a rapid increase in size, a painful lump, recurrence after a previ-
ous excision, or a size over 5 cm should prompt urgent referral to a specialized
center to rule out a malignancy [8]. Given the proximity of structures in this ana-
tomic area and the technical difficulties of a malignant neoplasm re-excision,
advance imaging should be considered early in sizeable lesions. In other words,
the classic 5 cm rule could underestimate the need for cross-sectional imaging in
this anatomic area.
Changes in the skin color should be considered with attention, given that mela-
noma is not an infrequent diagnosis around the foot. Moreover, a detailed physical
examination can give clues to the tumor extension, especially if a motor or sensorial
deficit is present. Soft tissue tumors should also be assessed in depth, tenderness,
pulsatility, and transillumination, which may be useful to suggest cystic lesions.
History of previous cancer, therapies (e.g., radiation), and risk factors (smoking)
should be obtained in all patients with a bone or soft tissue lesion. Acral metastases
are uncommon but should be among the differential diagnosis (mainly pulmonary
and renal carcinoma).
5 Imaging
All patients with a bone or soft tissue tumor and an uncertain diagnosis or a red flag
in the clinical presentation should be referred for radiographs (anteroposterior, lat-
eral, and oblique). Plain X-rays have at least moderate evidence to support its use in
evaluating all bone tumors of unknown origin. Similarly, in soft tissue tumors, they
can add information like the presence of phleboliths (in hemangiomas), calcifica-
tions, or cortical erosion of the underlying bone [9]. Signs of a more aggressive
lesion or malignancy include periosteal reaction, cortical erosion/breach, ill-defined
margins, and signs of a soft tissue mass and should prompt further investigations.
On the other hand, well-defined lesions with a sclerotic margin, without a periosteal
reaction, cortical disruption, or a soft tissue mass, orientate to a more chronic and
less aggressive process, usually benign.
Ultrasonography can be helpful in small and superficial soft tissue tumors by
distinguishing between benign lesions such as vascular malformations, lipomas or
simple cysts, and other lesions with a more solid component that warrant further
investigations. On the other hand, deep and larger than 5 cm tumors should be
assessed directly with cross-sectional imaging, as ultrasound could fail to discrimi-
nate in these lesions [9, 10].
Computed tomography (CT) scan and magnetic resonance imaging (MRI) are
the imaging of choice when it comes to a better assessment of bone and soft tissue
structures. CT provides an adequate assessment of bone involvement and cortical
disruption, as well as calcifications within the lesion that could orientate to a more
chronic process. MRI with gadolinium is the image of choice for soft tissue lesions
and to determine bone marrow changes within the bone and other processes such
as a stress fracture or osteomyelitis. MRI can also help to assess the extent of the
lesion in both bone and soft tissue tumors and give details about its relationship
with the surrounding tissues, being the imaging modality of choice for surgical
planning.
In case that a malignant lesion is suspected, further imaging is used to assess the
presence of metastatic disease. In bone sarcomas, a CT of the chest is used to rule
out a pulmonary compromise, as well as a whole-body bone scan with a radiotracer
(most commonly technetium-99) to assess for other skeletal lesions. In soft tissue
sarcomas, a CT of the abdomen and pelvis should be included. Similarly, a whole-
body MR or an 18-fluorine fluorodeoxyglucose (18F-FDG) positron emission
tomography (PET)/CT is useful for this purpose, with increased sensitivity, espe-
cially for axial metastatic disease [11, 12].
6 Biopsy
Obtaining a sample for histopathology is of crucial relevance in the diagnostic pro-

cess of musculoskeletal tumors around the foot and ankle as well as for other loca-
tions. This being said, the biopsy should be performed at least in communication
with the referral center, as it has been reported a higher biopsy related complication
rate when biopsies are performed in non-specialized centers [13].
Imaging is of particular importance when planning for a biopsy. Cross-sectional
imaging should help decide the biopsy tract and the lesion area that will be sampled
to avoid purely cystic or necrotic areas.
More important than the type of biopsy performed is that it complies with classic
oncologic principles such as: it should be minimally invasive; should be performed
by or in consultation with the surgeon/team that will perform the definitive manage-
ment; should not contaminate other compartments; should be in line with the defini-
tive/planned incision; should be representative of the lesion being biopsied; and
should achieve adequate hemostasis. According to local practice and preference,
after all this is reviewed, a decision whether a percutaneous or an open biopsy
should be performed. Percutaneous biopsy techniques with a core needle biopsy can
be performed in most tumors and are easily guided through ultrasound (soft tissue)
or CT (bone). They have shown to be accurate, with most studies reporting more
than 90% accuracy for bone and soft tissue tumors [14, 15], and have become the
initial approach in most scenarios. On the other hand, even though fine-needle aspi-
ration biopsy techniques have a role in general oncology and they are used in some
centers for musculoskeletal tumors, we discourage their use given the high variabil-
ity and lack of accuracy in some circumstances [16]. Open incisional biopsy remains
a valid and commonly used technique; however, it should be reserved after a previ-
ous non-diagnostic or discordant biopsy or in young patients where a general anes-
thetic will be needed anyway. In the same way, an excisional biopsy is usually
reserved for small tumors that can be easily excised with low risks and complying
with oncological principles.
7 Principles of Treatment
General management depends on the type of tumor and its grade. For clearly benign
lesions, including stage 1 latent bone lesions according to the Enneking staging
system, close observation is generally the rule if the patient remains asymptomatic.
Patients with benign but symptomatic lesions or active/aggressive benign bone
tumors that could progress with significant morbidity are generally managed surgi-
cally with either intralesional or marginal excision depending on the type of tumor,
its grade, and anatomic location, among others. On the other hand, wide resection is
generally reserved for malignant tumors; however, it can also be the technique of
choice in some benign aggressive lesions such as a giant cell tumor of bone with
extensive bone destruction and soft tissue mass. In the foot, a radical excision usu-
ally includes some sort of amputation, given that metatarsals are the only distinct
compartmental boundaries.
If limb salvage is not possible with safe margins in a high-grade malignant tumor,
amputation should be considered. Most below the knee amputations can give more
than acceptable function in association with adequate rehabilitation and access to
prosthesis if needed.
8 Common Types of Tumors
8.1 Giant Cell Tumor (GCT) of Bone
GCT of bone is an intermediate, locally aggressive bone tumor characterized for the
presence of classic multinucleated giant cells from which the tumor derives its
name, distributed in a stroma of ovoid mononuclear cells, which are the true neo-
plastic origin. It can metastasize in its benign form and has a malignant counterpart,
which is clinical and histologically different.
GCT of bone has a peak incidence in the third and fourth decade, and it is rare in
children with an open physis. Even though it has been described in practically every
bone of the skeleton, it is more frequent in the metaphyseal-epiphyseal region of
long bones, especially around the knee in the distal femur. From all cases of GCT of
bone, lesions in the foot and ankle had been reported to be up to 5% of cases, more
frequently in the talus, distal tibia, and calcaneus [17–19].
Most GCT of bone present as a lytic lesion with geographic margins that can be
expansile and are located eccentrically within the bone (Fig. 1). In the foot and
ankle region, these lesions tend to appear more aggressive on imaging, with a more
ill-defined margin, cortical disruption, and even soft tissue mass. On MRI, it has a
low signal on T1 sequences and a high signal on fluid sensitive sequences such as
T2, with avid enhancement on contrast-enhanced sequences.
Treatment for contained lesions (Campanacci I and II) [20] usually consists in
curettage and bone grafting or cement. Given the aggressive pattern and high
Fig. 1 35-year-old female with a bone tumor in her right ankle. (Left) AP X-ray and (center) coro-
nal STIR reconstruction, revealing a lytic lesion in the distal epiphysis and metaphysis of the tibia.
Biopsy showed a giant cell tumor of bone. (Right) AP X-ray after curettage with adjuvant treat-
ment, plus cement filling and plate fixation with good results
recurrence risks classically described for GCT of bone, the use of some adjuvant
treatment is recommended. In the foot and ankle, lesions tend to act even more
aggressively with a higher recurrence rate than for other anatomic areas, with up to
30–52% of recurrence rate [17, 21]. For this reason, wide excision with resection
and reconstruction and even amputation has to be considered in more advanced
lesions with extensive bone destruction. On the other hand, medical treatment with
neoadjuvant denosumab protocols has been used extensively in the last decade,
especially in cases with a soft tissue compromise.
8.2 Chondroblastoma
Chondroblastoma is a rare and benign bone tumor of chondroid origin that typically
arises in the epiphysis of long bones, especially tibia, femur, and humerus, but up to
13% of cases can involve the foot, specially tarsal bones [22, 23]. Its peak incidence
is during the second decade; however, it has been described at all ages, with a 2–3:1
male preponderance.
Most cases present with severe pain and limitation of movement. The radio-
graphic appearance is of a lytic lesion with well-defined margins. In MRI the pres-
ence of intense perilesional edema is frequent. It is most commonly found in the
posterior facet of the calcaneus and the posterior body of the talus close to the tib-
iotalar joint [24] and can be associated with cystic features and even a secondary
aneurysmal bone cyst (ABC) component.
Treatment in latent or active lesions usually consists of curettage and bone graft-
ing or cement filling with an adjuvant treatment such as phenol or cryotherapy.
Recurrence has ranged from 10% to 15% [23, 25], without a clear relationship with
its location or the presence of a secondary ABC [23].
8.3 Aneurysmal Bone Cyst (ABC)
ABC was initially considered to be a reactive phenomenon; however, the identifica-

tion of the constant involvement of the USP6 fusion oncogene led to a better under-
standing of this neoplastic, benign, but locally aggressive lesion [26]. ABC is
usually observed in the metaphysis of long bones, more frequently around the knee.
This being said, the foot and ankle involvement is considered infrequent, with
reports stating 2–9% of ABCs located in this region [24, 27, 28]. Secondary ABC
arises together with other bone tumors such as GCT of bone, chondroblastoma,
osteoblastoma, or fibrous dysplasia.
Most patients with ABC are young, with a peak incidence in the second decade.
Radiographic appearance includes an eccentric, expansile lytic lesion with cortical
thinning, located in the metaphysis of bone. MRI shows the classic fluid-fluid lev-
els, representing blood-filled compartments, and a CT scan is especially useful to
define the extent of the lesion and cortical compromise as for other lesions. When a
secondary component is present, the MRI will demonstrate an additional solid com-
ponent representing the primary tumor, especially in gadolinium-enhanced
sequences.
As with most benign lesions, management generally includes curettage with or
without bone grafting or cement augmentation. Reported recurrence rates have been
described as up to 20%, with most of them being during the first 2 years from the
initial surgical treatment [28]. Lesions with extensive bone loss are treated with
wide resection and reconstruction depending on the location. Other techniques,
such as embolization, radiofrequency ablation, or minimally invasive methods, have
also been described [24, 29].
8.4 Enchondroma
Enchondromas are one of the most common benign forms of cartilaginous neo-
plasms. They represent approximately 3% of all bone tumors and up to 15% of
benign bone tumors. This being said, the foot will host up to 6% of all enchondro-
mas, especially in the proximal phalanx [30].
Enchondromas are usually solitary tumors found incidentally, and therefore,
their true incidence is likely to be higher than reported. Most of them are asymptom-
atic and are found at any age but usually from 15–40 years. Enchondromas appear
as central and metaphyseal lesions, with a well-delimitated border and central min-
eralization. Calcifications can range in size from small punctuate to larger rings.
MRI will show a cartilaginous neoplasm signal pattern with low signal intensity on
T1 sequences and high signal intensity on T2-weighted sequences.
Various radiographic and clinical features can help differentiate a benign enchon-
droma from a more aggressive /malignant tumor; however, this remains a diagnostic
challenge, even for experienced specialists [31]. Painful and larger lesions, exten-
sive cortical compromise, and a large soft tissue mass should alert for the possibility
of malignant transformation; however, this is rare for isolated lesions.
As with most benign latent lesions, enchondromas that are asymptomatic can be
treated non-operatively with observation alone. Single lesions with a characteristic
radiographic appearance do not need to undergo a biopsy. Indications for surgical
treatment in an enchondroma are continuous symptoms, enlargement, or radio-
graphic changes during follow-up to rule out a low-grade malignant variant, impend-
ing fracture, or an actual fracture of the host bone. If surgical treatment is decided,
curettage and bone grafting or cement augmentation is usually the treatment of
choice, with a low rate of recurrence if done adequately and with the addition of
some form of adjuvant therapy.
Several syndromes have been described in patients with multiple enchondromas,
with recent classifications based on spinal involvement and genetic inheritance. The
two most frequently described syndromes are Ollier disease and Maffucci syn-
drome, both non-hereditary and without spinal involvement.
8.5 Osteochondroma
Osteochondromas are the most frequently biopsied bone tumors. It is usually located
in the metaphysis of long bones, especially around the knee, during the second
decade of life [32]. The foot and ankle region are relatively uncommon locations;
however, they usually cause significant symptoms that require treatment in contrast
to other anatomic areas.
Osteochondromas are usually diagnosed incidentally if they are small. However,
in the distal tibia, osteochondromas can cause deformity and significant symptoms
(Fig. 2). X-rays are the primary imaging modality, observing an osseous protuber-
ance arising from the bone that can be pedunculated or sessile but has medullary and
cortical continuity (Fig. 2). If there is a symptomatic or atypical lesion, MRI can
accurately characterize the lesion and its cartilage cap, with a high sensitivity and
specificity for malignant transformation, especially if the cap measures more than
2 cm [33].
Treatment usually consists in resection through the base of the lesion in case
of significant symptoms [34], with adequate results. Multiple hereditary exosto-
sis (MHE) is a rare autosomal dominant inherited syndrome in which patients
have multiple enchondromas with a higher risk of malignant transformation
(up to 5%).
Fig. 2 Coronal MRI

reconstruction and oblique
X-ray of the ankle from an
18-year-old male, with a
distal tibia
osteochondroma. A lateral
osseous protuberance is
observed in the distal tibia,
with slight fibular
deformity
8.6 Subungual Exostosis
A subungual exostosis is a benign, painful osteocartilaginous surface lesion of the

distal phalanx, mostly located in the great toe (80%); however, it can occur in any
toe or finger, producing nail deformation.
X-rays show an osseous proliferation attached to the distal phalanx’s side or
dorsum without cortical or medullary continuity (unlike classic osteochondroma).
Initially, these lesions were thought to be reactive; however, clonal cytogenetic find-
ings in recent years have confirmed a proper neoplastic process. As with most
benign lesions, marginal resection is usually adequate and curative.
8.7 Unicameral Bone Cyst (UBC)
UBCs are benign cystic lesions that are commonly seen in young patients. Their
most frequent location is in the metaphysis of long bones (femur or humerus); how-
ever, the calcaneus is also a common site (sixth in frequency), and it is the most
frequent location in the foot and ankle region.
Most of these lesions are found incidentally and are located in the anterolateral
aspect of the calcaneus. On plain X-rays, they are observed as lytic lesions with
well-defined margins and mild cortical thinning. MRI shows no solid component.
Most asymptomatic calcaneal UBC tends to be treated non-operatively, with
observation alone. Levy et al. [35] showed that only a small percentage (1%) had
spontaneous regression with observation, and for that reason, most symptomatic
large cysts, or those with a high risk for a pathological fracture, are treated with
some sort of intervention. Corticosteroid injection has shown radiographic healing
in 66% of patients, while open curettage and grafting have been considered the
traditional treatment with the best outcome described. Minimally invasive cannu-
lated screws decompression and limited curettage have also been shown to be a
valid technique for smaller lesions, especially in children [35].
8.8 Intraosseous Lipoma
Intraosseous lipomas are usually considered to be rare entities and are most com-
monly located in long bones or the calcaneus in the Ward’s triangle, just inferior to
the angle of Gissane [24, 36, 37].
It is unclear whether intraosseous lipoma has a predilection for a specific age or
gender; however, some studies have reported a predilection for males and adult life.
Most patients are symptomatic, with pain being the most frequent symptom, fol-
lowed by swelling or tenderness. On plain X-rays, they appear as a lytic cystic
lesion with well-defined sclerotic margins and calcifications within the margins.
MRI confirms the suspected lesion with an intense signal in T1- and T2-weighted
sequences, identical to subcutaneous fat.
Non-symptomatic lesions can be treated with observation, as some of them can
undergo spontaneous regression. Symptomatic and large lesions are usually treated
with open curettage and grafting, to prevent a pathological fracture. Lesions
extending the full breadth of the calcaneus laterally to medially in the coronal
plane and at least 30% of the length anteroposteriorly are considered to be of criti-
cal size and warrant surgical treatment to prevent fractures [38]. Recurrence rates
are very low.
8.9 Tenosynovial Giant Cell Tumor
Tenosynovial giant cell tumors are a group of lesions that arise from the synovium
of joints, bursae, or tendon sheaths that can be intra- or extra-articular and are clas-
sified by its clinical and biological behavior in localized (previously called giant cell
tumor of the tendon sheath) or diffuse type (previously called pigmented villonodu-
lar synovitis). In time, cytogenetic studies have confirmed its neoplastic nature and
common pathology, with a structural change involving the translocation of the
CSF1 gene, causing the synthesis of a large amount of CSF1 protein [39].
The localized form of tenosynovial giant cell tumor is more frequent around the
hand; however, another common location is the ankle associated with many of the
tendon sheaths. They can occur at any age but are more frequent in adult life with a
slight female preponderance. They present as a firm nodule, usually painless, that
can grow in time and cause symptoms when compressed by footwear. Surgical
resection usually gives a good outcome with a low recurrence risk if treated
adequately.
The diffuse form of tenosynovial giant cell tumor usually presents in younger
patients than its localized counterpart. The most commonly involved joints are the
knee and ankle, but the midfoot is also a frequently involved region [3]. Patients
present with pain, tenderness, swelling, and a limited range of motion. X-rays can
show signs of a soft tissue mass, with bone erosions and secondary degenerative
joint disease. MRI is the imaging modality of choice, showing the classic blooming
artifact on gradient echo sequences and low signal on T1- and T2-weighted
sequences due to hemosiderin deposits. Macroscopically, the synovium appears
brown, and there can be a multinodular appearance. Surgical resection is usually the
treatment of choice, with arthroscopic modalities having satisfactory outcomes in
limited disease but usually needing an open radical synovectomy in diffuse and
extensive lesions [40].
Recurrence can be common in diffuse forms (up to 40%) [41] but can be initially
controlled by surgical re-excision. Radiation has been used as an adjuvant therapy.
Molecular targeted therapy represents a new option for managing patients with
recurrent or inoperable disease and has shown promising results [42].
8.10 Plantar Fibromatosis
Plantar fibromatosis or Ledderhose disease is a benign fibroblastic proliferation

involving the plantar aponeurosis and is one of the most common soft tissue tumors
of the foot. It is more common in younger patients and can be painful with multiple
nodules in the medial and central band of the plantar aponeurosis, with a significant
proportion of patients presenting with bilateral disease (one-third).
It has been associated with Dupuytren’s contractures and Peyronie’s disease, as
well as with other systemic diseases (such as epilepsy, diabetes mellitus, and ciga-
rette smoking), although these last ones have not been widely validated.
Asymptomatic and small lesions can be managed with observation alone; how-
ever, symptomatic lesions might require surgical excision with partial or complete
resection of the plantar fascia. Direct and marginal excision of nodules has been
associated with an elevated recurrence risk [43, 44]; therefore, a more extensive
resection is usually needed with even a complete plantar fasciectomy indicated in
cases of recurrent disease. Other therapies, such as corticoid injections, extracorpo-
real shock wave therapy, and radiation therapy, have been used with variable success.
8.11 Ganglion
Ganglions are one of the most common soft tissue masses in the foot and ankle
region [3] and are considered to be a cystic degeneration more than a proper neo-
plastic condition. They appear as a firm superficial nodule that can cause symptoms
depending on their location. On clinical examination, the trans-illumination test can
confirm its purely cystic nature, and aspiration will reveal a gel-like fluid content,
confirming the diagnosis. Surgical excision is recommended in large symptomatic
lesions, and special care should be taken to remove the entire capsule and the stalk
of the tumor to avoid recurrent disease.
8.12 Lipoma
Lipoma is the most common mesenchymal soft tissue tumor and is composed of
mature adipocytes. It commonly arises in the foot’s dorsum and is usually a painless
subcutaneous mass but can cause symptoms when compressed by footwear. Clinical
examination usually reveals a superficial, small, and mobile mass. Ultrasound (in
small, superficial lesions) and MRI can be diagnostic, demonstrating a homogenous
lesion with an isointense signal to subcutaneous fat in all pulse sequences. Thick
septations, deep location, and contrast enhancement should raise suspicion for a
more atypical lesion [45].
Marginal excision is indicated in symptomatic lesions and is usually a curative
treatment with a low recurrence rate.
8.13 Soft Tissue Sarcoma
Soft tissue sarcomas are relatively uncommon, with fewer than 10% arising in the
foot and ankle [46]. Synovial sarcoma has been described as the most frequent his-
tology in many case series [46–48], followed by myxofibrosarcoma, clear cell sar-
coma, epithelioid sarcoma, and leiomyosarcoma.
Synovial sarcoma has a variable presentation but usually presents as a soft tissue
lump, which may or may not be painful, and is usually long-standing before starting
to grow significantly (Fig. 3). It can occur at any age and is equally distributed
Fig. 3 Lateral X-ray (Left) and sagittal T1 MRI reconstruction (right) from a 67-year-old male’s
left foot, who presented with a hind foot bone and soft tissue tumor. Percutaneous biopsy resulted
in a synovial sarcoma
Fig. 4 Same previous

case. Surgical specimen
after wide excision.
Pathology report revealed a
high-grade synovial
sarcoma with clear margins
in bone and soft tissue
Fig. 5 Same previous

case. Lateral X-ray of the
left foot after wide excision
and reconstruction with a
femoral head allograft,
with good results after
10 years
among males and females; however, most cases occur in adolescents or young
adults. Synovial sarcomas are among the soft tissue sarcomas considered to have a
relative predilection for lymphatic spread (compared to others).
Wide resection with limb salvage has become the treatment of choice for soft
tissue sarcoma of the extremities, even distally, without compromising oncologic
outcomes such as recurrence or survival [47] (Figs. 4 and 5). This has been achieved
on the foot and ankle region with a combination of adjuvant therapies such as radia-
tion therapy in selected cases and advances in plastic technique reconstruction with
free flap coverage. Radiation therapy has been used with caution in the distal
extremities, given the high rate of potential soft tissue complications. This being
said, the difficulties in achieving an adequate margin in this anatomic location might
outweigh the complications after radiation therapy, and therefore, postoperative or

preoperative radiation is usually indicated in high-grade tumors of significant size.
Overall, sarcomas of the distal extremities appear to have better survival than
sarcomas elsewhere. Cribb et al. [48] showed an overall mortality rate for distal
extremities sarcoma of 14%, while Zeytoonjian et al. [46] showed an overall mortal-
ity rate of 10% for foot and ankle sarcoma, against 26% for all sarcomas. This might
be explained by the relatively earlier presentation of these patients, given that foot
masses usually become symptomatic before tumors located elsewhere.
8.14 Bone Sarcoma
8.14.1 Osteosarcoma
Osteosarcoma (OS) is the most frequent primary bone malignancy, and it has a
bimodal occurrence with a peak incidence in the second decade. On the contrary,
osteosarcoma of the foot is very rare, with less than 1% of all osteosarcoma arising
in this location [49], and it is only slightly less uncommon in the distal tibia or fibula.
Radiographic appearance of a high-grade OS includes a lytic or sclerotic lesion
with an osseous matrix, ill-defined margins, and varying amounts of periosteal reac-
tion, including sunburst patterns or Codman’s triangle. On the other hand, low-
grade lesions might not show such a distinctive appearance. Because of the low
grade of suspicion for malignant bone sarcoma, delays in the treatment of osteosar-
comas of the foot and ankle region are often high.
Multi-agent chemotherapy and wide surgical excision are the mainstays of treat-
ment for these lesions, but the details of medical or surgical treatment are beyond
the scope of this review (Fig. 6).
8.14.2 Chondrosarcoma
Chondrosarcomas are (with Ewing’s sarcoma) the most frequent primary bone sar-
coma in the foot and ankle [50], but only 5% of these tumors occur in this region,
being the calcaneus the most common location. Chondrosarcomas characterize for
a peak incidence in middle age to older adults and are usually slow-growing
malignancies.
Differentiation of a benign cartilaginous neoplasm from a chondrosarcoma
remains a diagnostic challenge, even for experienced specialists [31]. Various radio-
graphic and clinical features can help orientate the diagnostic process, including the
patient’s age, pain during clinical examination, size of the lesion, cortical compro-
mise, soft tissue mass, and increased metabolic activity on bone scan or 18F-
FDG PET/CT.
The recommended treatment is wide resection for all high-grade chondrosar-
coma. Low-grade chondrosarcoma or atypical cartilaginous tumor could be treated
Fig. 6 7-year-old female patient with a left distal tibia high-grade conventional osteosarcoma.
(Left) Coronal T1 MRI reconstruction after neoadjuvant systemic chemotherapy. AP X-ray (cen-
ter) showing a bone transport technique as a reconstruction method after finishing her adjuvant
chemotherapy. (Right) Two years post-op AP X-ray, with a stable ankle arthrodesis and an intra-
medullary nail
with an aggressive curettage, plus adjuvant treatment and cement augmentation

with adequate recurrence rates and oncological outcomes [51, 52].
8.15 Ewing Sarcoma
Ewing sarcoma is a small round cell sarcoma showing a FET-ETS fusion gene
derived mostly from a translocation between the chromosomes 11 and 22 –
t(11;22)(q24;q12). It is more frequently located in the long bones, chest wall, and
spine; however, the foot and ankle region’s bones can be affected in up to 5% of
cases. The calcaneus, talus, and metatarsal are the most commonly involved
bones [50].
Classic radiographic appearance shows an ill-defined lesion with a permeated or
moth-eaten pattern of bone destruction. Soft tissue mass is usually present.
As with osteosarcoma, multi-agent chemotherapy and local ablation are the
treatment of choice. Surgical resection and radiation therapy are both forms of local
control, with surgical resection being the preferred one when surgery provides
acceptable morbidity and patient’s tolerance [53].
8.16 Metastatic Disease
Metastatic disease in the distal extremities is less frequent than in the proximal
appendicular or axial skeleton. Evans et al. [7] reported that only 0.5% of all osseous
metastases, from an extensive database including more than 2500 metastatic patients,
involved the foot. As described in other series for acrometastases [54], bronchogenic
cancer was the most common primary disease (27% of cases), while the rest were
secondary to other malignancies, including breast, prostate, kidney, and others.
Treatment for a symptomatic lesion should consider different factors such as the
histology of the primary lesion, expected survival, patient’s expectations and func-
tionality, and response to other nonsurgical therapies. This being said, most patients
can be managed locally with radiation therapy and marginal excision with or with-
out internal fixation and cementation in case of persistent symptoms or impending
fracture. Patients with oligometastatic disease and a primary histology that is non-
responsive to other therapies (such as renal or thyroid cancer) should be considered
for wide resection to avoid local progression and surgical failure.
9 Summary
Foot and ankle tumors are rare. Although most of the time they are benign, they
should not be underestimated, keeping in mind the basic oncological concepts of
initial management and referral to specialized centers in the case of malignant
lesions or locally aggressive behavior. Given this region’s unique anatomy, where
the soft tissue coverage is poor, the different pathologies’ treatments can be compli-
cated with difficult reconstructions and a higher percentage of complications.
References
1. Bos GD, Esther RJ, Woll TS. Foot tumors: diagnosis and treatment. Vol. 10, The Journal of the
American Academy of Orthopaedic Surgeons. 2002. p. 259–70.
2. Toepfer A, Harrasser N, Recker M, Lenze U, Pohlig F, Gerdesmeyer L, et al. Distribution
patterns of foot and ankle tumors: A university tumor institute experience. BMC Cancer.
2018;18(1).
3. Khan Z, Hussain S, Carter SR. Tumours of the foot and ankle. Vol. 25, Foot. 2015. p. 164–72.
4. Davis AM, Kandel RA, Wunder JS, Unger R, Meer J, O’Sullivan B, et al. The impact of
residual disease on local recurrence in patients treated by initial unplanned resection for soft
tissue sarcoma of the extremity. J Surg Oncol. 1997;66(2):81–7.
5. Chou LB, Ho YY, Malawer MM. Tumors of the foot and ankle: Experience with 153 cases.
Foot Ankle Int. 2009;30(9):836–41.
6. George A, Grimer R. Early symptoms of bone and soft tissue sarcomas: could they be diag-
nosed earlier? Ann R Coll Surg Engl. 2012;94:261.
7. Evans S, Ramasamy A, Jeys L, Grimer R. Delayed diagnosis in metastatic lesions of the foot.
Ann R Coll Surg Engl. 2014;96:536.
8. Grimer RJ, Briggs TWR. Earlier diagnosis of bone and soft-tissue tumors. J Bone Joint Surg
Br. 2010;92:1489.
9. Miller BJ. Use of Imaging Prior to Referral to a Musculoskeletal Oncologist. Vol. 27, Journal
of the American Academy of Orthopaedic Surgeons. 2019. p. E1001–8.
10. Nagano S, Yahiro Y, Yokouchi M, Setoguchi T, Ishidou Y, Sasaki H, et al. Doppler ultrasound
for diagnosis of soft tissue sarcoma: Efficacy of ultrasound-based screening score. Radiol
Oncol. 2015;49(2):135–40.
11. Harrison DJ, Parisi MT, Shulkin BL. The Role of 18F-FDG-PET/CT in Pediatric Sarcoma.
Vol. 47, Seminars in Nuclear Medicine. 2017. p. 229–41.
12. Wu Q, Yang R, Zhou F, Hu Y. Comparison of whole-body MRI and skeletal scintigraphy for
detection of bone metastatic tumors: A meta-analysis. Vol. 22, Surgical Oncology. 2013. p. 261–6.
13. Mankin HJ, Mankin CJ, Simon MA. The hazards of the biopsy, revisited: For the members of
the musculoskeletal tumor society. J Bone Jt Surg - Ser A. 1996;78(5):656–63.
14. De Marchi A, Brach Del Prever EM, Linari A, Pozza S, Verga L, Albertini U, et al. Accuracy
of core-needle biopsy after contrast-enhanced ultrasound in soft-tissue tumours. Eur Radiol.
2010;20(11):2740–8.
15. Shin HJ, Amaral JG, Armstrong D, Chait PG, Temple MJ, John P, et al. Image-guided percu-
taneous biopsy of musculoskeletal lesions in children. Pediatr Radiol. 2007;37(4):362–9.
16. Ogilvie CM, Torbert JT, Finstein JL, Fox EJ, Lackman RD. Clinical utility of percutaneous
biopsies of musculoskeletal tumors. Clin Orthop Relat Res. 2006 Sep;450:95-100.
17. Biscaglia R, Bacchini P, Bertoni F. Giant cell tumor of the bones of the hand and foot. Cancer.
2000;88(9):2022–32.
18. About the Foot and Ankle. Vol. 56, Radiologic Clinics of North America. 2018. p. 917–34.
19. Osman W, Jerbi M, Ben Abdelkrim S, Maaref K, Ben Maitigue M, Ben Ayèche ML. Giant
cell tumor of the lower end of tibia. Curettage and cement reconstruction. Foot Ankle Surg.
2015;21(1):e16–20.
20. Campanacci M, Baldini N, Boriani S, Sudanese A. Giant-cell tumor of bone. J Bone Jt Surg -
Ser A. 1987;69(1):106–14.
21. Rajani R, Schaefer L, Scarborough MT, Gibbs CP. Giant Cell Tumors of the Foot and Ankle
Bones: High Recurrence Rates After Surgical Treatment. J Foot Ankle Surg. 2015;54(6):1141–5.
22. Fink BR, Temple HT, Chiricosta FM, Mizel MS, Murphey MD. Chondroblastoma of the foot.
Foot Ankle Int. 1997;18(4):236–42.
23. Angelini A, Arguedas F, Varela A, Ruggieri P. Chondroblastoma of the Foot: 40 Cases From a
Single Institution. J Foot Ankle Surg. 2018;57(6):1105–9.
24. Reda B. Cystic bone tumors of the foot and ankle. Vol. 117, Journal of Surgical Oncology.
2018. p. 1786–98.
25. Ramappa AJ, Lee FYI, Tang P, Carlson JR, Gebhardt MC, Mankin HJ. Chondroblastoma of
bone. J Bone Jt Surg - Ser A. 2000;82(8):1140–5.
26. Oliveira AM, Chou MM. USP6-induced neoplasms: The biologic spectrum of aneurysmal
bone cyst and nodular fasciitis. Hum Pathol. 2014;45(1):1–11.
27. Park HY, Yang SK, Sheppard WL, Hegde V, Zoller SD, Nelson SD, et al. Current management of
aneurysmal bone cysts. Vol. 9, Current Reviews in Musculoskeletal Medicine. 2016. p. 435–44.
28. Chowdhry M, Chandrasekar CR, Mohammed R, Grimer RJ. Curettage of aneurysmal bone
cysts of the feet. Foot Ankle Int. 2010;31(2):131–5.
29. Rhee Y, Lee JD, Shin KH, Lee HC, Huh KB, Lim SK. Oncogenic osteomalacia associated
with mesenchymal tumour detected by indium-111 octreotide scintigraphy. Clin Endocrinol
(Oxf). 2001 Apr;54(4):551–4.
30. Chun KA, Stephanie S, Choi JY, Nam JH, Suh JS. Enchondroma of the Foot. J Foot Ankle
Surg. 2015;54(5):836–9.
31. Zamora T, Urrutia J, Schweitzer D, Amenabar PP, Botello E. Do Orthopaedic Oncologists
Agree on the Diagnosis and Treatment of Cartilage Tumors of the Appendicular Skeleton?
Clin Orthop Relat Res. 2017;475(9):2176–86.
32. Kitsoulis P, Galani V, Stefanaki K, Paraskevas G, Karatzias G, Agnantis NJ, et al.
Osteochondromas: Review of the clinical, radiological and pathological features. Vol. 22, In
Vivo. 2008. p. 633–46.
33. Bernard SA, Murphey MD, Flemming DJ, Kransdorf MJ. Improved differentiation of benign
osteochondromas from secondary chondrosarcomas with standardized measurement of carti-
lage cap at CT and MR imaging. Radiology. 2010;255(3):857–65.
34. Schulze S C, Valenzuela G G, Zamora H T. Manejo expectante de osteocondroma solitario
interóseo de la tibia distal: reporte de un caso y revisión de la literatura. Rev Chil Ortop y
Traumatol. 2018;59(03):100–4.
35. Levy DM, Gross CE, Garras DN. Treatment of Unicameral Bone Cysts of the Calcaneus: A
Systematic Review. Vol. 54, Journal of Foot and Ankle Surgery. 2015. p. 652–6.
36. Aumar DK, Dadjo YBA, Chagar B. Intraosseous Lipoma of the Calcaneus: Report of a Case
and Review of the Literature. J Foot Ankle Surg. 2013;52(3):360–3.
37. Chow LTC, Lee KC. Intraosseous lipoma: A clinicopathologic study of nine cases. Am J Surg
Pathol. 1992;16(4):401–10.
38. Narang S, Gangopadhyay M. Calcaneal intraosseous lipoma: A case report and review of the
literature. J Foot Ankle Surg. 2011;50(2):216–20.
39. Gouin F, Noailles T. Localized and diffuse forms of tenosynovial giant cell tumor (for-
merly giant cell tumor of the tendon sheath and pigmented villonodular synovitis). Vol. 103,
Orthopaedics and Traumatology: Surgery and Research. 2017. p. S91–7.
40. Noailles T, Brulefert K, Briand S, Longis PM, Andrieu K, Chalopin A, et al. Giant cell tumor
of tendon sheath: Open surgery or arthroscopic synovectomy? A systematic review of the
literature. Vol. 103, Orthopaedics and Traumatology: Surgery and Research. 2017. p. 809–14.
41. Mastboom MJL, Palmerini E, Verspoor FGM, Rueten-Budde AJ, Stacchiotti S, Staals EL,
et al. Surgical outcomes of patients with diffuse-type tenosynovial giant-cell tumours: an inter-
national, retrospective, cohort study. Lancet Oncol. 2019;20(6):877–86.
42. Staals EL, Ferrari S, Donati DM, Palmerini E. Diffuse-type tenosynovial giant cell tumour:
Current treatment concepts and future perspectives. Vol. 63, European Journal of Cancer.
2016. p. 34–40.
43. Carroll P, Henshaw RM, Garwood C, Raspovic K, Kumar D. Plantar Fibromatosis:
Pathophysiology, Surgical and Nonsurgical Therapies: An Evidence-Based Review. Vol. 11,
Foot and Ankle Specialist. 2018. p. 168–76.
44. Aluisio F V., Mair SD, Hall RL. Plantar fibromatosis: treatment of primary and recurrent
lesions and factors associated with recurrence. Foot Ankle Int. 1996 Nov;17(11):672-8.
45. Knebel C, Neumann J, Schwaiger BJ, Karampinos DC, Pfeiffer D, Specht K, et al.
Differentiating atypical lipomatous tumors from lipomas with magnetic resonance imaging: A
comparison with MDM2 gene amplification status. BMC Cancer. 2019;19(1).
46. Zeytoonjian T, Mankin HJ, Gebhardt MC, Hornicek FJ. Distal lower extremity sarcomas:
Frequency of occurrence and patient survival rate. Foot Ankle Int. 2004;25(5):325–30.
47. Branford-White H, Giele H, Critchley P, Cogswell L, Gibbons CLM, Dean BJF, et al.
Management and outcome of acral soft-tissue sarcomas. Bone Jt J. 2018;100B(11):1518–23.
48. Cribb GL, Loo SCS, Dickinson I. Limb salvage for soft-tissue sarcomas of the foot and ankle.
J Bone Jt Surg - Ser B. 2010;92(3):424–9.
49. Blscaglia R, Gasbarrini A, Böhling T, Bacchini P, Bertoni F, Picci P. Osteosarcoma of the bones
of the foot-an easily misdiagnosed malignant tumor. Mayo Clin Proc. 1998;73(9):842–7.
50. Mascard E, Gaspar N, Brugières L, Glorion C, Pannier S, Gomez-Brouchet A. Malignant
tumours of the foot and ankle. EFORT Open Rev. 2017;2(5):261–71.
51. Verdegaal SHM, Brouwers HFG, Van Zwet EW, Hogendoorn PCW, Taminiau AHM. Low-
grade chondrosarcoma of long bones treated with intralesional curettage followed by applica-
tion of phenol, ethanol, and bone-grafting. J Bone Jt Surg - Ser A. 2012;94(13):1201–7.
52. Schreuder HWB, Pruszczynski M, Veth RPH, Lemmens JAM. Treatment of benign and low-
grade malignant intramedullary chondroid tumours with curettage and cryosurgery. Eur J Surg
Oncol. 1998;24(2):120–6.
53. DuBois SG, Krailo MD, Gebhardt MC, Donaldson SS, Marcus KJ, Dormans J, et al.
Comparative evaluation of local control strategies in localized Ewing sarcoma of bone: A
report from the Children’s Oncology Group. Cancer. 2015;121(3):467–75.
54. Chung TS. Metastatic malignancy to the bones of the hand. J Surg Oncol. 1983;24(2):99–102.
Care and Management of Surgical
Wounds, Wounds Dehiscence, and Scars
Leonardo Parada and Günther Mangelsdorff
1 Introduction
Although the skin is not the key issue in foot and ankle surgery, wound healing has
a fundamental role for a successful outcome.
A wound that does not close properly can lead to severe problems with bone and/
or osteosynthesis hardware exposure, leading to known consequences such as infec-
tions, delayed consolidation, and the need for reoperations, among others.
A defective scar, from either a functional or an aesthetic point of view, could be
a nightmare for the surgeon. Even though the main problem may be resolved, a scar
that is annoying for the patient could be related to multiple consultations and dis-
crepancies with the result obtained.
Bearing these points in mind, it is essential to take serious precautions and man-
age surgical wounds with care, trying to procure the most effective results in the
context of global treatments.
Anatomical considerations and the considerable mobility exerted at the ankle
level make the management of wounds in this body segment even more challenging.
A separate topic corresponds to traumatic wounds that add even more significant
difficulties and usually require a plastic surgery specialist’s assistance to achieve a
suitable improvement.
L. Parada (*)
Department of Plastic Surgery and Burns, Hospital del Trabajador, Santiago, Chile
Department of Plastic Surgery, Clínica Las Condes, Santiago, Chile
G. Mangelsdorff
Department of Plastic Surgery and Burns, Hospital del Trabajador, Santiago, Chile
Department of Plastic Surgery, Clínica Santa Maria, Santiago, Chile

Switzerland AG 2022
90 L. Parada and G. Mangelsdorff
In this chapter, we will review practical recommendations to adequately treat

surgical wounds performed during foot and ankle surgery, both in elective and
trauma surgery, as well as advices to follow when complications such as dehis-
cences and pathological scars occur.
2 Relevant Anatomy
The lower limbs, especially the foot and ankle, are functionally very relevant and
highly demanded areas for developing the human standing characteristic. By being
upright, they support all body weight, generally for long periods, and, furthermore,
are responsible for producing our displacements.
Despite this, it could be stated that the ankle and the foot are relatively unprotected
areas highly exposed to trauma. The skin on the distal third of the leg and around the
ankle is thin, with a little subcutaneous tissue layer; moreover, essential structures
like bones and tendons are poorly covered and can be easily exposed in trauma.
Conversely, the glabrous skin of the sole possesses completely different charac-
teristics, being thick and firm, designed to resist weight. Unfortunately, its charac-
teristics are unique, and there are no similar structures that could replace it.
2.1 Irrigation
As in all the functioning of the human body and each surgical intervention, the
blood supply is central for a favorable result.
The foot and ankle are supplied by arteries dependent on three main axes, the
anterior tibial, posterior tibial, and peroneal arteries, each of which feeds specific
segments interconnected by vessels of a smaller caliber.
To better understand how a body segment is irrigated, it is essential to keep in
mind the concept of angiosome described by Ian Taylor [1]. An angiosome corre-
sponds to a three-dimensional anatomical unit of tissue supplied by a source artery.
In his experimental study, Taylor maps the whole body describing 40 territories or
angiosomes, of which 6 correspond to the foot and ankle. These angiosomes are
unrigid structures intercommunicated between adjacent angiosomes through a net-
work of so-called shock vessels. Specifically, at the ankle and foot level, six angio-
somes are described (Fig. 1).
• The posterior tibial artery originates three angiosomes that supply the medial
ankle and the sole through the calcaneal branch (heel), the medial plantar artery
(arch of the foot), and the lateral plantar artery (lateral midfoot and forefoot).
• The peroneal artery is the source of two angiosomes that supply the anterolateral
ankle and the lateral hindfoot, thanks to the anterior perforating branch (superior
anterolateral ankle) and the calcaneal branch (plantar heel).
Care and Management of Surgical Wounds, Wounds Dehiscence, and Scars 91
Fig. 1 A schematic representation of the angiosomes at the level of foot and ankle
• An angiosome that supplies the anterior ankle depends on the anterior tibial
artery and then like the dorsal artery of the foot that feeds the entire foot
dorsum [2].
Knowing these angiosomes allows for the correct planning of the location of the
surgical incisions. The usual designs consider these angiosomes, reducing the risk
of complications. In the case of traumatized feet or with chronic pathologies, such
as diabetic foot [3], that can alter the vasculature, an easy-to-use tool is mapping
these arteries with a portable Doppler pencil, noting alterations to the normal anat-
omy and allowing adjustment of surgical plans [2].
3 Wound Healing Process
To understand how to manage a wound, it is a prerequisite to have notions about the

normal healing process and the factors that can alter it.
Every time a wound occurs, our body triggers a series of processes that lead to
tissue repair and scar formation. This process has been divided into stages that help
understand it better, yet these stages are intertwined in a dynamic process [4, 5].
3.1 Phases of Wound Healing Process
• Hemostasis: While it is not considered a stage in the healing process, it is the first
to happen after any injury. Initially, vasoconstriction occurs, and the intrinsic and
extrinsic coagulation pathways are triggered. This process culminating in the
production of a clot acts as a bridge to the inflammatory phase.
• Inflammatory phase: Immediately after the injury, an inflammatory process
begins cleaning the wound of microorganisms and foreign bodies. After the ini-
tial vasoconstriction occurs vasodilation, an increase in the blood vessels perme-
ability, and an increased arrival of lymphocytes and macrophages releasing
cytokines and other biologically active agents.
• Proliferative phase: From the second day and approximately until the third week,
fibroblasts represent the predominant cells in the wound, producing collagen
deposits, granulatory tissue formation, angiogenesis, and finally
epithelialization.
• Maturation/remodeling phase: Finally, the repair process can be extended for up
to 1 or even 2 years. Initially, the scar is mostly composed of type III collagen,
achieving approximately 20% of healthy skin strength. This collagen predomi-
nantly changes to type I through remodeling, reaching 80% of the original
strength after 2–3 months. Later the scar begins to contract and never reaches the
initial strength of healthy tissue.
3.2 Factors Affecting Wound Healing
From a practical point of view, understanding the factors that can alter the wound
healing process is more important than understanding the physiological process of
wound repairs. Keeping these factors in mind is essential to avoid problems later.
• Oxygen: The cellular growth proper to the healing process is dependent on oxy-
gen, and adequate arterial oxygen pressure and tissue perfusion are fundamental
factors for tissue repair.
• Age: Age, by itself, affects healing. At an older age, the stages described previ-
ously begin late, occur more slowly, and generally do not obtain the same results
as at younger ages.
• Nutrition: Healing requires an increased production of cells and their products,
so a state of malnutrition will negatively affect the entire process. On the other
hand, poor nutrition due to excess has also shown an increase in complications
such as infections and dehiscences.
Ideally, a patient who will undergo elective surgery should arrive in good
nutritional condition at the surgery. In trauma cases, the nutritional status should
be evaluated, and the necessary corrections and supplements should be
adjusted early.
• Tobacco: The deleterious effects of tobacco are multifactorial. Nicotine is a vaso-

constrictor that decreases cell proliferation; carbon monoxide decreases oxygen
transport capacity; and tobacco also increases platelet aggregation and blood vis-
cosity. These and other facts explain why a single cigarette generates cutaneous
vasoconstriction for about 90 minutes.
The recommendation for elective surgeries is to stop smoking at least 4 weeks
before and 4 weeks after surgery.
• Infection: Infection prolongs the inflammatory phase, interfering with later
phases, especially collagen deposition, epithelialization, and contraction. In
addition, the granulatory tissue growing under local infection is of lower quality,
therefore being more abundant, edematous, hemorrhagic, and fragile, not allow-
ing an adequate closure of the wounds.
• In chronic wounds, attention should be paid to biofilm, although it does not
imply an active infection, alters, and inhibits wounds healing. Actions must be
taken to eliminate it.
• Radiation: Apart from the beneficial effects sought with radiotherapy, it also
causes deleterious effects on the tissues, altering the DNA, and reduces the irri-
gation, the deposit of collagens, and the tensile strength obtained. Unfortunately,
irradiated skin is chronically damaged, forever affecting the wound healing
processes.
• Chronic diseases: A series of chronic diseases alter the overall state of health and
wound healing. The classic example is diabetes mellitus, but others such as obe-
sity, COPD, cancer, liver and kidney failure, connective tissue diseases, and
venous and arterial failure, among others, are involved in alterations to the heal-
ing process and should be compensated as much as possible prior to any elective
surgery.
4 Elective Surgical Wounds
As previously mentioned, the anatomical characteristics at the foot and ankle require
the correct management of surgical incisions to achieve the best result.
4.1 Location of Incisions
The approach to be used will remain a fundamental matter for the orthopedic sur-
geon, who will consider anatomical factors, such as irrigation of the area and the
need for adequate access to the element to be intervened.
When deciding on these approaches, it is crucial always to be concerned about
the possible complications in the future and the soft tissue deficit existing at the
time or that could develop in the expected evolution of the wound, paying
particular attention to signs of skin suffering. In these cases, being aware of the
situation and the options to reconstruct later will always guide a fair decision-
making process.
In complex cases, it is always advisable to discuss the case with the plastic sur-
gery team if, in the future, the patient requires their assistance to reconstruct a skin
coverage deficit.
4.2 Incisions
In general, the incision should be the smallest to achieve adequate exposure,

limiting the scars’ extension. However, it is inadvisable to save on the incision
extension at the cost of having poor access and hindering subsequent repair and
results.
The skin must be handled with care avoiding unnecessary traumatization, han-
dling the skin with grasps pressing the dermis, and leaving the epidermis free is a
way to protect it, especially with delicate skin like those of aged people. Using
hooks to catch the skin, instead of grasps, is also an excellent alternative.
The use of skin retractors is recommended to avoid damage to the soft tissues.
These could be self-retaining retractors or individual elastic retractors (Lone Star™
Cooper Surgical™/CooperSurgical Inc., USA), which, given their versatility, can be
adjusted to any size and wound position.
The incision closure is presumably the most critical surgeon-dependent aspect to
achieve the best possible scar, this means making it as unnoticeable as possible, not
depressed, not raised, and similar in color to the surrounding skin [6]. With this, the
core objective is to close in layers and avoid, whenever possible, a closure only in a
single cutaneous plane. When facing deep planes, dead spaces are closed, avoiding
scar depression and reducing skin tension. Ideally, before placing the last suture line
over the skin, the wound margins should be seen practically closed, leaving minimal
tension on this layer (Fig. 2).
Fig. 2 Skin suture: before

performing the last suture
plane, for example, with a
running subcuticular
suture, the wound edges
have to be almost
completely opposite
without tension
4.3 Suture Materials
Absorbable suture materials are preferably used to target muscles, fascia, and sub-
cutaneous tissues. Our preferred material is polydioxanone (PDS™, Ethicon Inc.,
Somerville, NJ, USA), a strand of easy maneuverability that, being monofilament,
reduces trauma to tissues and risk of infection. Also, its durability profile allows
maintaining extended support while healing occurs.
A valid and high-quality alternative corresponds to polyglactin (Vicryl™,
Ethicon), probably the most used suture for deep planes. In very thin patients and
incisions over areas with scarce subcutaneous tissue between the skin and the
bone, it can be especially useful, since by being more flexible, it would be less
noticeable by patients. The use of a colorless strand prevents it from showing
through the skin.
For superficial layers, a continuous subdermal suture is recommended, avoiding
the excessive accumulation of knots, with 3–0 or 4–0 material depending on the
patient’s wound location and characteristics.
Finally, for the last plane, non-absorbable materials should be used that causes
the least possible inflammatory reaction. Nylon (Ethilon™, Ethicon) is usually the
first alternative, and in general, a 4–0 size should be adequate. However, in less
demanding areas such as the foot dorsum, smaller diameter sutures could be used.
On the contrary, in greater demand areas such as the sole or closed with a certain
degree of tension, larger sutures should be used. An alternative is polypropylene
(Prolene™, Ethicon), which advantage is having a higher tensile strength, being
useful when approaching tissues with some tension degree.
4.4 Suturing Technique
Before closing any wound, hemostasis should be appropriately checked in order to

stop any active bleeding. It is ideal to coagulate promptly only at the bleeding sites
and not aimlessly reducing the tissues’ irrigation, with the risks that it entails in
terms of infections and dehiscences.
For deep layers, inverted stitches are used in which the needle enters and exits
through a deep plane, leaving the knots inwards, which reduce the chances of
extrusion or even being felt by the patient, especially at the ankle in the case of
very thin patients. The steps to perform an inverted suture are demonstrated in
Fig. 3. When there is greater tension or risk of infection, it is advisable to use
simple interrupted stitches. Once the tension has been decreased, a continuous
suture could be used with the advantage of reducing time and resulting in
fewer knots.
There are different options for suturing skin, always remembering that wound
edges must be everted. The first corresponds to the simple interrupted stitches whose
advantage lies in its ease of execution, ability to adapt the tissues’ margins, and
a b
c d
Fig. 3 Inverted stitches are used to suture deep planes. (a) The needle penetrates from a deep
plane; (b) at the opposite edge, it enters from a superficial plane to a deep one; (c) edges are
approaching; (d) the knot is hidden inward
speed. An excellent option is to perform an intradermal suture in wounds well faced

in their deep layers, which generates a more aesthetic linear scar. It could be done
with absorbable material avoiding the need to remove stitches or with a non-
absorbable suture, in which case it can be removed deferred. It is important regard-
ing long incisions, to leave intermediate exits of the strand, in order to be able to
remove it easily.
In the case of wounds closed at higher tension, it is ideal to use a stitch that pro-
vides greater firmness and a coapted surface. In this case, vertical or horizontal
mattress points are the alternative of choice.
In the situation where one of the edges of the wound has borderline irrigation, it
is advisable to use a less ischemic technique, such as Gillies’ stitches in which the
suture enters and exits the surface on only one side and passes through the other
edge only by dermis (as in an intradermal suture). This same point is recommended
to close flap wounds.
Regarding surgical staples, no evidence shows the superiority of one method
over another [7–9] except for faster with stapling [10] and a trend towards better
aesthetics with suturing [11]. In our practice, the use of staples is unusual, and we
recommend always using them after correctly closing deep planes and removing
them promptly, no later than 10 days, to avoid excess marks on the skin.
4.5 Wound Dressing
Once the suture is finished, the skin must be protected. The ideal dressing generates
an environment with controlled humidity, which prevents desiccation and reduces
edema, with an easy application and removal, painless, and inexpensive.
In simple wounds that do not have a higher risk of complication, our recommen-
dation is to apply a skin protector and then cover with paper tape (Micropore™ 3 M,
Ltd., USA), applying at least four tape layers.
In the case of bruised or traumatized skin, it is important to use a product for
advanced wound management. At this point, the most used primary dressing is a
tulle gras, applied to the wound and covered with a secondary dressing. The telfa
has similar characteristics.
For highly exudative wounds, alginate or foam is the most suitable alternative.
In general, wound dressings should be changed every 3 to 5 days, depending on
the product used. When healthy skin has been noticed, it can continue using
paper tape.
Regarding the right time to wet a wound, we recommend not doing it for the first
48 to 72 hours, and then, for example, if using paper tape, it is possible to wet it with
extreme caution in order to completely dry it later. Other dressings require keeping
it dry until removal.
Other essential precautions are respecting rest, keeping the leg up, and evaluating
the use of compression bandages [12], all measures that reduce edema and its nega-
tive consequences.
In the same way, it is crucial to maintain adequate glycemic and nutritional man-
agement and suspend the use of tobacco.
4.6 Incisional Negative Pressure Wound Therapy
Negative pressure wound therapy (NPWT) since its introduction in 1997 [13] has
been a significant contribution to wound management. Traditionally it has been
used in open wounds, being widely accepted as a bridging or even definitive therapy.
Its applications have gradually expanded, including its use in closed surgical
wounds, known as incisional negative pressure wound therapy (iNPWT) described
by Gomoll et al. in 2006 [14] precisely in patients undergoing ankle and foot
surgery.
iNPWT refers to the application over closed wounds, acting as a dressing that
transmits pressure on the suture line.
The advantages it provides are fundamentally an improvement in the microcircu-
lation of the wound, a decrease in tension on the wound edges, a decrease in edema,
and a more effective obliteration of dead spaces [15].
Its use is increasingly popular, thanks to a decrease in dehiscences and wounds

infections [16–19]. Our group demonstrated a decrease in complications in the
donor area of the anterolateral thigh flap, allowing large defects to be closed with
minimal consequences [15]; however, systematic reviews have not been able to
strongly demonstrate a global utility of this therapy nor its clear cost-effectiveness
[20, 21].
We recommend the use of iNPWT in any high-risk injury:
• Closed with a certain degree of tension.
• Performed on traumatized tissues.
• Patients with risk factors for dehiscence (obese and smokers, among others).
• Presence of significant edema.
• Arthroplasty, considering that the consequences of a wound infection are so dire
that any preventive measures seem reasonable.
Its application is straightforward. There are ready-to-use devices such as the
VAC Prevena™ (KCI, San Antonio, Texas, USA). If this type of device is not avail-
able, it can be easily made with the material of a standard NPWT. Once the wound
is closed, both sides of the lesion are covered with a transparent dressing, leaving
only the suture line uncovered, and over this, the standard NPWT foam is placed
covering the sutured area and then is connected to the suction motor (Fig. 4). In
general, a pressure of −125 mm Hg continuously is the most suitable.
a b
Fig. 4 An incisional negative pressure wound therapy (NPWT) can be assembled using a tradi-
tional one. (a) Start protecting the edges of the wound with a transparent dressing, (b) cover with
foam over protected areas. In this case, a traditional NPWT is used to cover an open wound and an
incisional segment over a closed one
Its removal is recommended between 5 and 7 days later, being earlier in the case
of doubts about infection or other complications. A second cycle can then be applied
if the wound is not yet completely closed or if there are reasonable doubts of subse-
quent favorable evolution. If the wound is seen to be in good condition, it will be
possible to continue with the usual care.
4.7 Suture Removal
A frequent question for patients, and surgeons, is when to remove sutures.

The first thing to point out is that there is no standard recipe applicable to every
case, but rather, it will be customized according to the characteristics of the injury,
the quality of the tissues, and the technique used.
In general, at the ankle, they should remain in place for 10 to 14 days for
young patients and up to 21 days for older patients or in case of high-risk wounds
(fracture cases, limb with more edema, greater risk of dehiscence). On the dor-
sum, they could be removed between 7 and 10 days. On the contrary, those
located on the sole should be removed deferred, especially if the patient has the
authorization to support. In these circumstances we recommend not to do so,
before 21 days.
A suture that remains on the wound for a long time will leave more imprints,
especially marking each site where the suture passes through the skin. If a useful,
aesthetically result is sought, the sutures should be removed early; however, it
should never be done before ensuring that the wound will not become dehiscent. A
good alternative is to make partial removals, which reduce the areas where there
could be marks of the suture material in the scar but maintains adequate support.
After removal, reinforce the wound with paper tape or adhesive skin suture (Steri-
Strip™, 3 M).
4.8 Wound and Scar Care Management
Once the wound is closed and the stitches have been removed, it is still essential to
continue with the scar’s management in order to obtain the best possible result.
In this sense, there are three significant actions to develop:
• Adequate moistening, keeping the scar moisturized properly, promotes better
healing and a better aesthetic result. Simply use any moisturizer to achieve this
effect, to be used two to three times a day.
• Compression: It has been shown that a scar’s compression improves their quality
and prevents the appearance of complications such as hypertrophic scars. In case
of a normal scar, it is enough to cover it with a few layers of paper tape [22, 23]
that needs to be changed each 3 to 4 days.
• Of better quality is the use of the silicone sheet, which, due to its characteristics,
has been demonstrated as an excellent tool for the improvement of the quality of
scars [6]. It has the advantage of being self-adhesive and transparent.
• In both cases, we recommend its use for 2 to 3 months after surgery.
• Sun protection: One key point when looking for the least noticeable scar possible
is to protect it adequately from the sun. During all wound healing process, the
skin is much more vulnerable to the sun’s damaging effects and may become
hyperpigmented. We recommend the daily use of sunscreen, ideally SPF 50,
reapplying to the scar, at least three times a day and ideally every 2–3 hours if are
extensively exposed to the sun.
In the circumstance of presenting a pathological scar, this care should be rein-
forced, which will be reviewed later in this chapter.
5 Traumatic Wounds
A particular situation occurs with injuries originating after trauma. Open fractures,
ulcers, and degloving are common in this body segment. Any soft tissue injury
could complicate the orthopedic surgeons work and could be a risk factor for future
complications.
In general terms, the treatment is similar and follows the same rules previously
presented, with some necessary adaptations to remember:
• They should undergo surgical debridement, removing all necrotic tissue. If there
are tissues with borderline vitality, it is appropriate to keep it until the following
intervention.
• The ideal surgical incision could be located over injured areas and therefore not
available, needing to adjust in an individual approach.
• Avoid using braided sutures.
• Perform advanced wound care that protects and allows damaged skin to recover.
5.1 I Cannot Close the Wound
Unfortunately, a wholly unpleasant and not uncommon circumstance occurs when

the surgeon has finished performing the central actions of the surgery and proceeds
to close the wound, which is not possible or has to do it with extreme tension or with
injured tissues.
Faced with this situation, we recommend three actions:
• Try closing the wound with few single total stitches, separated and away from
the edges. Doing this makes possible to approximate the wound margins gener-
ously or even close it completely, avoiding future surgeries. An example is pre-

sented in Fig. 5.
• If there are not enough tissues to close, the ideal method is to try to cope the tis-
sues as much as possible and not leave them in a relaxed position, as they will
quickly retract and will be unavailable for future closures leaving a larger defect
and requiring the use of other reconstructive techniques.
• Ultimately, we recommend using NPWT or iNPWT, which helps to improve the
condition of the tissues, and in a future intervention, try a definitive closure or
request the plastic surgeon’s assistance for this.
In the case of having a soft tissue deficit and especially if it involves exposure of
noble structures or any hardware, the limb’s reconstruction should be performed as
early as possible [24]. Management in conjunction with the plastic surgeon is an
excellent alternative. If this is not possible, the NPWT gives a time window to
schedule the reconstruction.
A practical recommendation is always to take pictures of the injury to discuss the
case with the plastic surgeon and have reconstructive options planned for the next
intervention.
a b
Fig. 5 (a) Due to an accident, the patient develops an eschar on the lateral aspect of the foot. (b)
After resection, it is closed advancing skin flaps on both sides of the wound that are sutured in a
single plane with simple interrupted stitches. If a complete closure is not achieved, at least the skin
edges are approximated, preventing their retraction
6 Wound Dehiscence
6.1 Definition and Classification
Wound dehiscence corresponds to the partial or total disruption or opening of a

previously closed wound. A complication, with an incidence in the foot and ankle
surgery difficult to estimate, both due to a lack of consensus in defining dehiscence
and because of communications that use slightly broader expressions such as prob-
lems of the wound. Considering these factors, reports show an overall incidence of
4–6% [25], between 8.6% and 16.5% in fractures [18] up to values as high as 28%
in ankle arthroplasty [26].
To standardize concepts in 2018, the World Union of Wound Healing Societies
generates a consensus that defines dehiscence as the separation of the margins of a
closed surgical incision that involves the skin with or without exposure or protru-
sion of underlying tissue, organs, or implants. It can occur at single or multiple
regions or involve the entire length of the incision and one or all tissue layers [27].
In the same consensus, they adapt the Sandy Grading System for Surgical Wound
Dehiscence Classification [28], generating a new classification that allows an effi-
cient systematization and the treatment options suggested, which graduates surgical
wound dehiscences into four levels according to the depth of affected tissues:
• Grade 1: Epidermis only.
• Grade 2: Exposed subcutaneous tissue.
• Grade 3: Exposed subcutaneous tissue and fascia.
• Grade 4: With exposure of organs, viscera, bones, or implants.
• A: In addition to each of these degrees, add the presence or absence of signs and
symptoms of wound infection.
6.2 Risk Factors
There are several risk factors for the occurrence of operative wound dehiscence.
These factors can be:
• Related to the patient and modifiable: Obesity considering that the higher the
BMI, the greater the risk, malnutrition, especially protein deficit, anemia, diabe-
tes mellitus, smoking, and alcohol consumption.
• Related to the patient and difficulty or non-modifiable: Age over 65 years, emer-
gency surgery, and other comorbidities such as cancer, liver failure, kidney fail-
ure, use of steroids, and prior irradiation.
• Intraoperative: Prolonged duration of surgery, perioperative hypothermia, inad-
equate closure technique, non-obliteration of dead spaces, tension closure, and
wide dissections.
• Postoperative: Wound infection, premature removal of sutures, edema, failure to
rest, and other complications such as hematomas and seromas.
Managing these risk factors is essential to avoid complications. Optimizing the

patient’s global state prior to elective surgery, especially by stopping tobacco con-
sumption 1 month prior, making nutritional corrections, and maintaining controlled
comorbidities are unavoidable actions.
Similarly, after surgery, adequate care must be provided, generating a good fol-
low-up plan, especially in patients undergoing outpatient surgeries, reinforcing the
importance of complying with indications such as rest and wound care.
6.3 Treatment
If despite taking all possible safeguards a dehiscence occurs, which unfortunately is

not unusual in ankle and foot surgery, an adequate treatment can help resolve it
successfully.
Its management will depend on the extension and mainly on the depth of this and
the presence or not of wound infection.
We will systematize its management in the following aspects:
6.3.1 Prevention
Already stated in the risk factors section, we cannot fail to reinforce these measures,
which are by far the most important.
In addition to stopping tobacco consumption, optimizing nutritional status, and
compensating for any chronic disease, there are some specific actions to be carried
out by the medical team:
• Closure technique appropriate to the type of surgery and patient’s characteristic.
It is important to remember the closure by layers and avoid prolonged surger-
ies [29].
• Wound dressings: keep the wound closed, with dressings that maintain a con-
trolled moist environment. In the case of traumatic wounds, they should also
allow adequate recovery of the epidermis.
• Do not remove the dressing in the first 48 to 72 hours, at which time a re-
epidermization should have already occurred, thus reducing the risk of wound
infection.
• Use of iNPWT: its use on closed wounds is gradually gaining more acceptance;
the cause has been shown to reduce the risk of infection and complications, like
dehiscences. Its use is recommended in wounds or patients at high risk for dehis-
cence [18] [16].
• Prevention of edema: during the postoperative period through compression ban-
dages [7] and the limb’s elevation.
• Rest/immobilization: reinforcing the previous point, it is necessary to maintain
rest and eventually use immobilizers to avoid excessive movements subjecting
the wound to excessive stress.
6.3.2 Infection
In the case of wounds with local signs of infection, limited to the wound, the main
treatment tool corresponds to advanced dressings adapted to each wound’s needs.
The use of topical antimicrobial and antibiotic dressings for a limited period should
also be added [27].
In the case of systemic signs of infection or local signs that extend beyond the
wound’s limits, systemic antibiotic therapy is indicated.
Antibiotic therapy should be adjusted to the local epidemiological reality and, if
possible, guided by cultures, ideally of tissues, since those with superficial exudate
usually show cutaneous flora and do not represent accurately soft tissue infec-
tion status.
6.3.3 Superficial Dehiscence
Superficial dehiscences, grades 1 and 2, that is, that exposes even the subcutaneous
tissue, can be effectively treated with advanced dressings.
In most cases, products will be used to control the exudate and debride while
there are detritus and then continue with another dressing type that allows better
granulatory tissue growth.
In early dehiscence, generally linked to an inadequate closure technique, a pri-
mary delayed closure can be performed, as in totally clean wounds without other
associated complications. In all other circumstances, which covers most cases, a
closure by secondary intention is chosen.
6.3.4 Deep Dehiscence
For dehiscences of grades 3 and 4, that is, with exposure of fascia and other ele-
ments such as viscera, bones, and implants, in addition to what is exposed for those
more superficial parts, management is usually more aggressive and involves surger-
ies. Surgical toilets will be performed, removing all the devitalized tissue present.
The ideal situation in these circumstances is, when the wound is clean and without
other complications, to try a new closure by re-advancing the skin flaps and apply-
ing iNPWT.
In wounds that cannot be closed, an attempt should be made to advance the flaps
and approximate the tissues as much as possible to avoid their retraction. In a sec-
ond intervention, they can be re-advanced again and eventually achieve closure.
We strongly recommend using NPWT as bridging therapy in these circum-
stances, especially in dehiscences of great extension and with abundant exudate. If
bone or tendons are exposed, hydrophilic foam, VAC Whitefoam™ Dressing (KCI,
San Antonio, Texas, USA), should be used to prevent drying out (Fig. 6).
a b
Fig. 6 (a) A traumatic injury with exposure of bone and osteosynthesis hardware is appreciated.
(b) If it is not possible to close the wound, to avoid desiccation of the bone, a hydrophilic foam
(VAC Whitefoam™) is used together with a traditional VAC
In the case of contaminated wounds, between any toilets, it is advisable to use

NPWT with irrigation (VAC VERAFLO™ Therapy, KCI), which will help to clean
the wound and promote the development of granulatory tissue [30].
Finally, in these cases, it is possible to continue treating with wound dressings or
NPWT until a closure by second intention is achieved or when local conditions
allow performing a closure by the third intention. If there are no tissues available to
close the wound after extensive dehiscence, it will be necessary to work together
with the plastic surgeon who will eventually require the use of grafts or flaps for
definitive treatment [31].
7 When to Consult the Plastic Surgeon
By far, most of the wounds can be managed entirely and successfully by any ortho-
pedic surgeon, being quite unlikely to need a reconstructive specialist for their man-
agement. Nonetheless, this may be necessary, especially in foot and ankle injuries
due to the anatomical characteristics and frequently high-energy trauma.
A wound that does not close and has tendon, bone, or implants exposure can be
a disaster if it is not promptly well managed.
Although the orthopedist can successfully execute the first steps, it is very likely
that they will require a reconstructive plastic surgeon’s support for the correct treat-
ment. In these cases, we recommend that the consultation be as early as possible.
Depending on the characteristics of each hospital, it can be immediately during the
surgery. If this is not possible, a photograph will always be an excellent bridge to
discuss the case with the plastic surgeon and plan actions to follow.
We highly recommended consulting the plastic surgeon in the following
circumstances:
• Wide and deep dehiscences.
• Infected wounds.
• Traumatized surrounding tissues with signs of poor irrigation.
• Wounds with tendon, neurovascular structures, bone, or osteosynthesis materials
exposure.
• Patients with a clear history of previous hypertrophic or keloid scars.
Working together to plan a reconstructive option, basically, grafts or flaps will
give the best result for patients, minimizing the occurrence of significant complica-
tions such as osteomyelitis and its consequences.
8 Pathological Scar
Despite all care taken to manage wounds, some scars do not evolve favorably.
Beyond a bad aesthetic result, which can generate high psychosocial stress in the
patient, some scars transform into a new pathology, specifically hypertrophic and
keloid scars.
8.1 Hypertrophic and Keloid Scars
One of the most feared problems is when a scar evolves into a hypertrophic one or,
worse yet, to a keloid. Both carry a series of problems not only from an aesthetic
point of view, but they can also be symptomatic.
Traditionally, both types of scars have been considered as distinct entities char-
acterized by generating an excessive amount of scar. Hypertrophic scars are limited
to the original margins of the wound, unlike keloids that grow beyond the limits of
the initial wound; they also possess a genetic factor involved and can be symptom-
atic, mainly due to the pain and itching and, unfortunately, of very complex treat-
ment. An example of a scar with both a hypertrophic segment and also a keloid part
could be appreciated in Fig. 7.
In recent years, however, there is a tendency to consider both types of scars as a
continuum on the same spectrum, in which the initial state would correspond to the
Fig. 7 A lateral foot

surgical incision develops
an excessive pathological
scar of both types. (a) A
hypertrophic scar
respecting the original scar
boundaries. (b) A keloid
growing outside the
borders of the original scar
hypertrophic scar and its most severe level to the keloid [32]. All this is based on
physiopathological appraisals and histological findings.
Although there is still no complete understanding of these conditions, there are
related factors, mainly the tension over the wound. Indeed, those sutured under ten-
sion or in areas of great mobility where the tissues are exposed to forces have a
greater risk of progressing to hypertrophy in different degrees.
The treatment of these pathologies has several modalities. None of them are
100% effective. Among these, we can mention the infiltration with corticosteroids
infiltration compression, use of silicone sheets, cryotherapy, and laser, among oth-
ers, to reach the most effective keloid treatment that corresponds to the resection
followed by radiotherapy. All of these generally have discrete results, with high
recurrence rates, with radiotherapy being the most successful alternative in avoiding
keloid recurrence, with success rates close to 90%.
8.2 Prevention
For the ankle and foot specialist, perhaps the most relevant action is prevention and,
if one develops, its prompt referral to plastic surgery for definitive management.
The prevention actions will be grouped into two areas: patient with no history and
patient with a previous history.
8.2.1 Patient with No Previous History of Pathological Scars
This situation could occur in any patient and any scar; however, some risk factors
such as wounds closed at high tension, in highly traumatized tissues, or with a slow
healing process should make us suspect the appearance of problematic scars. In
these cases, we recommend being very strict in the care of scars, with the elements
already exposed, namely, adequate lubrication of the skin and the fundamental com-
pression of the scar with paper tape or silicone sheet [33].
If the problem is already established and a hypertrophic or keloid scar begins
developing, the ideal step is to address it promptly, so it is essential to warn the
patient to consult immediately if they notice that the scar begins to grow
abnormally.
If a scar is evidently hypertrophic, it should be immediately compressed, ideally
with a silicone sheet. After this, we believe the best course of action would be refer-
ring the patient to a specialist, generally plastic surgeons or dermatologists, to estab-
lish the appropriate treatment and perform a follow-up.
8.2.2 Patient with a Personal History of Hypertrophic/Keloid Scars
Although the ankle and foot are not among the most common areas of the body for
the development of this type of scar, if a patient has already developed them else-
where, especially a keloid previous history, they are at high risk of producing
another keloid if they suffer any additional skin injuries.
For patients with hypertrophic scars, we recommend closing the wound, han-
dling the tissues with care, avoiding over-trauma, achieving a tension-free closure,
and immediately starting compression with a silicone sheet. If in the healing process
it begins to hypertrophy, promptly refer to a plastic surgeon.
In terms of patients with keloids, extreme precautions must be taken. Even if it
sounds like a truism, the first action is to warn the patient about the risk of develop-
ing a new keloid, owing to the way they cicatrize and mostly independent of the
suture technique used.
At the time of surgery, we recommended using sutures that react as little as pos-
sible and that generate the minimum inflammatory effect on the wound. In this
sense, an excellent option is to use nylon to close deep planes, although it is non-
absorbable, since it avoids producing a reaction with tissues. It could be colorless
for more superficial planes. For the final closure of the skin, ideally perform intra-
dermal sutures avoiding multiple passes of the needle through the epidermis and
dermis, as would occur with simple stitches or staples, since in each of these points
a wound is produced with the risk of evolving into a keloid. Again, it is important to
compress the wound initially with paper tape and, after removing the sutures, start
using silicone.
All of the above can be accompanied by even more aggressive actions like infil-
tration of corticosteroids, generally triamcinolone, into the wound at the time of
closure or the early use of tapes impregnated with corticosteroids [34] to avoid the
appearance of a keloid; however, we recommend that under these circumstances
refer the patient previously to the plastic surgeon, for a joint treatment planning.
Once again, teamwork can deliver the best solutions for the patient.
9 Summary
The human being’s ability to stand lies mainly on the foot and ankle, so on a daily
basis, this body segment is overstressed and vulnerable to trauma. However, its
anatomical characteristics leave it relatively unprotected. The skin at the ankle is
very thin and bones and tendons can be easily exposed in any high-energy trauma
or also in case of complications from elective surgery. Thus, correctly managing
skin injuries is a skill to be developed by the foot and ankle surgeon.
The treatment of these wounds requires careful handling of the skin, making
sutures by layers and posteriorly with adequate wound healing dressings, in which
the use of negative pressure wound therapy plays an increasingly relevant role. The
early recognition of complications such as dehiscences is essential to treat them
successfully.
In the case of complex wounds and skin coverage deficits, working together with
the plastic surgeon is essential.
If, despite everything, the patient develops hypertrophic or keloid scars, nowa-
days, there are a series of treatments that allow them to be treated with good results.
References
1. Taylor GI, Palmer JH. The vascular territories (angiosomes) of the body: experimental study
and clinical applications. Br J Plast Surg. 1987;40:113–41.
2. Attinger CE, Evans KK, Bulan E, Blume P, Cooper P. Angiosomes of the foot and ankle and
clinical implications for limb salvage: reconstruction. Incisions, and Revascularization: Plast
Reconstr Surg. 2006;117:261S–93S.
3. Clemens MW, Attinger CE. Angiosomes and wound care in the diabetic foot. Foot Ankle Clin.
2010;15:439–64.
4. Broughton G, Rohrich RJ. Wounds and scars. Sel Read Plast Surg. 2005;10
5. Kaufman MG, Louis MR, Qiu SS, Buchanan EP. Wound healing. In: Fundam. Top. En Plast.
Surg. 1st ed. New York: Thieme, Stuttgart; 2018. p. 13–30.
6. Lee Peng G, Kerolus JL. Management of Surgical Scars. Facial Plast Surg Clin N Am.
2019;27:513–7.
7. Biancari F, Tiozzo V. Staples versus sutures for closing leg wounds after vein graft harvesting
for coronary artery bypass surgery. Cochrane Database Syst Rev. 2010;(5):CD008057.
8. Iavazzo C, Gkegkes ID, Vouloumanou EK, Mamais I, Peppas G, Falagas ME. Sutures versus
staples for the management of surgical wounds: a meta-analysis of randomized controlled tri-
als. Am Surg. 2011;77:1206–21.
9. Krishnan RJ, Crawford EJ, Syed I, Kim P, Rampersaud YR, Martin J. Is the risk of infec-
tion lower with sutures than with Staples for skin closure after Orthopaedic surgery? A Meta-
analysis of randomized trials. Clin Orthop. 2019;477:922–37.
10. Krishnan R, MacNeil SD, Malvankar-Mehta MS. Comparing sutures versus staples for
skin closure after orthopaedic surgery: systematic review and meta-analysis. BMJ Open.
2016;6:e009257.
11. Cochetti G, Abraha I, Randolph J, Montedori A, Boni A, Arezzo A, Mazza E, Rossi De

Vermandois JA, Cirocchi R, Mearini E. Surgical wound closure by staples or sutures?: system-
atic review. Medicine (Baltimore). 2020;99:e20573.
12. Winge R, Bayer L, Gottlieb H, Ryge C. Compression therapy after ankle fracture surgery: a
systematic review. Eur J Trauma Emerg Surg. 2017;43:451–9.
13. Argenta LC, Morykwas MJ. Vacuum-assisted closure: a new method for wound control and
treatment: clinical experience. Ann Plast Surg. 1997;38:563–76. discussion 577
14. Gomoll AH, Lin A, Harris MB. Incisional vacuum-assisted closure therapy. J Orthop Trauma.
2006;20:705–9.
15. Mangelsdorff G, Cuevas P, Rodriguez J, Pereira N, Ramirez E, Yañez R. Reduced antero-
lateral thigh flap donor-site morbidity using incisional negative pressure therapy. J Reconstr
Microsurg. 2019;35:229–34.
16. Agarwal A. Management of closed incisions using negative-pressure wound therapy in ortho-
pedic surgery. Plast Reconstr Surg. 2019;143:21S–6S.
17. Nam D, Sershon RA, Levine BR, Della Valle CJ. The use of closed incision negative-pressure
wound therapy in orthopaedic surgery. J Am Acad Orthop Surg. 2018;26:295–302.
18. Stannard JP, Volgas DA, McGwin G, Stewart RL, Obremskey W, Moore T, Anglen
JO. Incisional negative pressure wound therapy after high-risk lower extremity fractures. J
Orthop Trauma. 2012;26:37–42.
19. Wang C, Zhang Y, Qu H. Negative pressure wound therapy for closed incisions in orthopedic
trauma surgery: a metaanalysis. J Orthop Surg. 2019;14(1):427.
20. Norman G, Goh EL, Dumville JC, Shi C, Liu Z, Chiverton L, Stankiewicz M, Reid A. Negative
pressure wound therapy for surgical wounds healing by primary closure. Cochrane Database
Syst Rev. 2020;5(5):CD009261.
21. Iheozor-Ejiofor Z, Newton K, Dumville JC, Costa ML, Norman G, Bruce J. Negative pressure
wound therapy for open traumatic wounds. Cochrane Database Syst Rev. 2018;7(7):CD012522.
22. Atkinson J-AM, McKenna KT, Barnett AG, McGrath DJ, Rudd M. A randomized, controlled
trial to determine the efficacy of paper tape in preventing hypertrophic scar formation in surgical
incisions that traverse Langer??S skin tension lines. Plast Reconstr Surg. 2005;116:1648–56.
23. Gold MH, McGuire M, Mustoe TA, Pusic A, Sachdev M, Waibel J, Murcia C, International
Advisory Panel on Scar Management. Updated international clinical recommendations on scar
management: part 2--algorithms for scar prevention and treatment. Dermatol Surg Off Publ
Am Soc Dermatol Surg Al. 2014;40:825–31.
24. Soltanian H, Garcia RM, Hollenbeck ST. Current concepts in lower extremity reconstruction.
Plast Reconstr Surg. 2015;136:815e–29.
25. Lehtonen E, Patel H, Phillips S, Correia Pinto M, Naranje S, Shah A. Staple versus suture
closure for ankle fracture fixation: retrospective chart review for safety and outcomes. Foot.
2018;37:71–6.
26. Whalen JL, Spelsberg SC, Murray P. Wound breakdown after Total ankle arthroplasty. Foot
Ankle Int. 2010;31:301–5.
27. World Union of Wound Healing Societies. World Union of Wound Healing Societies
(WUWHS) consensus document. Surgical wound dehiscence: improving prevention and out-
comes. 2018;
28. Sandy-Hodgetts K. Clinical innovation: the Sandy grading system for surgical wound dehis-
cence classification — a new taxonomy. Wounds Int. 2017;2017(8):6–11.
29. Gowd AK, Bohl DD, Hamid KS, Lee S, Holmes GB, Lin J. Longer operative time is indepen-
dently associated with surgical site infection and wound dehiscence following open reduction
and internal fixation of the ankle. Foot Ankle Spec. 2020;13:104–11.
30. Kim PJ, Attinger CE, Constantine T, et al. Negative pressure wound therapy with instillation:
international consensus guidelines update. Int Wound J. 2020;17:174–86.
31. Ieropoli G, Villafañe JH, Zompi SC, Morozzo U, D'Ambrosi R, Usuelli FG, Berjano
P. Successful treatment of infected wound dehiscence after minimally invasive locking-plate
osteosynthesis of tibial pilon and calcaneal fractures by plate preservation, surgical debride-
ment and antibiotics. Foot. 2017;33:44–7.
32. Köse O, Waseem A. Keloids and hypertrophic scars: are they two different sides of the same
coin? Dermatol Surg. 2008;34:336–46.
33. Del Toro D, Dedhia R, Tollefson TT. Advances in scar management: prevention and man-
agement of hypertrophic scars and keloids. Curr Opin Otolaryngol Head Neck Surg.
2016;24:322–9.
34. Ogawa R, Akaishi S, Kuribayashi S, Miyashita T. Keloids and hypertrophic scars can now
be cured completely: recent Progress in our understanding of the pathogenesis of keloids and
hypertrophic scars and the Most promising current therapeutic strategy. J Nippon Med Sch
Nippon Ika Daigaku Zasshi. 2016;83:46–53.
Part II
Pediatric Orthopaedics and Traumatology
Biomechanics, Assessment,
and Management Principles for Pediatric
Foot Deformities
Vincent S. Mosca
We, as orthopedic surgeons, were obviously drawn to our profession by a desire to

help relieve musculoskeletal pain and related dysfunction using surgical techniques.
However, techniques change. Principles are forever. For such a complex anatomic
site as the child’s foot with its 26 bones and at least 19 major articulations and
almost innumerable congenital and developmental deformities and malformations,
one must, therefore, study principles. A principle is a basic generalization that is
accepted as true and can be used as a basis for reasoning or conduct.
The following principles were personally conceived, developed, organized,
explained, presented, and finally published in 2014 in my book, Principles and
Management of Pediatric Foot and Ankle Deformities and Malformations [1]. I am
pleased to share with you some of my excerpted principles in condensed form in
this book. Note that the number of the principle in this chapter does not necessarily
match the number of the principle in my book because all of them are not
included here.
1 Biomechanics
Biomechanics Principle #1
“The foot is not a joint!” In all congenital and developmental deformities and most
malformations of the child’s foot, there are at least two segmental deformities that
are often in rotationally opposite directions from each other, “as if the foot was
wrung out.” Before one can surgically treat the pain and disability associated with
V. S. Mosca (*)
Orthopedics, University of Washington School of Medicine, Seattle, WA, USA
Pediatric Orthopedic Surgeon, Seattle Children’s Hospital, Seattle, WA, USA

Switzerland AG 2022
116 V. S. Mosca
foot deformities and malformations, each segmental deformity and malformation

must be identified, characterized, and understood so a plan can be created to indi-
vidually, yet concurrently, manage each one.
Before treating deformities and malformations of the child’s foot, whether non-
operatively or operatively, a thorough and working knowledge of the normal anat-
omy of the child’s foot and ankle is required.
The average foot shape of a child is different than the average foot shape of an adult.
And the range of normal foot shapes in a child is different than the range of normal
foot shapes in an adult, though with significant overlap between age groups. For
example, many or most babies are flatfooted, a shape less commonly seen in adults.
Many babies have metatarsus adductus, a shape rarely seen in adults.
Age-related anatomic variations in the shape of the foot and the natural history of
each one must be appreciated. In most cases, anatomic variations in the shape of the
child’s foot change spontaneously to adult norms through normal growth and
development.
For example, most babies are flatfooted, whereas about 25% of adults are flat-
footed. Approximately 1 in 100 babies has metatarsus adductus, almost none receive
treatment, and very few adults have that foot shape. Knowledge of anatomic varia-
tions and their natural history should prevent unnecessary and potentially harmful
interventions.
One must understand subtalar joint positions and motions in a manner that super-
sedes the confusing and inconsistent terminology in the literature. The static defor-
mity positions of the subtalar joint can appropriately be described using the
terminology used for other joints, i.e., varus (the calcaneus angles inwards in rela-
tion to the talus) and valgus (the calcaneus angles outwards in relation to the talus).
Hindfoot varus is the static position of the subtalar joint found in cavovarus feet and
clubfeet. Hindfoot valgus is the static position of the subtalar joint seen in flatfeet,
skewfeet, and vertical tali. Some healthcare professionals use the term “pronated”
when referring to a foot with hindfoot valgus. I disagree. Forearms pronate and
supinate. There is a lot more going on in foot deformities with a valgus hindfoot
than can be captured with the simplistic and specific term “pronated.”
The motions that result in those static positions should, in my opinion, be
described using terms that recognize the unique and complex features of the sub-
talar joint. The subtalar joint differs from all other joints in the body in several
ways: it is not a hinge joint or a ball-and-socket joint; its axis is not in the sagittal,
coronal, or transverse plane; and it is a compound joint (several bones articulate)
rather than a diarthrodial joint (two bones articulate). The subtalar joint complex
is comprised of three bones (possibly four, if one includes the cuboid), several
important ligaments, and multiple joint capsules that function together as a unit.
Almost 200 years ago, Scarpa saw similarities between the hip joint and the sub-
talar joint complex. He coined the term “acetabulum pedis,” referring to a cuplike
Biomechanics, Assessment, and Management Principles for Pediatric Foot Deformities 117
structure made up of the proximal articular surface of the navicular, the spring
ligament, and the facets of the anterior end of the calcaneus. He compared the
femoral head to the talar head and the pelvic acetabulum to his so-called acetabu-
lum pedis. I believe that the unique term “inversion” best captures the three-
dimensional motions of the acetabulum pedis around the head of the talus that
result in the static position termed “varus.” The acetabulum pedis plantar flexes
(down), internally rotates (in), and supinates. Simply stated, inversion is a “down
and in” movement of the acetabulum pedis around the talus. Conversely, “ever-
sion” motion results in the static position termed “valgus.” It is a combination of
dorsiflexion (up), external rotation (out), and pronation of the acetabulum pedis
around the talar head. Simply stated, eversion is an “up and out” movement of the
acetabulum pedis around the talus.
A thorough and working knowledge of the biomechanics of the foot and of the sub-
talar joint complex in particular are mandatory for assessment and management of
foot deformities in children. The functions of the foot include provision of a stable,
but supple, platform that helps it accommodate to the changing terrain below and
propel the body in space. And the subtalar joint is the machinery used by the foot to
adapt to the ground during the early stance phase of gait and then convert to a rigid
lever during push-off.
The foot acts as the most efficient and effective lever for the generation of power
during push-off when the subtalar joint is inverted/locked and the foot is pointing
directly forward, i.e., perpendicular to the transverse axis of the knee joint. This is
the concept of lever arm function. Lever arm dysfunction can result from shortening
the lever arm and/or weakening the triceps surae. The lever arm is shortened when
the foot is externally rotated in relationship to the sagittal plane of the knee. This can
be due to an everted/unlocked subtalar joint and/or external tibial torsion. The force
coupling (force x distance to the center of the axis of motion, i.e., length of the lever
arm) can be further diminished by weakness of the triceps surae. This can occur if
the triceps surae is inappropriately lengthened and, thereby, weakened.
In the normal foot, the overall shape is determined by the shapes and interrelation-
ships of the bones, coupled with the strength and flexibility of the ligaments.
Muscles maintain balance, accommodate the foot to uneven terrain, protect the liga-
ments from unusual stresses, and propel the body forward.
Don’t use the term “pronated” as a substitute for the term “flatfoot.” There’s very
little pronation in a flatfoot, yet many healthcare professionals refer to a flatfoot as
a pronated foot. It’s true that pronation is one of the components of eversion of the
subtalar joint, but the dorsiflexion and external rotation components are far more
significant deformities. And the forefoot in a flatfoot is supinated! If it were not
supinated, but instead followed the subtalar joint into eversion/“pronation,” it might
be appropriate to use the term pronated. In that situation, however, the lateral fore-
foot would be elevated off the ground, a deformity that almost never exists except in
some cases of congenital subtalar synostosis.
118 V. S. Mosca
Another misnomer for flatfoot that is often used when discussing adult flatfoot is
“dorsolateral peritalar subluxation.” It is true that eversion of the subtalar joint
results in dorsal and lateral alignment of the navicular in relation to the head of the
talus, i.e., peritalar. But there is no subluxation of any component part of the subta-
lar joint complex with even severe eversion. Subluxation is defined as incomplete or
partial dislocation of a joint, i.e., only partial contact between articular surfaces that
normally have full contact. Think of Scarpa’s analogy of the hip and the acetabulum
pedis. Congenital and developmental hip subluxations occur, and these are charac-
terized by partial contact (incongruity) of the articular surfaces due to translation of
the femoral head from the center of the acetabulum. There is no analogy for that
pathology in the foot. Severe eversion, which might be called dorsolateral peritalar
positioning, is a rotational malalignment of the subtalar joint. It is perhaps analo-
gous to severe abduction or adduction of the hip without translational loss of contact
of the articular surfaces, i.e., without subluxation.
The term flatfoot has historical precedence and, though not specific, is associated
with a good visual for most people.
Cavus is defined as plantar flexion of the forefoot on the hindfoot. It does not
mean “high arch,” although that’s the resultant effect. There may be plantar flexion
of the medial column, the lateral column, or the entire forefoot on the hindfoot.
Coincidentally, the subtalar joint can be inverted, everted, or in neutral alignment.
And the ankle can be plantar flexed, dorsiflexed, or in neutral alignment. When
describing a cavus foot, it is best to describe all of its features. Some examples are
cavovarus, equinocavovarus, calcaneocavus, and transtarsal cavus. I’ve seen con-
genital and iatrogenic calcaneo-abducto-cavo-valgus.
The foot deformity may be the primary problem or the result of the primary prob-
lem, i.e., a neuromuscular disorder. Differentiation is important. A cavovarus foot
deformity is the result of a neuromuscular disorder until proven otherwise. This is
important to remember because a treatable neuromuscular disorder, such as a teth-
ered spinal cord or spinal tumor, is not necessarily readily apparent when a child
presents with a cavovarus foot deformity. However, it should be diagnosed and
treated before the foot deformity is treated. Further permanent neuromuscular dete-
rioration should be arrested as soon as possible. Flatfoot is most often either a nor-
mal anatomic variant or the primary problem. Examples of the latter include flexible
flatfoot with short Achilles tendon, tarsal coalition, congenital vertical talus, and
skewfoot. Flatfoot can also be associated with neuromuscular disorders, such as
cerebral palsy, but these underlying disorders are usually apparent.
2 Clinical Assessment
Assessment Principle #1
A complete and detailed clinical and radiographic assessment of the child’s foot is
required before treatment is instituted.
Clinical evaluation of the child’s foot begins with a clinical evaluation of the child.
Although the foot deformity or malformation is the reason for the requested evalu-
ation by you, children with these conditions often have underlying neuromuscular,
genetic, or chromosome disorders as well as other deformities and/or malforma-
tions of the lower extremities and spine. These must be recognized and factored into
the decision-making process to ensure that the most appropriate of the possible
non-operative and operative interventions are chosen.
Congenital and developmental deformities should be differentiated. Congenital
deformities are rarely progressive in their natural history, yet rarely regressive.
Tendons and joint capsules are usually co-contracted. For example, in a clubfoot
(congenital talipes equinocavovarus) in an older child that does not correct with
non-operative management, posterior ankle capsulotomy is often required in addi-
tion to Achilles tendon lengthening.
Developmental deformities, by definition, are progressive in their natural history,
though the rate of progression is variable. Contracture of tendons precedes contrac-
ture of joint capsules. In a developmental equinocavovarus foot deformity in an
older child, an Achilles tendon lengthening is usually enough to correct the equinus
deformity.
Static and progressive deformities should be differentiated, and the rate of progres-
sion established, if possible. As stated in Assessment Principle #3, most congenital
foot deformities are static, rather than progressive, in nature. Muscle imbalance is
the underlying problem in many acquired foot deformities. The muscle imbalance
can be static, as in children with myelomeningocele, lipomeningocele, and post-
infectious poliomyelitis, or it can be progressive, as in children with Charcot-Marie-
Tooth disease, muscular dystrophy, spinal cord tumors, tethered cord, and
diastematomyelia. Whether the muscle imbalance is static or progressive, the defor-
mity is likely to progress. Unfortunately, the rate of progression is rarely predictable
for either static or progressive muscle imbalances. Progression and increased time
to treatment will increase the complexity of reconstruction.
It is often more challenging to ascertain the history of pain and/or dysfunction that is
related to the foot deformity in a child than in an adult, but it’s worth the effort.
Reasons for children to be poor historians include that they are too young, “too ado-
lescent,” intellectually challenged, and neurologically impaired. The importance of
an accurate assessment of the pain and dysfunction is that there are many clinically
and radiographically apparent normal anatomic variations of the child’s foot. If the
pain location, severity, and temporal and activity-related patterns do not match the
known pain pattern of an identified deformity/condition, the two might not be related.
Assessment of pain must be specific – where, when, what level/severity, and what
associations. There are many anatomic variations of the foot, including a host of
120 V. S. Mosca
accessory ossicles, which could be the source of pain or merely incidental findings. It
is easy, for example, to ascribe reported foot pain to a tarsal coalition or an accessory
navicular that is identified on an x-ray. However, since most anatomic variations
including tarsal coalitions and accessory naviculars don’t hurt, it is important to know
the exact site(s) of pain, as well as the activities that insight and relieve the pain.
Severity of the pain should be quantified. Visual analog pain scales have been shown
to be reliable in even very young children. The pain location, pattern, and severity
must all match those of the presumed diagnosis. Chronic pain in a non-physiologic
distribution that occurs continuously during all waking hours and is reported to be of
an exaggerated severity suggests chronic regional pain syndrome, aka reflex sympa-
thetic dystrophy, reflex neurovascular dystrophy, and pain amplification syndrome.
If pain is a complaint, ask the child to point to the exact location(s). By having the
child identify the point(s) of maximal tenderness, you can start your physical exam-
ination away from that site(s) and learn about the surrounding area(s) before creat-
ing pain that might limit the rest of the examination. You can also quickly determine
if your working diagnosis (based on the history) is valid even before you touch
the foot.
Physical evaluation of the child’s foot begins with a physical evaluation of the child.
This includes a careful examination of the hips and spine in a newborn. Visual gait
analysis, torsional profile analysis, and angular alignment assessment are used for
older children and adolescents. Visual gait analysis is carried out by watching the
child walk, run, toe walk, heel walk, squat and stand, and hop on each foot. These
observations are used to evaluate symmetry, strength, coordination, and comfort.
The child’s torsional profile must be ascertained with the child prone on an exami-
nation table.
The foot must be clinically assessed in weight-bearing, not just on the exam table.
Do this first to learn about the true deformities and functions/dysfunctions of the
foot. The foot deformity will look very different when weight-bearing and non-
weight-bearing. A flatfoot looks better than it truly is when it is not bearing weight.
And a cavovarus foot looks worse than it truly is when non-weight-bearing. Pain
and/or disability are usually, if not always, experienced when weight-bearing.
Observation of the weight-bearing foot helps understand the pattern of pain and
disability.
Assessment of each of the segmental deformities of the foot and ankle is imperative
before planning treatment, as a plan needs to be established to correct each one.
The segments are:
1. Forefoot – pronated or supinated; plantar flexed (equinus) or dorsiflexed.
(a) Recall that alignment (and deformity) is defined as the relationship between
a more distal anatomic part and the next more proximal anatomic part.
Therefore, pronation or supination refers to the alignment of the forefoot in
relation to the midfoot/hindfoot, not the tibia/leg. This has been a source of
confusion for many who believe the forefoot in a flatfoot is neutrally aligned
(in relation to the tibia) when, in fact, it is supinated – in relation to the mid/
hindfoot.
2. Midfoot – abducted or adducted.
3. Hindfoot – varus/inverted or valgus/everted.
4. Ankle – varus or valgus; plantar flexed (equinus) or dorsiflexed (calcaneus).
Each segment of the foot should be evaluated for shape/deformity, flexibility, and
skin integrity. Documentation should be specific. Accurate assessment of the shape
of each segment of the foot is the first step.
For a cavovarus foot deformity, the segmental deformities are pronation of the
forefoot, adduction of the midfoot, varus of the hindfoot, and possibly equinus of
the ankle. Equally important is the flexibility of each segment. The first segment to
lose flexibility is the forefoot. Loss of flexibility of the hindfoot, which is assessed
by the Coleman block test, eventually follows.
Skin integrity should be assessed, as it can identify unsafe foot pressures. This is
especially important in children with insensate skin. In the cavovarus foot, exagger-
ated pressures are seen at the base of the fifth metatarsal and under the first and fifth
metatarsal heads.
The segmental deformities of a flatfoot include supination of the forefoot, abduc-
tion or straight alignment of the midfoot, valgus of the hindfoot, and equinus of the
ankle. Equally important is the flexibility of each segment. Flexibility of the hind-
foot is assessed in a different manner than that used for a cavovarus foot. There is
not a reliable “reverse” Coleman block test. Instead, toe standing and the Jack toe
raise test are utilized to assess hindfoot flexibility.
Evidence of exaggerated skin pressures in a flatfoot are identified under the
medial midfoot. The skin in this area is rarely stressed except when a flatfoot is
associated with contracture of the gastrocnemius or the entire triceps surae (Achilles
tendon).
The accurate assessment of subtalar motion is an inexact science, but you can better
at it by practicing. There are no studies documenting the accuracy of assessment of
subtalar motion. It is particularly challenging in very small feet and fat feet.
The best way to improve your skills for assessing subtalar joint motion is to
practice in the OR during a foot deformity correction operation while observing
your technique and the resultant motions of the subtalar joint under mini
fluoroscopy.
There may also be a deformity in the ankle joint. An ankle joint deformity may
coexist with a foot deformity or it may be an isolated deformity. It must be
differentiated.
The ankle joint is in valgus orientation to the anatomic axis of the tibia in all
newborns. In otherwise normal children, the distal fibula and lateral distal tibia grow
relatively faster than the medial distal tibia until about age 3–4 years at which point
122 V. S. Mosca
the ankle joint/tibial plafond becomes perpendicular to the tibia. It maintains that
anatomic alignment through skeletal maturity.
That spontaneous change from physiologic neonatal ankle valgus to neutral
alignment does not occur in children with myelomeningocele, lipomeningocele,
early onset poliomyelitis, other early onset flaccid paralytic conditions, and approx-
imately 66% of limbs with a clubfoot. The clinical assessment of ankle joint align-
ment and the differentiation from subtalar joint alignment are helpful in older
children, particularly in those with the stated underlying conditions. In spastic con-
ditions, such as cerebral palsy, normal spontaneous correction of neonatal ankle
valgus to neutral occurs.
The frontal plane angle between the ankle joint and a line connecting the distal
tips of the medial and lateral malleoli is 15 degrees. Therefore, with a valgus
ankle joint deformity of approximately 15 degrees, the line connecting the distal
tips of the medial and lateral malleoli is in a transverse plane that is perpendicular
to the tibia. When the ankle joint has assumed its adult alignment perpendicular
with the tibia, the distal tip of the lateral malleolus is closer to the floor and fur-
ther from the knee than the medial malleolus. This assessment of the relative
heights of the malleoli is helpful in the clinical determination of frontal plane
ankle alignment. It is particularly helpful in the clinical determination of the site
of hindfoot valgus deformity, which can exist in the ankle joint, the subtalar joint,
or in both joints.
The ankle joint can also have a procurvatum or recurvatum deformity. These are
almost always acquired deformities. A flat-top deformity of the talus can occur fol-
lowing both non-operative and operative treatment of clubfoot deformity and result
in a true or “functional” procurvatum deformity of the ankle. Iatrogenic posterior
distal tibial physeal arrest following clubfoot surgery can cause a true procurvatum
deformity.
The Achilles tendon or gastrocnemius muscle may be contracted. The presence of a
gastrocnemius or an Achilles tendon contracture must be identified and differenti-
ated from each other.
Many foot deformities do not cause pain or functional disability unless they are
accompanied by a contracture of the heel cord (the gastrocnemius alone or the entire
triceps surae/Achilles tendon). The ankle joint should have at least 10° of dorsiflex-
ion with the knee extended and the subtalar joint in neutral alignment. The
Silfverskiold test should be used to determine if there is a contracture of the heel
cord and, if so, whether the contracture is of the gastrocnemius alone or the Achilles
tendon. This will ensure that the proper tendon is lengthened if surgery is indicated,
thereby avoiding under- or overlengthening. The Silfverskiold test must be mastered.
The cavus foot presents a different challenge to the assessment of a possible heel
cord contracture. Cavus means plantar flexion of the forefoot on the hindfoot, i.e.,
equinus of the forefoot. Therefore, assessment of ankle equinus can only be per-
formed by isolating the hindfoot. The forefoot should be obscured from your vision
with your hand so that only the hindfoot can be seen.

A detailed examination of strength, sensation, reflexes, and vascularity is required.
This is particularly true for the cavovarus foot but is important for all foot deformi-
ties. Don’t rely on EMG findings or on someone else to do it.
Signs and symptoms must match the presumed pathology, so ensure that you have
enough clinical information before focusing on a radiographic finding.
There are many common anatomic foot variations, such as tarsal coalitions and
accessory naviculars, that do not cause pain or functional disability in most affected
individuals. Therefore, it’s important to ensure that the signs and symptoms match
those associated with the radiographic finding. If they don’t, the two are unrelated,
and a more thorough investigation is required.
3 Radiographic And Other Imaging Assessment

All standard initial/screening radiographs for assessment of foot deformities should
be obtained in weight-bearing, or simulated weight-bearing if the former is not pos-
sible because of young age or inability to stand.
This is the radiographic version of Assessment Principle #9. The appropriate
clinical assessment of foot deformities is performed in weight-bearing. Radiographs
must, therefore, be obtained in weight-bearing to correlate the anatomic alignment
of the bones and joints with the outward appearance of the foot. Specialized views,
such as oblique views, can be taken non-weight-bearing because they are used to
identify anatomic abnormalities other than bone and joint alignment. The standard
radiographic views for assessing foot deformities are standing AP, lateral, and
(medial or standard) oblique. Additional views include lateral oblique, Harris axial,
and Saltzman views.
The foot-CORA method should be used pre-, intra-, and postoperatively for the
most objective evaluation of foot deformities and malformations.
There are several radiographic features of the foot bones in children that make it
unreliable or impossible to apply the CORA method, as used in the long bones of
the extremities, to the assessment of pediatric foot deformities. These features jus-
tify a unique CORA method for assessment of pediatric foot deformities.
The basis of the “foot-CORA” method is the assessment of the relationship
between the axis of the talus and the axis of the first metatarsal in the transverse
(AP) and sagittal (lateral) planes. Unlike the ossification centers of the bones of the
midfoot, those of the metatarsals, talus, and calcaneus are present at birth and reli-
ably represent the shapes of the incompletely ossified bones. The first metatarsal is
a proxy for the calcaneopedal unit (CPU), which is the term for all the bones of the
foot except the talus. The major deformities of subtalar varus/inversion and valgus/
124 V. S. Mosca
eversion exist between the CPU and the talus. The foot-CORA method readily iden-
tifies and defines those deformities by an intersection of those axis lines in the head
of the talus in the AP plane. The lines are adducted in varus/inversion deformities
and abducted in valgus/eversion deformities.
There may also be static deformities in the shapes of the small bones within the
CPU. Based on the acknowledged challenges of assessing them directly, the foot-
CORA method assessment of the relationship between the axis of the talus and that
of the first metatarsal accurately identifies those as well, by proxy.
The CORA in a long bone is the site of deformity and the ideal site for deformity
correction by means of an osteotomy. The foot-CORA for varus and valgus hindfoot
deformities, that is in the talar head, is the site of deformity but never the site for
deformity correction. Instead, soft tissue procedures and/or osteotomies of the peri-
talar structures are performed to align the axes of the talus and the first MT at the
foot-CORA. The talus-first metatarsal angle can be used to quantify the degree of
inversion and eversion deformities before and after correction.
The center of the medial cuneiform (within the CPU) is the foot-CORA for the
two most common midfoot deformities, cavus and metatarsus adductus. Like the
CORA in long bones, the medial cuneiform is the site of deformity and the ideal site
for deformity correction for these deformities.
There will be a projectional artifact on the lateral radiograph of a foot with a varus
or valgus hindfoot deformity and an adduction or abduction midfoot deformity.
Therefore, order specifically positioned views.
When a foot is C-shaped due to inversion or eversion of the hindfoot and adduc-
tion or abduction of the midfoot, the lateral x-ray creates an unusual appearance of
the hindfoot. The reason is that an x-ray beam cannot simultaneously pass perpen-
dicular to the forefoot and the hindfoot when there is a curve in the plane of the
beam. Therefore, order specifically positioned views to see each segment in a true
lateral projection. The radiology technicians can easily visualize the forefoot and
will generally aim the x-ray beam perpendicular to the metatarsals. That creates a
rotational projectional artifact of the hindfoot in varus/inversion and valgus/ever-
sion hindfoot deformities and in adduction and abduction midfoot deformities.
Recall that one component of inversion is internal rotation of the subtalar joint/
acetabulum pedis in relation to the talus/ankle and that one component of eversion
is external rotation of the subtalar joint/acetabulum pedis in relation to the
talus/ankle.
Finally, be aware that the best way to assess proper hindfoot positioning for a
lateral radiograph is to note the relationship between the distal fibula and tibia. The
posterior cortex of the distal fibula metaphysis and the posterior ossification margin
of the distal tibial epiphysis are colinear in a true lateral x-ray of the hindfoot/ankle.
It is unreliable to use the shape of the dome of the talus to determine a true lateral
projection, because the ossification of the dome is not particularly dome-shaped in
young children. Furthermore, there are many instances in which the dome had been
crushed, devascularized, or otherwise injured, thereby flattening its dome shape.
And, as has just been discussed, flattening of the dome can be a projectional artifact.
Therefore, use the distal fibula to tibia relationships to determine if the projection is
a true lateral of the hindfoot/ankle.
Don’t forget about ankle radiographs.
Ankle radiographs (standing AP, lateral, mortis) are not a standard part of every
assessment of a foot deformity or malformation but should be ordered if clinically
indicated. See Assessment Principle #13.
CT scan in all three orthogonal planes and with 3D reconstruction is the best imag-
ing modality for more detailed assessment of complex foot deformities and malfor-
mations. It is the definitive imaging study for the diagnosis and management of
tarsal coalitions.
For most deformities and malformations, plain radiographs provide enough
information to corroborate the physical examination findings. CT scans show the
shapes of bones and the alignment of joints in three dimensions, the exact informa-
tion needed to assess the more complex deformities and malformations, particularly
those that have been operated on previously. MRI scans are best for the assessment
of soft tissue pathology, which is not the intent of structural assessment. The exor-
bitant cost of an MRI (even in comparison with a CT scan) makes it fiscally irre-
sponsible to obtain this study without careful consideration of the indications and
the information desired, considerations that apply to all imaging studies. CT scans
use ionizing radiation but at a distance far from the most radiation sensitive parts of
the body.
Importantly, the CT scan is the definitive imaging study for the diagnosis and
management of talocalcaneal tarsal coalitions, because the published criteria for
choosing the appropriate treatment modality are based on CT scan findings.
Fibrocartilaginous as well as osseous coalitions can be easily identified on CT scans.
MRI is rarely helpful for assessment of pediatric foot deformities and malforma-
tions. Radiographs and CT scans are most helpful for these indications.
MRI scans are useful in assessing soft tissue abnormalities, such as infections
and soft tissue tumors. The exorbitant cost of an MRI of the foot might be justified
in the assessment of a complex deformity or malformation in a very young child
who has minimal ossification of the tarsal bones.
4 Management
Management Principle #1
The decision (to operate) is more important than the incision (i.e., the surgical tech-
nique). And the decision to operate on a foot deformity or malformation is based on
126 V. S. Mosca
(1) the known natural history of the condition, (2) the symptomatic and/or func-
tional responses to non-operative treatment (where appropriate), and (3) the reported
risks and complications of surgery. A “well-executed” operation for the right indica-
tion is far better for the patient than the “most skillfully executed operation in the
history of surgery” for the wrong indication. The best surgeon is not necessarily the
most skillful, but the one who knows when to operate. Of course, it’s nice to make
the best decisions and be technically excellent. We all strive for that combination of
knowledge and skills.
A less than ideal surgical outcome can be due to a poor technique, a poor technician,
or both.
This principle assumes that the patient satisfies reasonable indications for the
technique in question. A surgical or non-surgical (e.g., Ponseti) technique is devel-
oped and, hopefully, tested by the originator before it is presented to the medical
community. There is perhaps no technique that is so simple or foolproof that mere
knowledge of the concept allows another surgeon to perform the procedure as well
as the originator. And for some/many techniques, attention to all the fine details of
the procedure is critical for success. Failure to perform the procedure as described
by the originator might result in a good outcome, but a poor outcome cannot auto-
matically be attributed to the technique. It can only, perhaps, be considered a poor
technique if other surgeons skillfully follow the fine details of the procedure (as
published and without modifications) and fail to achieve outcomes comparable to
the originator. Before abandoning or modifying a procedure that has been shown by
others to be effective, make sure to perform it as described by the originator.
Personal observation of, or tutoring by, an expert might be required, depending on
the complexity and uniqueness of the technique.
You can’t un-operate on anyone. Foot deformities and malformations are never
lethal. Non-operative treatment might prolong the temporary pain and disability but
might eliminate both, thereby avoiding the reported risks and complications of
surgery.
The (surgical) treatment could be worse than the condition itself.
No operation is without potential risks and complications that are unacceptable if
the natural history of the condition or the response to non-operative treatment pro-
vides favorable outcomes with little to no long-term disability. Non-operative treat-
ment corrects a high percentage of many congenital deformities (clubfoot and
metatarsus adductus) and/or resolves pain and functional disability in a high percent-
age of certain other conditions (tarsal coalition, juvenile hallux valgus, and acces-
sory navicular). Natural history trumps all treatment modalities. Many anatomic
variations correct spontaneously through normal growth and development (flexible
flatfoot, metatarsus adductus, and position calcaneovalgus) or persist without result-
ing in pain or functional disability (flexible flatfoot, metatarsus adductus, skewfoot).
Modalities that correct structural deformities: (1) natural history, (2) physical
stretching, (3) serial casting, and (4) surgery.
Surgery is the final common pathway for foot deformities that do not correct
spontaneously or respond fully to non-operative treatment. Surgical techniques
include soft tissue releases and/or plications, osteotomies, and, rarely, arthrodeses.
Tendon transfers do not correct structural deformities.
As a corollary, natural history is the only modality that results in permanent
deformity correction. There is a risk of deformity recurrence following all treatment
modalities.
A commonly held belief by some healthcare professionals and most grandpar-
ents is that special “orthopedic shoes” and orthotics correct foot deformities in chil-
dren. There is no scientific evidence to support that belief. The myth has been
perpetuated because those devices have been credited with the deformity correction
that has, in fact, occurred as a result of the natural history of the condition.
Modalities that correct dynamic deformities: (1) focal injection of tone-reducing
medication into muscles (such as BOTOX) and (2) muscle-balancing tendon
surgery.
Tendon lengthening/weakening, shortening, and transfer techniques are more
permanent solutions to muscle imbalance, but they are not entirely reliable, pre-
dictable, or definitive. The main problem with a dynamic deformity is that it is the
result of the problem (an underlying neuromuscular disorder) and not the primary
problem. After tendon surgery, the child still has the underlying nerve or muscle
disorder. Therefore, recurrence of deformity and overcorrection are real
possibilities.
Modalities that maintain deformity correction: (1) focal injection of tone-reducing
medication into muscles, (2) physical stretching, (3) special shoes/braces, (4)
orthotics, and (5) balanced muscles.
Surgically balanced muscles can maintain deformity correction, but achieving
balance is an art and may not be achievable. Maintaining muscle balance is particu-
larly challenging in progressive neuromuscular disorders.
Treatment (non-operative and/or operative) is indicated for:
1. Congenital deformities and malformations that are known, or expected, to cause
pain and/or functional disability unless corrected.
(a) These include congenital clubfoot, congenital vertical talus, rigid metatarsus
adductus, rigid skewfoot, polydactyly, and macrodactyly. They are treated
well before they become symptomatic.
128 V. S. Mosca
2. Developmental deformities that are creating pain and/or functional disability.

(a) These include cavovarus foot, flexible flatfoot with short Achilles tendon,
idiopathic equinus, tarsal coalition, accessory navicular, spastic and para-
lytic foot deformities, and iatrogenic deformities.
For both pain and functional disability, the treatment is disease-specific and can
be non-operative and/or operative.
Surgical treatment is indicated for:
1. Congenital deformities and malformations that do not, or cannot, correct with
non-operative treatment and are known to cause pain and/or functional disability
unless corrected.
(a) These include congenital clubfoot and vertical talus that do not respond to
non-operative (Ponseti and reverse Ponseti) management, macrodactyly,
longitudinal epiphyseal bracket of the first metatarsal, and polydactyly.
2. Progressive cavovarus foot deformities that are associated with pain and/or func-
tional disability.
3. Other developmental, persistent, and recurrent deformities that do not adequately
respond to prolonged attempts at non-operative treatment designed to relieve
pain and/or diminish or relieve functional disability that are related to the
deformity.
(a) These include skewfoot, recurrent and overcorrected congenital clubfoot
and vertical talus, idiopathic equinus, flexible flatfoot with short Achilles
tendon, tarsal coalition, accessory navicular, juvenile hallux valgus, and
spastic and paralytic foot deformities.
Provide clear, accurate, and reasonable expectations to the patient and family of the
short- and long-term outcomes of non-operative and operative management.
Foot deformities and malformations are rarely “cured”, i.e., made normal. But
long-term comfort and function can be anticipated for many or most of them. For
deformities that are due to neuromuscular disorders, the foot deformity is the
result of the problem and not the primary problem. Recurrence of deformity and
the need for future treatment can be anticipated in many of these cases. Normal
growth and development of a foot with a primary deformity can have an antici-
pated or unanticipated effect on the long-term outcome of the intervention. Share
your predictions about future comfort and function and about the need for future
treatment with the patient and family. That way there should be few surprises
down the line.
A surgical plan for each of the segmental deformities and muscle imbalances needs
to be established before proceeding with surgery.
This means creating a list of the multiple related and unrelated procedures that
are to be performed either during a single operative session or sequentially in cases
of staged procedures. Some deformities are not evident until others are corrected.
This needs to be anticipated before the start of the operation, based on one’s knowl-
edge and understanding of deformities, with a surgical plan ready for each addi-
tional deformity that might be identified intraoperatively. Be prepared, rather than
surprised.
Correct deformity at the site of the deformity, unless the only option is arthrodesis
of the subtalar joint.
That means:
1. Perform a calcaneal lengthening osteotomy (CLO) rather than posterior calca-
neal medial displacement osteotomy (PCDO) for valgus/eversion deformity of
the hindfoot. The former procedure (CLO) corrects all components of subtalar
joint eversion at the site of deformity, whereas the latter procedure (PCDO) cre-
ates a compensatory deformity to “correct” valgus alignment of the hindfoot.
2. Perform a plantar-medial soft tissue release (PMR) of the subtalar joint rather
than posterior calcaneal lateral displacement osteotomy (PCDO) for varus/inver-
sion deformity of the hindfoot. The former procedure (PMR) corrects all compo-
nents of subtalar joint inversion at the site of deformity, whereas the latter
procedure (PCDO) creates a compensatory deformity to “correct” varus align-
ment of the hindfoot.
3. Perform a medial cuneiform opening wedge osteotomy rather than first metatar-
sal osteotomy for cavus deformity (plantar flexion deformity of the first ray).
The foot-CORA for cavus is in the medial cuneiform.
4. Perform a medial cuneiform opening wedge osteotomy and cuboid closing
wedge osteotomy rather than metatarsal osteotomies or tarsometatarsal capsu-
lotomies for metatarsus adductus. The foot-CORA for metatarsus adductus is in
the medial cuneiform.
Preserve joint motion (particularly subtalar joint motion) in the feet of children and
adolescents by utilizing soft tissue releases/plications and osteotomies instead of
arthrodeses.
Arthrodesis of the subtalar joint results in debilitating stress transfer to adjacent
joints, particularly the ankle joint, leading to premature degenerative arthritis.
Arthrodesis also has a detrimental effect on future growth and development of the
foot. The subtalar joint is the shock absorber of the foot and, in fact, the entire lower
extremity. Preserve its function at all costs.
Use biologic, rather than technologic, interventions, i.e., rearrange and/or reshape
anatomic parts rather than replace or interfere with them.
The overall reported short-term complication rate of subtalar arthroereisis with
synthetic implants is 3.5–30%, with more recent reports of 3.5–11%. However, the
130 V. S. Mosca
actual rates are much higher if one includes the inappropriate implantation of these
devices into normal physiologic flexible flatfeet, a practice employed by some
healthcare providers. Complications can be categorized as surgeon error, biomateri-
als problems, biologic problems, and inappropriate implantations. Long-term out-
come studies have not been reported. Pain after insertion of these implants may be
greater than the pain that predated their implantation. This is particularly concern-
ing if none preexisted, as when they are implanted in normal, physiologic flexible
flatfeet.
Correct deformities and balance muscle forces.
1. Deformity correction will not correct muscle imbalance.
Deformity correction without muscle balancing can result in recurrent deformity.
If muscle imbalance created the deformity, as is usually the case in cavovarus foot
deformities, persistence of the muscle imbalance will recreate the deformity, despite
adequate initial deformity correction.
2. Tendon transfers will not correct structural deformities.
Muscle balancing without deformity correction will create a balanced deformity.
That’s not the goal.
The calcaneocuboid joint is the most distal site at which the lateral column of the
foot can be shortened or lengthened to realign the talonavicular joint/acetabulum
pedis in a foot with a varus/inverted or a valgus/everted hindfoot deformity. The
body of the cuboid is too far distal.
The medial cuneiform is the foot-CORA for cavus and for metatarsus adductus.
Osteotomies in the medial cuneiform can and should be used to correct forefoot
pronation and supination, midfoot adduction and abduction, as well as combina-
tions of those deformities.
When treating pronation (plantar flexion of the first ray) and supination (dorsi-
flexion of the first ray) deformities of the forefoot, it is important to recognize the
alignment of the midfoot, i.e., adduction or abduction. Knowledge of this second
plane alignment can help determine whether an opening or closing wedge osteot-
omy should be used. Opening wedge osteotomies of the medial cuneiform to dorsi-
flex or plantar flex the first ray inadvertently create mild abduction of the midfoot,
whereas closing wedge osteotomies inadvertently create mild adduction of the mid-
foot. This can be used to your advantage or detriment. For the supination forefoot
deformity in a skewfoot, a plantar-based closing wedge osteotomy will pronate the
forefoot but increase the midfoot adduction. The better choice is a dorsomedially
based opening wedge osteotomy that will pronate the forefoot and abduct the
adducted forefoot.

The iliac crest is the ideal bone graft source for foot deformity correction surgery in
children and adolescents. Allograft has advantages over autograft.
Principles of tendon transfers:
1. Move the right tendon to the right location at the right tension.
2. Tendon transfers will not correct structural deformities.
3. Tendon transfers are based on existing and anticipated patterns of muscle
imbalance.
4. Tendon transfers are much more challenging with joint preserving
reconstruction.
Correct deformities in a complex multi-segmental foot/ankle deformity in the
proper order.
1. Cavovarus – forefoot before hindfoot.
2. Equinocavovarus – cavovarus before equinus.
3. Planovalgus – hindfoot before forefoot.
4. Equinoplanovalgus – planovalgus concurrent with equinus.
5. Planovalgus or cavovarus deformity with real or apparent ipsilateral tibial tor-
sion – foot deformity before tibial deformity.
6. Coincident subtalar joint and ankle joint valgus – ankle before foot.
Order of events during complex foot reconstruction surgery:
1. Expose and prepare everything before completing anything.
2. Perform and stabilize deformity corrections.
3. As you proceed, close incisions that will no longer be accessed.
4. Set proper tension on tendon lengthenings/plications/transfers.
5. Close final incisions.
Reference
1. Mosca VS. Principles and management of pediatric foot and ankle deformities and malforma-
tions. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2014.
Clubfoot
Dalia Sepúlveda Arriagada and Nicolas Valdivia Rojo
Summary Clubfoot or congenital talipes equinovarus is the most common con-

genital deformity affecting the lower extremities. It can occur in approximately 50%
bilaterally and is more frequent in males.
Despite its frequency, its etiology is not completely clear. What is recognized is
that there is a group of genes that jointly influence the appearance of this deformity.
The gold standard for treatment of idiopathic clubfoot is the Ponseti technique,
which presents studies with long follow-up and which confirms it as a safe, low
cost, reproducible technique with very good results.
1 Introduction
Clubfoot or talipes equinovarus is one of the most common pediatric orthopedic

disorders. It affects approximately 1 per 1000 live newborns [1]. In the world about
174,000 children are born with this pathology, and of these, approximately 90% are
born in developing countries [2]. It is currently the leading cause of disability in
these countries and carries a heavy social stigma if left untreated.
About 80% of patients with clubfoot present in isolation, the remainder being
associated with chromosomal or genetic abnormalities, neurological disorders,
D. Sepúlveda Arriagada (*)

Private Practice, COTI Chile, Santiago, Chile
N. Valdivia Rojo
Servicio de Salud Bio bio, Concepción, Chile
Hospital Base Los Angeles, Concepción, Chile
Sanatorio Alemán, Concepción, Chile

Switzerland AG 2022
134 D. Sepúlveda Arriagada and N. Valdivia Rojo
arthrogryposis, myelomeningocele, or muscular dystrophies. A family history of

clubfoot is found in only about 25% of cases [3].
Approximately 50% affect both feet, and in the case of being unilateral, it slightly
more frequently affects the right lower extremity [4]. The Polynesian race has the
record of having an affection seven to eight times greater than the rest of the world
population.
Its etiology is not very clear, but apparently genetic inheritance and maternal
smoking are the factors that recur most frequently in clubfoot without associated
pathologies or syndromes.
In the last 20 years, the treatment of clubfoot has changed radically, taking a
conservative line less and less surgical. In the past, wide posteromedial releases
became very common (generating greater scarring, stiffness, and painful arthrosis
in the long term); nowadays, they are in frank withdrawal, to the point of being
considered contraindicated in the management of children with clubfoot.
Currently the gold standard for the treatment of clubfoot is the Ponseti
method; it is a very minimally invasive method that consists of serial manipula-
tion of the foot using modeling casts that progressively correct the deformity and
culminate with percutaneous tenotomy of the Achilles tendon (95% of the cases).
The correction must be maintained with the use of an orthosis designed by Dr.
Ponseti and must be worn until at least 4 years of age. This method has gained
more and more followers due to its good long-term results and the low rate of
complications [5].
The objective of this chapter is to understand the specific characteristics of club-
foot and the pillars for its diagnosis, its causes, and specific treatment, as well as to
show some other types of clubfoot.
2 Diagnosis
In order to make an accurate diagnosis of clubfoot, one must initially recognize

what deformities are present. Its diagnosis is clinical, and no additional examination
is required. Radiographic study has proven not to be necessary because it does not
change the form of treatment according to Ponseti’s method.
Classically, clubfoot is described as a set of deformities recognized by the old
mnemonic CAVE, midfoot cavus, forefoot adductus, varus, and hindfoot equinus.
For this to occur, it is accepted that there is an anomalous position of the tarsal
bones (described below) (Figs. 1, 2, 3, 4, and 6).
In addition to these characteristics, we can find a foot generally smaller than the
contralateral foot (in unilateral cases), a thinner calf due to the presence of shorter
gastrocnemius (occupying only 1/3 of the calf length), and hypodevelopment of the
lateral compartment of the leg.
Histological and imaging studies with 3D magnetic resonance imaging show less
muscle volume throughout the calf, increased subcutaneous adipose tissue, smaller
tibia and fibula, abnormal tendon insertions, shortened ligamentous structures, and
Clubfoot 135
Figs. 1, 2, 3, and 4 Four examples of clubfoot patients
smaller diameter, with abundant fibrous tissue (medial and posterior areas of the
foot); this includes shortening of the tendons: posterior tibial, Achilles, deltoid, and
calcaneal navicular plantar ligament. Finally, hypoplasia or vascular alterations in
the calf territory such as absence of posterior tibial artery [6–9].
3 Etiology
The etiology of clubfoot is well studied, but its origin is not completely clear
(assuming that we are talking about the most prevalent orthopedic deformity in
pediatrics). A precise origin is not yet known for the group of patients with idio-
pathic clubfoot which corresponds to 80% of the cases. Researchers have proposed
several theories (lack of intrauterine mobility, neurological, vascular, alterations in
the connective system and genetic), histological and structural alterations that affect
the whole leg and not only the foot are described in several publications [10], so the
genetic theory of those genes responsible for the development of the lower limbs is
the one that is currently being studied.
There are several reviews with twin patients, where the concordance rate is 2.9%,
while monozygotes present 32.5% [11]. On the other hand, having a direct relative
(sibling or parent) with clubfoot has a 10 to 20% higher risk of suffering the defor-
mity versus the general population.
In recent years, anatomical and genetic studies have made considerable progress
regarding the origin of this pathology [11].
Genetics plays a crucial role in the appearance of clubfoot; however, there is no
single gene involved or predominant in the presence of this deformity. There is a
wide group of genes involved in clubfoot such as HOXD13, NAT2 (associated with
smoking), PITX1, TBX4, HOXC13, UTX, CHD1, RIPPLY2, CAND2, andWNT7.
In addition, it is highlighted that there are two regions on chromosomes 3 and 13
suggesting that clubfoot was related to a single major gene but with multigenic
susceptibility [12, 13].
The HOX gene family (homeobox family genes) plays an essential role in the
morphogenesis process of embryonic development. It determines the correct forma-
tion of the axial skeleton and limbs. Several publications have found a genetic sus-
ceptibility locus where the presence of clubfoot is associated with the HOX domain.
Based on the emerging evidence, we can assume that disruption of the HOXA,
HOXC, and HOXD gene clusters may play a role in the etiology and pathogenesis
of clubfoot.
The CASP gene family plays an essential role in apoptosis, necrosis, and inflam-
mation. This family was studied by Heck’s group, since its activity was correlated
with the development of the members.
There is a group of genes of the collagen family also associated with the origin
of clubfoot. Recent studies [14] comparing a healthy population versus a population
with idiopathic clubfoot show an overexpression of COL1A1 (including mutations
of COL1A1), which would correlate even more with the presence of clubfoot.
Mutations of the GLI3 gene would also be involved in the appearance of idio-
pathic clubfoot. It is noteworthy that this group of genes interacts with HOXD13
with the GLI3 promoter. This was proven by observing that GLI3 mRNA levels and
the levels of its expression protein were elevated in rat models of clubfoot.
This would mean that HOXD13 is a transcription factor of GLI3. Its low levels
(HOXD13) could lead to elevated levels of GLI3 expression during limb formation
which would play an important role in the occurrence of clubfoot.
The role of the T-box gene family would play important roles in embryogenesis
and morphogenesis. There are only associations of mutations of these genes with
the appearance of clubfoot.
The transcription factors PITX1-TBX4 are responsible for early limb develop-
ment. There are numerous reports about mutations at this level where less muscle
development and the classic phenotype of clubfoot are observed in both rats and
humans [15]. Studies by Gurnett, Alvarado, and Dobbs show that there is a close
relationship of this pathway with the development of clubfoot and even with the
presence of congenital vertical talus.
The family of genes in charge of encoding the troponin and tropomyosin pro-
teins, responsible for muscle contraction, would also be involved in the presence of
clubfoot, which clinically would be responsible for the shortening and poor
Clubfoot 137
development of the musculature around the calf. This group of genes could also be
responsible in cases of syndromic clubfoot associated with distal arthrogryposis.
Variations in genes at this level (MYH3, TPM2, TNNT3, TNNI2, and MYH8)
would result in muscle contractures at this level. It is unclear which specific altera-
tions would lead to the development of distal arthrogryposis or clubfoot.
The presence of hypoplasia or muscle atrophy around the calf which is main-
tained over time [16], which is also replaced by fat, has been demonstrated in some
MRI studies. On the other hand, studies rule out the presence of histological altera-
tions that suggest a neuromuscular origin of this pathology [17]. This would lead to
think of a genetic origin mainly oriented to this group of genes as the ones respon-
sible for clubfoot.
As we can see, there are multiple gene families involved in the etiopathogenesis
of VEP. It is clear that external stimuli (tobacco or others) could influence the abnor-
mal expression of these genes, so the multifactorial theory is the one that is cur-
rently most supported, and it would not be only one responsible for the presence of
this disease.
4 Functional Anatomy
The detailed analysis of the multidirectional movements in the multiple joints of the
normal foot, which we know and call the functional anatomy of the foot, is the fun-
damental pillar of the principle of the correction of the clubfoot with the conserva-
tive method technique of Dr. Ignacio Ponseti; he was the one who used the normal
kinematics proper and exclusive to the joints surrounding the talus to simultane-
ously reduce the many deformities of the clubfoot.
5 Normal Anatomy
The subtalar joint complex is one of the most complex and difficult to explain joints
in the entire human skeleton. It plays a fundamental role in the adaptation of reac-
tion forces to the ground during lower extremity rotation and gait, as well as in the
adaptation of a movable foot to surfaces inclined to the ground plane.
The talus has three articular facets, posterior, medial, and anterior, and two func-
tional components.
–– Talocalcaneal joint is housed in the posterior articular facet, which is oblique in
the coronal plane and saddle-shaped in the sagittal plane.
–– Talocalcaneonavicular joint or “acetabulum pedis” sits on the anterior and medial
facets (Fig. 5).
–– Interosseous talocalcaneal ligament constitutes the center of rotation of the sub-
talar joint consisting of two bands: “acetabulum pedis” and Interosseous
ligament.
Fig. 5 Anatomy diagram of the acetabulum pedis (talocalcaneonavicular joint). Drawing by Dr.
Estefanía Birrer
6 Subtalar Kinematics
Functionally, all the bones of the foot move as a unit around the talus. There is very
little intertarsal motion [18] (Inman 1976).
The foot normally moves around the two functional entities of the subtalar joint,
the talar calcaneal joint and the “acetabulum pedis” (talocalcaneonavicular), with
the interosseous ligament as the center of rotation.
On the other hand, the subtalar axis is not fixed but a dynamic axis that allows
displacement and sliding around the limiting or restraining mechanism of the inter-
osseous ligaments, as determined by Inman, Husen, and Van Langelann [19–21].
The motion achieved by the subtalar joint in this oblique plane is supination and
pronation. Supination consists of the kinematically coupled movements of adduc-
tion, inversion, and plantar flexion, and pronation consists of the kinematically
coupled movements of abduction, eversion, and dorsiflexion.
Correction of the rearfoot and midfoot can be fully achieved by abduction of the
forefoot. Pressure thus applied on the first metatarsal lever can “motorize” the
motion of the calcaneus pedis, thus demonstrating that abduction and eversion are
“kinematically coupled.”
7 Kinematic Coupling
It is common for orthopedic surgeons to analyze joint movements in reference to

standard body planes: coronal, sagittal, and axial. Thus, we have adduction/abduc-
tion, inversion/eversion, and plantar flexion/dorsiflexion of the foot.
Clubfoot 139
But when a joint is in the oblique plane, as is the case with the subtalar joint, all
these movements are inextricably linked to each other, or “kinematically coupled.”
Therefore, calcaneal abduction cannot occur without simultaneous eversion and
extension. The Ponseti technique allows correction by simultaneously producing
the movements in the oblique plane, using abduction as the motor [21–28].
With this explanation of the functional anatomy of the foot, it is possible to
understand why abduction of the foot alone simultaneously leads to abduction of
the calcaneus and why the entire block pedis during Ponseti manipulation, including
the calcaneus, moves or follows in conjunction around the talus.
The Ponseti technique, as we can see, is both simple and profoundly complex.
The forefoot is abducted around the talus, which must be kept in the shroud and held
in that reduction position by pressure on its head and counterpressure on the widest
part of the tibial malleolus, thus obtaining simultaneous abduction, eversion, and
extension (dorsiflexion) of the foot with heel valgus.
The normal maximum reduction of the talus in the tibioperoneal mortise of an
infant provides full range of motion of the subtalar joint, also reducing the scaphoid
at the head of the talus and obtaining full eversion and pronation with dorsiflexion
of the calcaneus which simultaneously corrects heel varus.
The clubfoot is not adequately corrected until full abduction is obtained, and
calcaneal extension or dorsiflexion occurs primarily during extreme abduction. An
infant’s foot normally abducts 70°–80°, and the single correction of the clubfoot to
a neutral or functional position is not sufficient to achieve all kinematically coupled
movements, for this reason recurrence is inevitable [29].
Based on this same mechanism of the kinematic coupling of the tarsal bones, it
is also possible to understand the error of the Kite technique [29–32] and other simi-
lar treatments, which attempt to correct the foot sequentially, dividing or separating
the combined movements into their component parts. Fixing the calcaneus when
displacing the forefoot does nothing but block its normal kinematically coupled
movement, and then we have to accept that the pseudo correction of the badly
manipulated foot only obeys to an iatrogenic deformation of the tarsal bones; for
example, blocking the abduction of the calcaneus causes an iatrogenic deformation
of the midtarsal bones and joints creating the “bean-shaped or bunioned foot.”
8 Classification
The clubfoot can be classified in different ways:

–– According to its origin or association to other diseases or syndromes: idiopathic,
complex, and syndromic.
–– Severity classification: Pirani (currently most used), Dimeglio.
The most currently used classification is that of Pirani, which has a greater
interobserver similarity than Dimeglio’s classification, and some publications state
that both age and the Pirani score at the beginning of treatment could even suggest
the number of casts to be used. The important point is that the higher the Pirani
score, the longer the treatment (higher number of casts) and the higher the risk of
recurrence.
9 Pirani Score (Fig. 6)
10 Treatment
The treatment of congenital clubfoot with Ponseti’s method is one of the treatments
with the longest follow-up in the world of pediatric orthopedics; in fact, its first
publications date back to 1996; however, the method was only adopted and accepted
by orthopedic doctors in the world in the last two decades. Since the beginning of
the twenty-first century, the news has spread both in the scientific field of specialists
and in the social networks of parents with children treated with the bloodless method
of Dr. Ignacio Ponseti [20, 33–35].
The excellent functional results of the feet treated with the method slowly con-
vinced parents and orthopedic surgeons of its superiority over any of the surgical
techniques in vogue in the last half of the twentieth century, techniques that never
came close to the near 100% success achieved with Dr. Ignacio Ponseti’s method
and technique (Evans, Crawford, Turco).
It is recommended that parents start treatment after the first 2 to 3 weeks of the
child’s life, once the mother, child, and family unit becomes stable and once they
have been informed and explained in great detail the strict route already mapped out
for the successful correction of their child’s feet.
The method of reduction, to a normal position and appearance, consists first of a
very specific and efficient technique of manipulations that return the calcaneal foot
(block pedis) to its normal location below the subtalar joint. The advantage and
multidirectional kinematic capacity of the subtalar joint (explained in the functional
anatomy section) is used to this effect, which progressively allows all components
of the clubfoot deformity to be corrected simultaneously.
11 Description of the Two-Handed Manipulation Technique
This is the classic form recommended by Dr. Ponseti whereby the soft tissues of the
medial aspect of the foot that are firm and thickened and which cause the retraction
and adduction deformity of the forefoot are stretched or elongated (etiology).
The procedure room in which the procedure will be performed should maintain
as comfortable an environment as possible, both for the child and accompanying
person and for the operators of the treating medical team. The orthopedist or
Clubfoot 141
Fig. 6 Pirani Score

operator can be seated or standing and positions himself on the side of the foot to be
manipulated; his assistant should not interfere in this positioning and should be
positioned on the opposite side to the operator who will perform the manipulations;
the assistant’s task is fundamental, because he must neutralize the limb to be cor-
rected by firmly holding the knee and only the tip of the toes. The operator then first
looks, touches, and then looks for the bony prominences of the tibial (medial) and
peroneal (lateral) malleoli as a reference, as well as the prominence of the head of
the talus which is located immediately below the lateral or peroneal malleolus just
below the anterior ankle interline [36].
The operator supports the tip of the thumb of the hand opposite to the foot that is
treating on the lateral prominence of the head of the talus, at the same time that with
the index and/or middle fingers of the same hand takes and makes counterpressure
on the widest and posterior aspect of the tibial malleolus lodging, controlling and
stabilizing completely the talus inside the tibioperoneal mortise.
The opposite hand (hand on the same side as the foot being corrected) grasps
with the middle and index fingers the medial and plantar aspect of the midfoot and
forefoot up to the scaphoid and with the thumb of the same hand embraces the dor-
sum covering up to the level of the toes and metatarsals. Next, combine a firm but
delicate traction maneuver and then move the foot in supination and abduction seek-
ing to align the midfoot and forefoot with the rearfoot (Fig. 7); this maneuver is held
and repeated for a few seconds until the child tolerates it; ideally the child should
not cry (Figs. 8, 9, and 10).
A frequent error during this manipulation and application of the Ponseti tech-
nique is pronating the forefoot, which worsens the cavus and keeps the calcaneus in
varus. Other errors during the application of the technique include pressure on the
calcaneocuboid joint instead of the heel head, also known as the Kite error, which
blocks calcaneal abduction and prevents correction of heel varus and foot adduction
and may even damage the Lisfranc joint (be careful and respect the area of the
thumb that presses on the small head of the talus in infants starting treatment); it can
also be observed that by seeking abduction of the foot without properly containing
the head of the talus in the mortise, a posterior translation of the peroneal malleolus
Fig. 7 Kinematic of the subtalar joint. Midfoot and forefoot move around green dot. Recreation
of the Ponseti method motion
Clubfoot 143
Fig. 8 Manipulation with

two hands, holding the
forefoot as described in
Fig. 7. Foot position after
casting
is produced by rotating the talus and opening the syndesmosis, while the calcaneus
will fail to correct itself and will remain in varus. On the other hand, if the operator
asserts the calcaneus during the manipulation, which tends to correct the foot and
does not allow it to follow the movement spontaneously offered by the subtalar
joint, he will also be blocking the correction of the varus to valgus instead of
improving it.
Finally, you should not apply forces against plantar flexion with fulcrum in the
ankle without first having corrected the abduction and varus of the calcaneus; some
less experienced operators believe that this could correct the equinus; however, this
bad manipulation leads to a rocker deformity by stress and breakage of the Lisfranc
joint. This same bad anti-equinus force can compromise the future congruence of
the talus in the mortise causing a flat talus by compromise of its ossification nucleus
very moldable and sensitive at that stage of the child’s life, and that is thus com-
pressed between the anterior zone of the mortise and the calcaneus [29].
On average, after five sessions with progressive serial casts containing the abduc-
tion obtained after manipulation with the Ponseti technique, the foot should reach
the next stage of treatment consisting of a transcutaneous tenotomy of the tricipital
tendon or Achilles tendon (Figs. 11 and 12).
Figs. 9 and 10 Another case before and after casting
Fig. 11 Correct 15–25 degrees of abduction in each cast. Before tenotomy, abduction external
rotation should be 60–70 degrees with valgus heel and 90° of ankle dorsiflexion
12 Description of One-Handed Manipulation
In this one-handed technique, the operator faces the child and rests the index finger
of the hand opposite to the foot to be treated on the head of the talus and embraces
the foot with the thumb on the plantar and medial aspect at the level of the scaphoid;
applying with this one-handed gripper, a slight traction is made while bringing the
rest of the foot in supination and abduction, thus achieving the same as with the
Clubfoot 145
Fig. 12 Final cast, after

Achilles tenotomy
two-handed technique. If the assistant does not exercise good firm control of the leg
during this maneuver, with only one hand, the same effect of external rotation of the
tibioperoneal mortise can be generated instead of stretching the medial and plantar
soft tissues of the foot, with the same risk of producing a posterior displacement of
the peroneal malleolus. It is advisable to be used in very young children who offer
less resistance, and a single hand can do the maneuver as if turning a key in a lock
to achieve the task (Fig. 13).
13 Casting
13.1 Materials
It is necessary to have cotton for the protection of the patient’s skin, which should
ideally be hypoallergenic soft and come prepared in bandages of width and length
appropriate to the size of the foot we are going to treat. Traditional plaster bandages
(plaster of Paris) are needed of 5, 7.5, and 10 cm wide according to the size of the
foot, leg, and thigh. Other necessary items are scissors plaster spreaders and forceps
to open and remove casts of appropriate size to the dimensions of the child under
treatment (Fig. 14).
Warm water is needed as well that does not offer burns risk.
Fig. 13 One-handed
manipulation technique
14 Procedure
On a healthy, clean, and dry skin, place the protective material you have at your
disposal, which should cover the entire limb leaving it long in excess both in the
toes and thigh.
Add a small piece of padding around the heel, malleoli, popliteal fosa and fibu-
lar head.
Being the cast operators in the positions indicated in the previous paragraph, ide-
ally with the patient calm, you must begin to roll the cast from the tip of the toes,
covering them and moving proximally after giving about three cast revolutions in
Clubfoot 147
Fig. 14 Casting and cast removal materials
Fig. 15 Cast molding around the talar head, forefoot, and medial malleolus
each section of the limb until the tibial tuberosity, taking care to remove excess air
and water with a dragging maneuver in each cast revolution.
The operator applies the cast at this time, neatly demarcating the areas and points
of anchorage of the cast to the ankle and foot – forefoot, heel, anterior ankle, and
malleoli – maintaining the reduction of the talus and giving the degree of correction
corresponding to the degree of correction achieved at the time of this procedure and
immobilization (Ponseti 1,2,3, 4,....) (Fig. 15).
The forefoot should be molded until obtaining in a lateral view a triangular sec-
tion and perfectly flat finish dorsal and plantar; the leg should also be molded to the
tibia as straight as possible, avoiding that it adopts a curved shape as a banana by its
anterior face (frequent error).
Wait a few minutes maintaining the reduction position achieved until the plaster
dries out. Continue casting in the same way above the knee until reaching the root
of the thigh. At this stage, do not forget to remove the air at each turn, mold the
popliteal fosa, and leave the knee flexed at 90°.
It is customary that some operators, when finishing the boot below the knee,
make cuts of 1.5 cm, radial and perpendicular to the circular section of the cast at
the level of the proximal tibia. This is in order to prevent the formation of a waist
that could compress and/or embed in the child’s skin producing compression and
even a wound.
At the end of the cast, the toes end should be trimmed, leaving only the third
phalanx uncovered, keeping the plantar support a little longer, so that the toes are
restricted to perform plantar flexion (Figs. 16 and 17).
Fig. 16 Photos of casting procedure at different stages
Fig. 17 Ponseti cast in position 3, with details of the plaster finish

Clubfoot 149
15 Percutaneous Tenotomy of the Achilles Tendon
Immediately after corrective casts, it is time to decide on percutaneous or transcuta-

neous tenotomy; for this purpose, it is required that all components of the deformity
are already corrected (achieve a minimum of 60° of foot abduction, complete cor-
rection of the cavus and a hindfoot ideally in valgus or neutral) (except for the
equinus). A dorsiflexion of less than 20 degrees is an indication for Achilles lenght-
ening (surgery needed in 95–99% of cases).
Percutaneous tenotomy of the Achilles tendon is a quick and simple procedure,
which can be performed under local anesthesia in a procedure box with sterile tech-
nique or in the ward under general anesthesia or sedation (this varies between dif-
ferent health centers).
The patient should be positioned so that the operator feels comfortable and
safe in the procedure to be performed, which will certainly be different if this
procedure is done under local or general anesthesia. With the foot in maximun
dorsiflexion, insert a scalpel N°11 or an ophthalmologic straight scalpel 2 cm proxi-
mal to its insertion in the calcaneus along the medial border of the Achilles tendon.
Then proceed to rotate the blade laterally and transect the tendon completely. A
sudden loss of resistance reflecting the complete section of the tendon will be felt
and heard, and an increase in dorsiflexion of at least 10 to 20° will be observed
(Fig. 18).
After the tenotomy, apply the post-tenotomy cast. This cast is placed in 60°–70°
of foot abduction and maximum ankle dorsiflexion (minimum 20°). The cast,
always with the knee included, should remain in place for 3–4 weeks.
16 Abductor Orthosis
The use of the abductor orthosis is intended to maintain the correction of the affected
foot(s). It has no corrective function. There are several models and designs of brace
in the market (Mitchell, Dobbs, handmade, etc.); the important thing is that it com-
plies with certain characteristics included in Dr. Ponseti’s design.
The ideal brace is one that is as anatomical as possible, made of soft materials
that do not injure the skin, durable, easy to install, as comfortable as possible, ide-
ally with adjustable degrees of abduction, with a resistant bar, hopefully telescopic,
and affordable. The length of the bar should be equivalent to the distance of the
midpoint between shoulders (adjustable and rigid models are available). The posi-
tion of the brace boots should ideally have 10° to 15° of dorsiflexion. In the case of
unilateral clubfoot, it should be positioned in 60° of abduction in the affected foot
and 35–40° in the healthy foot (Figs. 19 and 20).
Fig. 18 Photos showing different ways of performing the Achilles tenotomy with n°11 blade.
Posterior view post-tenotomy showing heel in valgus and dorsiflexion greater than 20°
Fig. 19 Ponseti bar

Clubfoot 151
Fig. 20 Ponseti bar examples
The brace use starts immediately after the last cast.

The first 3 to 4 months of splint use should be 23 hours/day, and then the number
of hours should be reduced according to various factors (age, motor development,
reliability of use, number of casts needed before the tenotomy, etc.), until reaching
12–14 hours/day (at this stage rather during nights and naps) at least until
4 years of age.
17 Recurrences
A recurrence is defined as the appearance of any of the previously corrected club-

foot deformities. It is initially characterized by loss of dorsiflexion of the foot due
to increased tension of the gastrosoleus complex which leads to plantar flexion of
the calcaneus, which progresses to hindfoot varus, forefoot adduction and
finally cavus.
The severity of the relapse depends directly on the time of evolution. In some
occasions only loss of dorsiflexion will be evident. In others, all the deformities
present in clubfoot can reappear.
It should be remembered that the relapses are an evolutionary process, where
gastrosoleus complex shortening is present. This shortening worsens with the longi-
tudinal bone growth which in turn ncreases the ankle plantar flexion (Fig. 21).
Fig. 21 Late relapse in patient with previously treated clubfoot. Note the subtle adductus in the
left foot
It is a mistake to consider that the clubfoot is a “foot deformity,” but it is a sign

of a disease that affects the entire limb.
The early identification of a relapse will allow simpler and less invasive
treatments.
Recurrences can be found from 11 to 48% of corrected feet [37, 38]. In spite of
a correct management and an adequate adherence to the brace use, the appearance
of recurrences is quite frequent.
The main reasons for recurrence are incomplete correction of the foot (not com-
plying with the principles of the Ponseti method), poor adherence to the brace use,
and failures in the strict follow-up of these patients. Poor adherence to bracing is
directly correlated with the educational and socioeconomic level of the parents.
As is well known, the Ponseti method is often promoted as a conservative and
minimally invasive method, but even the staunchest proponents of the method
acknowledge that at least one surgical procedure should be performed: Achilles
tenotomy (95%), tibialis anterior tendon transfer (15–40%), and even a second
Achilles tenotomy [39].
When evaluating a patient with a recurrence, it is extremely important to assess
the correct use of the abduction splint and its adherence. Understanding the family
environment and evaluating the various difficulties (economic, logistical, religious,
etc.) or any other variable that could hinder the correct use of the orthosis should be
identified and discussed with the parents patient.
Correct bracing is a critical step. The orthosis should be the right one, with an
adequate fit, and the parents themselves should demonstrate how to install it in order
to correct key points of its use.
A foot with recurrence is approached in exactly the same way as an uncorrected
foot, that is, it begins with the installation of molding casts and correcting each of
the deformities present in the foot, achieving an abduction of 60°. Once achieved,
the dorsiflexion of the foot is evaluated. If 15 or more degrees of dorsiflexion are
achieved, the bracing protocol is initiated; if this is not achieved, Achilles lengthen-
ing tenotomy should be performed. It is recommended to perform the classic tech-
nique of single tenotomy in children under 3 years of age, or triple tenotomy in
older patients.
Clubfoot 153
Fig. 22 Corrected feet and long-term follow-up
After the age of 4 years, the splint can be discontinued since recurrences are
uncommon (5–10% of cases). If a contracted Achilles tendon is observed achieving
10° of ankle dorsiflexion, 1 more year of brace use is recommended. In addition,
daily Achilles stretching exercises are prescribed (Fig. 22).
The indication to perform an anterior tibial tendon transfer is very specific. It
should be performed only in children older than 4 years of age who present a
dynamic supination. Those patients have to have all other deformities corrected. It
should be kept in mind that this procedure is not useful to correct any deformity but
only helps to maintain the correction of the deformity together with the splint.
18 Complex Clubfoot
We speak of complex clubfoot when we have an idiopathic clubfoot, and that due to
a bad manipulation of the foot and/or incorrectly installed casts generated changes
in the structure of the affected foot.
It is described as a foot that characteristically has a midfoot flexion (a midfoot
plantar crease is evident) and a shortened hallux in hyperextension. The foot may be
swollen and even have trophic changes in the skin if it was recently casted (Fig. 23).
Its management depends on the general condition of the foot. If the foot presents
skin lesions, edema, or erythema and is currently being treated with casts, it is
Fig. 23 Photo of left

complex clubfoot
recommended to suspend the installation of casts. It is advisable to wait 3–4 weeks

(or even longer if necessary) until the foot is in optimal condition to reinstall a cast.
The technique of manipulation and correction of a complex clubfoot consists of
placing one thumb under the head of the first metatarsal and the other under the head
of the fifth metatarsal, pushing the forefoot in dorsiflexion, and the index and mid-
dle fingers push the heel in the opposite direction, sliding the talus into the ankle and
thus avoiding flattening it. To prevent the foot from slipping into the cast (these feet
are very short and difficult to manipulate), it is recommended that the cast have 100
to 120° of knee flexion.
Once the plantar crease (secondary to midfoot flexion) is corrected, with the
rearfoot in neutral, achieve 30º of forefoot abduction and 0º of ankle dorsiflexion.
It is at this point that the Achilles tendon tenotomy is performed. The abduction
splint should not go beyond 35° of abduction since the forefoot can commonly
present a lateral crease suggestive of hypercorrection of the forefoot. The protocol
of splinting in the complex foot has no other differences compared to the idiopathic
clubfoot.
19 Syndromic Clubfoot
Syndromic clubfoot, as the name implies, is a clubfoot associated with another

pathology, whether neuromuscular, neurological, or genetic syndrome. In recent
years, Ponseti’s method has been extrapolated to be used in other pathologies such
as spinal dysraphism and arthrogryposis, but there is still no consensus on when this
method can be applied.
References
1. Dobbs MB, Gurnett CA. Update on clubfoot: etiology and treatment. Clin Orthopaed relat res.
2009;467(5):1146–53. https://doi.org/10.1007/s11999-009-0734-9.
2. Owen RM, Capper B, Lavy C. Clubfoot treatment in 2015: a global perspective. BMJ Glob
Health. 2018;3(4):e000852. https://doi.org/10.1136/bmjgh-2018-000852. PMID: 30233830;
PMCID: PMC6135438.
Clubfoot 155
3. Gurnett CA, Boehm S, Connolly A, Reimschisel T, Dobbs MB. Impact of congenital talipes
equinovarus etiology on treatment outcomes. Dev Med Child Neurol. 2008;50(7):498–502.
https://doi.org/10.1111/j.1469-8749.2008.03016.x. PMID: 18611198.
4. Miedzybrodzka Z. Congenital talipes equinovarus (clubfoot): a disorder of the foot but not the
hand. J Anat. 2003;202(1):37–42. https://doi.org/10.1046/j.1469-7580.2003.00147.x. PMID:
12587918; PMCID: PMC1571059.
5. Laaveg SJ, Ponseti IV. Long-term results of treatment of congenital club foot. J Bone Joint
Surg Am. 1980;62(1):23–31. PMID: 7351412.
6. Duce SL, D’Alessandro M, Du Y, Jagpal B, Gilbert FJ, Crichton L, Barker S, Collinson JM,
Miedzybrodzka Z. 3D MRI analysis of the lower legs of treated idiopathic congenital tali-
pes equinovarus (clubfoot). PLoS One. 2013;8(1):e54100. https://doi.org/10.1371/journal.
pone.0054100. Epub 2013 Jan 30. PMID: 23382871; PMCID: PMC3559654.
7. Ippolito E, De Maio F, Mancini F, Bellini D, Orefice A. Leg muscle atrophy in idiopathic
congenital clubfoot: is it primitive or acquired? J Child Orthop. 2009;3(3):171–8. https://
doi.org/10.1007/s11832-009-0179-4. Epub 2009 May 6. PMID: 19418086; PMCID:
PMC2686819.
8. Merrill LJ, Gurnett CA, Siegel M, Sonavane S, Dobbs MB. Vascular abnormalities cor-
relate with decreased soft tissue volumes in idiopathic clubfoot. Clin Orthop Relat Res.
2011;469(5):1442–9. https://doi.org/10.1007/s11999-010-1657-1. Epub 2010 Nov 2. PMID:
21042891; PMCID: PMC3069258.
9. Dobbs MB, Gordon JE, Schoenecker PL. Absent posterior tibial artery associated with idio-
pathic clubfoot. A report of two cases. J Bone Joint Surg Am. 2004;86(3):599–602. https://doi.
org/10.2106/00004623-200403000-00022. PMID: 14996890.
10. Dobbs MB, Walton T, Gordon JE, Schoenecker PL, Gurnett CA. Flexor digitorum
accessorius longus muscle is associated with familial idiopathic clubfoot. J Pediatr

Orthop. 2005;25(3):357–9. https://doi.org/10.1097/01.bpo.0000152908.08422.95. PMID:
15832155.
11. Pavone V, Chisari E, Vescio A, Lucenti L, Sessa G, Testa G. The etiology of idiopathic con-
genital talipes equinovarus: a systematic review. J Orthop Surg Res. 2018;13(1):206. https://
doi.org/10.1186/s13018-018-0913-z. PMID: 30134936; PMCID: PMC6104023.
12. Gurnett CA, Alaee F, Kruse LM, Desruisseau DM, Hecht JT, Wise CA, Bowcock AM, Dobbs
MB. Asymmetric lower-limb malformations in individuals with homeobox PITX1 gene muta-
tion. Am J Hum Genet. 2008;83(5):616–22. https://doi.org/10.1016/j.ajhg.2008.10.004. Epub
2008 Oct 23. PMID: 18950742; PMCID: PMC2668044.
13. Alvarado DM, Buchan JG, Frick SL, Herzenberg JE, Dobbs MB, Gurnett CA. Copy number
analysis of 413 isolated talipes equinovarus patients suggests role for transcriptional regulators
of early limb development. Eur J Hum Genet. 2013;21(4):373–80. https://doi.org/10.1038/
ejhg.2012.177. Epub 2012 Aug 15. PMID: 22892537; PMCID: PMC3598331.
14. Zhao XL, Wang YJ, Wu YL, Han WH. Role of COL9A1 genetic polymorphisms in develop-
ment of congenital talipes equinovarus in a Chinese population. Genet Mol Res. 2016;3:15(4).
https://doi.org/10.4238/gmr15048773. PMID: 27819742.
15. Alvarado DM, McCall K, Aferol H, Silva MJ, Garbow JR, Spees WM, Patel T, Siegel M,
Dobbs MB, Gurnett CA. Pitx1 haploinsufficiency causes clubfoot in humans and a clubfoot-
like phenotype in mice. Hum Mol Genet. 2011;20(20):3943–52. https://doi.org/10.1093/hmg/
ddr313. Epub 2011 Jul 20. PMID: 21775501; PMCID: PMC3177645.
16. Ippolito E, De Maio F, Mancini F, Bellini D, Orefice A. Leg muscle atrophy in idiopathic
congenital clubfoot: is it primitive or acquired? J Child Orthop. 2009;3(3):171–8. https://
doi.org/10.1007/s11832-009-0179-4. Epub 2009 May 6. PMID: 19418086; PMCID:
PMC2686819.
17. Herceg MB, Weiner DS, Agamanolis DP, Hawk D. Histologic and histochemical analysis
of muscle specimens in idiopathic talipes equinovarus. J Pediatr Orthop. 2006;26(1):91–3.
https://doi.org/10.1097/01.bpo.0000188994.90931.e8. PMID: 16439910.
18. Inman VT. The joints of the ankle. Williams & Wilkins; 1976.
19. Ponseti IV. Congenital clubfoot. Fundamentals of treatment. Oxford: Oxford Medical
Publications; 1996.
20. Ponseti IV, Smoley EN. Congenital club foot: the results of treatment. Bone Joint Surg.
1963;45-A:261–27.Plaster cast treatment of clubfoot.
21. van Langelaan EJ. A kinematical analysis of the tarsal joints. An X-ray photogrammetric
study. Acta Orthop Scand Suppl. 1983;204:1–269. PMID: 6582753.
22. The Ponseti method of manipulation and casting Morcuende 1994. J Pediatr Orthop Part
B. 1994;3:161–7.
23. Close JR, Inman VT, Poor PM, Todd FN. The function of the subtalar joint. Clin Orthop Relat
Res. 1967;50:159–79. PMID: 6029014.
24. Huson A. Functional anatomy of the foot. In: Jahs JH, editor. Disorders of the foot and ankle,
vol. 1. 2nd ed. Philadelphia: Saunders; 1991.
25. Kapandji IA. The Physiology of the joints. 2nd ed. Churchill Livingstone.
26. Ponseti IV. Congenital clubfoot. Fundamentals of treatment. Oxford, New York: Oxford
University Press; 1996.
27. Sarrafian SK. Biomechanics of the subtalar joint complex. Clin Orthop Relat Res.
1993;290:17–26. PMID: 8472445.
28. Sarrafian SK. Functional anatomy of the foot and ankle. 2nd ed. J.B.Lippincott Company.
29. Ponseti IV. Common errors in the treatment of congenital clubfoot. Int Orthop.
1997;21(2):137–41. https://doi.org/10.1007/s002640050137. PMID: 9195271; PMCID:
PMC3616653.
30. Kite JH. The clubfoot. New York London: Grune & Stratton; 1964.
31. Kite JH. Nonoperative treatment of congenital clubfoot. Clin Orthop. 1972;
32. Manter JT. Movements of the Subtalar and transverse Tarsal Joints. The Anatomical Record.
1941;80(4)
33. Ponseti IV, Campos J. The classic: observations on pathogenesis and treatment of congeni-
tal clubfoot. 1972. Clin Orthop Relat Res. 2009;467(5):1124–32. https://doi.org/10.1007/
s11999-009-0721-1. Epub 2009 Feb 14. PMID: 19219518; PMCID: PMC2664437.
34. Miller NH, Carry PM, Mark BJ, Engelman GH, Georgopoulos G, Graham S, Dobbs MB. Does
strict adherence to the ponseti method improve isolated clubfoot treatment outcomes? a two-
institution review. Clin Orthop Relat Res. 2016;474(1):237–43. https://doi.org/10.1007/
s11999-015-4559-4. Epub 2015 Sep 22. PMID: 26394639; PMCID: PMC4686485.
35. Arana Hernández EI, Cuevas De Alba C. Método de Ponseti en el tratamiento del pie equino
varo: técnica de enyesado y tenotomía percutánea del tendón de Aquiles. Orthotips. 2015;11(4)
36. Morcuende JA, Abbasi D, Dolan LA, Ponseti IV. Results of an accelerated Ponseti pro-
tocol for clubfoot. J Pediatr Orthop. 2005;25(5):623–6. https://doi.org/10.1097/01.
bpo.0000162015.44865.5e. PMID: 16199943.
37. Ponseti IV. Common errors in the treatment of congenital clubfoot. Int Orthop.
1997;21(2):137–41. https://doi.org/10.1007/s002640050137. PMID: 9195271; PMCID:
PMC3616653.
38. Morcuende JA, Dolan LA, Dietz FR, Ponseti IV. Radical reduction in the rate of extensive
corrective surgery for clubfoot using the ponseti method. Pediatrics. 2004;113:376. https://doi.
org/10.1542/peds.113.2.376.
39. Eidelman M, Kotlarsky P, Herzenberg JE. Treatment of relapsed, residual and neglected
clubfoot: adjunctive surgery. J Child Orthop. 2019;13(3):293–303. https://doi.
org/10.1302/1863-2548.13.190079.
Pediatric Metatarsus Adductus
and Cavovarus Foot
Maryse Bouchard
1 Metatarsus Adductus
1.1 Introduction
Metatarsus adductus is the most common congenital foot deformity [1]. It consists
of medial angulation of the forefoot relative to the hindfoot. The longitudinal medial
arch is present, and the hindfoot alignment is neutral to valgus [1] (Fig. 1). The true
incidence remains unknown with reports from 0.1% to 12% [2–4]. Associations
with twin births [3] and hip dysplasia [5] have been reported, although the latter has
been refuted in more recent studies [6, 7].
1.2 Etiology
The etiology of metatarsus adductus is unknown. Given the deformity often resolves
spontaneously, intra-uterine positioning is suspected as a possible cause [3, 8, 9].
Other theories include anomalous morphology of the medial cuneiform [10] and
muscle imbalance of the tibialis anterior, tibialis posterior, or abductor hallucis
[5, 11–13].
M. Bouchard (*)
The Hospital for Sick Children, Division of Orthopaedic Surgery, University of Toronto,
Toronto, ON, Canada

Switzerland AG 2022
158 M. Bouchard
Fig. 1 Plantar and posterior photographs of an infant with right metatarsus adductus deformity.
The foot has a curved convex lateral border and neutral hindfoot alignment. (From the private col-
lection of Maryse Bouchard, MD)
1.3 Anatomy
The foot with metatarsus adductus presents with a medially deviated forefoot rela-
tive to the hindfoot creating a convex curved lateral border. There is full ankle and
subtalar motion, and hindfoot is in neutral to slight valgus [14].
On anteroposterior (AP) radiographs of the foot, there is often a trapezoidal
shape to the medial cuneiform [15]. Instead of a square bone with its distal and
proximal articular surfaces being parallel to one another, the distal articular surface
is angulated medially resulting in a varus alignment of the first metatarsal (Fig. 2)
[10]. There may also be milder adductus through the lesser metatarsals. The hind-
foot alignment is normal on AP and lateral foot radiographs [14].
1.4 Diagnosis
Metatarsus adductus is a clinical diagnosis based on the shape of the foot.

Radiographs are not necessary for diagnosis. Radiographs are indicated in the case
of significant residual deformity and pain in the older child or adolescent and if
surgical intervention is being considered [1].
The majority of metatarsus adductus deformities in children resolved spontane-
ously by age 3–4 years [8, 16]. In a prospective natural history study by Rushforth
Pediatric Metatarsus Adductus and Cavovarus Foot 159
Fig. 2 AP radiograph of
an older child’s foot with
metatarsus adductus. Note
the medially deviated distal
articular surface (red line)
contributing to the
adducted alignment of the
first metatarsal. Normally,
the distal and proximal
articular surfaces are
parallel to one another
(yellow dashed and solid
lines, respectively). (From
the private collection of
Maryse Bouchard, MD)
et al. with mean follow-up of 7 years, 86% of 83 children with metatarsus adductus
(130 feet) received no treatment and developed normal foot shapes. Ten percent had
persistent moderate deformities but were asymptomatic, and 4% of feet were
deformed and stiff [8]. In a cohort of 335 children with flexible metatarsus adductus
studied by Ponseti and Becker, 88% of feet improved by age 4 years, with only 12%
requiring corrective casting. No poor long-term results or functional disabilities in
patients with mild or moderate residual deformity have been reported [8, 16, 17].
There are two commonly used classifications for metatarsus adductus [18–20].
One classification is based on severity and is determined by the heel bisector when
examining the foot’s plantar surface anatomy (Fig. 3) [20]. The other is based on
flexibility of the foot deformity [18]. Metatarsus adductus is defined as flexible if
the forefoot can be passively abducted beyond the midline heel bisector rendering
the lateral border concave (Fig. 4) [14]. A partly flexible foot can be abducted only
160 M. Bouchard
Fig. 3 The heel bisector method. Severity is determined by how medial a line bisecting the heel
ends in the toes distally. The closer the line ends to the fifth ray, the more severe the deformity. Red
lines denote the heel bisector. (From the private collection of Maryse Bouchard, MD)
Fig. 4 Clinical photos

demonstrating a foot with
flexible metatarsus
adductus. Using the
calcaneal cuboid joint as
the fulcrum, the foot is
abducted. Note the curved
lateral border is now
corrected denoting a
flexible foot (yellow lines).
(From the private
collection of Maryse
Bouchard, MD)
to the midline, with the lateral border only correcting to straight. An inflexible, or
rigid, foot is one that cannot be abducted to the midline, and the lateral border
remains convex [14].
1.5 Non-operative Management
Given the high rate of spontaneous resolution of metatarsus adductus [15–17, 21],
observation is recommended for children under the age of 1 year, especially when
the deformity is flexible [22]. Although passive stretching exercises are commonly
performed, there is no evidence of their efficacy [4, 16]. In a study of 94 newborns
with metatarsus adductus who were randomized to a parental stretching program or
observation, there was no significant difference in resolution or rate of correc-

tion [23].
Other non-operative modalities for management for metatarsus adductus include
orthoses, corrective shoes, and corrective casts. The efficacy of shoes and orthoses
in correcting metatarsus adductus has never been clearly demonstrated, and some
authors believe excessive manipulation into valgus can create harm to the foot caus-
ing an iatrogenic skewfoot deformity [4, 16, 24]. A recent systematic review dem-
onstrated no evidence for treatment of flexible metatarsus adductus and only limited
evidence for partly flexible feet with no supportive high-level studies [22].
Multiple studies have shown efficacy of manipulation and serial casting for the
correction of partly flexible and rigid deformities and recommend initiation under
the age of 1 year [16, 18, 24, 25]. No upper age limit has been reported, and there is
no clear indication to initiate treatment before the age of 6 months [1]. The tech-
nique for manipulation and casting is important to avoid excessive valgus of the
hindfoot. Ponseti and Becker originally describe a technique with long-leg casts
where the fulcrum of the manipulation is on the lateral border of the foot at the
cuboid [16]. An abduction moment is applied at the medial aspect of first metatarsal
head while maintaining the hindfoot in neutral [16]. Orthoses and shoes are often
used after correction to decrease the risk of recurrence. Recurrence ranges between
8% and 37% [2, 18, 26].
Katz et al. published on the use of short-leg casts for correction of partly flexible
and rigid deformities and reported similar correction and recurrence rates to studies
using long-leg casts [25]. Herzenberg et al. prospectively randomized 27 infants
with residual metatarsus adductus deformity aged 3–9 months to treatment with
either serial plaster casts or a triplanar-hinged orthoses. There was no difference in
outcomes or rate of correction; however, parental compliance was critical for suc-
cess with the orthosis [27].
1.6 Surgical Management
Although surgery is rarely indicated for metatarsus adductus in children, many

operative procedures have been recommended for resistant deformities [1].
Described soft tissue procedures include release of the abductor hallucis and medial
midfoot capsulotomies [12, 13]. When capsulotomies were combined with intermeta-
tarsal ligament releases, there was a 41% long-term complication rate with skin
sloughing, avascular necrosis of the middle and lateral cuneiforms, prominence of the
first metatarsal-tarsal joint, and early degenerative changes [28]. Hallux valgus has
been reported after abductor hallucis release [12]. For children between 1 and 3 years
old with rigid deformities rendering who recur after casting and bracing and have
persistent problems with shoe wear and skin breakdown, this author has performed
mini-open distal abductor hallucis recessions followed by use of straight last shoes for
6 months. Anecdotally, this small improvement in flexibility of the first ray resolved
symptoms, and no hallux valgus has occurred in short- to medium-term follow-up.
162 M. Bouchard
If an older child experiences ongoing pain and disability from residual metatar-
sus adductus deformity, surgery may be indicated after failure of non-operative
interventions such as insoles and shoe modification. On standing radiographs of the
foot, skewfoot deformity should be ruled out. Corrective osteotomies are ideally
performed at the apex of deformity. In metatarsus adductus, the site is typically the
misshapen trapezoidal medial cuneiform [14]. This author’s preferred technique is
therefore a medial opening wedge osteotomy of this bone. In more severe or rigid
deformities, additional closing wedge osteotomy of the cuboid or base of second,
third, or fourth metatarsals may be required [29–32] (Fig. 5). It is important to rec-
ognize the high risk of resulting shortening due to osteotomies of the first
a b
Fig. 5 Medial opening wedge medial cuneiform osteotomy for correction of residual metatarsus
adductus in the older child. (a) Direction of the osteotomy aiming to wards the second tarsometa-
tarsal joint. (b) Distraction of the osteotomy to achieve correction of the adducted first ray. (c)
Placement of tricortical allograft. Internal fixation can be added if there is insufficient press-fit of
the graft. (From the private collection of Maryse Bouchard, MD)
metatarsal. Shortening from nonunion or physeal injury is reported in 5–30% of

patients [33]. Recently, good results have been reported with percutaneous lesser
metatarsal osteotomies and first tarsometatarsal joint capsule release in children
with a mean age of 5.7 years and mean follow-up of 55 months [34].
2 Cavovarus Foot
2.1 Introduction
The cavovarus foot is challenging to treat. The concurrent deformities in the fore,
mid-, and hindfoot are typically coupled with muscle imbalance and joint contrac-
tures. Successful correction relies on determining the underlying diagnosis and the
application of deformity-based principles to select the appropriate surgical
procedures.
2.2 Etiology
Cavovarus foot deformity is rare in children under 3 years. Incidence in adults is

10–20% [35–38]. In up to two-thirds of patients, the underlying etiology is second-
ary to a spinal cord or neuromuscular disorder, with Charcot-Marie-Tooth (CMT)
disease, a hereditary sensorimotor neuropathy (HSMN), being one of the most com-
mon causes [36, 37, 39]. CMT rarely presents in children under age 10 years and is
causative in approximately half of adults with a neuromuscular cavovarus foot [37,
40]. Other common pathologies include tethered cord, myelodysplasia, and post-
traumatic injuries [37, 39, 41]. Poor prognosis is associated with early age of onset.
The subtle, flexible cavovarus foot may be a normal variant, but a neuromuscular
etiology in all cavovarus feet must be considered and ruled out [36]. Table 1 includes
a comprehensive list of differential diagnoses.
Establishing the etiology is important to understand the natural history of the
deformity and risk of recurrence. Some conditions are static (cerebral palsy (CP),
post-traumatic injury), while others are progressive (HSMN and tethered cord) [37,
39, 42]. However, typically bilateral, cavovarus deformities can be unilateral in
hemiplegic CP, poliomyelitis, peripheral nerve lesions or tumors, or after compart-
ment syndrome or trauma [37, 39, 41, 42].
2.3 Anatomy
Muscle imbalance in the cavovarus foot causes deformities of the fore-, mid-, and
hindfoot and if left untreated can progress to rigid deformities.
164 M. Bouchard
Table 1 Differential diagnosis for cavovarus foot deformity

Brain Cerebral palsy
Friedrich’s ataxia
Tumor
Spinocerebellar degeneration
Spine Tumor
Spinal dysraphism (tethered cord, myelomeningocele,
diastematomyelia)
Spinal muscular atrophy
Poliomyelitis
Peripheral nervous Hereditary sensorimotor neuropathy (Charcot-Marie-Tooth)
system Traumatic or neoplastic nerve lesions
Muscle and tendon Leg compartment syndrome
Residual clubfoot deformity
Muscular dystrophy
Bone Tarsal coalition
Post-traumatic (fracture malunion)
Weakness of the foot intrinsics leads to shortening of the plantar fascia and the
short flexors of the toes, thereby increasing the height of the medial arch [39].
Plantarflexion of the first ray, also described as pronation of the forefoot, is further
accentuated by the relative over-pull of peroneus longus versus the tibialis anterior
[14]. Flexibility of the plantarflexed first ray is assessed manually by elevating the
first metatarsal head. If the arch can be completely flattened, the forefoot pronation
is flexible, and the hindfoot will remain aligned in valgus [43].
In stance, the weight through a normal-shaped foot is evenly distributed as a tri-
pod between the first and fifth metatarsal heads and the heel. When there is exces-
sive plantarflexion of the first ray, the foot rolls onto the lateral border and the heel
is forced into varus alignment to keep all three points on the ground [44]. The flex-
ibility of the hindfoot varus is assessed with the Coleman block test [45]. This
author performs a modified version of the Coleman block test as described by
Mosca where only the fourth and fifth metatarsal heads are placed on a 2.5 cm block
[14]. With the first ray in its plantarflexed position, the heel will correct to its normal
valgus if the hindfoot deformity is flexible [39, 44, 46] (Fig. 6). If the hindfoot varus
is rigid, the heel remains in varus or only partially corrects to neutral. Relative
weakness of tibialis anterior versus the tibialis posterior and peroneus longus fur-
ther contributes to hindfoot varus [44].
Dynamic supination occurs when there is over-pull of tibialis anterior compared
to peroneus brevis. This can be appreciated in gait or with active dorsiflexion of the
ankle on seated exam [44, 47]. A fixed supination in stance phase and at rest occurs
with a rigid hindfoot varus deformity or when there is excessive over-pull of tibialis
posterior over the peroneals [47]. When the hindfoot is in varus, the Achilles tendon
exacerbates the supination deformity acting as a secondary inverter [37, 44].
Fig. 6 Photograph
demonstrating the modified
Coleman block test
showing correction of
hindfoot varus to valgus.
This is therefore a flexible
hindfoot deformity. (From
the private collection of
Maryse Bouchard, MD)
Fig. 7 When examining for equinus, be sure to evaluate the hindfoot relative to the tibia. If severe
cavus is present, this can confuse the examiner as it gives the appearance of equinus. The horizon-
tal yellow line represents the axis of the tibia. The vertical yellow line shows the inclination of the
hindfoot and the blue the inclination of the forefoot. The red line represents the plantar aspect of
the foot. Relative to the tibial axis, if referencing the red line, it would suggest significant lack of
dorsiflexion at the ankle. Manually covering the forefoot can help visualize the true hindfoot posi-
tion. In this patient, the hindfoot is dorsiflexed (yellow lines), and therefore correction of the cavus
and not Achilles lengthening is required. (From the private collection of Maryse Bouchard, MD)
Assessment for equinus contracture can be challenging in feet with severe cavus
as the midfoot deformity gives the appearance that the ankle cannot dorsiflex above
neutral [46]. A more accurate examination of ankle equinus can be achieved by
manually covering forefoot to better visualize only the hindfoot position versus the
tibial axis (Fig. 7). The Silfverskiold test must also be performed to determine if the
166 M. Bouchard
contracture is due to the entire triceps surae complex or the gastrocnemius alone, as
this will inform selection of the appropriate surgical procedure [47]. The Silfverskiold
test assesses ankle dorsiflexion with the knee in flexion relaxing the gastrocnemius
and with the knee in extension tensioning the gastrocnemius as it crosses the knee
joint. If equinus is present when the knee is in extension, but improves or resolves
when the knee is flexed, the gastrocnemius is predominantly shortened [14].
Toe deformities can result from the relative weakness of the long toe extensors
and flexors versus the intrinsics [47, 48]. Most common are toe flexion contractures
(hammer toes) and claw toes [39, 46, 48]. A hammer toe is flexible if it straightens
with a “push-up test,” when the examiner elevates the metatarsal head manually.
2.4 Diagnosis
A thorough history and physical examination, and elucidation of the underlying

etiology, are imperative to inform optimal management of the cavovarus foot.
Focused history should include the onset and progression of deformity, pain, dis-
ability, problems with shoe wear, and presence of neurologic symptoms such pares-
thesias [43]. The surgeon should confirm the family history, birth and developmental
history, past surgical history, and any antecedent trauma [39].
Foot position in stance and during gait is necessary to identify static and dynamic
deformities. A high-steppage gait with recruitment of toe extensors is typical in
CMT [39]. Assessment of the feet for calluses and evaluation of the patient’s shoes
for wear patterns will improve understanding of the deformity [36]. With long-
standing cavovarus deformity, ankle instability can develop and should be tested for
[43]. Passive range of motion of the for-, mid-, and hindfoot should be performed as
described above to determine the flexibility of identified deformities. The spine and
hips must also be examined [44].
A complete neurological exam is required including manual strength testing,
sensory examination, and deep tendon reflex testing of the upper and lower extremi-
ties [29, 37, 47]. Assessment of muscle bulk is important as conditions such as CMT
can present with muscle wasting of the calves and hand intrinsics [43].
Weight-bearing AP and lateral radiographs of the foot and ankle are essential to
assess the cavovarus deformity [39, 42, 44]. Hindfoot alignment is best evaluated on
a Saltzman view [43].
There are many angles described to assess foot deformities. This author prefers
measures that identify the location of the deformity as they inform the surgical plan.
Assessment of midfoot deformity on the AP and lateral views is determined by the
intersection of the longitudinal axes of the first metatarsal and talus. The angle
between these axes on both views is normally 0–5 degrees [36, 39] (Fig. 8a and b).
The location of the intersection, as opposed to the magnitude of angle, identifies the
site or apex of deformity. In a cavovarus foot, this is typically in the medial cunei-
form [14]. When there is hindfoot varus, the intersection on the AP view may occur
in the head of the talus [14]. On the lateral, calcaneal pitch (normal 20–30 degrees)
may be decreased if equinus is present or increased if there is calcaneocavus [36,

39] (Fig. 8b). On the Saltzman view, the axis of the calcaneus to the tibia is normally
in slight valgus but may be in varus in a cavovarus foot [35, 47] (Fig. 8c).
When a clinical Coleman block test is equivocal, Saltzman x-rays taken with the
foot on and off the Coleman block are helpful to confirm if hindfoot alignment has
improved [14, 45] (Fig. 8c).
In especially rigid deformities, tarsal coalitions and degenerative changes should
be ruled out on radiographs. If suspected, or in cases of severe deformity, a CT scan
can be helpful [41, 44]. Magnetic resonance imaging (MRI) of the ankle or foot is
rarely indicated [4].
a b
Fig. 8 (a) AP weight-bearing foot radiograph with first metatarsal-talar angle with intersection in
the talar head demonstrating the site of hindfoot varus deformity (yellow lines). (b) Lateral weight-
bearing foot radiograph with first metatarsal-talar angle with intersection in the medial cuneiform
demonstrating the site of cavus deformity (yellow lines). The lateral calcaneal pitch is also demon-
strated and in normal range (orange lines). (c) Saltzman view radiographs on and off a Coleman
block. Note improvement of the calcaneal-tibial alignment (green lines) and foot position when
positioned on the Coleman block. This confirms improvement of hindfoot varus and flexibility of
the hindfoot deformity. (From the private collection of Maryse Bouchard, MD)
168 M. Bouchard
Acetabular dysplasia can occur in patients with CMT. A screening AP pelvis

radiograph is recommended [36, 39]. Additional diagnostic investigations may
include electromyography, nerve conduction studies, radiographs of the spine, and/
or MRI of the brain, spine, or affected extremity [36, 39, 41]. Referral to neurology
is also recommended.
2.5 Non-operative Management
For progressive cavovarus foot conditions, there is a very limited role for non-
operative intervention. Physical therapy [36], orthotics [35–37], bracing, casting
[48, 49], and botulinum toxin [50] have all been described without success at cor-
recting or preventing worsening of the cavovarus deformity [39].
D’Astorg et al. published a series of 23 children (35 feet) with cavovarus feet
treated with serial casting and turnbuckle bracing [49]. Bracing and casting achieved
better outcomes than bracing alone. After 4.5 years, 10 feet required surgery. No
patient required triple arthrodesis. This is the only study to date supportive of non-
operative intervention [49].
Accommodative orthotics or gait aids may have a role in the mild non-progressive
deformity [36, 37].
2.6 Surgical Management
In almost all cavovarus feet, surgical correction is recommended. Goals of surgery

are to achieve a plantigrade, supple foot to alleviate pain, improve function, and
prevent development of rigid deformities and degenerative changes [46]. In the
child or adolescent, with rare exception, procedures should be joint and physeal
sparing [35, 37, 38, 43, 46].
Surgical correction may involve a combination of soft tissue releases, tendon
transfers, and osteotomies. Determining the necessary procedures will depend on
the flexibility of the deformities and their location. When deformities are flexible,
soft tissue procedures are typically sufficient, while rigid deformities require the
addition of bony procedures [36, 39, 42].
The order in which procedures are performed is important to ensure optimal
deformity correction. Performing soft tissue before bony procedures helps avoid
unnecessary bony overcorrection [14]. Tendon transfers should be secured after
deformity correction is achieved to avoid overly taught or lax tension [14, 37, 39,
51]. Osteotomies should be done at the site of deformity or as close to it as possible
to avoid creating secondary deformities [14, 37, 51].
Consider staging procedures in severe rigid feet. Performing simultaneous soft
tissues and osteotomies may not allow for full and immediate deformity correction
due the tight plantarmedial skin [14, 43]. By staging the plantarmedial soft tissue
releases in a first surgery then allowing the patient to walk in a short-leg cast allows
for gradual stretching of the skin and soft tissues. When the second surgery for the
required osteotomies and tendon transfers is performed 2–3 weeks later, there is
now more flexibility in the foot and improved ability to obtain full correction
[14, 43].
There are many procedures described in the literature and in textbooks.
Determining the optimal treatment for individual cavovarus feet can be challenging.
Each foot is different in etiology, flexibility, severity, and muscle imbalance and
requires careful assessment. A one-size-fits-all approach is not adequate. This
author determines the operative plan based on five questions to assess and qualify
the deformities present in the cavovarus foot [43].
2.6.1 Is the Forefoot Pronation Flexible or Rigid?
First, the surgeon must assess if there is adduction of the first ray in addition to
plantar flexion. Secondly, through manual testing, they must determine if the prona-
tion is flexible or rigid.
In flexible deformities, soft tissue releases are sufficient. As described above, the
weakened plantar intrinsic muscles and plantar fascia shorten elevating the arch.
The abductor hallucis is typically spared in CMT and therefore can cause adduction
of the first ray. If only plantarflexion is present, the plantar fascia is released. If there
is adduction and plantarflexion, through a medial incision, the plantar fascia and
three bellies of the abductor hallucis are released from the calcaneus, decompress-
ing the tarsal tunnel [14, 35]. Care must be taken not to injure the lateral and medial
plantar nerves [35].
To augment a relatively weak peroneus brevis and to minimize the plantarflexion
moment of the peroneus longus on the first ray, the longus can be transferred to the
brevis. This can be performed through a lateral approach at the midfoot or postero-
laterally if performing a concurrent calcaneal osteotomy. A side-to-side tenodesis or
Pulvertaft weave may be used to dock the longus tendon to the brevis [42, 43, 46].
If the forefoot pronation is rigid, a dorsiflexion osteotomy through the apex of
the deformity is required in addition to the above soft tissue releases [14]. A variety
of midfoot osteotomies, in isolation or in combination, have been described to cor-
rect cavus including first and lesser metatarsal osteotomies, cuboid closing wedges,
and medial cuneiform dorsiflexion opening and closing wedges [52].
In most cavovarus feet, the apex of the midfoot deformity as described above is
in the medial cuneiform [36, 41]. This author therefore performs a plantarmedial-
based opening wedge osteotomy of the medial cuneiform to correct both the plan-
tarflexion and adduction of the first ray [14, 43]. A tricortical triangular piece of
allograft is used [14, 43], but autograft is an equal alternative [41]. As this osteot-
omy is under tension, fixation of the graft or bone is rarely required [14]. If unstable,
a Steinman pin is usually sufficient [52].
170 M. Bouchard
2.6.2 Is the Hindfoot Varus Flexible or Rigid?
Flexibility of the hindfoot varus is assessed clinically and/or radiographically by the

Coleman block test. If the hindfoot varus corrects to valgus, it is considered flexible
and is treated by correcting the forefoot pronation that is driving the deformity as
described above [14, 43].
If the hindfoot does not correct into valgus on the Coleman block, additional soft
tissue releases and a lateralizing posterior calcaneal displacement osteotomy are
needed [14, 43, 52]. The tibialis posterior requires lengthening or a recession [53],
and release of the talonavicular joint capsule, sparing the lateral aspect, may be
needed in particularly rigid feet [14, 47]. For the lateral displacement posterior cal-
caneal osteotomy, this author prefers a percutaneous minimally invasive technique
using a cooled Shannon burr. There is little published on results in children [54];
however, the adult literature strongly supports the technique with equivalent defor-
mity correction, less postoperative pain, swelling and wound issues, and no
increased infection or neurovascular injury rates [55, 56] (Fig. 9). Alternatively, this
author uses a posterolateral open approach, taking care to preserve the sural nerve
and peroneal tendons [43]. To prevent unwanted lengthening or shortening of the
calcaneus, the osteotomy is made in the plane of the metatarsal heads, as opposed to
perpendicular to the lateral wall of the calcaneus [14].
Fig. 9 (a) Intraoperative photograph of the percutaneous technique for calcaneal displacement
osteotomy with a cooled Shannon burr. (b) Intraoperative radiographs demonstrating the percuta-
neous osteotomy of the posterior calcaneus, using a Williger to translate and final screw fixation.
(From the private collection of Maryse Bouchard, MD)
Other osteotomies of the calcaneus have been described. The Dwyer osteotomy
is a biplanar calcaneal osteotomy that adds a lateral closing wedge to the slide, and
Malerba described a concurrent translational and rotational “Z” cut osteotomy [35,
41, 46, 47]. The Z osteotomy provides the most powerful correction but also has the
highest complication rate [57].
2.6.3 Is There Dynamic or Fixed Supination of the Foot?
When there is dynamic supination resulting from relative overpower of tibialis ante-
rior to peroneus brevis, a tendon transfer should be performed though this is not
routinely needed in patients with CMT.
To correct dynamic supination, the tibialis anterior should be transferred in full
or partially to the dorsolateral foot [14]. Selecting the appropriate transfer technique
depends on the degree of eversion weakness and severity of deformity. This author
prefers a split transfer to the lateral cuneiform when there is ≥4 out of 5 peroneal
strength on manual testing [43]. If there is weak or no peroneal function (<4 out of
5), a full transfer can be performed with docking as far lateral as the cuboid if neces-
sary for optimal muscle balance [43].
If the supination is fixed, and the eversion and dorsiflexion function are weak or
absent, consider full or partial tibialis posterior tendon transfer through the interosse-
ous membrane to the lateral cuneiform [39, 42, 48]. Consider transfer to the cuboid
if there is no eversion function. It is important to include plantar fascia, abductor
hallucis, and talonavicular joint capsule releases as needed, and to ensure correction
of the hindfoot varus is also achieved, to avoid recurrence or persistence of deformity.
Dreher et al. report improved active balanced dorsiflexion in swing phase and
maintained active plantarflexion with total split posterior tibialis tendon transfers in
adults with CMT [42]. There is no literature supporting this technique routinely in
children, and there is scant evidence on the minimum age to perform a tibialis pos-
terior transfer. Turner and Cooper describe a cohort of 33 patients with equinovarus
from multiple etiologies in children aged 1–25 years [58]. Overcorrection occurred
predominantly in children with spastic CP and spina bifida. Age at the time of sur-
gery was not reported. Aydin et al. report on 24 patients with post-traumatic foot
drop (75%) and myelodysplasia (25%) aged 7–18 years [59]. No patient developed
a flatfoot after a mean of 32 months follow-up. To avoid overcorrection, this author
reserves full transfers of the tibialis posterior to children aged 8 years and older and
selects split transfers when there is significant risk of muscle imbalance such as in
spastic or myelodysplastic conditions [43].
2.6.4 Is There Concurrent Equinus?
In a cavovarus foot without equinus, Achilles lengthening is contraindicated as the

tendon acts as the counterforce in the correction of the cavus after the plantarmedial
tissues are released from the calcaneus [48]. If there is equinus based on clinical and
172 M. Bouchard
radiographic assessment, the appropriate lengthening should be performed. If the

gastrocnemius alone is tight, a recession of this muscle (Strayer) is done [35]. If
there is <10 degrees of equinus with the knee extended, this author performs a
recession of the gastrocnemius and soleus (Vulpius), or a percutaneous or mini-
open tendoachilles release, such as the double-cut lengthening described by Mosca
[14, 43]. If equinus is ≥10 degrees with the knee extended and there is little risk of
overlengthening, an open z-lengthening of the tendon is preferred [43].
2.6.5 Are There Toe Deformities and Are They Flexible or Rigid?
If hammer toes are present and remain flexible as per the push-up test, percutaneous
long toe flexor tenotomy performed distally, with temporary pinning as needed, is
indicated [42, 43]. For a flexible first claw toe, most surgeons perform a modified
Jones procedure (first interphalangeal joint fusion with EHL transfer to dorsal meta-
tarsal neck) with good results [36, 37, 39, 46]. For flexible lesser claw toes, a variety
of tendon transfers have been described including the Girdlestone-Taylor (flexor
digitorum longus [FDL] to the extensor hood [36, 39] and extensor digitorum lon-
gus [EDL] to the neck of the metatarsals [39, 46, 48]) but with less predictable
outcomes. Alternatively, a Hibbs transfer of the EDL to the cuboid or the peroneus
tertius can be performed with percutaneous tenotomy of the distal FDL tendons
[14]. If the toe deformities are rigid and symptomatic, an arthrodesis [39] or resec-
tion arthroplasty of the affected joints is necessary.
2.7 Intraarticular and Tibial Deformity
The surgeon must also assess for concurrent coronal and/or rotational deformity of
the distal tibia. A supramalleolar osteotomy may be required if present [42, 44].
Similarly, the chronic lateral overloading of the foot and ankle from the rigid hind-
foot varus alignment may lead to lateral ankle instability [44, 47]. If present on
examination and the ankle joint is healthy, a lateral ligament repair should be con-
sidered especially if laxity persists after deformity correction [43]. The modified
Brostrom, Brostrom-Gould, and repairs with allo- and autograft augment have been
described for this indication [35, 41, 44]. Lateral ankle instability with concurrent
degenerative ankle joint changes typically does not occur until adulthood and often
requires arthrodesis or arthroplasty.
2.8 Gradual Deformity Correction
For the isolated cavovarus foot, indications for gradual deformity correction with a
circular external fixator are rare and should only be employed if severe deformities
cannot be corrected acutely, in patients whose feet are significantly shortened from
prior surgeries, or have a poor soft tissue envelope preventing standard surgical
approaches [60, 61]. In cases with concurrent equinus, an external fixator may be
more useful [60, 61]. Typically under 8–10 years of age, correction by soft tissue
distraction is possible. Osteotomies through the calcaneus or midfoot can be added
in older children with acute or gradual correction [43]. The typical complications of
external fixators remain, such as pin site infections and pain, and residual stiffness
and recurrence are common [51, 60].
2.9 Arthrodesis and Midfoot Wedge Resections
Arthrodesis and large wedge resections should only be considered in the older child
with severe rigid deformity [43].
Classically, severe midfoot deformity was corrected with a dorsal or dorsolateral
closing wedge resection through the joints or tarsal bones. Multiple techniques have
been described including the Cole, Jahss, Japas, or Akron dome [46, 51, 53].
Although powerful, the foot is left stiff and shortened [39]. Better results and lower
recurrence are reported in patients over 8 years of age with non-progressive disor-
ders [37, 39, 51].
Other described resection techniques include navicular excision and dorsolateral
cuboid closing wedge as described by Mubarak and Dimeglio in a small series of patients
with good results at 5 years [62]. Shariff et al. obtained good results with partial or com-
plete excision of the base of the fifth metatarsal in adults with residual lateral overloading
after cavovarus deformity correction with a triple fusion or osteotomies [47, 63].
Arthrodesis is not recommended before the age of 10–12 years [39, 64]. There is
scant literature on the outcomes of arthrodesis in the pediatric foot and minimal
evidence supporting its use in isolated cavovarus deformity. Specifically in adults
with CMT undergoing triple arthrodesis, satisfaction ranges from excellent to good
with development of adjacent joint disease in 24–77% [65–69]. Saltzman et al.
reported on their 40-year follow-up of triple arthrodesis in adult patients and found
75% good and 25% fair outcomes at 25 years, whereas at 40 years, 28% had good
results, 69% were fair, and 3% had poor results [65]. Aarts et al. reported 58% of
adult patients at 7.5 years following triple fusion showed no signs of adjacent joint
disease [66]. Generally results are better in the setting of non-progressive motor
conditions and if sensation is spared [53]. It is important for the surgeon to remem-
ber that the arthrodesis alone will not correct the forefoot pronation or muscle
imbalance and should be addressed separately as described above [53].
2.10 Postoperative Protocol
Most patients are placed in a short-leg cast after surgery. If only soft tissue releases
were performed, weight-bearing is allowed [43]. If tendon transfers or osteotomies
were required, the patient is non-weight-bearing for a minimum of 6 weeks [14, 42,
174 M. Bouchard
43]. If the etiology of the cavovarus foot is progressive, they are transitioned to
custom articulated ankle-foot-orthosis for maintenance of deformity correction [37,
39, 43]. Monitoring and surveillance of the children throughout growth to watch for
and, if needed, manage recurrence are critical. Transition to an adult surgeon should
be made for ongoing care if the underlying etiology is progressive [43].
3 Summary
Spontaneous resolution of the metatarsus adductus can occur up to age 4 years, and
minor residual deformity rarely leads to disability. The cavovarus foot can be chal-
lenging to manage. It requires an understanding of the etiology, concurrent deformi-
ties, and muscle imbalances to determine the optimal treatment. Recurrence in
progressive deformities is common, and close follow-up is mandatory.
References
1. Mosca V, Bouchard M. Chapter 28: The foot. In: Weinstein SL, Flynn JM, editors. Lovell and
Winter’s pediatric orthopedics. 8th ed. Philadelphia: Lippincott Williams and Wilkins; 2020.
p. 1431–4.
2. Wynne-Davies R. Family studies and the cause of congenital club foot. Talipes equinovarus,
talipes calcaneo-valgus and metatarsus varus. J Bone Joint Surg Br. 1964;46:445–63.
3. Hunziker UA, Largo RH, Duc G. Neonatal metatarsus adductus, joint mobility, axis, and rota-
tion of the lower extremity in preterm and term children 0–5 years of age. Eur J Pediatr.
1988;148:19–23.
4. Kite JH. Congenital metatarsus varus. J Bone Joint Surg Am. 1967;49:388–97.
5. Kumar SJ, MacEwen GD. The incidence of hip dysplasia with metatarsus adductus. Clin
Orthop Relat Res. 1982;164:234–5.
6. Gruber MA, Lozano JA. Metatarsus varus and developmental dysplasia of the hip: is there a
relationship? Orthop Trans. 1991;15:336.
7. Kollmer CE, Betz RR, Clancy M, et al. Relationship of congenital hip and foot deformities: a
national Shriner’s Hospital survey. Orthop Trans. 1991;15:96.
8. Rushforth GF. The natural history of hooked forefoot. J Bone Joint Surg Br. 1978;60-B:530–2.
9. Wynne-Davies R, Littlejohn A, Gormley J. Aetiology and interrelationship of some common
skeletal deformities. (Talipes equinovarus and calcaneovalgus, metatarsus varus, congenital
dislocation of the hip, and infantile idiopathic scoliosis). J Med Genet. 1982;19:321–8.
10. Morcuende JA, Ponseti IV. Congenital metatarsus adductus in early human fetal development:
a histologic study. Clin Orthop Relat Res. 1996;333:261–6.
11. Browne RS, Paton DF. Anomalous insertion of the tibialis posterior tendon in congenital meta-
tarsus varus. J Bone Joint Surg Br. 1979;61:74–6.
12. Asirvatham R, Stevens PM. Idiopathic forefoot-adduction deformity: medial capsulotomy
and abductor hallucis lengthening for resistant and severe deformities. J Pediatr Orthop.
1997;17:496–500.
13. Mitchell GP. Abductor hallucis release in congenital metatarsus varus. Int Orthop.
1980;3(4):299–304. https://doi.org/10.1007/BF00266025. PMID: 7399770
tions. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2014. p. 21, 26, 32–33,
43, 45, 68–69, 145–160, 176–177, 226–235.
15. Cappello T, Mosca VS. Metatarsus adductus and skewfoot. Foot Ankle Clin. 1998;3:683–700.
16. Ponseti IV, Becker JR. Congenital metatarsus adductus: the results of treatment. J Bone Joint
Surg Am. 1966;48:702.
17. Farsetti P, Weinstein SL, Ponseti IV. The long-term functional and radiographic outcomes
of untreated and non-operatively treated metatarsus adductus. J Bone Joint Surg Am.
1994;76:257–65.
18. Bleck EE. Metatarsus adductus: classification and relationship to outcomes of treatment. J
Pediatr Orthop. 1983;3:2–9.
19. Bleck EE. Developmental orthopaedics. III. Toddlers. Dev Med Child Neurol. 1982;24:533.
20. Smith JT, Bleck EE, Gamble JG, et al. Simple method of documenting metatarsus adductus. J
Pediatr Orthop. 1991;11:679–80.
21. Ghali NN, Abberton MJ, Silk FF. The management of metatarsus adductus et supinatus. J
Bone Joint Surg Br. 1984;66:376–80.
22. Williams CM, James AM, Tran T. Metatarsus adductus: development of a non-surgical
treatment pathway. J Paediatr Child Health. 2013;49(9):E428–33. https://doi.org/10.1111/
jpc.12219. Epub 2013 May 6. PMID: 23647850.
23. Eamsobhana P, Rojjananukulpong K, Ariyawatkul T, Chotigavanichaya C,
Kaewpornsawan K. Does the parental stretching programs improve metatarsus adduc-
tus in newborns? J Orthop Surg (Hong Kong). 2017;25(1):2309499017690320. https://doi.
org/10.1177/2309499017690320. PMID: 28215117.
24. Berg EE. A reappraisal of metatarsus adductus and skewfoot. J Bone Joint Surg Am.
1986;68:1185–96.
25. Katz K, David R, Soudry M. Below-knee plaster cast for the treatment of metatarsus adductus.
J Pediatr Orthop. 1999;19(1):49–50. PMID: 9890286.
26. McCauley J Jr, Lusskin R, Bromley J. Recurrence in congenital metatarsus varus. J Bone Joint
Surg Am. 1964;46:525–32.
27. Herzenberg JE, Burghardt RD. Resistant metatarsus adductus: prospective randomized
trial of casting versus orthosis. J Orthop Sci. 2014;19(2):250–6. https://doi.org/10.1007/
s00776-013-0498-7. Epub 2013 Nov 19. PMID: 24248551.
28. Stark JG, Johanson JE, Winter RB. The Heyman-Herndon tarsometatarsal capsulotomy for
metatarsus adductus: results in 48 feet. J Pediatr Orthop. 1987;7:305–10.
29. McHale KA, Lenhart MK. Treatment of residual clubfoot deformity—the “bean-shaped”
foot—by opening wedge medial cuneiform osteotomy and closing wedge cuboid osteotomy.
Clinical review and cadaver correlations. J Pediatr Orthop. 1991;11:374–81.
30. Anderson DA, Schoenecker PL, Blair VPI. Combined lateral column shortening and medial
column lengthening in the treatment of severe forefoot adductus. Orthop Trans. 1991;15:768.
31. Conklin MJ, Kling TF. Open-wedge osteotomies of the first cuneiform for metatarsus adduc-
tus. Orthop Trans. 1991;106.
32. Feng L, Sussman M. Combined medial cuneiform osteotomy and multiple metatarsal oste-
otomies for correction of persistent metatarsus adductus in children. J Pediatr Orthop.
2016;36(7):730–5. https://doi.org/10.1097/BPO.0000000000000559. PMID: 26057072.
33. Holden D, Siff S, Butler J, et al. Shortening of the first metatarsal as a complication of meta-
tarsal osteotomies. J Bone Joint Surg Am. 1984;66:582–7.
34. Knörr J, Soldado F, Pham TT, Torres A, Cahuzac JP, de Gauzy JS. Percutaneous correction
of persistent severe metatarsus adductus in children. J Pediatr Orthop. 2014;34(4):447–52.
https://doi.org/10.1097/BPO.0000000000000122. PMID: 24276227.
35. Kim BS. Reconstruction of cavus foot: a review. Open Orthop J. 2017;11:651–9. https://doi.
org/10.2174/1874325001711010651.
36. VanderHave KL, Hensinger RN, King BW. Flexible cavovarus foot in children and adoles-
cents. Foot Ankle Clinic N Am. 2013;18(4):715–26.
37. Schwend R, Drennan J. Cavus foot deformity in children. J Am Acad Orthop Surg.
2003;11(3):201–11.
38. Dwyer FC. The present status of the problem of pes cavus. Clin Orthop. 1975;106:254–75.
39. Lee MC, Sucato DJ. Pediatric issues with cavovarus foot deformities. Foot Ankle Clin.
2008;13(2):199–219, v. https://doi.org/10.1016/j.fcl.2008.01.002.
176 M. Bouchard
40. Alexander IJ, Johnson KA. Assessment and management of pes cavus in Charcot-Marie-Tooth
disease. Clin Orthop Relat Res. 1989;246:273–81.
41. DeVries JG, McAlister JE. Corrective osteotomies used in cavus reconstruction. Clin Podiatr
Med Surg. 2015;32(3):375–87. https://doi.org/10.1016/j.cpm.2015.03.003.
42. Dreher T, Beckmann NA, Wenz W. Surgical treatment of severe cavovarus foot deformity in
Charcot-Marie-Tooth disease. JBJS Essent Surg Tech. 2015;5(2):e11. https://doi.org/10.2106/
JBJS.ST.N.00005.
43. Bouchard M. Assessment and Management of the Pediatric Cavovarus Foot. Instruct Course
Lect. 2020;69:321–90.
44. Krause F, Seidel A. Malalignment and lateral ankle instability: causes of failure from the varus
tibia to the cavovarus foot. Foot Ankle Clin. 2018;23(4):593–603. https://doi.org/10.1016/j.
fcl.2018.07.005.
45. Coleman SS, Chestnut WJ. A simple test for hindfoot flexibility in the cavovarus foot. Clin
46. Barton T, Winson I. Joint sparing correction of cavovarus feet in Charcot-Marie-Tooth dis-
ease: what are the limits? Foot Ankle Clin. 2013;18(4):673–88. https://doi.org/10.1016/j.
fcl.2013.08.008.
47. Kaplan JRM, Aiyer AA, Cerrato RA, Jeng CL, Campbell JT. Operative treatment of the cav-
ovarus foot. Foot Ankle Int. 2018;39(11):1370–82.
48. Wicart P. Cavus foot, from neonates to adolescents. Orthop Traumatol Surg Res.
2012;98(7):813–28. https://doi.org/10.1016/j.otsr.2012.09.003.
49. d’Astorg H, Rampal V, Seringe R, Glorion C, Wicart P. Is non-operative management of child-
hood neurologic cavovarus foot effective? Orthop Traumatol Surg Res. 2016;102(8):1087–91.
50. Burns J, Scheinberg A, Ryan MM. Randomized trial of botulinum toxin to prevent pes cavus
progression in pediatric Charcot-Marie-Tooth disease type 1A. Muscle Nerve. 2010;42:262–7.
51. Weiner DS, Jones K, Jonah D, Dicintio MS. Management of the rigid cavus foot in children and
adolescents. Foot Ankle Clin. 2013;18(4):727–41. https://doi.org/10.1016/j.fcl.2013.08.007.
52. Mubarak SJ, Van Valin SE. Osteotomies of the foot for cavus deformities in children. J Pediatr
Orthop. 2009;29:294–9.
53. Simon A-L, Seringe R, Badina A, Khouri N, Glorion C, Wicart P. Long term results of the revis-
ited Meary closing wedge tarsectomy for the treatment of the fixed cavavarus foot in adolescent
with Charcot-Marie-Tooth disease. Foot Ankle Surg. 2018;15: pii: S1268-7731(18)34087-9.
54. Uglow MG. Percutaneous pediatric foot and ankle surgery. Foot Ankle Clin. 2016;21(3):577–94.
https://doi.org/10.1016/j.fcl.2016.04.005. Epub 2016 Jun 29. PMID: 27524707.
55. Mourkus H, Prem H. Double calcaneal osteotomy with minimally invasive surgery for the
treatment of severe flexible flatfeet. Int Orthop. 2018;42(9):2123–9. https://doi.org/10.1007/
s00264-018-3910-2. Epub 2018 Mar 26. PMID: 29582117.
56. Gutteck N, Zeh A, Wohlrab D, Delank KS. Comparative results of percutaneous calcaneal
osteotomy in correction of hindfoot deformities. Foot Ankle Int. 2019;40(3):276–81. https://
doi.org/10.1177/1071100718809449. Epub 2018 Nov 9. PMID: 30413133.
57. Pfeffer GB, Michalski MP, Basak T, Giaconi JC. Use of 3D prints to compare the efficacy
of three different calcaneal osteotomies for the correction of heel varus. Foot Ankle Int.
2018;39(5):591–7.
58. Turner JW, Cooper RR. Anterior transfer of the tibialis posterior through the interosseous
membrane. Clin Orthop Relat Res. 1972;1(2):41–9.
59. Aydin A, Topal M, Tuncer K, Canbek U, Yildiz V, Kose M. Extramembranous transfer of
the tibialis posterior for the treatment of drop foot deformity in children. Arch Iran Med.
2013;16(11):647–51.
60. Grill F, Franke J. The Ilizarov distractor for the correction of relapsed or neglected clubfoot. J
Bone Joint Surg Br. 1987;69:593–7.
61. Ferreira RC, Costo MT, Frizzo GG, et al. Correction of neglected clubfoot using the Ilizarov
external fixator. Foot Ankle Int. 2006;27:266–73.
62. Mubarak SJ, Dimeglio A. Navicular excision and cuboid closing wedge for severe cavovarus
foot deformities: a salvage procedure. J Pediatr Orthop. 2011;31:551–6.
63. Shariff R, Myerson MS, Palmanovich E. Resection of the fifth metatarsal base in the severe
rigid cavovarus foot. Foot Ankle Int. 2014;35(6):558–65.
64. Penny JN. The neglected clubfoot. Tech Orthop. 2005;20(2):153–66.
65. Saltzman CL, Fehrle MJ, Cooper RR, et al. Triple arthrodesis: twenty-five and forty-four-year
average follow-up of the same patients. J Bone Joint Surg Am. 1999;81-A(10):1391Y1402.
66. Aarts CAM, Heesterbeek PJC, Jaspers PEM, Stegeman M, Louwerens JWK. Does osteoarthri-
tis of the ankle joint progress after triple arthrodesis? A midterm prospective outcome study.
Foot Ankle Surg. 2016;22:265–9.
67. Wukilch DK, Bowen JR. A long-term study of triple arthrodesis for correction of pes cav-
ovarus in Charcot-Marie-Tooth disease. J Pediatr Orthop. 1989;9:433–7.
68. Wetmore RS, Drennan JC. Long-term results of triple arthrodesis in Charcot-Marie-Tooth dis-
ease. J Bone Joint Surg Am. 1989;71:417–22.
69. Mann DC, Hsu JD. Triple arthrodesis in the treatment of fixed cavovarus deformity in adoles-
cent patients with Charcot-Marie-Tooth disease. Foot Ankle. 1992;13(1):1–6.
Pediatric Flexible and Rigid Flatfoot
Kyle M. Natsuhara and Jacob R. Zide
1 Introduction
Children and adolescents commonly present to orthopedic providers with concerns

about a flatfoot deformity. While the etiology and management of flatfeet in this
population differ substantially from that in adults, there is a lack of consensus as to
what constitutes a consistent definition of the deformity as well as what the optimal
treatment should be. The majority of flatfoot deformities in children are flexible,
painless, and functional and do not require any treatment whatsoever [1, 2].
Despite the fact that most patients with flatfeet will never develop symptoms,
there still exists a widespread negative sentiment associated with the “low-arched”
foot. The genesis of this is unclear, but it may stem somewhat from historic military
reports. In 1944, it was reported that foot symptoms were the cause of 30–40% of
US Army medical discharges. Among soldiers with foot symptoms, many had flat-
feet which led to the assumption that it was the flatfoot that was the source of pain
and disability [3]. This simplistic interpretation resulted in a lingering stigma still
present today and may, in part, explain parental concerns for future pain, physical
dysfunction, or deformity progression in children with asymptomatic flatfeet.
A small percentage of children with flexible flatfeet are symptomatic, and when
this is the case, treatment is often indicated. Additionally, a subset of patients with
K. M. Natsuhara
Department of Orthopaedic Surgery, Baylor University Medical Center, Dallas, TX, USA
J. R. Zide (*)
Department of Orthopaedic Surgery, Baylor University Medical Center, Dallas, TX, USA
Department of Orthopaedic Surgery, UT Southwestern Medical School, Dallas, TX, USA
Department of Surgery, Texas A&M Health Science Center College of Medicine,
Dallas, TX, USA

Switzerland AG 2022
180 K. M. Natsuhara and J. R. Zide
painful flatfeet have rigid deformities suggesting an underlying disorder that war-
rants further investigation and treatment.
2 Etiology-Pathophysiology
The challenge of creating an agreed upon definition of the pediatric flatfoot has
resulted in an unusually wide range of prevalence of 0.6–77.9% found in the litera-
ture [1, 2]. Moreover, the reporting is inconsistent, and disparities related to variable
sampling, different assessment measures, and age groups must be taken into
account [2].
Before defining what constitutes a pathologic flatfoot, it is crucial to understand
what comprises the normal development and common variations of a child’s foot.
Infants are born with flatfeet, and the longitudinal arch forms over the course of the
first decade of life [4, 5]. In a Cochrane review, children aged 2–6 years were found
to have a mean flatfoot prevalence of 46.3% [2]. In studies that investigated children
ages 8–13 years old, the mean prevalence decreased to 14.2% [2]. A study by
Pfeiffer et al. investigated 835 children aged 3–6 years and observed that boys and
obese children were at higher risk for flatfeet than girls and normal weight children
[4]. In fact, boys were twice as likely as girls to have a flatfoot deformity, and chil-
dren who were obese were three times as likely as those with a healthy weight [4].
El et al. found that hypermobility, based on Beighton’s assessment method, was a
risk factor for pediatric flatfoot [6].
The conundrum of the pediatric flexible flatfoot is that there remains no under-
standing as to why some patients become symptomatic while others do not.
Furthermore, when patients are symptomatic, the underlying source of pain has not
been fully elucidated and is likely multifactorial. It has been postulated that increased
hindfoot valgus and collapse of the longitudinal arch elevate stress within the sub-
talar joint which in turn provokes synovial and ligamentous irritation at the subtalar
and midtarsal joints. This irritation, along with overload of the intrinsic muscula-
ture, may be one source of hindfoot pain associated with the deformity [7].
Certain clinical characteristics such as a short Achilles tendon associated with a
flexible flatfoot have been correlated with symptoms and are reported to have an
increased prevalence of pain and disability [1]. Some radiographic parameters also
correspond to symptomatology. For example, a study of 135 pediatric patients over
the age of 7 with idiopathic flexible flatfeet demonstrated that increased lateral dis-
placement of the navicular on the AP radiograph (measured by talonavicular cover-
age) was found to relate to the presence of symptoms [8]. This study found that no
other measurements of hindfoot alignment including longitudinal arch, lateral col-
umn length, or pronation/supination of the forefoot correlated to symptomatology [8].
In contrast to flexible flatfeet, rigid flatfeet occur at a lower prevalence but are
more often symptomatic. There are multiple causes of rigid flatfeet in children and
adolescents, with tarsal coalitions being the most common [1, 9]. However, in
patients without an identifiable structural cause, one must consider and rule out
Pediatric Flexible and Rigid Flatfoot 181
other potential underlying pathologies including but not limited to neoplastic, neu-
rologic, and rheumatologic etiologies [1, 9]. Peroneal and Achilles spasticity are
also associated with rigid flatfoot deformities, so it is important to identify neuro-
logic conditions such as cerebral palsy, hypoxic brain injury, Chiari malformation,
syrinx, trauma, and central nervous system tumors [9, 10].
3 Anatomy
The medial longitudinal arch develops during the first decade of life along with the
bones, muscles, and ligaments of the foot. Maintenance of the longitudinal arch is
thought by some to rely on muscular strength and that a flexible flatfoot is the result
of subclinical muscle weakness [1, 7]. Others theorize that while the surrounding
musculature functions to support balance, propel the body forward, and navigate
uneven terrain, the shape of the longitudinal arch is truly determined by the bone-
ligament complex [1, 7]. Despite the lack of consensus on how the longitudinal arch
is maintained, the biomechanical function of the bony ligamentous complex is well
understood.
In early stance phase, the hindfoot complex of the flexible flatfoot is aligned in
accentuated valgus with the transverse tarsal joint unlocked. As stance phase pro-
gresses, the transition to a locked transverse tarsal joint and varus hindfoot position
requires increased intrinsic muscle activity to stabilize the hindfoot joints at toe off.
It is thought that these demands on the intrinsic musculature may subsequently lead
to foot fatigue and pain.
Contractures of the gastroc-soleus complex and peroneal tendons play an impor-
tant role in flatfoot deformities. The decrease in calcaneal pitch seen in a flatfoot
allows for shortening and contracture of the gastroc-soleus. In concert with the val-
gus alignment of the hindfoot, the shortened Achilles acts as a deforming force,
driving the calcaneus further into valgus and equinus. Contractures of the peroneus
brevis are associated with midfoot abduction deformity. Whether these contractures
are a primary force that drive and exacerbate the deformity or a consequence of the
foot position is not known.
Overt peroneal tendon spasticity as a primary cause of flatfoot deformity in the
pediatric flatfoot is well described but poorly understood. It has been theorized that
the peroneals are dynamically contracted due to subtalar pain and eventually become
shortened [9].
Tarsal coalitions are the most common cause of a rigid flatfoot deformity. They
are thought to be the product of failure of mesenchymal segmentation and are char-
acterized by a fibrous, cartilaginous, or osseous connection between two or more
tarsal bones [11, 12]. The most common coalitions are calcaneonavicular (CN) and
talocalcaneal (TC). While it is thought that coalitions are present from birth in car-
tilaginous form, ossification of the coalition occurs between the ages of 8 and 12
years and correlates closely with the most common age range for symptomatic clin-
ical presentation [11].
4 Diagnosis
4.1 History
Children and adolescents commonly present for evaluation secondary to parental

concern regarding the cosmetic appearance of the foot or the potential for future
disability rather than for pain or dysfunction. Determining whether or not the patient
is symptomatic is the most important part of the interaction as it guides all further
discussion with the patient and family.
The physician should inquire as to recurrent injuries, calluses, or skin irritation.
Difficulties with shoe wear, walking bare foot, or walking on uneven surfaces may
also provide clues regarding the underlying diagnosis. A history of frequent ankle
sprains with activity is common in the setting of a coalition since the hindfoot can-
not properly accommodate to the inversion and eversion stresses typically seen in
sports. Additionally, adolescents with a stiff hindfoot often describe worsening of
their symptoms with a corrective arch support [1, 2, 13].
When pain is present, identifying its precise location is critical in the diagnosis of
flatfoot deformity. Most frequently, pain is found at the plantarmedial aspect of the
midfoot as a result of the talar head pressing into the floor, but sinus tarsi pain and
calcaneofibular impingement symptoms are common as well [1, 10, 13]. Occasionally,
pain along the course of the posterior tibial tendon (PTT) may be present. True
pathology of the PTT however is essentially a nonissue in the pediatric population
except in cases of trauma or iatrogenic injury. In the setting of a tarsal coalition, pain
may be localized to the coalition itself. Rigid deformities also commonly present
with anterior ankle pain as a result of stress transfer from the stiff hindfoot [10, 13].
Flatfeet may be associated with rheumatologic, neoplastic, traumatic, neuro-
logic, or connective tissue disorders so it is important to ask if there is any known
patient or family history related to such conditions. Of note, night pain, swelling,
warmth, and redness are all unusual in both flexible and rigid flatfoot, and the pres-
ence of these symptoms warrants investigation for other potential underlying
pathology [1].
4.2 Exam
The physical examination begins with evaluation of the patient’s entire lower
extremity for additional sources of angular or rotational deformity that may be
related to the presenting foot symptoms. Genu valgus or external tibial torsion can
make a flatfoot appear exaggerated when standing [13]. Assessing the child’s gait
pattern especially when their attention is elsewhere, such as when they first walk
into an exam room, is helpful as children often alter their gait when being observed.
Asymmetry in gait or inability to perform a heel or toe walk may indicate an under-
lying neuromuscular disorder that requires further evaluation [10]. The patient’s
shoes should be examined for clues of abnormal wear due to an underlying
deformity. Asymmetric medial wear of the sole of the shoe is common in patients
with a flexible flatfoot, and when the Achilles tendon is tight, wear can be seen at
the medial midfoot [7]. Finally, one should examine the patient for signs of liga-
mentous laxity and other connective tissue disorders such as Ehlers-Danlos, Marfan
syndrome, or Down syndrome.
Recognition of a contracture of the gastroc-soleus complex is important since
pediatric patients with a flatfoot and associated short Achilles tendon are often
symptomatic [1, 2, 13]. The Silfverskiöld test is used to differentiate between an
isolated gastrocnemius contracture and a contracture of the entire gastroc-soleus
complex. During this examination maneuver, it is important to restrict dorsiflexion
through the subtalar joint by locking it in a neutral or slightly inverted position, thus
isolating sagittal motion of the talus. When less than 10 degrees of ankle dorsiflex-
ion is obtained with the knee in both flexion and extension, the entire gastroc-soleus
complex is contracted. If more than 10 degrees of ankle dorsiflexion is obtained
with the knee in flexion, but dorsiflexion beyond 10 degrees is not possible with the
knee in extension, the gastrocnemius alone is affected [1, 4, 13].
One of the primary goals of the diagnostic process is determining whether a
flatfoot is flexible or rigid because this has a substantial impact on the treatment
algorithm. There are several ways to assess for flexibility. First, a double-limb heel
rise should elicit correction of the hindfoot to a varus heel position through contrac-
tion of the posterior tibialis if the deformity is flexible. Performing a heel rise with-
out correction of the hindfoot into a varus position is suspicious for a rigid deformity.
Another method to check for rigidity is to manually assess subtalar joint motion
with the patient seated and the ankle in neutral dorsiflexion. Maintaining neutral
dorsiflexion during this maneuver is key as it minimizes the coronal plane motion
contribution from the tibiotalar joint by bringing the wider anterior portion of the
talar dome into the mortise. Perhaps the simplest way to evaluate hindfoot flexibility
is to observe the patient’s resting foot position when seated with the feet dangling
off the edge of the bed. A patient with a stiff hindfoot will often have a resting foot
position that is dorsiflexed and everted compared to the other side, assuming no
contralateral hindfoot stiffness (Fig. 1).
There is an approximately 50% incidence of bilateral tarsal coalitions so it is of
course necessary to examine the contralateral foot [14]. Patients with TC coalitions
may have a palpable eminence inferior to the medial malleolus and may also be
tender to palpation in the sinus tarsi. CN coalitions may be palpable as well and are
confluent with the anterior process of the calcaneus [12].
4.3 Imaging
Symptomatic patients should be assessed with standard weight-bearing ankle

(anteroposterior [AP] and mortise) and foot (AP, 45° external rotation oblique, and
lateral) radiographs to evaluate for signs of planovalgus alignment and assess for a
coalition or other osseous abnormality. The AP foot radiograph is used to analyze
talonavicular joint alignment as the navicular is laterally positioned relative to the
Fig. 1 Resting foot

position of a patient with a
rigid flatfoot on the
patient’s right side. The
resting foot position of the
rigid hindfoot (patient’s
right) is dorsiflexed and
everted compared to the
contralateral side
head of the talus in a flatfoot. This can be difficult to interpret however in the pedi-
atric population since the navicular does not normally ossify until the age of
3–4 years, and ossification begins asymmetrically toward its lateral aspect [7].
Alternatively, the AP talus-first metatarsal angle may be used to evaluate the talona-
vicular joint relationship (Fig. 2), but it may be unreliable, as in the case of metatar-
sus adductus and skewfoot deformity [7].
On the lateral view, the lateral talus-first metatarsal angle (Meary’s angle),
formed by lines drawn through the mid-axis of the talus and the mid-axis of the first
metatarsal, is evaluated (Fig. 3) [7, 15]. In a flatfoot deformity, there is an apex
plantar break in this angle, but it is important to note that this measurement has been
shown to vary off the neutral axis up to 13 degrees even in “normal” feet [15]. The
lateral radiograph of a flatfoot will also reveal an equinus position of the calcaneus,
measured by the calcaneal pitch (Fig. 4). The average calcaneal pitch in the pediat-
ric population is approximately 17 degrees [15].
It is often possible to identify a CN coalition on the oblique view of the foot (Fig. 5),
whereas an axial or Harris heel view of the hindfoot has traditionally been obtained to
help identify a middle facet TC coalition or dysmorphic middle facet. It should be
noted that literature examining the utility of the Harris view has found that it is poor
for diagnostic purposes in children and adolescents [16]. Other radiographic features
suggestive of a coalition may be seen on the lateral view and include talar beaking (TC
and CN coalitions), a C sign (TC coalition), or an anteater sign (CN coalition).
The C sign, formed by the medial outline of the talar dome and the posteroinfe-
rior outline of the sustentaculum tali (Fig. 6), is not always present in TC coalitions
and may also be seen in children with flexible flatfeet who do not have a coalition
[17]. One study used computed tomography (CT) scans to verify the presence of a
TC coalition and correlated them with the identification of a C sign on the lateral
Fig. 2 Standing
anteroposterior (AP) foot
radiograph demonstrating
the AP talus-first
metatarsal angle, formed
by lines drawn through the
mid-axis of the talus and
the mid-axis of the first
metatarsal
Fig. 3 Standing lateral

foot radiograph
demonstrating the lateral
talus-first metatarsal angle
(Meary’s angle), formed by
lines drawn through the
mid-axis of the talus and
the mid-axis of the first
metatarsal
radiograph. They found that a “true C sign,” defined as complete or a near complete
(with a linear interruption and rarefaction of the edges), was present in only 41% of
patients with a TC coalition. However, if a true C sign was present, then it was 97%
specific for a TC coalition [17].
Whether or not a coalition is identified on plain radiographs, advanced imaging
with CT or magnetic resonance imaging (MRI) is mandatory for the complete
Fig. 4 Standing lateral

foot radiograph
demonstrating the
calcaneal pitch, which is
the angle between the
horizontal line parallel to
the ground and the line
drawn between the plantar
prominence of the
calcaneus proximal to the
calcaneocuboid articular
surface and the plantar
aspect of the most plantar
prominence of the
calcaneal tuberosity
Fig. 5 Oblique foot

radiograph demonstrating a
calcaneonavicular coalition
Fig. 6 The C sign (arrows)

is formed by the medial
outline of the talar dome
and the posteroinferior
outline of the
sustentaculum tali
a b
Fig. 7 CT scan demonstrating a talocalcaneal medial facet coalition on the coronal view (a) and
associated narrowing of the posterior facet on the sagittal view (b)
workup of a rigid hindfoot. These studies are important to accurately evaluate the
characteristics of a coalition as well as to identify the presence of a second ipsilateral
coalition which occurs in 20% of cases [18]. We recommend bilateral ankle CT scans
to assess for contralateral pathology and as a comparison to the unaffected side since
subtle differences in the relationships of the joint surfaces may be difficult to identify.
CT is especially helpful to aid surgical planning for a TC coalition as morphology of
the coalition, joint space narrowing of the posterior facet, and extension of the coali-
tion into the posterior facet are all important factors to guide treatment (Fig. 7).
If no coalition is identified on advanced imaging studies, exam findings concern-

ing for rigidity warrant further workup with neurological consultation.
Electromyography can be a useful objective tool to confirm and quantify spasticity
affecting the hindfoot.
5 Conservative Treatment
The first line of treatment for pediatric flexible flatfeet is always nonsurgical. When
asymptomatic, observation alone is the rule as orthoses will neither help correct
alignment nor prevent future pain and dysfunction. Despite this, intervention is
often requested by parents or suggested by other medical providers, and in this set-
ting, it is essential to provide patient and parental education and reassurance.
When symptomatic, pain can often be lessened through the use of in-shoe pre-
fabricated or custom orthoses to invert the hindfoot, offload the plantarmedial soft
tissues, and decrease exaggerated muscle activity [1, 2, 13]. While most physicians
find orthoses and arch supports to be a useful treatment tool, there are mixed results
in the literature regarding their effectiveness and the overall quality of evidence is
poor [2]. In one of the few randomized controlled studies, Whitford and Esterman
showed that although orthoses improved pain and physical function, the improve-
ment was not statistically significant compared to the control group with no treat-
ment. They also showed there was no benefit to custom orthoses over prefabricated
inserts [19]. A 2010 Cochrane Review concluded that due to the heterogeneity of
the studies evaluating nonoperative management in pediatric flatfoot patients, there
was no clear evidence to support that foot orthoses affect the long-term shape of the
foot or decrease potential future disability [2]. However, there was limited evidence
that orthoses and supportive shoes improve pain and function, although there were
varying degrees of baseline symptoms in the patients included. Despite a lack of
evidence, over-the-counter foot orthoses may help reduce pain and relieve activity
related symptoms. They certainly seem to be a reasonable and relatively inexpen-
sive adjunct to the initial management of flexible flatfeet [2, 13, 20].
Pain is more common in flexible flatfeet with a short Achilles tendon, so heel
cord stretching should be part of the treatment plan for these patients [1, 2, 10, 13].
The patient should perform heel cord stretching with the knee extended and the
subtalar joint in neutral to slightly inverted alignment as this helps to isolate motion
to the tibiotalar joint and avoids dorsiflexion through the everted subtalar joint [1, 7].
When a flatfoot is rigid, the foot shape cannot be manipulated with a corrective
orthotic device. In fact, adding material to the arch may actually exacerbate symp-
toms by increasing pressure under the head of the talus [7]. Instead, it may be worth-
while to first treat symptomatic tarsal coalitions with 4–6 weeks of immobilization
with a walking boot or short leg cast. A University of California Berkeley
Laboratories (UCBL) orthosis is another alternative. These rigid orthoses can be
cumbersome and painful for some, but for those patients who find them comfort-
able, they can provide relief and may be used for long-term stabilization of the
hindfoot. Nonoperative interventions as a whole are valuable in the setting of a
symptomatic tarsal coalition and have shown durable pain relief in approximately
50% of patients at 1.5 year follow-up after initial presentation [21].
6 Surgical Management, Timing, and Post-op Protocol
6.1 Flexible Flatfoot
The primary indication for surgery is pain specifically related to the flatfoot that
affects the patient’s ability to participate in activities and failure of at least 3–6
months of nonsurgical treatment. As a result of the variability in the literature of
both the definition of the flexible flatfoot and surgical results, more specific surgical
indications are debatable [2, 7].
The mainstay of surgical treatment is a combination of soft tissue procedures and
osteotomies for rebalancing and realigning the foot. Other bony procedures includ-
ing osseous excision and arthrodesis procedures have been described for manage-
ment of the deformity but are not recommended in the treatment of an otherwise
uncomplicated flexible flatfoot. Excision procedures have been largely abandoned
due to their destructive nature. Hindfoot arthrodesis procedures are not typically
indicated in an otherwise healthy patient with a flexible flatfoot because the decrease
in mobility and shock absorbing capacity of the hindfoot can increase the risk of
adjacent joint degeneration, especially in children [7].
Osteotomies have the benefit of realigning the foot without sacrificing mobility.
The most popular techniques are the calcaneal lengthening osteotomy (CLO) with
or without a concomitant plantarflexion producing cuneiform osteotomy and the
calcaneo-cuboid-cuneiform osteotomy [1, 7, 13].
Evans originally described the CLO in 1975, and it was later modified by Mosca
in 1995 [22, 23]. Lateral column lengthening occurs via the use of a distraction
wedge osteotomy of the anterior calcaneus between the anterior and middle facets.
The location of the osteotomy positions the center of rotation near the center of the
talar head rather than the medial cortex of the calcaneus, and the opening wedge
trapezoid-shaped graft produces lengthening and adduction of the calcaneus. The
result is correction of hindfoot valgus and restoration of talar head coverage via cor-
rection of midfoot abduction. One of Mosca’s modifications to allow distraction of
the osteotomy included releasing the lateral plantar fascia and abductor digiti min-
imi aponeurosis [23]. His study reported satisfactory clinical and radiographic out-
comes in 29 of 31 patients at an average of 32 months follow-up [23]. Figure 8
demonstrates an example of this procedure.
Rathjen and Mubarak first reported the technique of combining of a medial dis-
placement calcaneal osteotomy, an opening wedge cuboid osteotomy, and a plantar-
based closing wedge osteotomy of the medial cuneiform to correct severe valgus
deformity in the pediatric population [24]. This calcaneo-cuboid-cuneiform osteot-
omy technique is alternatively referred to as the “triple C.” The medial displacement
calcaneal osteotomy provides correction of heel valgus; the cuboid opening wedge
lengthens the lateral column, helps to realign the talonavicular joint, and dorsiflexes
a b
Fig. 8 Preoperative anteroposterior (a) and lateral (b) radiographs demonstrating severe flatfoot
deformity. Postoperative anteroposterior (a) and lateral (b) radiographs of the same foot after cal-
caneal lengthening osteotomy showing correction of the deformity
the talus; and the plantarflexion medial cuneiform osteotomy introduces increased
arch height and corrects forefoot supination. Rathjen and Mubarak reported “good”
or “excellent” outcomes in 23 of the 24 patients included in their original study at
an average of 18 months follow-up [24].
Moraleda et al. compared the modified Evans CLO and the triple C osteotomy in
symptomatic pediatric patients with flexible flatfeet who had failed nonsurgical
management. They found that both techniques obtained good clinical and radio-
graphic results with an average follow-up of 2.7 years in the triple C group and 5.3
years in the CLO group. In their prospective series, the CLO provided better correc-
tion of talonavicular subluxation and of the talus-first metatarsal angle, but it was
associated with a slightly increased complication rate. It should be noted that greater
than 10% subluxation of the calcaneocuboid joint was included as a potential com-
plication and was present in 51.5% feet of the CLO group [25]. Other studies have
shown that calcaneocuboid subluxation after calcaneal lengthening osteotomy
improves and often resolves over time, and therefore it is not clear if the subluxation
noted intraoperatively has a significant clinical consequence [25, 26]. Other compli-
cations associated with the CLO procedure included nonunion, neuropraxia of the
popliteal portion of the sciatic nerve, pain and stiffness of the subtalar joint, and
delayed wound healing [25]. Complications with the triple C group included wound
complications and delayed union [24, 25].
A variety of bony and soft tissue procedures are added to the CLO and triple C
procedures to help remove deforming forces and balance the foot reconstruction.
Contracture of part or all of the gastroc-soleus complex is often present and contrib-
utes to the deformity because of the increased lateral line of pull of the Achilles seen
in patients with valgus heel alignment. The Silfverskiöld test should be performed
intraoperatively to determine whether a contracture is present and an Achilles
lengthening or gastrocnemius recession should be performed [1, 23, 24].
Z-lengthening of the peroneus brevis removes its deforming force on the midfoot
and decreases resistance to lateral column distraction. Mosca also recommends
recession of the abductor digiti minimi [27]. The posterior tibial tendon and spring
ligament/talonavicular joint capsule will be redundant after correcting the bony
alignment and should be imbricated to reset their tension and maintain deformity
correction. Finally, if there is residual forefoot supination after correction of the
hindfoot deformity, a plantarflexion medial cuneiform osteotomy is performed to
bring the metatarsal heads into a neutral alignment and recreate the longitudinal
arch of the foot through plantarflexion of the first ray [24].
A more controversial surgical option is the arthroereisis procedure which involves
inserting a bioabsorbable, silicone, or titanium cone-shaped implant into the sinus
tarsi. This may be performed in conjunction with other bony and soft tissue surgeries
or as a stand-alone. The device functions by restricting external rotation of the subtalar
joint and results in elevation the arch and improved talonavicular congruity. However,
the popularity of arthroereisis has declined due to implant pain, risk of misplacement
or displacement of the device, subtalar joint degeneration, and incomplete deformity
correction or recurrence [1, 7, 13]. In a critical review of the literature including 76
small studies, satisfactory patient-reported outcomes were reported between 79 and
100% with improvement of most radiographic measures. However, there was a com-
plication rate of 5–19% with an unplanned removal rate between 7 and 19% [28].
Overall, there is insufficient evidence to support its use for adolescent deformity.
6.2 Rigid Flatfoot
A rigid flatfoot may be the result of a variety of causes, some obvious and others
less so. If nonoperative treatment fails to provide satisfactory relief, surgery may be
considered only after an underlying source of the rigidity has been identified, as this
will significantly impact surgical planning. Here we will discuss options for surgical
treatment in the setting of TC or CN coalitions as well as the flatfoot with a neuro-
genic cause.
6.2.1 Talocalcaneal Coalition
Multiple techniques have been described for TC coalition resection along with
methods to prevent regrowth by coating the resection surfaces with bone wax and/
or interposing fat graft or tendon into the defect [1, 13, 29]. Historically, subtalar or
triple arthrodesis was the standard surgical treatment for a TC coalition. While
arthrodesis procedures still have an important role in their management, the concern
for long-term adjacent joint degeneration and functional issues associated with a
rigid hindfoot led to a transition toward the goal of motion restoration and preserva-
tion in the adolescent population [29].
Results of motion sparing surgery for TC coalitions were initially mixed so studies
began to focus on appropriate indications to guide the decision of joint preservation
rather than sacrifice. In a widely referenced article, Wilde et al. concluded that middle
facet coalitions with a cross-sectional area measuring 50% or more than that of the
adjacent posterior facet were associated with poorer outcomes after coalition resec-
tion [30]. Although many still use this guideline, the use of coalition size as an indica-
tion was based on an incidental finding of the study and has largely not been validated
in the literature [30–32]. Multiple studies have shown that when TC coalitions are
appropriately excised, approximately 90% of patients report decreased levels of pain
and significant improvement in outcome scores, even in patients with large coalitions
measuring more than 50% of the surface area of the middle facet [29, 31, 32]. While
there are no formal published guidelines for resection versus arthrodesis, our recom-
mendation is that all adolescent TC coalitions indicated for surgery should be resected
unless (1) there is narrowing of the subtalar joint space on CT scan (essentially indi-
cating subtalar arthritis) or (2) if the coalition involves any portion of the posterior
facet. If either of these two are the case, then subtalar arthrodesis is preferred.
When one does decide to proceed with resection, it is essential to take the time
to excise the coalition completely in order to prevent recurrence and improve clini-
cal outcomes. Assessing the adequacy of a TC coalition resection during surgery
can be difficult. Kemppainen et al. found that use of intraoperative CT scan improved
resection quality and altered surgical decision-making with 21% of their cases
requiring further resection [33]. Presently, there are no studies of long-term clinical
outcomes available to justify the increased cost and radiation incurred by use of
intraoperative CT.
When a TC coalition is present in the setting of planovalgus deformity, it is
important to discern whether the source of the pain is related to the deformity, to the
coalition, or to both as correction of the foot alignment is often necessary for pain
relief, whether or not the coalition is resected [34]. This differentiation of symptoms
is helpful for surgical planning as well as for guiding patient and family expectations.
Surgical treatment of a TC coalition with an associated flatfoot deformity

depends on whether or not the coalition is amenable to resection. When joint pres-
ervation is possible, resection of the coalition may proceed concomitantly with the
osteotomies and soft tissue procedures described in the flexible flatfoot section of
the chapter. If the coalition is unresectable, subtalar arthrodesis with correction of
hindfoot alignment either through the subtalar joint or via additional calcaneal oste-
otomy is preferred. Other bony and soft tissue procedures are included as necessary.
In the specific setting of an osseous coalition, one may consider performing the
flatfoot correction and leaving the bony coalition intact since it essentially repre-
sents an already fused subtalar joint.
It has been shown that CLO fully corrects the flatfoot deformity even when a
bony TC coalition is left unresected [34]. Mosca and Bevan reported on a cohort
of patients with planovalgus deformity associated with TC coalitions that were
treated with CLO, with or without coalition resection. Treatment was based on the
patient’s individual signs, symptoms, and imaging, and they showed that CLO
provided good deformity correction and pain relief. Most importantly, their algo-
rithmic approach demonstrated that treatment of the valgus deformity is just as
important as the management of the coalition itself and the coalition cannot nec-
essarily be assumed to be the primary pain generator among symptomatic
patients [34].
6.2.2 Calcaneonavicular Coalition
Symptomatic CN coalitions are treated with resection and interposition after failing
conservative management. Extensor digitorum brevis (EDB), fat graft interposition,
and bone wax have all been described to decrease recurrence rate and provide long-
term pain relief [11].
Mubarek et al. noted that the calcaneocuboid bony prominence after interposi-
tion of the EDB can lead to shoe wear difficulties and cosmetic differences in the
lateral contour of the foot [11]. They also used a cadaver model to demonstrate that
when EDB muscle belly was used for interposition, it filled an average of 64% of
the resected gap, which could potentially allow partial regrowth of the coalition
[11]. In the same study, fat graft was found to fill 100% of the resection gap.
Cosmetically, harvest of fat graft from a remote site (usually the medial calf or the
gluteal fold) avoids the change in contour of the lateral hindfoot seen after harvest
of the EDB muscle but requires a second surgical site and can leave a scarred soft
tissue dimple at the harvest site [11].
Masquijo et al. performed a retrospective study comparing fat graft, EDB, and
bone wax interposition after CN coalition resection and found that fat graft and
bone wax interposition techniques provided greater pain relief, resulted in better
functional scores, and avoided more coalition reossification than the EDB technique
[35]. Their study did not discuss whether or not the size of the EDB was adequate
to fill the defect left by the resection.
Percutaneous and arthroscopic resection techniques have been proposed for CN

coalitions in small patient cohorts with good short-term results, but long-term fol-
low-up with regard to pain relief or recurrence has not yet been reported [20].
As with a TC coalition, flatfoot deformities may occur along with a CN coalition.
The location of pain, symptomatology, and physical examination findings deter-
mine if the coalition can be treated in isolation or if correction of the deformity is
necessary as well. Flatfoot correction in the setting of a CN coalition may be per-
formed as described in the flexible flatfoot section above either concurrently or as a
staged procedure [27].
6.2.3 Neurogenic Flatfoot
The neurogenic flatfoot often presents as a severe deformity with variable patterns
of contracture, spasticity, and weakness. This poses a difficult challenge with con-
cerns for recurrence, undercorrection, and overcorrection [10].
In Mosca’s study describing his modified CLO technique, there were 24 flatfeet
treated with an underlying neurogenic disorder (16 with a myelomeningocele and 8
with cerebral palsy). Of these, only two patients had unsatisfactory outcomes [23].
Subsequently, Ettl et al. reported on 24 children (28 feet) with cerebral palsy that
were treated with CLO and organized the results based on ambulatory status [36].
Although they had good results in the ambulatory group, 44% of the nonambulatory
group had relapse and unsatisfactory outcomes. Therefore, they recommended
against CLO in nonambulatory children with cerebral palsy and severe planovalgus
deformities [36].
Correction of deformity through the use of fusion procedures such as a triple
arthrodesis may lead to a more predictable result in these patients and can provide
good long-term patient satisfaction [37]. However, one must recognize and counsel
patients and parents that fusions have been shown to lead to progressive adjacent
joint degeneration even in the low-demand neurogenic population [37].
7 Summary
Pediatric and adolescent flatfoot deformities can be flexible or rigid and present
with a variable degree of symptomatology. The flexible pediatric flatfoot is usually
painless and does not require treatment other than reassurance and education.
Occasionally, flexible flatfeet can be symptomatic, and a trial of generic orthoses is
the preferred first-line treatment option. If the patient continues to have pain and
disability after a concerted attempt at nonsurgical management, surgical correction
may be indicated. This most commonly consists of a combination of soft tissue
procedures and osteotomies. It is crucial for the surgeon to be diligent and confirm
that the deformity is the true source of the patient’s pain since conditions aside from
the flatfoot can occur concurrently and may be overlooked.
Rigid flatfeet are more commonly symptomatic than their flexible counter-
parts. When a rigid flatfoot is identified, identification and appropriate treatment
of the source of the deformity are critical. Surgery must be tailored to the specific
underlying cause, and although there are some promising short-term surgical
results, studies are needed to confirm long-term outcomes for this challenging
pathology.
References
1. Bouchard M, Mosca VS. Flatfoot deformity in children and adolescents: surgical indications
and management. J Am Acad Orthop Surg. 2014;22(10):623–32.
2. Evans AM, Rome K. A Cochrane review of the evidence for non-surgical interventions for
flexible pediatric flat feet. Eur J Phys Rehabil Med. 2011;47(1):68–9.
3. Ilfeld FW. Pes planus: military significance and treatment with simple arch support. J Am Med
Assoc. 1944;124(5):281–3.
4. Pfeiffer M, Kotz R, Ledl T, Hauser G, Sluga M. Prevalence of flat foot in preschool-aged chil-
dren. Pediatrics. 2006;118(2):634–9.
5. Gould N, Moreland M, Trevino S, Alvarez R, Fenwick J, Bach N. Foot growth in children age
one to five years. Foot Ankle. 1990;10(4):211–3.
6. El O, Akcali O, Kosay C, Kaner B, Arslan Y, Sagol E, et al. Flexible flatfoot and related factors
in primary school children: a report of a screening study. Rheumatol Int. 2006;26(11):1050–3.
7. Mosca VS. Flexible flatfoot in children and adolescents. J Child Orthop. 2010;4(2):107–21.
8. Moraleda L, Mubarak SJ. Flexible flatfoot: differences in the relative alignment of each
segment of the foot between symptomatic and asymptomatic patients. J Pediatr Orthop.
2011;31(4):421–8.
9. Luhmann SJ, Rich MM, Schoenecker PL. Painful idiopathic rigid flatfoot in children and ado-
lescents. Foot Ankle Int. 2000;21(1):59–66.
10. Dare DM, Dodwell ER. Pediatric flatfoot: cause, epidemiology, assessment, and treatment.
Curr Opin Pediatr. 2014;26(1):93–100.
11. Mubarak SJ, Patel PN, Upasani VV, Moor MA, Wenger DR. Calcaneonavicular coalition:
treatment by excision and fat graft. J Pediatr Orthop. 2009;29(5):418–26.
12. Takakura Y, Sugimoto K, Tanaka Y, Tamai S. Symptomatic talocalcaneal coalition its clinical
significance and treatment. Clin Orthop. 1991;269:249–56.
13. Ford SE, Scannell BP. Pediatric flatfoot. Foot Ankle Clin. 2017;22(3):643–56.
14. Cowell H, Elener V. Rigid painful flatfoot secondary to tarsal coalition. Clin Orthop.
1993;177:54–60.
15. Davids JR, Gibson TW, Pugh LI. Quantitative segmental analysis of weight-bearing radiographs
of the foot and ankle for children: normal alignment. J Pediatr Orthop. 2005;25(6):769–76.
16. Lee M, Harcke H, Bassett G. Subtalar joint coalition in children: new observations. Radiology.
1989;172(3):635–9.
17. Moraleda L, Gantsoudes GD, Mubarak SJ. C sign: talocalcaneal coalition or flatfoot defor-
mity? J Pediatr Orthop. 2014;34(8):814–9.
18. Clarke DM. Multiple tarsal coalitions in the same foot. J Pediatr Orthop. 1997;17(6):777–80.
19. Whitford D, Esterman A. A randomized controlled trial of two types of in-shoe orthoses in
children with flexible excess pronation of the feet. Foot Ankle Int. 2007;28(6):715–23.
20. Bauer K, Mosca VS, Zionts LE. What’s new in pediatric flatfoot? J Pediatr Orthop.
2016;36(8):865–9.
21. Shirley E, Gheorghe R, Neal KM. Results of nonoperative treatment for symptomatic tarsal
coalitions. Cureus. 2018;10(7):e2944.
22. Evans D. Calcaneo-valgus deformity. J Bone Joint Surg Br. 1975;57(3):270–8.

23. Mosca V. Calcaneal lengthening for valgus deformity of the hindfoot. Results in children who
had severe, symptomatic flatfoot and skewfoot. JBJS. 1995;77(4):500–12.
24. Rathjen K, Mubarak SJ. Calcaneal-cuboid-cuneiform osteotomy for the correction of valgus
foot deformities in children. J Pediatr Orthop. 1998;18(6):775–82.
25. Moraleda L, Salcedo M, Bastrom TP, Wenger DR, Albiñana J, Mubarak SJ. Comparison of the
calcaneo-cuboid-cuneiform osteotomies and the calcaneal lengthening osteotomy in the surgi-
cal treatment of symptomatic flexible flatfoot. J Pediatr Orthop. 2012;32(8):821–9.
26. Ahn JY, Lee HS, Kim CH, Yang JP, Park SS. Calcaneocuboid joint subluxation after the calca-
neal lengthening procedure in children. Foot Ankle Int. 2014;35(7):677–82.
tions. Philadelphia: Lippincott Williams & Wilkins; 2014.
28. Metcalfe SA, Bowling FL, Reeves ND. Subtalar joint arthroereisis in the management of pedi-
atric flexible flatfoot: a critical review of the literature. Foot Ankle Int. 2011;32(12):1127–39.
29. Gantsoudes GD, Roocroft JH, Mubarak SJ. Treatment of talocalcaneal coalitions. J Pediatr
Orthop. 2012;32(3):301–7.
30. Wilde P, Torode I, Dickens D, Cole W. Resection for symptomatic talocalcaneal coalition. J
Bone Joint Surg Br. 1994;76(5):797–801.
31. Khoshbin A, Law PW, Caspi L, Wright JG. Long-term functional outcomes of resected tarsal
coalitions. Foot Ankle Int. 2013;34(10):1370–5.
32. Mahan ST, Spencer SA, Vezeridis PS, Kasser JR. Patient-reported outcomes of tarsal coali-
tions treated with surgical excision. J Pediatr Orthop. 2015;35(6):583–8.
33. Kemppainen J, Pennock AT, Roocroft JH, Bastrom TP, Mubarak SJ. The use of a portable
CT scanner for the intraoperative assessment of talocalcaneal coalition resections. J Pediatr
Orthop. 2014;34(5):559–64.
34. Mosca VS, Bevan WP. Talocalcaneal tarsal coalitions and the calcaneal lengthening osteot-
omy: the role of deformity correction. JBJS. 2012;94(17):1584–94.
35. Masquijo J, Allende V, Torres-Gomez A, Dobbs MB. Fat graft and bone wax interposition pro-
vides better functional outcomes and lower reossification rates than extensor digitorum brevis
after calcaneonavicular coalition resection. J Pediatr Orthop. 2017;37(7):e427–31.
36. Ettl V, Wollmerstedt N, Kirschner S, Morrison R, Pasold E, Raab P. Calcaneal lengthening for
planovalgus deformity in children with cerebral palsy. Foot Ankle Int. 2009;30(5):398–404.
37. Saltzman CL, Fehrle MJ, Cooper RR, Spencer EC, Ponseti IV. Triple arthrodesis: twenty-five
and forty-four-year average follow-up of the same patients. JBJS. 1999;81(10):1391–402.
Foot Osteochondrosis
Pablo J. Echenique Díaz and Pablo Schaufele Muñoz
1 Introduction
Osteochondrosis is a focused alteration of the endochondral ossification process. It

is manifested by a variety of diseases that affect growing cartilage [1].
There are two areas of specialized growth cartilage present at the ends of devel-
oping bones: the physis, responsible for longitudinal growth, and the epiphyseal
cartilage (epiphyseal-articular cartilage complex), responsible for the bone end
shapes. In both areas, the growing cartilage is replaced by bone through a sequen-
tial process of cell proliferation, cell hypertrophy, extracellular matrix synthesis,
and matrix mineralization, where vascular invasion contributes to endochondral
ossification. Through this process, a continuous addition of cartilage is achieved,
which will be replaced by bone, thus allowing the individual to carry weight while
growing. Both the chondrocytes of the epiphysis and those of the physis are orga-
nized in different zones. The resting zone contains chondrocytes that divide slowly
and are precursors of the proliferative zone, in which cells divide rapidly forming
easily identifiable columns at the physiological level, while in the epiphyseal
growth zones, this column formation is less obvious, and they tend to form groups.
Finally, hypertrophic chondrocytes mature and secrete a highly specialized matrix,
whose function is to promote calcification of the cartilage that serves as a template
for bone formation by osteoblasts. In the calcification zone, the osteoclasts reab-
sorb the transverse septa, allowing vascular and osteoprogenitor cell invasion into
P. J. Echenique Díaz (*)

Universidad Austral de Chile, Valdivia, Chile
Hospital Base Valdivia, Los Ríos, Chile
P. Schaufele Muñoz
Universidad de Concepción, Concepción, Chile
Hospital Clínico Regional de Concepción Dr. Guillermo Grant Benavente, Biobío, Chile

Switzerland AG 2022
198 P. J. Echenique Díaz and P. Schaufele Muñoz
the gaps formed by the hypertrophic chondrocytes [2, 3]. Vascular endothelial
growth factor secreted by mature chondrocytes appears to be the factor responsi-
ble for vascular invasion of growth cartilage, a factor necessary for endochondral
ossification. When this angiogenesis is interrupted by any mechanism, whether
genetic, biochemical, or mechanical, a thickening of the growth cartilage occurs
due to the persistence and expansion of the hypertrophic layer (osteochondro-
sis) [4].
Multiple local factors have been identified as responsible for the proliferation
and differentiation of chondrocytes and subsequent ossification at the growth plate.
Thus, regulation mechanisms are described through expression mediators of at least
60 specific genes [5, 6], some of them related to osteochondrosis such as ATP6V0D2
and TMSB4. In addition, gene transcription factors and molecules secreted by
chondrocytes and other perichondrial cells are part of this complicated local control
network. The most important are Indian Hedgehog ligating protein (IHH), parathy-
roid hormone-related peptide (PTHrP), and transforming growth factor beta
(TGF-beta).
There are other factors that may have a role in the etiology of osteochondrosis
such as inheritance, anatomical features, repetitive trauma, dietary factors, and
alterations in the irrigation of epiphyseal or physiological cartilage that coincide
with the period of rapid growth. This pathology has been studied in animals and
humans, finding similarities in its presentation and origin.
At least two hypotheses indicate a vascular origin of this alteration. The first
one is based on a study carried out in birds, which experimentally demonstrates
that when the apoptosis of the vascular endothelium that covers the vascular
channels of the cartilage is artificially induced, a lesion of the surrounding carti-
lage is initiated that ends up showing an aspect very similar to the lesion observed
in mammals. Hypothetically, a focused interruption of the irrigation of the growth
cartilage causes the necrosis of the chondrocytes near the metaphyseal side of the
physis (where the ischemia would be greater). This can create an abnormal bone
matrix plate, impervious to penetration by the capillaries of the ossification front.
Such a barrier would isolate a group of hypertrophic chondrocytes on the epiphy-
sis side thus creating a thick mass of abnormal physiological cartilage in the
affected area, stopping its ossification. The second vascular theory attributes
repeated microtraumas to the metaphysical blood vessels that can disrupt the
irrigation of the ossification front, causing a failure to differentiate hypertrophic
cartilage and leaving an abnormally thickened area of physeal cartilage as a
result. This theory is based on experimental studies and evidence from animal
studies.
Siffert in 1981 classified osteochondroses into three groups [7]. The first group
originates in the cartilage of the articular epiphyseal complex, basically secondary
to necrosis of the articular hyaline cartilage or epiphyseal nucleus (Köhler’s disease
of the tarsal navicular, Freiberg’s disease of the second metatarsal). The second
group affects the growth cartilage of the apophyses that are zones of tendon inser-
tion, being osteochondrosis by traction (Sever’s disease of the calcaneus, Iselin’s
disease, Sinding-Larsen-Johansson’s disease of the inferior pole of the patella).
Finally a third group, that classifies alterations of the spine and long bones physis
(Blount’s disease, Scheuermann’s disease).
Foot Osteochondrosis 199
DE CUVELAND E, HEUCK F 1953 Willich – Wagner – Buchmann Kontjetny

(Maleolo medial)
1925 1928 1933 1926
Freiberg – Renander
Köhler (I) 1920 1924
Haglund – Sever 1908 Grashey 1933
1907 1912
Thiemann
1909
Monro – Kappis – Garcia-Diaz

1738 1922 1928 Wagner
Panner
1928
1921
Köhler II – Freiberg
Silverskiöld Isellin Lewin – Küntscher 1913 1914
1926 1912 1929 1939
Fig. 1 Osteochondrosis of the foot bones described with author’s name and date of publication.
(Copyright 2020, Dr. Pablo Echenique Díaz. Used with permission from Dr. Pablo Schaufele Muñoz)
In this chapter the osteochondroses that are presented in the bones of the foot are
reviewed (Fig. 1), except for the osteochondrosis and osteochondral lesions of the
talus that will be the subject of another chapter of this work.
2 Diagnosis
The diagnosis of these diseases is eminently clinical, in the presence of pain in the
growing foot, with its own characteristics for the different entities. In imaging stud-
ies [8], it is difficult to make a diagnosis in the early stages, with evidence of soft
tissue edema and increased joint space. However, in more advanced stages, signs of
necrosis are observed, with the appearance of sclerosis, irregularity of the edges of
the ossification nuclei, fragmentation, deformity, and finally collapse. Later, scar-
ring and recovery to its normal shape occur, which occurs during the remaining
growth within months or years.
The radiographs in standard projections, comparative of both extremities, allow
the follow-up.
Computed tomography (CT) can contribute to the differential diagnosis and
quantify the three-dimensional extent of bone involvement. It allows evaluating the
evolution of the fragmentation and articular free bodies and showing osteolytic
images of another origin. It is also capable of defining in detail the resulting deformity.
Magnetic resonance imaging (MRI) is also useful for differential diagnosis.
Usually, low-signal intensity images are observed in T1 and T2 sequences, consis-
tent with avascular necrosis. In the early stages, the findings are variable and show
the bone marrow with an isointense signal, highlighting a decreased signal area in
T1-weighted images at the level of the transition zone between normal and ischemic
tissue. Hyperintense images in T2 and STIR show diffuse edema, an early but
unspecific finding. Therefore, there may be cases of heterogeneous images, depend-
ing on the degree of necrosis in the different areas of the affected bone. In addition,
there is the sign of a double line in cancellous bone, evident in T2 sequence, with a
hyperintense internal line and a hypointense peripheral line, which indicate hyper-
vascular granulation tissue and necrosis, respectively. The addition of gadolinium
would not produce signal reinforcement in the necrotic zone [9].
Nuclear medicine has been successfully used in the diagnosis of this type of
disease [10], especially three-phase bone scintigraphy, with pinhole collimator-
enhanced images, and tomographic images with SPECT. These tests demonstrate
the lowest radiopharmaceutical uptake in necrotic bone and its recovery later in the
healing stage. However, their specificity and sensitivity are surpassed by the MRI.
3 Sever’s Disease
The picture of heel pain in children and adolescents was described initially by
Haglund in 1907 and later characterized by Sever in 1912 as an inflammatory dis-
ease of the posterior process of the calcaneus, secondary ossification center in which
the Achilles tendon is directly inserted.
This apophysitis of the calcaneus is the most frequent cause of pain in the heel in
adolescents. It affects mainly to the active population of children between 6 and 13
years. The disease is intermittent and self-limited, without evidencing sequels, last-
ing until the physis closure. Although it has been demonstrated that it affects the
quality of life of the affected ones, the parents are usually more worried than
patients. Its prevalence goes between 2% and 16% of the consultations by muscular
skeletal pathology in children, with bilateral presentation in 60–65% of the cases.
The apophysis grows on the posterior inferior part of the calcaneus, between 4
and 7 years in girls and between 7 and 10 years in boys. Characteristically it is
developed from several nuclei of ossification that converge and fuse with the tuber-
osity of the calcaneus at the age of 12–13 years in girls and from 15 years in boys.
The Achilles tendon is inserted in the cartilaginous surface of the most proximal
portion of the apophysis, and the plantar fascia and the musculature originate in the
lowest part of the apophysis [11].
The most accepted theory about the etiology of the calcaneal apophysitis is an
overuse syndrome, related to chronic repeated microtraumas, by traction or impact
along the calcaneal process, or through the union with the Achilles tendon.
Intrinsic and extrinsic biomechanical alterations have been described in patients
with Sever’s disease. Intrinsic factors include increase in plantar pressure [12],
greater body mass index, decreased capacity of impact absorption because of con-
ditions like genu varum, cavus foot, flat foot and short Achilles tendon. On the
other hand, extrinsic factors include, intense practice of sports with great impact
such as jogging and jumping, sports on hard surfaces and the use of inadequate
sports shoes. The repeated presence of these factors would take tissues to the
limit, causing the appearance of injuries such as microfractures secondary to com-
pression or traction.
The diagnosis of this disease is eminently clinical. It can affect one or both
feet. The patients refer pain in the posterior plantar part of the heel, during physi-
cal activity and relieves with rest. Normally, they do not refer pain at night.
Several weeks can pass before the first consultation. In the physical examination,
there is absence of edema and erythema or increase in local temperature. Three
diagnostic maneuvers have been validated with a high sensitivity and specificity
[13]: (1) monopodal heel load (painful in 100% of cases). (2) pain on direct pos-
terior calcaneus palpation (positive in 80% of cases), and (3) pain on simultane-
ous medial and lateral posterior calcaneal tuberosity compression (positive in
97% of cases).
The radiological findings in calcaneal apophysitis have been cause of contro-
versy for decades. At the moment it is accepted that the greater radiological
density of the apophysis compared with the calcaneal tuberosity is not an
apophyisitis sign, but is secondary to the orientation of its trabeculae. Some
trabeculae are oblique that provide resistance to the Achilles tendon traction and
other perpendicular giving resistance to compression. Some authors describe
fragmentation of the apophysis of the calcaneus, with the appearance of a frag-
ment in the lowest part of the apophysis. Another interesting factor is that Sever’s
disease only appears in a specific period of development coinciding with the
stages I to III of calcaneus ossification, described by Nicholson [14, 15].
Therefore, in patients with a suspicion of Sever’s disease in a more advanced
stage of ossification of the calcaneus, other etiologies must be ruled out. In MRI
images it is possible to rule out other diagnoses and detect stress fractures
(Fig. 2).
Fig. 2 Sever’s disease in male patient with heel pain, fragmentation, and increase of radiological
bone density is observed in posterior apophysis of the calcaneus, frequent finding in asymptomatic
patients. MRI shows signs of bone edema in the posterior apophysis and in the posterior tuberosity
around the physis. (Copyright 2020, Dr. Pablo Schaufele Muñoz. Used with permission from Dr.
Pablo Schaufele Muñoz)
The treatment of this self-limited condition is aimed at reducing pain. The rec-
ommendation is to limit the sport activity that causes the symptoms, while the crisis
lasts or until the child feels comfortable, or can change to another activity that pro-
duces less discomfort. Symptoms are intermittent and it is important to warn and
educate family and sports coaches accordingly [16]. The use of sports shoes that
reduce impact, viscoelastic heel pads, orthopedic insoles, therapeutic bandages in
conjunction with local ice, nonsteroidal anti-inflammatory drugs, and elongation
exercises for the gastro-soleus system are useful [17, 18]. In severe cases that do not
respond to these measures, a walking boot or a plaster boot can be used for 2–4
weeks [19]. There are reports of the benefit of prolotherapy consisting of local injec-
tions of substances that would activate healing (good results in follow-up to 1 year
in cases of Osgood Schlatter osteochondrosis) [20]. More studies of high method-
ological quality are needed to include this therapeutic alternative in the pediatric
population with benign musculoskeletal pain refractory to treatment. The authors
have an ongoing study of prolotherapy in Sever’s disease (Dr Pablo Schaufele) with
dextrose at 12.5% with promising results so far.
4 Köhler’s Disease
Navicular osteochondrosis was described by Köhler in 1908. It has been described

in children from 2 to 9 years of age. It is more common in boys than in girls (6:1),
and it may present bilaterally in 20–30% of the cases. It refers to history of isolated
trauma or repetitive microtraumas in 35–50% of the cases [21]. It is a self-limited
condition and usually without sequelae. Köhler’s disease has been associated with
patients with delayed ossification of the navicular, which would increase the risk of
injury due to ischemia or venous congestion in a mostly cartilaginous bone. The
navicular is subject to continuous compression forces between the talus and the
forefoot, that could end up in avascular necrosis. The extensive presence of blood
vessels ensures the complete recovery of the bone structure.
The symptoms of Köhler’s disease are gait claudication and occasionally inabil-
ity to carry weight due to pain in the medial longitudinal arch of the foot. Edema,
increased local temperature, and erythema may occur. Compression of the navicular
and the talonavicular joint can be painful. If pain is found in the rest of the tarsal,
subtalar, and talar joints, an inflammatory disease should be suspected. On the other
hand, if a rigid flat foot is found, a tarsal coalition should be suspected. The labora-
tory tests and clinical evolution will serve to rule out cases of osteomyelitis or septic
arthritis, which can also occur with pain and claudication in this area.
Two patterns of radiological presentation are described. The first is with an
increase in the bone density of the navicular (sclerosis) without loss of shape. The
second is characterized by thinning or flattening in the proximal-distal direction of
Fig. 3 Bilateral weight-bearing foot X-rays of a 4-year-old patient with Köhler’s disease.
Significant reduction in size and sclerosis of the navicular nucleus in the right foot (label DER) is
observed. In addition, there is a slight tendency to cavus foot in the affected foot. (Copyright 2020,
Dr. Pablo Echenique Díaz. Used with permission from Dr. Pablo Echenique Díaz)
the navicular (Fig. 3). In cases where the diagnosis is doubtful, the CT or MRI study
can be useful, allowing the identification of arthritis, posterior tibial tendonitis, os
naviculare, infection, tarsal coalition, or tumor pathology. It is recommended that
radiographic control be performed for follow-up until healing, which usually takes
up to a year. After 6 months to 4 years from the onset of symptoms, the radiological
appearance becomes normal [22].
Treatment of Köhler’s disease consists of immobilization with a short walking
boot for 4–8 weeks, with unloading and use of canes if necessary. After this, the use
of an insole or brace with medial arch support is recommended. In most cases, when
the cast is removed, the foot is already asymptomatic [23]. Exceptional cases are
described that result in degenerative changes in the talonavicular joint, which could
require surgery in the long term.
5 Freiberg’s Disease
Alfred Freiberg [24] reported in 1914 a series of six patients who presented a similar
pattern of infarction of the second metatarsal head, with flattening and collapse of
the head resulting in progressive degenerative changes.
Freiberg’s disease [25] is the fourth most frequent osteochondrosis. It is described
as a condition of the heads of the minor metatarsals. It involves almost exclusively
the head of the second metatarsal (80%), rarely the third metatarsal (27%), and
more rarely the fourth or fifth metatarsal (3%). It is usually unilateral and affects
only one metatarsal. It is the only osteochondrosis that preferentially affects the
female sex (5:1), between 10 and 18 years of age, the majority of cases being around
12 years of age. The disease can remain asymptomatic for a long time, being diag-
nosed in older patients by presenting symptoms in advanced stages.
It most frequently affects patients who present a short first metatarsal, an unfa-
vorable biomechanical situation that results in a second metatarsal overload. In
addition, the second ray is the least mobile of the forefoot, exposing it increased
pressure, thus contributing to the disease. The metatarsal heads have two sources of
arterial irrigation, the dorsal metatarsal arteries, originating from the dorsalis pedis
artery, and the plantar metatarsal arteries, originating from the posterior tibial artery.
These vessels are anastomosed in two places near the metatarsal heads in a vascular
ring, forming an extensive extra-bony arterial network around them. Small branches
of this network run distally and penetrate the metaphysis near the insertion of the
joint capsule and ligaments. This network irrigates the distal metaphysis, the growth
cartilage, the epiphyseal growth nucleus, and the subchondral bone of the epiphysis
[26]. Villadot and Villadot proposed that mechanical compression and repeated
trauma of the arteries that irrigate the metatarsal head can cause vessel spasm and
thrombosis of these vessels, with consequent necrosis of the metatarsal head.
Possible causes have also been linked to vascular anatomical variations, iatrogenic
complication, diabetes mellitus, systemic lupus erythematosus, and hypercoagula-
bility syndromes.
The diagnosis of Freiberg’s disease is based on clinical history, physical exami-
nation, and radiological findings. Patients typically report intermittent pain and lim-
ited mobility of the affected metatarsophalangeal joint. In some cases, they report a
history of trauma prior to the onset of symptoms. Pain increases with activity or
weight-bearing and is relieved by rest. Discomfort increases when wearing high-
heeled shoes or walking barefoot.
A mild limp is found secondary to pain, increased temperature and soft tissue
edema. These findings are secondary to metatarsophalangeal joint synovitis. Pain
can be elicited by dorsal or plantar palpation of the affected metatarsal joint.
Early stage radiological studies can only identify an increase in the space of
the involved metatarsophalangeal joint and signs of edema of the periarticular
soft tissues. In advanced stages, X-rays show sclerosis and flattening due to col-
lapse of the metatarsal head. In lateral oblique projection, more information can
be obtained about the extent of the metatarsal head damage. MRI is useful for the
differential diagnosis in early stages, in which X-rays are normal, doubtful, or
with atypical changes. It should be noted that a normal variant with bilateral flat-
tening of the head of the second metatarsal associated with a widening of the
joint space has been reported as a finding in asymptomatic patients. Differential
diagnoses are stress fractures of the metatarsals, osteomyelitis of the metatarsal
head, idiopathic metatarsophalangeal synovitis or capsulitis, tendonitis of exten-
sors or flexors, injury of collateral ligaments or plantar plate of the metatarso-
phalangeal joint, Morton’s neuroma, metatarsalgia or stress injury, juvenile
idiopathic arthritis or Still’s disease, and subacute inflammatory periostitis,
among others.
In 1957, Smillie [27] described the first classification of Freiberg’s disease, still
in use (Fig. 4). In stage I, a subchondral fracture is observed in the ischemic and
sclerotic epiphysis. In stage II there is an alteration of the articular surface of the
epiphysis. After the cancellous bone resorption, the central part of the metatarsal
head begins to collapse, leaving a bone bridge in the plantar area unharmed.
Progressive bone resorption gives way to stage III, which is when the metatarsal
head sinks into the metatarsal neck, keeping the neck edges intact but prominent on
Fig. 4 Diagram of
Smillie’s classification in
five progressive stages for
Freiberg’s disease, useful
in treatment planning.
Upper row: anteroposterior
metatarsal view. Lower
row: lateral metatarsal
view. (Copyright 2020, Dr.
Pablo Schaufele Muñoz.
Used with permission from
Dr. Pablo Schaufele
Muñoz)
I II III IV V
each side. In stage IV, the plantar rim collapses and a subchondral fracture occurs,
creating free articular fragments. The anatomy is lost. In stage V, the final stage,
osteoarthritis appears, with marked flattening and deformity of the metatarsal head
with joint space narrowing.
Although there are no prospective studies to determine the effectiveness of con-
servative management of Freiberg’s disease, most authors recommend it in Smillie
stages I to III [28]. The success of the conservative treatment is related to the pro-
gression of the disease, having great importance to the early diagnosis, despite the
fact that most of the symptomatic patients have radiological evidence of articular
free bodies (stage IV), while most of the asymptomatic patients did not have free
bodies. Immobilization, discharge, and activity restriction are the pillars of conser-
vative treatment in the acute stage. The use of a walker boot or surgical shoe, with
or without canes, is recommended for a period of 2–6 weeks, or until symptoms
subside. Alternative treatments such as corticosteroid and anesthetic infiltrations,
nonsteroidal anti-inflammatory analgesics, physiotherapy, and ultrasound have
been described as effective in the acute phase of the disease. The patient should be
advised to limit participation in sports and not to wear high-heeled shoes until the
disease is completely resolved. Alternative low-impact activities such as swimming,
cycling, and water aerobics are recommended for very active adolescents. To
decrease the pressure on the affected metatarsal head, the use of a brace or insole is
recommended to elevate and thus unload the metatarsal head. This, in combination
with stretching exercises, can alleviate pain and prevent the claw deformity of the
affected toe. Shoes with thick, rigid soles or rocker bottoms are also useful. It is
recommended to maintain this treatment until radiological evidence of healing,
which usually takes 2–3 years.
Surgical management is indicated in advanced cases (stages IV and V) and in
those that do not respond to conservative management. The surgical techniques
described can be divided into two groups: those that preserve the joint and those that
sacrifice the joint. There is no consensus on which procedure to choose. Recent
studies show that the techniques that preserve the joint would have better results
(over 90% success) in relation to those that sacrifice the joint (70% success) [29], so
the latter would be less recommended. The surgical complications are persistence of
pain, joint stiffness, floating toe, transfer metatarsalgia, dorsiflexion weakness and
painful scar.
Freiberg recommended removal of the free joint bodies. Many authors agree with
this behavior, noting improvement of symptoms in most cases. Other authors also
recommend a partial synovectomy. It has also been proposed to add a head decom-
pression, performed by perforating it with a drill or Kirschner wire. This procedure
should be performed preferably before significant structural changes occur showing
good results [30].
According to Smillie, a devitalized bone curettage, reduction of the collapsed
joint surface, and filling of the defect with autologous cancellous bone graft should
be considered. This principle has been considered in recent works applying the
technique of osteochondral autotransplantation and replacement with osteogenic
implants [31]. In 1979, Gauthier [32] designed a dorsal closing wedge osteotomy of
the metatarsal neck, as a variation of a Weil’s osteotomy, including part of the
necrotic zone and also resecting free bodies and osteophytes. This technique man-
ages to dorsally rotate the intact plantar articular cartilage. Given its good results, it
has become the most used technique nowadays, being used as reference to evaluate
other techniques (Fig. 5). Different forms of fixation are described, from sutures,
cerclages, Kirschner wires, resorbable wires, plates, and screws, all with good
results and few complications [33, 34]. These osteotomies produce shortening,
either by resecting a segment of the metatarsal neck or by sliding. This shortening
a b c
Fig. 5 (a) 24-year-old patient with Freiberg’s disease in stage IV. (b) Debridement of free articular
fragments and necrotic bone was performed. (c) Finally, a dorsal subtraction wedge osteotomy was
performed, fixed with two mini fragment screws, which allows dorsal reorientation of the articular
surface. (Copyright 2020, Dr. Pablo Echenique Díaz. Used with permission from Dr. Pablo
Echenique Díaz)
is 2.3 mm on average, with few clinical consequences. Pedobarographic studies

have shown a reduction in the pressure load on the operated metatarsal. The appear-
ance of floating toes is reported as a complication, but the appearance of transfer
metatarsalgia is not mentioned. Osteotomies without fixation have been used, but it
has not proven to be the optimal approach to the problem.
Kehr [35], in 1982, described an interposition arthroplasty for Freiberg’s dis-
ease. This technique is recommended if the whole joint surface is compromised.
After debridement of the metatarsal head, the extensor tendon and the joint capsule
are interposed in the joint. An alternative to this procedure is to perform a “U”
capsulotomy which is placed over the metatarsal head, holding it in place with a
pull-out suture on the sole of the foot, over a button or pad. It is also possible to
carve a periosteal and adipose flap, with less morbidity and excellent results [36].
In recent years, mini-invasive arthroscopic techniques have been developed, per-
forming the interposition of the extensor digitorum brevis for this purpose, with
good results [37].
Historically, the resection of the metatarsal head was reported. This technique
leads to the appearance of transfer metatarsalgia and hyperkeratosis, shortened and
floating toe, hallux valgus, alteration of the metatarsal parabola, and gait alteration.
It has been proposed to perform joint replacement arthroplasties [38], with total sili-
cone prosthesis or partial prosthesis, which could work in some patients. However,
in young and active patients, complications are frequent: bone resorption at the
interface with the implant, loosening and fracture of the prosthesis that forces the
removal of the implant, synovitis, stiffness, loss of stability, floating toe, etc.
Recently it has been reported the use of synthetic joint covering implants (NEXA
OsteocureTM [39], Cartiva [40]) initially designed for the treatment of hallux rigi-
dus, with good results. Prospective, comparative studies are needed to weigh the
results and draw conclusions. In joints with very severe osteoarthritis, with or with-
out dorsal toe dislocation, another option is to perform a debridement of the meta-
tarsal head and resection of the base of the proximal phalanx, in conjunction with
syndactylization to the adjacent toe. This procedure can improve symptoms and
preserves the metatarsal parabola.
6 Iselin’s Disease
In 1912, Hans Iselin described a traction apophysitis at the base of the fifth metatar-
sal. It occurs infrequently in adolescent athletes and is more common in boys than
in girls. It is a benign and self-limited condition, caused by the traction of the pero-
neus brevis, whose tendon is inserted into it [41]. The apophysis is located longitu-
dinally on the lateral plantar surface at the fifth metatarsal base. Sports that involve
running, jumping, or lateral pivoting movements can predispose child to develop
this disease, but it must be distinguished from other pathologies of the base of the
fifth metatarsal, such as acute or stress fractures, and supernumerary bones (os ves-
alianum). The diagnosis is clinical and radiological [42]. The symptoms are pain at
the base of the fifth metatarsal, which is exacerbated with activity and subsides with
rest. Palpation of the tuberosity can reproduce the pain. Increased local temperature,
erythema, and edema can be found. Eversion against resistance and maximum foot
inversion can also evoke the symptoms [43]. It appears normally at age 10 in girls
and at age 12 in boys. A thin ossification is observed with an oblique orientation to
the axis of the diaphysis, located at the lateral plantar edge of the proximal tuberos-
ity of the fifth metatarsal. The secondary nucleus fuses with the rest of the metatar-
sal about 2–4 years after its appearance [44]. Treatment consists of limiting physical
activity and restraining from sport. Functional bandaging and foot orthoses can
decrease the traction of the peroneus brevis tendon. In refractory cases, a short
walking cast boot can be used for 2–4 weeks [45]. Surgical treatment has been
reported in an exceptional way, with resection of loose bone fragments and fenestra-
tions that accelerate the fusion of the apophysis.
7 Cuneiform Osteochondrosis
An extremely rare disease, cuneiform osteochondrosis first reported in 1930 by

Harbin M. and Zollinger R. [46] and later by Buchman J. [47] in 1933. It most often
affects boys (80%) between 5 and 13 years of age (most often 4–6 years). Most cases
correspond to the medial cuneiform [48], to a lesser extent to the middle and rarely to
the lateral. It can be bilateral in half of the cases. Patients report discomfort around
the medial or dorsal side of the midfoot. The pain increases with activity and is
relieved with rest. It has been postulated that this disease may be underdiagnosed,
given the age of the patients and the null or low intensity of the symptoms. In X-rays,
a decrease in the size of the affected cuneiform is characteristic of the disease. The
changes are recovered within 6–24 months. It is possible to find its association with
navicular osteochondrosis. Consider differential diagnosis with lesions that may have
a similar radiological appearance (Ewing’s sarcoma, eosinophilic granuloma) and
rule out osteomyelitis. An erroneous diagnosis can delay treatment or subject the
patient to unnecessary surgery. Treatment is aimed at reducing impact, activities, and
treating pain [49].
8 De Cuveland’s Disease
It is an osteochondrosis of the tibial medial malleolus described in 1953 [50]. The

triggers of this condition would be the sport, especially with boot-type footwear, the
calcaneus valgus, and the presence of an accessory nucleus of ossification. Clinically
it is characterized by pain and slight local soft tissue edema, presenting pain to pal-
pation and with foot eversion. In the radiography, irregular ossification is evident,
and many times the presence of an accessory ossification nucleus can be seen [51].
The MRI helps with diagnostic confirmation and shows malleolar fragmentation
and bone edema. The treatment is symptomatic, sport rest, with improvement in
100% of the cases [52].
9 Sesamoid Osteochondrosis
The medial sesamoid is the most affected, described in 1925 by A. Renander, who
published two cases. It is characterized by pain at progressive pressure and stress-
related discomfort, especially with dorsiflexion of the first toe. Foot radiograph
shows a fragmented bone, sclerotic and slightly enlarged or reduced. Changes are
evident 6–12 months after symptoms start. MRI confirms the previous diagnosis,
showing bone fragmentation and edema. The differential diagnosis is with sesamoid
bone fracture, sesamoiditis, arthritic changes, and bi- or tripartite sesamoid. The
treatment is based on rest and orthoses (cushioning or unloading insoles) with very
good response. The few cases that do not respond are managed with walking boots
or short boot casts. In rare cases, sesamoidectomy is necessary [53].
10 Osteochondrosis of the First Metatarsal Base
Described by Grashey in 1933, it occurs between the ages of 6 and 13 years [54]. It
is characterized by insidious discomfort or pain and swelling over the base of the
first metatarsal which interrupts physical activity. The radiography shows a frag-
mented, dense, and flattened epiphysis. Its treatment includes non weight bearing in
a boot for 3 weeks. Its resolution takes between 4 and 6 months.
11 Osteochondrosis of the First Metatarsal Head
First described by Kontjetny and Wagner [55] in the years 1927 and 1930, respec-
tively. Clinically it is similar to Freiberg’s disease, characterized by first metatarso-
phalangeal joint swelling and increased local temperature. Pain at palpation and
mobilization of the joint is always present. The radiographic study may initially
show an increase in comparative size of the head of the affected metatarsal and a
subchondral radiolucent line, to later account for signs of necrosis and lytic changes.
MRI shows bone edema. The recommended treatment is non-weight-bearing, rest,
and analgesia. Then, at 10–12 weeks, it is changed to partial load with a walking
boot. The pain resolves completely within 6–8 months. However, there is a chance
of having persistent pain, even requiring surgery. Smillie’s classification for
Freiberg’s disease, which is also used for osteochondrosis of the third metatarsal
head (Panner) and the fourth and fifth metatarsal head (Ehrlach), is useful in decid-
ing on the indication for surgery.
12 Thiemann’s Disease
It is a form of genetic multifocal osteochondrosis [56] to be considered in the dif-

ferential diagnosis of juvenile arthritis. Described in 1909, it is considered an idio-
pathic avascular necrosis with progressive affection of the interphalangeal joints
(feet and hands). It can start at 4 years old, but the usual age of onset is around 13
years old. It is characterized by a painless increase in volume in the proximal inter-
phalangeal joint; however, it can present as a painful swelling with joint stiffness
that increases with cold. The radiological image shows alterations in the epiphysis
and metaphysis of the phalanxes (of the feet and hands), with widening, flattening,
and the appearance of scalloped and irregular edges. Its handling is symptomatic
and has a favorable evolution.
13 Summary
Osteochondroses are a group of abnormalities of the endochondral ossification pro-

cess of the growing skeleton. We will review the current knowledge and most
accepted theories about the etiology and treatment of those that occur in the ankle
and foot. Most of these diseases are rare and produce self-limited pain and func-
tional limitation.
References
1. Achar S, Yamanaka J. Apophysitis and osteochondrosis: common causes of pain in growing

bones. Am Fam Physician. 2019;99(10):610–8.
2. McCoy AM, Toth F, Dolvik NI, Ekman S, Ellermann J, Olstad K, Ytrehus B, Carlson
CS. Articular osteochondrosis: a comparison of naturally-occurring human and animal dis-
ease. Osteoarthr Cartil. 2013;21(11):1638–47.
3. Ytrehus B, Carlson CS, Ekman S. Etiology and pathogenesis of osteochondrosis. Vet Pathol.
2007;44(4):429–48. https://doi.org/10.1354/vp.44-4-429.
4. Sun MM, Beier F. Chondrocyte hypertrophy in skeletal development, growth, and disease.
Birth Defects Res C Embryo Today. 2014;102(1):74–82.
5. Mirams M, Ayodele BA, Tatarczuch L, Henson FM, Pagel CN, Mackie EJ. Identification of
novel osteochondrosis – associated genes. J Orthop Res. 2016;34(3):404–11.
6. Liu CF, Samsa WE, Zhou G, Lefebvre V. Transcriptional control of chondrocyte specification
and differentiation. Semin Cell Dev Biol. 2017;62:34–49.
7. Siffert RS. Classification of the osteochondroses. Clin Orthop Relat Res. 1981;158:10–8.
8. West EY, Jaramillo D. Imaging of osteochondrosis. Pediatr Radiol. 2019;49(12):1610–6.
9. Enge Junior DJ, Fonseca EKUN, Castro ADAE, Baptista E, Santos DDCB, Rosemberg
LA. Avascular necrosis: radiological findings and main sites of involvement – pictorial essay.
Radiol Bras. 2019;52(3):187–92.
10. Danger F, Wasyliw C, Varich L. Osteochondroses. Semin Musculoskelet Radiol.
2018;22(1):118–24.
11. Arbab D, Wingenfeld C, Rath B, Lüring C, Quack V, Tingart M. Osteochondrosen des kindli-
chen Fußes [Osteochondrosis of the pediatric foot]. Orthopade. 2013;42(1):20–9. German.
12. Rodríguez-Sanz D, Becerro-de-Bengoa-Vallejo R, López-López D, Calvo-Lobo C, Martínez-
Jiménez EM, Perez-Boal E, Losa-Iglesias ME, Palomo-López P. Slow velocity of the center of
pressure and high heel pressures may increase the risk of Sever’s disease: a case-control study.
BMC Pediatr. 2018;18(1):357.
13. Perhamre S, Lazowska D, Papageorgiou S, Lundin F, Klässbo M, Norlin R. Sever’s injury: a
clinical diagnosis. J Am Podiatr Med Assoc. 2013;103(5):361–8.
14. Duong M, Nicholson A, Li S, Gilmore A, Cooperman D, Liu R. Relationship of Sever’s dis-
ease with skeletal maturity and implications for radiographic findings. Pediatrics. 2018;142
(1_MeetingAbstract):278.
15. Nicholson AD, Liu RW, Sanders JO, Cooperman DR. Relationship of calcaneal and iliac
apophyseal ossification to peak height velocity timing in children. J Bone Joint Surg Am.
2015;97(2):147–54.
16. James AM, Williams CM, Haines TP. Health related quality of life of children with calcaneal
apophysitis: child & parent perceptions. Health Qual Life Outcomes. 2016;14:95.
17. James AM, Williams CM, Haines TP. Effectiveness of footwear and foot orthoses for calcaneal
apophysitis: a 12-month factorial randomised trial. Br J Sports Med. 2016;50(20):1268–75.
18. Wiegerinck JI, Zwiers R, Sierevelt IN, van Weert HC, van Dijk CN, Struijs PA. Treatment of
calcaneal apophysitis: wait and see versus orthotic device versus physical therapy: a pragmatic
therapeutic randomized clinical trial. J Pediatr Orthop. 2016;36(2):152–7.
19. Ramponi DR, Baker C. Sever’s disease (calcaneal apophysitis). Adv Emerg Nurs
J. 2019;41(1):10–4.
20. Topol GA, Podesta LA, Reeves KD, Raya MF, Fullerton BD, Yeh HW. Hyperosmolar dextrose
injection for recalcitrant Osgood-Schlatter disease. Pediatrics. 2011;128(5):e1121–8.
21. Chan JY, Young JL. Köhler disease: avascular necrosis in the child. Foot Ankle Clin.
2019;24(1):83–8.
22. Tuthill HL, Finkelstein ER, Sanchez AM, Clifford PD, Subhawong TK, Jose J. Imaging of
tarsal navicular disorders: a pictorial review. Foot Ankle Spec. 2014;7(3):211–25.
23. Sferopoulos NK. Tarsal navicular osteonecrosis in children. Int J Ortho Res. 2019;2(1):1–5.
24. Freiberg A. Infraction of the second metatarsal bone a typical injury. Surg Gynecol Obstet.
1914;19:191–3.
25. Carter KR, Chambers AR, Dreyer MA. Freiberg infarction. [Updated 2020 Aug 10]. In:
StatPearls [Internet]. Treasure Island: StatPearls Publishing; 2020 Jan-.
26. Petersen WJ, Lankes JM, Paulsen F, Hassenpflug J. The arterial supply of the lesser metatarsal
heads: a vascular injection study in human cadavers. Foot Ankle Int. 2002;23(6):491–5.
27. Smillie IS. Freiberg’s infarction. J Bone Joint Surg (Br). 1957;39:580.
28. Longworth R, Short L, Horwood A. Conservative treatment of Freiberg’s infraction using
foot orthoses: a tale of two prescriptions presented as a case study to open debate. The Foot
(Edinb). 2019;41:59–62.
29. Schade VL. Surgical management of Freiberg’s infraction: a systematic review. Foot Ankle
Spec. 2015;8(6):498–519.
30. Viladot A, Sodano L, Marcellini L. Joint debridement and microfracture for treat-
ment late-stage Freiberg-Kohler’s disease: long-term follow-up study. Foot Ankle Surg.
2019;25(4):457–61.
31. Miyamoto W, Takao M, Miki S, Kawano H. Midterm clinical results of osteochondral
autograft transplantation for advanced stage Freiberg disease. Int Orthop. 2016;40(5):
959–64.
32. Gauthier G, Elbaz R. Freiberg’s infraction: a subchondral bone fatigue fracture. A new surgical
treatment. Clin Orthop Relat Res. 1979;(142):93–5.
33. Trnka HJ, Lara JS. Freiberg’s infraction: surgical options. Foot Ankle Clin. 2019;24(4):669–76.
34. Balakumar B, Maripuri SN, Kotecha A, et al. The functional outcome of four-in-one tech-
nique: dorsal closing-wedge & shortening osteotomy, debridement, micro-fracture in the treat-
ment of Freiberg’s disease. MOJ Clin Med Case Rep. 2017;7(6):315–9.
35. Kehr LE. A new surgical technique for the correction of Freiberg’s deformity. J Am Podiatry
Assoc. 1982;72(3):130–4.
36. Abdul W, Hickey B, Perera A. Functional outcomes of local pedicle graft interpositional
arthroplasty in adults with severe Freiberg’s disease. Foot Ankle Int. 2018;39(11):1290–300.
37. Lui TH. Arthroscopic interpositional arthroplasty of the second metatarsophalangeal joint.
Arthrosc Tech. 2016;5(6):e1333–8.
38. Miller ML, Lenet MD, Sherman M. Surgical treatment of Freiberg's infraction with the use of
total joint replacement arthroplasty. J Foot Surg. 1984;23(1):35–40.
39. Kilmartin TE, Posmyk L. Synthetic cartilage implant hemiarthroplasty for second MTP joint
osteoarthrosis. J Foot Ankle Surg. 2020;59(5):942–8.
40. Brandao B, Fox A, Pillai A. Comparing the efficacy of Cartiva synthetic cartilage implant
hemiarthroplasty vs osteotomy for the treatment of conditions affecting the second metatarsal
head. Foot (Edinb). 2019;41:30–3.
41. Forrester RA, Eyre-Brook AI, Mannan K. Iselin’s disease: a systematic review. J Foot Ankle
Surg. 2017;56(5):1065–9.
42. Kishan TV, Mekala A, Bonala N, Sri PB. Iselin’s disease: traction apophysitis of the fifth meta-
tarsal base, a rare cause of lateral foot pain. Med J Armed Forces India. 2016;72(3):299–301.
43. Deniz G, Kose O, Guneri B, Duygun F. Traction apophysitis of the fifth metatarsal base in a
child: Iselin’s disease. BMJ Case Rep. 2014;2014:bcr2014204687.
44. Ralph BG, Barrett J, Kenyhercz C, DiDomenico LA. Iselin’s disease: a case presentation of
nonunion and review of the differential diagnosis. J Foot Ankle Surg. 1999;38(6):409–16.
45. Sylvester JE, Hennrikus WL. Treatment outcomes of adolescents with Iselin’s apophysitis. J
Pediatr Orthop B. 2015;24(4):362–5.
46. Harbin M, Zollinger R. Osteochondritis of the growth centers. Surg Gynec Obstet.
1930;51:145–61.
47. Buchman J. Osteochondritis of the internal cuneiform. J Bone Joint Surg Am. 1933;15:225–32.
48. Godoy IRB, Yamada AF, Skaf A. MRI findings of intermediate cuneiform osteochondrosis as
a rare cause of foot pain in a child. Radiol Case Rep. 2020;15(6):765–8.
49. Sferopoulos NK. Juvenile osteochondrosis of the cuneiform bones. Clin Res Pediatr.
2019;2(2):1–4.
50. de Cuveland E, Heuck F. Osteochondropathie eines akzessorischen Knochenkernes am
Malleolus tibiae (des sog. Os subtibiale) [Osteochondropathy of accessory apophyseal
ossification center on malleolus tibiae, so-called os subtibiale]. Fortschr Geb Rontgenstr.
1953;79(6):728–32. Undetermined Language.
51. Turati M, Glard Y, Griffet J, Afonso D, Courvoisier A, Bigoni M. Osteochondrosis of the
medial malleolar epiphysis: a case report and review of the literature. Int J Surg Case Rep.
2017;39:176–80.
52. Farsetti P, Dragoni M, Potenza V, Caterini R. Osteochondrosis of the accessory ossification
centre of the medial malleolus. J Pediatr Orthop B. 2015;24(1):28–30.
53. Bartosiak K, McCormick JJ. Avascular necrosis of the sesamoids. Foot Ankle Clin.
2019;24(1):57–67.
54. Souverijns G, Peene P, Cleeren P, Raes M, Steenwerckx A. Avascular necrosis of the epiphysis
of the first metatarsal bone. Skelet Radiol. 2002;31(6):366–8.
55. Wagner A. Isolated aseptic necrosis in the epiphysis of the first metatarsal bone. Acta Radiol.
1930;os-11(1):80–7.
56. Damseh N, Stimec J, O’Brien A, Marshall C, Savarirayan R, Jawad A, Laxer R, Kannu
P. Thiemann disease and familial digital arthropathy – brachydactyly: two sides of the same
coin? Orphanet J Rare Dis. 2019;14(1):156.
Fibular Hemimelia: Principles
and Techniques of Management
Philip K. McClure and John E. Herzenberg
1 Introduction
Fibular hemimelia (FH), also known as congenital fibular deficiency, has an annual
incidence of approximately one in 50,000 live births (~75 cases per year in the
United States; about 330 cases per year in Latin America and the Caribbean) [1].
The classic hallmark is a variable degree of absence of the fibula. In some cases,
however, the fibula appears near normal in length and shape. The degree of fibular
involvement does not necessarily predict the severity of other, arguably more impor-
tant, factors.
The known manifestations of fibular hemimelia include foot deformity
(equinovalgus and sometimes equinovarus), central or lateral ray deficiency, tarsal
coalitions, ankle stiffness/deformity, anteromedial tibial bowing, cruciate ligament
insufficiency or absence, genu valgum (often due to hypoplastic lateral femoral con-
dyle), and leg length discrepancy. The skin at the apex of the tibial bow often has a
characteristic dimple. While it is primarily a unilateral lower extremity phenome-
non, upper extremity manifestations may include syndactyly, cleft hand, and ulnar
hemimelia [2, 3]. Bilateral cases occur but are less common than unilateral cases.
Rodriguez-Ramirez et al. [4] examined the prevalence of associated congenital
osseous anomalies in patients with fibular hemimelia and found that lateral femoral
condyle hypoplasia was the most common associated anomaly (93%) followed by
ball-and-socket ankle joint (80%), congenital short femur (72%), tarsal coalition
(51%), and forefoot ray deletion (44%) [4]. While ray deficiency has often been
assumed to be limited to the lateral rays, a subset of patients have intact lateral
P. K. McClure (*) · J. E. Herzenberg

International Center for Limb Lengthening, Rubin Institute for Advanced Orthopedics, Sinai
Hospital of Baltimore, Baltimore, MD, USA
e-mail: [email protected]; [email protected]; http://www.
limblength.org; http://www.limblength.org

Switzerland AG 2022
214 P. K. McClure and J. E. Herzenberg
Fig. 1 Ten-month-old female with fibular hemimelia (FH) and congenital femoral deficiency
(CFD). AP (a) and lateral (b) view radiographs demonstrate leg length discrepancy, anterior bow-
ing of the tibia, and equinus position of the foot. (c) and (d) Two-year-old with FH and CFD. Mild
genu valgum and ankle valgus are present on AP and lateral view long leg images. (e) and (f)
Twelve-year-old with limb length discrepancy, genu valgum, and talocalcaneal coalition with
resultant ball-and-socket ankle joint. (Used with permission from the Rubin Institute for Advanced
Orthopedics, Sinai Hospital of Baltimore)
columns and appear to have central ray deletions [5]. Equinovalgus is much more
common than equinovarus. Absence of the anterior cruciate ligament (ACL) is com-
mon and may require reconstruction, either as a preparatory surgery for lengthening
or for symptomatic treatment of instability. ACL deficiency can contribute to ante-
rior subluxation of the tibia during tibial lengthening due to the deforming force of
the proximal gastrocnemius tendons that cross the knee to insert on the posterior
femoral condyles.
Fibular hemimelia has a very broad phenotype, as demonstrated in Fig. 1. This
spectrum should be considered carefully in the settings of family preferences, func-
tional needs, anticipated outcomes, and available resources. It is safe to say that if a
surgeon always treats fibular hemimelia using the same formulaic method, at least
some of the patients are being poorly served. Not every case is reconstructible to the
level of desired function, nor is amputation an appropriate automatic response to all
cases. Careful assessment of the patient is required, but extensive discussion with
family and caregivers is equally important for appropriate care. Prosthetic-mediated
reconstruction (amputation) is widely available in the United States and has predict-
able outcomes in most surgeons’ experience [3, 6–14]. Limb reconstruction requires
more from all parties involved, including the family, the patient, the surgeon, and
the therapists. Similar to traumatic reconstruction, the end outcomes remain similar
in the short to medium term: true long-term outcomes are not yet available for either
route of treatment [10, 13].
Ideally, the patient and family will meet with a surgeon who is experienced in
both amputation and reconstruction early in the child’s first year of life. While there
is generally no need for early intervention (prior to 1 year of age), developing a
trusting relationship is critical to optimize the care delivered. The surgeon must
strive to understand the family’s desires (and the realism thereof), while delivering
realistic expectations and risks for both pathways. Whether reconstruction or ampu-
tation is chosen, the patient will require a long-term care relationship with a dedi-
cated physician and medical team.
2 Classification
Classifications are an important component of any orthopedic pathology. In the

effort to categorize, these systems can serve two major functions: demonstrating the
spectrum of disease and directing treatment depending on classification type. In the
Fibular Hemimelia: Principles and Techniques of Management 215
a b
c d
e f
Fig. 1 (continued)
end, classifications are simply educational tools intended to highlight important

components of the pathology at hand. While some are closer than others to directing
treatment, classifications should not be used as a cookbook. The only recipe for suc-
cess in complex congenital deformity is an in-depth understanding of the pathology,
investing appropriate time to understand the patient’s/family’s goals, and careful
execution of surgical techniques. Where the goals of treatment are function based,
classification systems are required that evaluate the potential functional contribu-
tions of each component of fibular hemimelia rather than encouraging myopic focus
on individual variations.
Coventry and Johnson developed the first classification system for fibular hemi-
melia and separated their cohort into three groups (Fig. 2) [15]:
Type I Type II Type III
Fig. 2 Coventry and Johnson classification of fibular hemimelia: Type 1: unilateral fibular defi-
ciency (partial), mild bowing and/or shortening, and mild-to-no foot deformity. Type 2: total or
near total fibular absence, skin dimpling at the apex of the anterior tibial bow, deformed foot and
ankle with absent rays. Type 3: bilateral Type 1 or Type 2 deformities, or association with other
congenital differences. (Copyright 2020, Rubin Institute for Advanced Orthopedics, Sinai Hospital
of Baltimore)
• Type 1: Partial unilateral absence of fibula; normal or slight bowing of the tibia
with some shortening of the limb; the foot is normal or slightly deformed.
• Type 2: Fibula is completely or almost absent; anterior bowing of the tibia with
skin dimpling; deformed ankle joint; deformed foot with absent rays.
• Type 3: Bilateral Type 1 or 2.
While this classification highlights a subset of known pathology present in fibu-
lar hemimelia, the focus on the amount of fibula present is of historical interest only.
Perhaps the most important component is the focus on the amount of deformity in
the foot/ankle.
The Achterman and Kalamchi classification, proposed in 1979, moved even fur-
ther away from a functional assessment of the limb (Fig. 3) [16]. The simplicity of
the classification system makes it attractive to orthopedists who do not routinely
evaluate FH, but the utility is questionable. They divided the patients into two
groups with one subdivision:
• Type 1: Incomplete fibular deficiency
–– 1A: Proximal fibular epiphysis distal to proximal tibial epiphysis, distal fibu-
lar physis proximal to dome of talus
–– 1B: 30–50% shortening of the fibula without a distal talofibular articulation.
• Type 2: Complete fibular deficiency, with or without a small distal fibular remnant
In 2003, Stanitski and Stanitski proposed the first functional classification of
fibular hemimelia (Fig. 4) [17]. While it focuses on radiographic components, the
system was an important move toward functional evaluation. The system requires
evaluation of each of four components:
Normal Type II
Type IA Type IB
3-year-old child
Fig. 3 Achterman and Kalamchi classification of fibular hemimelia: Type 1: partial fibular defi-
ciency, subdivided into 1A and 1B. Type 1A: Proximal fibula distal to proximal tibial physis, distal
fibular physis proximal to ankle joint. Type 1B: 30 to 50% fibular deficiency, no talofibular articu-
lation. Type 2: Total absence of fibula, possible fibular anlage/remnant. (Copyright 2020, Rubin
Institute for Advanced Orthopedics, Sinai Hospital of Baltimore)
1. Fibula: Normal, partially absent, or completely absent

2. Ankle joint: According to the morphology of the tibiotalar joint: horizontal, val-
gus, or ball-and-socket joint
3. Tarsal bones: Tarsal coalition present or absent
4. Foot: Numbers of rays
Moving closer to a direct functional evaluation, Birch et al. proposed a system
focused on the clinical evaluation of the affected foot and severity of expected limb
length discrepancy (Fig. 5) [18]. As the classification system evolved, the indica-
tions for reconstruction widened to some degree [3, 19]. Built in a retrospective
manner, the original classification sought to evaluate what was done and determine
if predictive factors may have been present. The three-ray “cutoff” was not intended
to be used as a standalone metric, but it was reported that it did often reflect the
overall status of the foot (personal communications with John G. Birch, November
20, 2020).
• Type 1: The primary feature of Type 1 is a functional foot, which can function as
a stable weight-bearing platform. While exceptions certainly occurred, this crite-
rion was most often met when three or more rays of the foot were present. After
the foot is evaluated, the implications of leg length discrepancy are considered:
–– Type 1A: <6% leg length inequality; the treatment is orthosis or contralateral
epiphysiodesis.
–– Type 1B: Six to 10% leg length inequality; the treatment is epiphysiodesis ±
lengthening.
Fibula
Normal Type Type Type
(Nearly normal) (Small) (Absent)
Tibiotalar joint
H V S
(Horizontal - (Valgus) (Spherical)
Normal)
Presence of tarsal coalition
S C
(Without) (With)
Number of rays
5 4 3 2 1
Fig. 4 Four components of the Stanitski classification: (1) Fibula: normal, partially absent, or
completely absent. (2) Tibiotalar joint: Ball-and-socket, valgus, neutral. (3) Presence or absence of
tarsal coalition. (4) Foot: numbers of rays. (Copyright 2020, Rubin Institute for Advanced
At least three rays and functional upper extremity
Type 1A Type 1B Type 1C Type 1D
Overall length
(pelvic crest
to tibial plafond)
compared with
contralateral side
> 30%
11–30%
6–10%
< 6%
Contralateral side
Two or fewer rays
Functional Non-functional
upper extremity upper extremity
Type 2A Type 2B
Fig. 5 Birch classification of fibular hemimelia. Type 1: foot in stable weight-bearing position,
three or more rays. Type 1 is further broken down by percentage of limb length discrepancy. Type
1A: <6% limb length difference; Type 1B: 6% to 10% limb length difference; Type 1C: 11% to 30%
limb length difference; Type 1D: >30% limb length difference. Type 2: nonfunctional foot (fewer
than three rays, poor position). Type 2 is subdivided into Types 2A and 2B according to the func-
tionality of the upper extremity. Type 2A: functional upper extremity; Type 2B: nonfunctional upper
extremity. (Copyright 2020, Rubin Institute for Advanced Orthopedics, Sinai Hospital of Baltimore)
–– Type 1C: 11 to 30% leg length inequality; the treatment is one or two length-
ening procedures ± epiphysiodesis or extension orthosis.
–– Type 1D: >30% leg length inequality; the treatment proposed is more than
two lengthening procedures or amputation or extension orthosis.
• Type 2: Nonfunctional foot. Type 2 is subdivided into Types 2A and 2B accord-
ing to the functionality of the upper extremity.
–– Type 2A: Upper extremities are functional; therefore, the treatment proposed
is early amputation.
–– Type 2B: Upper extremities are nonfunctional, and foot amputation is contra-
indicated, as the foot must act as a replacement for the upper extremity.
The system did not evaluate the future potential of the foot after reconstruction,
which remains to be demonstrated in future research. As it stands, the Birch classi-
fication represents the most important effort to evaluate the functional potential of
the foot and ankle in fibular hemimelia and represents a critical moment in the
understanding of congenital deformity treatment.
A more recent classification proposed by Paley focuses primarily on surgical
treatment and subclassification of pathology centered around the ankle joint (Fig. 6)
[20, 21]. The classification differentiates fibular hemimelia based on four hindfoot/
ankle components:
• Type 1: Stable normal ankle.
• Type 2: Dynamic valgus ankle.
• Type 3: Fixed equinovalgus ankle. Type 3 is divided into four subtypes according
to the location of the valgus deformity.
–– Type 3a: Ankle type
–– Type 3b: Subtalar type
–– Type 3c: Combined ankle and subtalar type
–– Type 3d: Talar body type
• Type 4: Fixed equinovarus ankle (clubfoot).
In this classification system, each type indicates a certain reconstruction
approach:
• Type 1: Tibial lengthening, tendo Achilles lengthening as needed, depending on
ankle examination.
• Type 2: Supramalleolar reorientation osteotomy, tibial lengthening, tendo
Achilles lengthening.
• Type 3: Classic SUPERankle Reconstruction: peroneal tendon/Achilles length-
ening, fibular anlage resection, reorientation osteotomies of the distal tibia/hind-
foot as needed.
–– 3a: Supramalleolar osteotomy
–– 3b: Subtalar osteotomy
–– 3c: Supramalleolar and subtalar osteotomy
–– 3d: Opening wedge osteotomy of talar body
Type 1: Stable normal ankle Type 2: Dynamic valgus ankle
LDTA = ADTA =
85 – 90° 80 – 85°
Type 3: Fixed equinovalgus ankle

3A: Ankle type 3B: Subtalar type
ADTA ≥ 90° ADTA < 90°
3C: Combined ankle and

subtalar type 3D: Talar type
ADTA ≥ 90° ADTA < 90°
Type 4: Fixed equinovarus ankle Ossified bone

(clubfoot type)
Non-ossified bone
ADTA ≥ 90°
Fig. 6 Paley classification of fibular hemimelia. Type 1: normal ankle. Type 2: dynamic valgus
ankle. Type 3: rigid equinovalgus ankle. Type 3 is further subdivided according to the location of
the valgus into 3A (ankle), 3B (subtalar), 3C (combined ankle and subtalar), and 3D (talar). Type
4: clubfoot type (equinovarus). (Copyright 2020, Rubin Institute for Advanced Orthopedics, Sinai
Hospital of Baltimore)
• Type 4: Initial Ponseti casting following typical technique and progression. This
treatment protocol will often convert a Type 4 into a Type 3 and is then treated
with a SUPERankle procedure at 12–18 months of age.
A thoughtful surgeon will interpret the Paley classification in the setting of antic-
ipated outcomes of reconstruction, as well as other factors including family prefer-
ence and the care environment. When focusing on reconstructive surgery for the
foot and ankle, we use the Paley classification and will do so for the remainder of
the chapter.
3 Clinical Assessment of a Child with FH
Children with fibular hemimelia should be seen in the neonatal period to allow the
surgeon to begin discussing treatment options with the parents; a few patients will
present with a prenatal diagnosis [22]. Unfortunately, a large percentage of parents
do not have accurate information about the diagnosis and prognosis and also feel
significant guilt about their child’s condition. It is imperative that adequate time be
allotted to the family in clinic so that all questions are answered.
The initial physical examination is important. A complete orthopedic exam
should be completed, including overall height/length measurements, upper extremi-
ties, and cervical/thoracic/lumbar spine with evaluation of signs of neuraxial abnor-
malities. The range of motion of the hips must be assessed, as well as the alignment
and stability of the knee. Obviously, the foot and ankle will be a critical component
of the examination, focusing on range of motion, neurologic status, and deformity.
Based on clinical and radiographic evaluation, an outline or life plan should be
made of various surgical options, including prosthetic and reconstructive pathways.
The family should leave the initial visit with a basic understanding of the risks and
benefits of each pathway that are specific to the child. Depending on their level of
comfort and understanding, clinical follow-up prior to the child’s first birthday may
be necessary to revisit the decision-making process.
4 Radiographic Assessment of a Child with FH
In the neonatal period, radiographs of the foot and ankle will be of limited value, but
a supine anteroposterior (AP) radiographic view of the legs can aid the surgeon in
predicting future leg length discrepancy, which is a core component of decision-
making. During the first year of life, a supine AP view radiograph of the legs is often
enough to generate a rough outline for the family. If a decision has been made for
reconstruction, a long lateral view radiograph can be helpful to evaluate foot posi-
tion, knee laxity, and/or contracture. These radiographs should be assessed for evi-
dence of knee and hip pathology in addition to detailed analysis of leg length
discrepancy. The child’s length/height can be used to predict adult height, but this
should be done cautiously as small errors will be magnified significantly. While
questions have been raised about the accuracy of the multiplier method for predic-
tion of leg length discrepancy for treatment with epiphysiodesis, we use this method
for initial evaluation as it is simple and allows prediction without multiple radio-
graphs temporally spaced [23–25]. The Multiplier app is available as a free down-
load through the Apple App Store and Google Play. For predicting adult height, we
reference the height based on the long leg.
The combination of anticipated leg length discrepancy and predicted adult height
is helpful for building a treatment framework for the family. The predicted leg
length discrepancy generates a ballpark estimate of lengthening/epiphysiodesis
options, and predicted adult height creates an environment in which the family can
consider the effects of either strategy on adult height.
In older children, the initial radiographic examination includes full-length stand-
ing AP and lateral view radiographs. The AP film should be obtained with an ade-
quately sized lift under the short leg to level the pelvis (Fig. 7). Ideally, the lateral
view radiograph is obtained in full extension, though this can be technically diffi-
cult. In older patients, standing long leg films are more dependable for leg length
discrepancy determination, as well as evaluation of coronal and sagittal deformity.
As demonstrated by Manner et al., various degrees of tibial spine deficiency on the
coronal view indicate likely knee instability and may be accompanied by sublux-
ation on the long leg lateral view (Fig. 8) [26].
Typical findings in mild cases include valgus alignment of the extremity, gener-
ally driven by a hypoplastic lateral condyle. This is not universal, however, and the
temptation to skip formal deformity analysis including the tibia should be resisted.
In our practice, a complete deformity analysis is conducted on each radiograph
according to the system described in The Art of Limb Alignment [27]. An anterome-
dial tibial bow may contribute to the overall valgus alignment, as can the proximal
tibial physis. A skin dimple on the anteromedial surface of the tibia is a common
clinical sign of the radiographic anteromedial bow (Fig. 9).
The radiographic appearance of the hindfoot varies widely depending on age.
Nearly all children with fibular hemimelia have a tarsal coalition, most commonly
between the talus and calcaneus. This coalition can be in a near-anatomic position
(Fig. 10) or a side-by-side position (double-barrel shotgun appearance, (Figs. 11
and 12) indicating a need for subtalar osteotomy. The surgeon should avoid the
temptation to rule out tarsal coalition on the radiographs of a young child (Fig. 13),
as this near universal association becomes more obvious with increasing age. The
anatomy of the forefoot has been shown to be more varied than previously outlined.
The classical teaching that ray deficiencies are lateral in fibular hemimelia has been
called into question [5]. The prognostic importance of this finding remains to be
determined.
a b
Fig. 7 In older children, the AP view radiograph should be obtained with an adequately sized lift
under the short leg to level the pelvis. (a) An inadequate lift was used when obtaining this radio-
graph, but it was accepted as no surgery was planned before the next follow-up visit. (b) At the next
follow-up visit, the previous film was used to guide proper lifting, which allows for easier evalua-
tion of leg length discrepancy as well as more accurate assessment of acetabular coverage. (Used
with permission from the Rubin Institute for Advanced Orthopedics, Sinai Hospital of Baltimore)
Normal 12-Year-Old Type I
Narrow femoral intercondylar

notch and lateral tibial
spine hypoplasia
Type II Type III
Narrow femoral intercondylar Absent femoral intercondylar

notch, lateral tibial spine notch and flattening of
aplasia, and medial tibial tibial spines
spine hypoplasia
Fig. 8 Radiographic findings of ligamentous deficiency of the knee in fibular hemimelia. Type 1:
narrowing of intercondylar notch and hypoplasia of the lateral tibial spine. Type 2: further narrow-
ing of the intercondylar notch (with decreased notch height), aplasia of lateral tibial spine, hypo-
plasia of medial tibial spine. Type 3: absence of femoral notch, flattening of tibial spines. (Copyright
2020, Rubin Institute for Advanced Orthopedics, Sinai Hospital of Baltimore)
Magnetic resonance imaging (MRI) can be useful in evaluating the knee and
ankle in fibular hemimelia, particularly during the first years of life. The primary
utility lies in the ability to accurately evaluate unossified portions of the ankle and
hindfoot, though useful information regarding the anatomic location of neurovascu-
lar structures and knee anatomy is also available (Figs. 14 and 15) [28]. Further
information can be garnered intraoperatively using ankle arthrography, which gen-
erates a smooth “reference line” for the orientation of the ankle joint on the AP and
lateral views during reorientation osteotomy. This can help to differentiate between
ankle valgus and subtalar valgus (Fig. 16).
a b
c d
Fig. 9 (a) and (b) Clinical photos of moderate deformity secondary to fibular hemimelia.
Equinovalgus of the foot and skin dimple at the apex of an anteromedial tibial bow. (c) and (d)
More severe deformity secondary to fibular hemimelia, with apical dimple and equinovalgus foot
deformity. (Used with permission from the Rubin Institute for Advanced Orthopedics, Sinai
5 Principles of Treatment
Comprehensive treatment of the child affected by fibular hemimelia is required to

optimize outcomes, either with reconstruction or prosthetic-mediated plans.
Through the reconstructive route, the goals of treatment are to create a lower limb
with a stable hip, knee, and ankle:
1. Correct the foot (typically equinovalgus) into a stable, plantigrade position.
2. Equalize lower limb lengths by skeletal maturity.
Fig. 10 Lateral radiograph

of the tibia and foot shows
the hindfoot in near normal
orientation (vertically
stacked), suggesting
supramalleolar valgus.
(Used with permission
from the Rubin Institute
for Advanced Orthopedics,
Sinai Hospital of
Baltimore)
3. Restore normal limb alignment.

4. Ligamentous reconstruction of the unstable knee.
In reconstruction-mediated treatment, the ankle remains the center of attention.
A general rule is that a stiff ankle remains stiff throughout treatment and, in fact,
will get stiffer. The central goal is to obtain and maintain a plantigrade position. A
plantigrade foot with minimal motion can remain functional for a long time, as
evidenced by outcomes from ankle fusion in other patient populations [29, 30].
Whether a stiff ankle and foot is better than the absence of a foot and ankle should
likely be left up to the family to decide.
As implied by the Birch classification, the total amount of leg length discrepancy
predicted at adulthood is a factor in counseling families regarding the expected
course of reconstruction. As a rule of thumb, each lengthening can be estimated to
gain 5 cm, though it is often possible to exceed this goal at experienced centers. In
both small and large discrepancies (<5 cm and >20 cm), contralateral epiphysiode-
sis can be a useful component to achieve the desired outcome.

of the tibia and foot shows
the talus and calcaneus
superimposed, suggesting
a subtalar origin of the
valgus deformity. (Used
with permission from the
Rubin Institute for
Advanced Orthopedics,
Sinai Hospital of
Baltimore)
Outside of correction of the anteromedial bow, our center has moved away from
large lengthening at the time of ankle reconstruction, as the immobilization of the
hindfoot during lengthening appears to exacerbate postoperative stiffness.
Correction of a large anteromedial bow is accomplished with an Ilizarov-type fix-
ator with an oblique hinge or with hexapod frames. The majority of severe antero-
medial bows are associated with very stiff hindfeet. In less severe anteromedial
bows, the correction can be achieved with the shortening osteotomy realignment
distal tibia (SHORDT) procedure. Based on extrapolation from adult trauma litera-
ture, caution is advised if more than 1–2 cm of shortening is required to correct the
deformity, as the soft tissues may not tolerate the abrupt change [31, 32]. It is cer-
tainly possible that the safe limit is even lower for limbs that have “dense” tissue.
Figure 17 shows radiographs of a patient after undergoing shortening osteotomy
Fig. 12 AP view tibia and

ankle radiograph
demonstrates the talus and
calcaneus side by side,
suggesting subtalar valgus
deformity. (Used with
permission from the Rubin
Institute for Advanced
Orthopedics, Sinai
with deformity correction at another institution, with resultant soft-tissue necrosis

and physeal closure. We tend to use the SHORDT procedure mainly for Paley Type
2 FH with mild to moderate deformity only (Figs. 18 and 19).
Depending on the total amount of length needed, this outline can be followed:
First Lengthening Plan for frame/device applied and removed prior to 4 years of age
(typically initiating treatment shortly after third birthday). This ensures that the child
will have no memory of this first lengthening. This lengthening is not included when
planning treatment for mild cases. Currently, there are no viable surgical options for
this first lengthening other than external fixation, though internal plates may eventu-
ally be small enough to help reduce the fixator-related complications in this group.
a b
Fig. 13 (a) AP view radiograph of the tibia to include the foot shows ball-and-socket ankle joint.
The coalition becomes more obvious as ossification progresses during normal development. (b)
Lateral view radiograph with the classic “C” sign of the talocalcaneal coalition. A talonavicular
coalition is also present. (Used with permission from the Rubin Institute for Advanced Orthopedics,
Sinai Hospital of Baltimore)
Second Lengthening Initiated after age 8 years to allow involvement of the patient
in the decision-making progress. The key psychological milestone that we assess
for in our clinic is the ability to understand the concept of a short-term loss in
exchange for a long-term gain – meaning that the patient understands the setback of
surgical procedures in exchange for a longer leg.
a b
Fig. 14 (a–c) Supramalleolar valgus demonstrated on sequential magnetic resonance imaging

evaluations (Paley Type 3A – ankle type). (Used with permission from the Rubin Institute for
Advanced Orthopedics, Sinai Hospital of Baltimore)
Fig. 15 Subtalar valgus

demonstrated on sequential
magnetic resonance
imaging scans (Paley Type
3B). (Used with
Orthopedics, Sinai
Subsequent Lengthening Procedures Depending on the goals in each case, addi-

tional lengthening can be done in 2- to 4-year intervals, allowing the soft tissue (and
family) to rest and recover. Delaying the final lengthening until after physeal closure
allows for internal lengthening, which has been shown to be the preferred option for
patients, along with decreased minor complications [33, 34]. Importantly, the inci-
dence of major complications from internal lengthening procedures is not less when
compared to external fixator-mediated correction, indicating that these procedures
should remain in the hands of experienced centers despite wide familiarity with the
surgical technique of intramedullary rodding [34–36].
During lengthening, the surgeon must pay careful attention to the regenerate as
it forms, initially appearing at 3- to 4-week post-osteotomy. In addition to managing
the regenerate, the surgeon and physical therapy team need to pay very close atten-
tion to the position and range of motion of the knee and ankle during lengthening.
a b
Fig. 16 (a) Supine full-length radiograph of an 18-month-old female demonstrates equinovalgus

position of the foot. (b) An ankle arthrogram obtained in the operating room demonstrates supra-
malleolar valgus. (Used with permission from the Rubin Institute for Advanced Orthopedics, Sinai
The knee more than the ankle is subject to forces strong enough to lead to disloca-
tion, and this risk can be mitigated by extension bracing, close monitoring, and
specialized physical therapy. The knee range of motion must be assessed at every
clinical evaluation. During femoral and tibial lengthening, we use a custom knee
device to maintain full extension, as flexion contracture is a harbinger of impending
knee dislocation [37]. This is of particular importance in femoral lengthening. Tibial
lengthening adds risk of ankle equinus, and therapy along with splinting is an
important factor to minimize the occurrence.
Fig. 17 Care should be

taken to avoid extensive
exposure and soft-tissue
stripping during
reconstruction. Patient
shown underwent
concurrent medial and
lateral approaches to the
ankle for the shortening
osteotomy realignment
distal tibia (SHORDT)
procedure at another
institution. Resultant skin
necrosis and physeal
closure can lead to a more
complex reconstructive
plan or amputation –
depending on patient and
family preferences. (Used
with permission from the
Rubin Institute for
Sinai Hospital of
Baltimore)
6 Surgical Techniques for FH
6.1 Lengthening for Paley Type 1
Mild cases of FH are amenable to standard lengthening techniques, with less need
for soft-tissue management procedures. All children and adults with FH have some
tightness of the Achilles tendon, and limb lengthening will increase this tightness.
At the time of tibial lengthening, we recommend performing a triceps surae length-
ening procedure. We recommend an open Vulpius procedure and a prophylactic
anterior compartment fasciotomy (Fig. 20). The posterior tibial neurovascular
a b c
Guidewire
perpendicular Wedge Tibia secured
to tibia removed with plate
and screws
Guidewire
parallel to
plantar aspect
of foot
a c
Guidewire
perpendicular
to tibia
Tibia secured
with plate
and screws
Guidewire
parallel to
plantar aspect
of foot
Tibiopla
n
angle = tar Tibioplantar
100° angle = 90°
Fig. 18 (a–c) Illustration shows the shortening osteotomy realignment distal tibia (SHORDT)
procedure. (Copyright 2020, Rubin Institute for Advanced Orthopedics, Sinai Hospital of
Baltimore)
bundle is often in close proximity to the triceps surae tendon, so this procedure must
be done under direct vision, not percutaneously. The fasciotomy decreases but does
not eliminate the risk of compartment syndrome (a known complication of tibial
osteotomy). An additional benefit of anterior compartment fasciotomy is that it
allows the anterior compartment musculature to bulge out, especially if the longitu-
dinal incision in the fascia is combined with a short, transverse cruciate incision.
a b
Fig. 19 (a) Preoperative radiograph of fibular hemimelia. Note the shortening of the fibula relative
to the tibial plafond. (b) Postoperative radiograph obtained 3 months after shortening osteotomy
realignment distal tibia (SHORDT) procedure. Note the position of the fibular physis relative to the
ankle joint line. (Used with permission from the Rubin Institute for Advanced Orthopedics, Sinai
This bulging of the anterior compartment musculature will create the impression of
a larger diameter calf, which is desirable because all patients with FH have a smaller
ipsilateral calf due to the combined bone and soft-tissue hypoplasia.
The fixator may need to be extended to include the foot to prevent ankle equinus
during lengthening. If the surgeon elects to avoid fixator extension to the foot, a
temporary extra-articular screw (from the calcaneus to the tibia, posteriorly) or a
lateral plate may be used. Therapy is also an option and can serve as the primary
preventative measure [38]. The surgeon must maintain a watchful eye and be will-
ing to intervene if equinus develops in the absence of internal or external bridging.
If the frame is extended to the foot, it may be removed to minimize stiffness after
the lengthening goal is obtained, provided there is no unresolved flexion contracture
of the knee.
Monolateral fixators are not appropriate for lengthening in fibular hemimelia,
due to a high rate of iatrogenic deformity secondary to tight lateral structures and a
tendency to drift into valgus [39]. While technical modifications can be made to
limit this complication, the near universal availability of ring external fixation
Incision
Proximal
extension
of fasciotomy
Ant.
Lat.
Skin
incision
Distal
b extension
Small incision of fasciotomy
created in fascia
c
Longer end of
fasciotome inserted
under fascia
Fig. 20 Prophylactic anterior compartment fasciotomy may reduce the risk of compartment syn-
drome; the anterior prominence of the muscle may be desirable from a cosmetic standpoint. (a) A
1- to 2-cm incision is made just lateral to the tibial crest. (b) Fascia is opened after exposure with
blunt dissection. (c) Fasciotome is then inserted under the fascia. (d) Fasciotome is advanced
proximally. The fasciotome should remain as medial as possible (right of the crest). Ant., anterior
compartment; Lat., lateral compartment. (Copyright 2020, Rubin Institute for Advanced
Fasciotome
advanced
proximally
and
distally
under guidance
of touch
Fig. 20 (continued)
systems, and their versatility, argues against the use of monolateral fixation for tibial
lengthening.
Figure 21 shows a typical lengthening with external fixation for FH. In most pure
external fixation cases, three pins/wires are used proximally, three pins/wires are
used in the distal segment, and foot fixation may be included. The proximal and
distal rings should be placed so that there is plenty of room to allow for better
recruitment of soft tissue into the lengthening. The greater the distance between
fixation points, the more soft tissue is available to accommodate the lengthening
(less soft tissue strain, defined as the amount of tissue change required along the
direction of force divided by the initial ring spacing).
For skeletally mature patients in whom there is no longer a viable proximal tibial
growth plate, it is attractive to use intramedullary (IM) telescopic nails. Two sys-
tems, the PRECICE (NuVasive, Inc., San Diego, CA, USA) and the FITBONE
(Orthofix, Lewisville, TX, USA), are now widely available. An important technical
point of intramedullary distraction osteogenesis is to make the multiple drill holes
in preparation for osteotomy prior to reaming the canal for nail placement. This is
in an effort to encourage the reamings to exit anteriorly to stimulate new bone for-
mation at the lengthening site.
In the developing world, implantable telescopic lengthening nails are generally
unavailable, so the lengthening over nail (LON) technique is useful. The external
a b
Fig. 21 Standing long leg films of a 12-year-old girl (a), after distraction osteogenesis of the tibia
and distal femoral guided growth (b), after frame removal (c), and after neutralization of the axis
through growth modulation (d). (Used with permission from the Rubin Institute for Advanced
c d
Fig. 21 (continued)
fixator that is applied for the LON technique can be a simple frame with two points
of fixation at either end (Fig. 22). The rate of lengthening is adjusted according to
bone formation. After lengthening is achieved, the patient undergoes distal locking
and frame removal (performed in that order in the operating room to prevent short-
ening). The majority of the consolidation phase then occurs under the protection of
the nail, without need for an external fixator. It is important to place the external
fixation points outside the planned pathway of the nail and to maintain the lengthen-
ing axis of the fixator parallel to the nail axis to minimize the risk of mechanical
interference.
Fig. 22 Lengthening over

nail technique. (Copyright
2020, Rubin Institute for
Sinai Hospital of
Baltimore)
In both internal lengthening nails and LON, blocking screws (Poller screws) can
be used to prevent mechanical axis deviation during lengthening. If needed in the
LON technique, these screws can be inserted at the time of frame removal. Figure 23
shows lengthening with a PRECICE using a posterior blocking screw in the proxi-
mal fragment to prevent procurvatum. The recent development of an internal length-
ening plate allows avoidance of external fixators for tibial lengthening prior to
skeletal maturity (Fig. 24).
a b
Fig. 23 Lateral views of the tibia during distraction of a tibial osteotomy. A posterior blocking
screw is present in the proximal fragment to drive the nail into the anterior cortex, limiting the
risk of procurvatum deformity. (a) Immediate postoperative radiograph. (b) Radiograph
obtained 2 weeks postoperative. (c) Radiograph obtained 6 months after the procedure. (Used
with permission from the Rubin Institute for Advanced Orthopedics, Sinai Hospital of
Baltimore)
Fig. 23 (continued)
6.2 Lengthening Plus Ankle Realignment for Paley Type 2
The flexible valgus deformity of the ankle should be corrected prior to lengthening
to avoid complications of asymmetric muscle pull during lengthening. Reorientation
osteotomy of the supramalleolar distal tibia should be completed prior to lengthen-
ing (Fig. 25). In the same setting, intramuscular lengthening of the peroneal tendons
can help to rebalance the soft tissues around the ankle.
A supramalleolar rotational dome osteotomy is appropriate in mature patients.
The SHORDT procedure is more appropriate for younger children with remodeling
Fig. 24 Internal
lengthening with the
a b
PRECICE plate. In this
case, the anterolateral soft
tissues allowed adequate
coverage of the implant,
and the position resists
tendency toward valgus in
tibial lengthening. (a)
Immediate postoperative
radiograph. (b) One-month
postimplantation with
7-day latency. (Used with
Orthopedics, Sinai
potential, but long-term outcomes are unknown (Fig. 18). From a soft-tissue stand-
point, the medial osseous shortening generates a relative lengthening of the poste-
rior tibialis muscle; at the same time, the peroneal tendons are stretched during the
reorientation. For this reason (among others), we reserve the SHORDT correction
for mild cases.
6.3 Lengthening Plus SUPERankle Reconstruction

for Paley Type 3
For the rigid equinovalgus type, we use a modified Paley SUPERankle approach.
Children can undergo this surgery as young as 1 or 2 years of age. The goal is
to create a plantigrade foot and realign the foot relative to the distal tibia. The
ankle joint and its ligaments are not opened during this extra-articular
reconstruction.
Supra-
malleolar
dome Valgus
osteotomy deformity
planned corrected
30°
Fig. 25 (a) Focal dome osteotomy of the distal tibia and fibula allows realignment of the dynamic
valgus ankle in patients who are deemed too skeletally mature to undergo surgical correction that
requires joint remodeling (shortening osteotomy realignment distal tibia [SHORDT]). Copyright
2020, Rubin Institute for Advanced Orthopedics, Sinai Hospital of Baltimore. (b) Supramalleolar
rotational dome osteotomy in a skeletally mature individual with fibular hemimelia. (Used with
permission from the Rubin Institute for Advanced Orthopedics, Sinai Hospital of Baltimore)
6.3.1 Surgical Technique for Type 3a (Figs. 26 and 27)
Positioning
Supine position, bump under the ipsilateral sacrum, and tourniquet control.
Surgical Approach
Longitudinal (straight) incision is made laterally from the mid-calf to just above the
sole of the foot. The peroneal tendons are cut with a Z-technique and later repaired
a
Peroneal
longus
tendon c
divided Extent of
proximally membrane
and anlage
resection
b
Peroneal
brevis
tendon
divided
distally
Sites of mid-
diaphyseal
and
d supramalleolar
Path of osteotomies
Achilles
tendon
Z-lengthening
e e
K-wires K-wires
inserted inserted
Fig. 26 (a–m) SUPERankle surgical technique for supramalleolar type fibular hemimelia (Paley
Type 3A – ankle type). PRN, when necessary. (Copyright 2020, Rubin Institute for Advanced
f
Acute
opening wedge
osteotomy
performed
g
Bone graft
inserted
h
Tendons sutured
i
K-wires advanced
Fig. 26 (continued)
j
Achilles tendon repair
augmented with resected
membrane PRN
k
Fixator
applied
l
Mid-diaphyseal
opening wedge
osteotomy performed
m
Gradual alignment
and lengthening
completed
Fig. 26 (continued)
a b
c d
Fig. 27 Case example of an 18-month-old boy with Paley Type 3A fibular hemimelia. (a) and (b)
Preoperative AP (a) and lateral (b) view radiographs showing equinovalgus foot/ankle deformity
with anterior tibial bowing. (c–e) Distal tibial osteotomy of SUPERankle procedure. (f) Hinge
position outside the convexity to allow lengthening and deformity correction. (g) and (h)
Postoperative imaging of the SUPERankle procedure. (i) and (j) Two-week postoperative imaging
showing correction and lengthening. (k) and (l) AP (k) 3-month postoperative imaging after frame
removal. Note the complete correction of the tibia and the ankle. (Used with permission from the
Rubin Institute for Advanced Orthopedics, Sinai Hospital of Baltimore)
e f
g h
Fig. 27 (continued)
i j
Fig. 27 (continued)
in the lengthened configuration. In some cases, only one peroneal tendon is present.
If there is a distal anlage of the fibula, it may be left in place. Anterior compartment
fasciotomy is performed. The superficial peroneal nerve is identified and protected.
The anterior compartment muscles are dissected off of the fibular cartilage anlage
and off of the intermuscular septum.
The intermuscular septum is resected from the ankle proximally up to the mid-
portion of the tibia at the apex of the anterolateral bow. The resected intermuscular
septum is placed in a sterile specimen cup and covered with saline, as it may be
needed for repair and elongation of the Achilles tendon. There is no need to resect
the anlage proximal to the anterior tibial bow, nor is there any need to decompress
the peroneal nerve proximally.
The sural nerve is identified and protected. The Achilles tendon and posterior
tibial neurovascular bundle are also identified. Avoid damage to the posterior tibial
nerve, which is often in close proximity to the Achilles tendon. In some cases, the
posterior tibial nerve is quite large – a nerve stimulator can help distinguish tendon
from nerve. Do not be tempted to lengthen a structure before finding all of the ten-
dons, nerves, and blood vessels. The flexor hallucis longus is identified and used as
a guide to the posterolateral corner anatomy. Through this posterolateral approach,
the posterior tibial nerve is decompressed into the tarsal tunnel distally as far as it
can be visualized. The Achilles tendon is very short; the tendon available for length-
ening can be made longer by scraping the distal muscle belly proximally to expose
more of the tendon and prepare it for Z-lengthening. Despite this, it is sometimes
necessary to create a tendon graft from the resected intermuscular septum to obtain
sufficient Achilles tendon elongation. The foot is then placed into the maximum
equinus and valgus position. Two 1.8-mm diameter Kirschner wires (K-wires) are
inserted from the plantar surface of the heel, across the calcaneus and talus, across
the ankle joint, and approximately 5–10 mm into the distal tibia. This pins the ankle
in the maximum valgus/equinus position.
Osteotomy
A distal tibial subperiosteal dissection is performed. Great care should be taken

to avoid damage to the growth plate’s perichondrial ring. Mini-Hohmann retrac-
tors are placed anteriorly and posteriorly. An oscillating saw is used to make an
oblique cut from posterolateral to anteromedial, but the anteromedial cortex is
left intact. To correct the equinovalgus position of the hindfoot, the osteotomy is
levered open from the posterolateral direction with an osteotome or laminar
spreader. The osteotomy is held open with a cortical allograft (e.g., small piece of
fibular allograft). The two K-wires are passed across the osteotomy and up into
the distal half of the tibia, stopping just short of the anterolateral bow in the apex
of the diaphysis. The K-wires are bent outside the skin of the heel and can be
incorporated into the frame (if planned) or left outside the skin for removal if the
frame is not going to be used. The foot is now corrected and plantigrade relative
to the distal tibia.
The tourniquet can be let down for the closure. The Achilles and peroneal ten-
dons are repaired in their lengthened configuration. The incision is closed over a
small drain to prevent compartment syndrome and wound hematoma. At this point,
the operation can conclude and a long leg, bivalved cast can be applied. The cast and
pins are removed in 6 weeks, and then the patient can attend physical therapy ses-
sions for the ankle.
Frame Application
Four to 6 months after the initial procedure, the tibia can be lengthened with an
Ilizarov or hexapod external fixator through an osteotomy made at the apex of the
anterolateral bow. Alternatively, the fixator may be applied at the same time as the
SUPERankle reconstruction and used to correct the apex anteromedial bow with
1–2 cm of lengthening. The frame is removed after healing of the diaphyseal corti-
cotomy is achieved, and a long leg cast is applied for 3–4 weeks. After cast removal,
the patient undergoes mobilization and rehabilitation of the ankle to try to regain as
much motion as possible.
6.3.2 Surgical Technique for Type 3b (Figs. 28 and 29)
Positioning and Surgical Approach
The positioning and approach are the same as described for Type 3a.
Osteotomy
An oblique subtalar osteotomy is performed. The osteotomy should initiate in the

sinus tarsi, exit medially in the region of a typical talocalcaneal joint, and terminate
posteriorly just anterior to the Achilles insertion. The cartilaginous anlage of the
fibula is dissected and excised around. After the osteotomy is complete and the sur-
geon is able to fully mobilize the hindfoot, K-wires are initially inserted in a similar
manner to Type 2A with the foot in the maximally deformed position (equinus and
valgus). The distal half of the calcaneus and foot is translated medially and angu-
lated to make the K-wires face directly upward toward the talus. The reduction of
the “side-by-side” position of the talocalcaneal block reduces the overall valgus
position of the foot. A bone graft can be placed posteriorly to improve the equinus
position. A large piece should not be used, as it adds to overall soft-tissue tension.
The fixation is then driven across the osteotomy into the talus. In some cases, suf-
ficient purchase is available in the talus. For very young children, better purchase
can be achieved by driving the wires across the ankle joint into the distal tibia. The
tourniquet is released, and the closure proceeds as described for Type 3A, including
external fixator application to correct the mid-diaphyseal deformity.
a. c.
Peroneal Extent of
longus membrane
tendon and anlage
divided resection
proximally
b.
Peroneal
brevis
tendon
divided
distally
Site of mid-
diaphyseal
osteotomy
d.
Path of
Achilles
tendon Site of subtalar
Z-lengthening osteotomy
e.
Acute translation
and angulation
osteotomy
performed
Fig. 28 (a–l) SUPERankle surgical technique used to treat subtalar type fibular hemimelia (Paley Type
3B). PRN, when necessary. (Copyright 2020, Rubin Institute for Advanced Orthopedics, Sinai Hospital
of Baltimore)
f.
Bone graft
inserted
g.
K-wires inserted
h.
Tendons
sutured
i.
Achilles
tendon repair
augmentated
with resected
membrane PRN
j.
Fixator k.
applied Mid-diaphyseal
opening wedge
osteotomy
performed
l.
Gradual
alignment and
lengthening
completed
Fig. 28 (continued)
a b
c d
Fig. 29 Subtalar deformity in a 6-year-old male (Paley Type 3B). The osteotomy is performed
through the talocalcaneal coalition. (a) and (b) AP (a) and lateral (b) views demonstrate residual
valgus deformity after previous supramalleolar osteotomy at age 2 years. (c) K-wire guidance for
planned osteotomy line. (d) After osteotomy completion, the distal fragment is translated medially
and positioned into varus with the aid of a laminar spreader. (e) Fibular allograft placed to maintain
correction in conjunction with retrograde K-wires. (f) and (g) Final position after deformity cor-
rection and fixation. (Used with permission from the Rubin Institute for Advanced Orthopedics,
e f
Fig. 29 (continued)
6.3.3 Surgical Technique for Type 3c (Fig. 30)
Osteotomy
An ankle arthrogram is helpful to determine the position of the ankle joint intraop-
eratively. The supramalleolar osteotomy and the subtalar osteotomy are then per-
formed. As the subtalar osteotomy can be more difficult to control, this deformity is
corrected first, translating the distal fragment medially and opening posteriorly. The
subtalar coalition osteotomy is provisionally held with bone graft and K-wires. The
position of the ankle is then corrected, typically with a posterolateral opening wedge
osteotomy to correct valgus and procurvatum of the joint surface demonstrated dur-
ing the arthrogram. A fibular allograft is then introduced into the opening wedge,
and the K-wires from the heel are driven into the tibia. At the completion of correc-
tion, the wires cross the subtalar coalition osteotomy, the ankle joint, and the distal
tibial osteotomy. If there is too much tension on the soft tissues, the supramalleolar
osteotomy may be fashioned as a closing wedge type rather than an opening wedge
type. Generally this is done through the same lateral incision to limit risk for soft-
tissue compromise between medial and lateral incisions.
6.3.4 Surgical Technique for Type 3d (Fig. 31)
Diagnosing Type 3d
This subtype is extremely rare and can be diagnosed in younger children through
MRI evaluation or in older children through computed tomography. The distinctive
feature of this deformity is a wedge-shaped talar body.
Osteotomy
The opening wedge procedure is similar to the technique described for Type 3b
(subtalar type). However, the osteotomy used in Type 3d cases does not pass com-
pletely through the medial side.
a. c.
Peroneal Extent of
longus membrane
tendon and anlage
divided resection
proximally
b.
Peroneal
brevis
tendon
divided
distally
Site of mid-
diaphyseal
osteotomy
Site of
d. supramalleolar
Path of osteotomy
Achilles
tendon Site of subtalar
Z-lengthening osteotomy
e.
Acute subtalar
osteotomy completed
along with translation
and angulation
Fig. 30 (a–o) SUPERankle surgical technique that is used to treat combined ankle/subtalar type
fibular hemimelia (Paley Type 3C). (Copyright 2020, Rubin Institute for Advanced Orthopedics,
f.
Subtalar
bone graft
inserted
g.
K-wires inserted
h.
Acute
supramalleolar
opening wedge
osteotomy
performed
i.
Supramalleolar
bone graft inserted
j.
K-wires advanced
Fig. 30 (continued)
l.
Achilles
tendon repair
k. augmented
Tendons with resected
sutured membrane
PRN
m.
Fixator
applied
n.
Mid-diaphyseal opening
wedge osteotomy
o.
Gradual
alignment and
lengthening
completed
Fig. 30 (continued)
Fig. 31 Surgical technique

that is used to treat talar
body type fibular
hemimelia (Paley Type
3D). (Copyright 2020,
Rubin Institute for
Sinai Hospital of
Baltimore) Bone
Opening graft
wedge
osteotomy
Wire
6.4 Initial Nonsurgical Treatment for Type 4 (Clubfoot Type)
Fewer than 15% of FH cases can be classified as Type 4; therefore, treatment must
be individualized. In the authors’ experience, the initial treatment is nonsurgical and
should follow Ponseti principles. It is unclear why the Ponseti method is able to
correct the varus and internal rotation deformity, as the Ponseti technique ostensibly
works through the subtalar joint. In our experience, all children with Type 4 FH
have a subtalar joint coalition. After casting and tenotomy, the deformity is con-
verted to an equinovalgus type, which can be corrected using the SUPERankle
approaches described previously.
6.5 Additional Procedures
Valgus at the knee is common in fibular hemimelia and is amenable to growth mod-
ulation as long as the physes are open. While the valgus is classically distal femoral
in nature, the proximal tibia should also be evaluated to avoid creating the “bad
combination” of distal femoral valgus and proximal tibial varus in the uncommon
case of tibial-driven valgus. The optimal timing of growth modulation for valgus at
the knee is debatable. Whether there is a long-term impact on trochlear formation is
unknown. Rebound is common in younger patients [40–42]. The cause of progres-
sive valgus has not been clearly elucidated and has been attributed to lateral femoral
condyle hypoplasia traditionally. Additional factors could be the fibrous band of the
fibular anlage and/or the Cozen phenomenon post-lengthening (Fig. 32).
a b
Fig. 32 (a) Preoperative standing full-length imaging of a 6-year-old male. (b) Full-length stand-
ing AP view radiograph after 6 cm of lengthening and placement of tension-band plate. Note the
mild knee flexion contracture but normalized medial proximal tibial angle. (c) Six months after
frame removal. Note the correction of the distal femur and the normalized lateral distal femoral
angle. Progressive recurrence of proximal tibial valgus, possibly from a Cozen-type phenomenon.
(d) Placement of tension-band plate on medial proximal tibia. (e) Improvement of proximal tibial
valgus after placement of tension-band plate. (Used with permission from the Rubin Institute for
Advanced Orthopedics, Sinai Hospital of Baltimore)
c d
Fig. 32 (continued)
Fig. 32 (continued)
7 Postsurgical Care
The most critical component of postoperative care is physical therapy. We require

3 to 5 days per week of supervised physical therapy, depending on knee stability,
family compliance, and previous lengthening experience. In addition to the super-
vised sessions, families are prescribed a home exercise program to help minimize
complications. In tibial lengthening, these programs focus on prevention of equi-
nus deformity (if not otherwise prevented with extra-articular screw or bridging the
frame) and knee flexion contracture. Flexion contractures of the toes are also pos-
sible but have less severe consequences than knee and ankle complications. We
include a splinting and stretching protocol for the toe flexors in our tibial
lengthening protocol. Physical therapy continues until the completion of lengthen-

ing and restoration of normal range of motion in all joints. Nighttime extension
splinting is helpful for the knee and is used for all tibial and femoral lengthening
patients [37, 43]. This splinting device can be modified as needed to accommodate
an external fixator.
Weight-bearing depends on the patient’s size and anticipated compliance.
Additional factors are choice of lengthening device. External fixators typically
allow full weight-bearing as tolerated. Titanium intramedullary rods are restricted
to 10 to 20 kg weight-bearing, while stainless steel intramedullary rods tolerate
65–110 kg, depending on diameter. We encourage patients to continue to use
crutches for balance even if full weight-bearing is permitted.
We recommend a latency period of 7 days. If the patient experienced previous
premature consolidation despite good compliance, we shorten the latency. Poor soft
tissue, repeated lengthening, and a requirement for more soft-tissue dissection dur-
ing osteotomy all factor into a potential decision to extend the latency period. Our
typical distraction rate is 0.75–0.8 mm/day completed over three or four sessions
per day depending on device used. If the ankle joint was bridged with a fixator, the
foot fixation may be removed at the termination of the distraction period to allow
ankle range of motion and minimize stiffness, provided there is no knee flexion
contracture. If a syndesmotic wire or screw was used to maintain the ankle mortise,
it should be kept in place until frame removal to avoid the potential complication of
fibular shortening.
8 Outcomes
An initial single-center report by McCarthy et al. in 2000 found improved outcome

scores in an amputation group when compared with a lengthening group [7].
Lengthening was done either with the Wagner device or Ilizarov method, and results
were not broken down according to each strategy. Wagner lengthening has been
shown to yield higher complication rates [14, 44]. Perhaps the most important dis-
tinction between the reconstructive protocol presented in this chapter and the
lengthening in the study by McCarthy et al. is the presence of adjacent joint recon-
struction in the modern method. McCarthy et al. reported that a valgus ankle was a
risk factor for poor result in their lengthening patients, but it does not appear that
ankle correction was pursued pre-lengthening [7]. Prior to the McCarthy et al. arti-
cle, several other single-center studies reported similar findings [11, 45].
Reconstruction management for mild fibular hemimelia is well established as a
realistic option with good to excellent outcomes [8, 12, 46–49]. Oberc and Sulko
evaluated 31 patients who had undergone a variety of treatments for fibular hemi-
melia [12]. Overall, they found improved outcomes in patients treated with amputa-
tion instead of reconstruction; however, the group with the best outcomes was in
fact a subset of the reconstruction patients. They found the highest satisfaction and
functional scores were in patients treated with a combination of lengthening and
epiphysiodesis, resulting in nearly equal leg lengths. The authors did note that in the
lengthening-only cohort, residual leg length discrepancy exceeding 5 cm appeared
to be a major factor in functional outcomes. In their series, a “nonfunctional” foot
was considered an indication for amputation, though the definition was somewhat
unclear [12].
In 2010, El-Sayed et al. reported the results of their comprehensive reconstruc-
tion protocol that focused on the Ilizarov lengthening method and centralization of
the ankle [48]. A total of 157 patients with Kalamchi Type 2 fibular hemimelia were
reviewed, with an average lengthening gain of 13.6 cm. Patient outcomes were
reported by means of a distributed satisfaction survey. Of the 119 surveys returned,
70 (59%) reported excellent results, and good results were reported in an additional
49 (41%). They reported that two patients with psychiatric conditions refused to
participate in the survey, likely indicating that the authors felt the reported outcome
would have been poor if the survey had been completed. Twenty-two patients either
declined to participate or returned incomplete surveys and could not be included.
All parents were reported to be happy with the final results. While cultural factors
play a large role in family acceptance of amputation, this study highlights the pos-
sibility of good results in severe cases with a comprehensive reconstruction
protocol.
Catagni et al. have reviewed their experience in two reports [9, 46]. Catagni et al.
presented their modifications of the Delmonte classification as follows:
• Grade I – mild shortening of fibula associated with tibial shortening, mild defor-
mity, and stable knee/ankle joints.
• Grade II – Severe fibular shortening, no functional lateral malleolus, equinoval-
gus foot deformity with ray deficiencies. Tibial and femoral deformities may also
be present.
• Grade III – Absent fibula, severe deformity and shortening, equinovalgus foot,
and/or dislocated ankle, with femoral involvement.
Each grade was treated with a specific approach, including lengthening alone for
Grade I and initial brace management followed by initiation of deformity correction
at age 10–12 years for Grade II. For Grade III, treatment included initial ankle soft-
tissue release at 3–6 months of age followed by a series of lengthening procedures
initiating at age 5–8 years. The details of their reconstructive protocol are
shown below:
• Grade I: Simple lengthening, no bridge to foot.
• Grade II:
–– Stage 1 – Ankle orthosis with shoe lift after walking age.
–– Stage 2 – Tibial deformity correction and lengthening at age 10–12 years,
with foot included in the frame. Foot fixation was included for stability and
gradual reduction of the deformity. Fibular transport was also included as
needed. The authors noted that lengthening should be less aggressive with
more severe foot deformity.
–– Stage 3 – Second lengthening, bridging to femur if double-level lengthening
is planned.
• Grade III:
–– Stage 1 – Ankle release at 3–6 months of age with correction of deformity.
–– Stage 2 – Lengthening at 5–6 years of age, bridge to foot, with correction of
deformity and more conservative lengthening if foot deformity present.
–– Stage 3 – Lengthening at 8–10 years of age, with or without femoral
lengthening.
In their initial report, 29 patients with Grade I were treated with a range of
lengthening from 4 to 37 cm [46]. In the initial series, they reported good joint func-
tion in all patients, with all patients satisfied with functional and cosmetic results.
Seven Grade II patients had competed treatment. Complication rates were higher in
Grade II, but all patients were reported to have met the goals of treatment. Four
Grade III patients had completed treatment, complications were again higher, and
outcomes were not specifically reported [46].
A follow-up study in 2011 reviewed outcomes of 32 patients with Grade III fibu-
lar hemimelia [9]. Outcomes were scored based on limitation of function (on a
4-point scale) and pain (on a 5-point scale). Most patients had moderate limitation
of activity and minimal to no pain. Twenty-four of 32 patients were satisfied. In the
end, 17 patients were reported to have a satisfactory outcome in the surgeons’ inter-
pretation (no need for braces and no residual need for surgical care), and an addi-
tional 8 patients had relatively good outcomes (still required brace wear for daily
activity). Two patients underwent late Syme amputation. The authors noted that the
majority of patients were “quite active” with minimal pain, but the details of activity
level were not clearly defined. Ankle valgus deformity was noted to be a risk factor
for poor outcome [9].
The use of the above described SUPERankle procedure has been evaluated as a
means to limit the effect of ankle valgus deformity on reconstructive outcomes [50].
Twenty-nine consecutive patients were managed according to the Paley classifica-
tion. Excellent results were reported in 55%, good results in 22%, fair results in
15%, and poor results in 7%. The authors attributed improvements in outcomes
when compared to historical controls to management of the ankle deformities with
pre-lengthening reconstruction [50].
A 2019 comparison between amputation and reconstruction published by Birch
et al. reviewed the outcomes of amputation-mediated treatment and reconstructive
surgery for fibular hemimelia [13]. Both institutions involved were highly special-
ized: one with an on-site prosthetics department and the other with a very high
concentration of surgical experience with congenital pathology. Minor differences
were identified but felt to be clinically insignificant between the outcomes of each
approach. Self-selected walking speed was 1.13 m/s in the reconstruction group
versus 1.20 m/s in the amputation group. Both differed significantly from control
patients at 1.25 m/s. This difference, though statistically significant, was not felt to
be of clinical importance. Paired with the evidence by Pate et al. that outcomes trend
toward control subjects with increasing age in fibular hemimelia [51], this is a very
positive indication for the long-term health of patients affected by fibular hemime-
lia. Based on data presented by Birch et al., fears regarding the long-term impact of
multiple procedures on quality of life for children appear to be groundless, as
reported mental health outcomes in both groups were equivalent [13]. Whether
these results can be reproduced outside of highly specialized centers is not clear
based on available evidence.
9 Summary
A wide range of complications can occur with reconstruction and lengthening of

limbs affected by fibular hemimelia. Pin infections are common. Residual leg length
discrepancy, delayed union, joint stiffness, refractures, knee subluxation, residual
foot deformities, and psychological impacts have all been reported. In the end, at
least when performed in experienced centers, the outcomes of reconstruction are
generally comparable to amputation, while avoiding the need for lifelong prosthetic
care [13]. As might be expected for a rare pathology, this may not be reproducible
in the more generalized experience [52]. Patients and families should be counseled
carefully regarding surgical and nonsurgical treatment options, ideally at experi-
enced centers. Outcomes data are emerging to support either reconstruction or
amputation-mediated treatment, but overly rosy or dark representation of either
method is unjustified. Both amputation and reconstruction have meaningful risks
and benefits when managed properly; to be fair to our patients, we must represent
both in a complete and unbiased discussion.
References
1. Bedard T, Lowry RB, Sibbald B, Kiefer GN, Metcalfe A. Congenital limb deficiencies in
Alberta-a review of 33 years (1980-2012) from the Alberta Congenital Anomalies Surveillance
System (ACASS). Am J Med Genet A. 2015;167A:2599–609.
2. Stevens PM, Arms D. Postaxial hypoplasia of the lower extremity. J Pediatr Orthop.
2000;20:166–72.
3. Birch JG, Lincoln TL, Mack PW, Birch CM. Congenital fibular deficiency: a review of thirty
years’ experience at one institution and a proposed classification system based on clinical
deformity. J Bone Joint Surg. 2011;93:1144–51.
4. Rodriguez-Ramirez A, Thacker MM, Becerra LC, Riddle EC, Mackenzie WG. Limb
length discrepancy and congenital limb anomalies in fibular hemimelia. J Pediatr Orthop
B. 2010;19:436–40.
5. Reyes BA, Birch JG, Hootnick DR, Cherkashin AM, Samchukov ML. The nature of foot ray
deficiency in congenital fibular deficiency. J Pediatr Orthop. 2017;37:332–7.
6. Calder P, Shaw S, Roberts A, Tennant S, Sedki I, Hanspal R, et al. A comparison of functional
outcome between amputation and extension prosthesis in the treatment of congenital absence
of the fibula with severe limb deformity. J Child Orthop. 2017;11:318–25.
7. McCarthy JJ, Glancy GL, Chang FM, Eilert RE. Fibular hemimelia: comparison of outcome
measurements after amputation and lengthening. J Bone Joint Surg Am. 2000;82:1732.
8. Changulani M, Ali F, Mulgrew E, Day JB, Zenios M. Outcome of limb lengthening in fibular
hemimelia and a functional foot. J Child Orthop. 2010;4:519–24.
9. Catagni MA, Radwan M, Lovisetti L, Guerreschi F, Elmoghazy NA. Limb lengthening and
deformity correction by the Ilizarov technique in type III fibular hemimelia: an alternative to
amputation. Clin Orthop. 2011;469:1175–80.
10. Patel M, Paley D, Herzenberg JE, McCarthy JJ, Glancy GL, Chang FM, et al. Limb-lengthening
versus amputation for fibular hemimelia. J Bone Joint Surg Am. 2002;84:317–9.
11. Naudie D, Hamdy RC, Fassier F, Morin B, Duhaime M. Management of fibular hemimelia:
amputation or limb lengthening. J Bone Joint Surg Br. 1997;79:58–65.
12. Oberc A, Sulko J. Fibular hemimelia – diagnostic management, principles, and results of treat-
ment. J Pediatr Orthop B. 2013;22:450–6.
13. Birch JG, Paley D, Herzenberg JE, Morton A, Ward S, Riddle R, et al. Amputation versus
staged reconstruction for severe fibular hemimelia: assessment of psychosocial and quality-of-
life status and physical functioning in childhood. JBJS Open Access. 2019;4:e0053.
14. Choi I, Kumar S, Bowen J. Amputation or limb-lengthening for partial or total absence of the
fibula. J Bone Joint Surg Am. 1990;72:1391–9.
15. Coventry MB, Johnson EW. Congenital absence of the fibula. J Bone Joint Surg Am.
1952;34(A):941–55.
16. Achterman C, Kalamchi A. Congenital deficiency of the fibula. J Bone Joint Surg Br.
1979;61-B:133–7.
17. Stanitski D, Stanitski C. Fibular hemimelia: a new classification system. J Pediatr Orthop.
2003;23:30–4.
18. Birch JG, Lincoln TL, Mack PW. Functional classification of fibular deficiency. In: Herring
JA, Birch JG, editors. The child with a limb deficiency. Rosemont: American Academy of
Orthopaedic Surgeons; 1998. p. 161–70.
19. Hamdy RC, Makhdom AM, Saran N, Birch J. Congenital fibular deficiency. J Am Acad Orthop
Surg. 2014;22:246–55.
20. Herzenberg JE, Paley D, Gillespie R. Limb deficiency. In: Staheli LT, editor. Pediatric ortho-
paedic secrets. 2nd ed. Philadelphia: Hanley & Belfus, Inc.; 2003. p. 406–16.
21. Paley D. Surgical reconstruction for fibular hemimelia. J Child Orthop. 2016;10:557–83.
22. Radler C, Myers AK, Hunter RJ, Arrabal PP, Herzenberg JE. Prenatal diagnosis of congenital
femoral deficiency and fibular hemimelia. Prenat Diagn. 2014;34:940–5.
23. Aguilar JA, Paley D, Paley J, Santpure S, Patel M, Herzenberg JE, et al. Clinical validation of
the multiplier method for predicting limb length discrepancy and outcome of epiphysiodesis,
part II. J Pediatr Orthop. 2005;25:192–6.
24. Mills G, Nelson S. An improved spreadsheet for calculating limb length discrepancy and epi-
physiodesis timing using the multiplier method. J Child Orthop. 2016;10:313–9.
25. Makarov MR, Jackson TJ, Smith CM, Jo C-H, Birch JG. Timing of epiphysiodesis to cor-
rect leg-length discrepancy: a comparison of prediction methods. J Bone Joint Surg Am.
2018;100:1217–22.
26. Manner HM. Dysplasia of the cruciate ligaments: radiographic assessment and classification.
J Bone Joint Surg Am. 2006;88:130.
27. Standard SC, Herzenberg JE, Conway JD, Siddiqui NA, McClure PK, Assayag MJ. The art of
limb alignment. 9th ed. Baltimore: Rubin Institute for Advanced Orthopedics, Sinai Hospital
of Baltimore; 2020.
28. Laor T, Jaramillo D, Hoffer FA, Kasser JR. MR imaging in congenital lower limb deformities.
Pediatr Radiol. 1996;26:381–7.
29. de l’Escalopier N, Badina A, Padovani JP, Harroche A, Frenzel L, Wicart P, et al. Long-
term results of ankle arthrodesis in children and adolescents with haemophilia. Int Orthop.
2017;41:1579–84.
30. Trichard T, Remy F, Girard J, Soenen M, Duquennoy A, Migaud H. [Long-term behavior of
ankle fusion: assessment of the same series at 7 and 23 year (19–36 years) follow-up]. Rev
Chir Orthop Reparatrice Appar Mot 2006;92:701–7.
31. El-Rosasy MA. Acute shortening and re-lengthening in the management of bone and soft-
tissue loss in complicated fractures of the tibia. J Bone Joint Surg Br. 2007;89:80–8.
32. Mahaluxmivala J, Nadarajah R, Allen PW, Hill RA. Ilizarov external fixator: acute shorten-
ing and lengthening versus bone transport in the management of tibial non-unions. Injury.
2005;36:662–8.
33. Landge V, Shabtai L, Gesheff M, Specht SC, Herzenberg JE. Patient satisfaction after limb
lengthening with internal and external devices. J Surg Orthop Adv. 2015;24:174–9.
34. Black SR, Kwon MS, Cherkashin AM, Samchukov ML, Birch JG, Jo C-H. Lengthening in
congenital femoral deficiency: a comparison of circular external fixation and a motorized intra-
medullary nail. J Bone Joint Surg Am. 2015;97:1432–40.
35. Laubscher M, Mitchell C, Timms A, Goodier D, Calder P. Outcomes following femoral length-
ening: an initial comparison of the Precice intramedullary lengthening nail and the LRS exter-
nal fixator monorail system. Bone Joint J. 2016;98-B:1382–8.
36. Szymczuk VL, Hammouda AI, Gesheff MG, Standard SC, Herzenberg JE. Lengthening with
monolateral external fixation versus magnetically motorized intramedullary nail in congenital
femoral deficiency. J Pediatr Orthop. 2019;39(9):458–65.
37. Bhave A, Shabtai L, Ong P-H, Standard SC, Paley D, Herzenberg JE. Custom knee device for
knee contractures after internal femoral lengthening. Orthopedics. 2015:e567–72.
38. Belthur MV, Paley D, Jindal G, Burghardt RD, Specht SC, Herzenberg JE. Tibial lengthening:
extraarticular calcaneotibial screw to prevent ankle equinus. Clin Orthop. 2008;466:3003–10.
39. Leyes M, Noonan KJ, Forriol F, Cañadell J. Statistical analysis of axial deformity during dis-
traction osteogenesis of the tibia. J Pediatr Orthop. 1998;18:190–7.
40. Westberry DE, Carpenter AM, Prodoehl J. Correction of genu valgum in patients with con-
genital fibular deficiency. J Pediatr Orthop. 2020;40:367–72.
41. Boakes JL, Stevens PM, Moseley RF. Treatment of genu valgus deformity in congenital
absence of the fibula. J Pediatr Orthop. 1991;11:721–4.
42. Leveille LA, Razi O, Johnston CE. Rebound deformity after growth modulation in patients
with coronal plane angular deformities about the knee: who gets it and how much? J Pediatr
Orthop. 2019;39:353–8.
43. McGrath MS, Mont MA, Siddiqui JA, Baker E, Bhave A. Evaluation of a custom device for
the treatment of flexion contractures after total knee arthroplasty. Clin Orthop Relat Res.
2009;467:1485–92.
44. Dahl MT, Fischer DA. Lower extremity lengthening by Wagner’s method and by callus dis-
traction. Orthop Clin North Am. 1991;22:643–9.
45. Cheng JC, Cheung KW, Ng BK. Severe progressive deformities after limb lengthening in type-
II fibular hemimelia. J Bone Joint Surg Br. 1998;80:772–6.
46. Catagni MA, Bolano L, Cattaneo R. Management of fibular hemimelia using the Ilizarov
method. Orthop Clin North Am. 1991;22:715–22.
47. Başbozkurt M, Yildiz C, Kömürcü M, Demiralp B, Kürklü M, Ateşalp AS. Fibular hemimelia:
Ilizarov sirküler eksternal fiksatörü ile tedavi sonuçlari [Management of fibular hemimelia
with the Ilizarov circular external fixator]. Acta Orthop Traumatol Turc. 2005;39:46–53.
48. El-Sayed MM, Correll J, Pohlig K. Limb sparing reconstructive surgery and Ilizarov length-
ening in fibular hemimelia of Achterman-Kalamchi type II patients. J Pediatr Orthop Part
B. 2010;19:55–60.
49. El-Tayeby HM, Ahmed AARY. Ankle reconstruction in type II fibular hemimelia. Strateg
Trauma Limb Reconstr. 2012;7:23–6.
50. Kulkarni RM, Arora N, Saxena S, Kulkarni SM, Saini Y, Negandhi R. Use of Paley classifica-
tion and SUPERankle procedure in the management of fibular hemimelia. J Pediatr Orthop.
2019;39:e708–17.
51. Pate JW, Hancock MJ, Tofts L, Epps A, Baldwin JN, McKay MJ, Burns J, Morris E, Pacey
V. Longitudinal fibular deficiency: a cross-sectional study comparing lower limb function of
children and young people with that of unaffected peers. Children (Basel). 2019;6:45.
52. Elmherig A, Ahmed AF, Hegazy A, Herzenberg JE, Ibrahim T. Amputation versus limb recon-
struction for fibula hemimelia: a meta-analysis. J Pediatr Orthop. 2020;40:425–30.
Brachymetatarsia: Surgical Management
with Internal and External Fixation
Noman A. Siddiqui
1 Introduction
Brachymetatarsia is a term used to describe a shortened metatarsal in the foot. This

condition can be congenital or acquired and occurs due to premature closure of the
metatarsal epiphysis [1]. Sarrafian described a normal pedal protrusion of metatar-
sal length with the second metatarsal being the longest and the fifth being the short-
est [2]. This protrusion creates a parabolic arch described by Lelie‘vre [3]. In
brachymetatarsia one or more (brachymetapodia) metatarsals are shortened with
respect to this normal pedal metatarsal positioning. This condition can be unilateral
or bilateral and has a higher predilection in females by almost 5:1 [4–6] and occurs
in less than 1 in 1000 [1].
The most common metatarsal affected by this condition is the fourth [6–8], fol-
lowed by the first metatarsal [6, 7]. Jones et al. noted in a meta-analysis of 771
metatarsals that underwent surgical intervention; the fourth metatarsal was affected
73% of the time followed by the first metatarsal (19%) [6]. Congenital conditions
were implicated as the primary reason for surgical intervention in the review. Other
case reports have identified certain conditions and syndromes such as Trisomy 21,
monosomy X, pseudohypoparathyroidism, pseudopseudohypoparathyroidism,
Adams-Oliver syndrome, Cohen syndrome, diastrophic dysplasia, and many other
disorders [5, 9, 10].
Acquired brachymetatarsia occurs due to premature epiphyseal closure due to
trauma, infection, idiopathic, and iatrogenic causes [1]. This type of
N. A. Siddiqui (*)
International Center for Limb Lengthening/Rubin Institute for Advanced Orthopedics, Sinai
Hospital of Baltimore, Baltimore, MD, USA

Switzerland AG 2022
274 N. A. Siddiqui
brachymetatarsia presentation is more common and will often present as unilater-

ally. Idiopathic causes such as trauma or shortening of the first metatarsal from
overzealous tarsometatarsal arthrodesis or shortening from hallux valgus correction
are other sources of brachymetatarsia of the first metatarsal (Fig. 8a).
2 Anatomy
The metatarsals are important for toe off and help distribute the weight of the limb
equally as gait progresses. The metatarsals form from the mesoderm approximately
5 weeks after fertilization from the lateral condensation. This continues to form
primary ossification centers by week 9 until birth [2]. The secondary ossification
centers are usually visualized by age 3 and ossify by 17–21 years of age.
Since the first and fourth metatarsals are most commonly involved in this con-
dition, it is important to be familiar with some important anatomic features. The
first metatarsal is a long bone that articulates proximally with the medial cunei-
form and in some cases with the second metatarsal. The distal end of the metatar-
sal articulates with the hallux. In terms of overall size, it is the shortest metatarsal
but critical for function of the foot. It has an independent axis of rotation which
allows it the most mobility compared to the lesser metatarsals. The first metatarsal
has intrinsic muscular attachments from the abductor hallucis muscle medially,
extensor hallucis brevis, and the dorsal interosseus muscle laterally. Extrinsic ten-
dons of the peroneus longus and tibialis anterior tendon attach directly to the base
plantar and dorsally, respectively. The arterial supply of the metatarsal is robust,
and it receives perfusion from the distal branches of the dorsalis pedis and medial
plantar artery. The interconnections between the dorsal metatarsal arteries, plantar
metatarsal arteries, and deep perforating branches provide a network of flow that
supplies blood to the base, shaft, and metatarsal head. The nerve supply to the first
metatarsal is provided by the sensory branches of the superficial peroneal nerve to
the dorsum of the first metatarsal, the terminal aspect of the great saphenous
nerve, and medial plantar nerve. Motor branches from the deep peroneal and
medial plantar nerve provide function to the muscular attachments to the intrinsic
muscles of the foot.
The fourth metatarsal is a long bone that articulates proximally with the cuboid
and fifth metatarsal laterally, the lateral cuneiform and third metatarsal medially. At
the metatarsophalangeal joint, it articulates with the proximal phalanx. Its intrinsic
muscular attachments include the dorsal and plantar interosseous muscles. The arte-
rial supply of the metatarsal receives perfusion from the dorsal and plantar metatar-
sal arteries. The nerve supply to the fourth metatarsal is provided by the sensory
branches of the superficial peroneal nerve to the dorsum of the metatarsal, along
with the lateral plantar nerve.
Brachymetatarsia: Surgical Management with Internal and External Fixation 275
3 Diagnosis
The diagnosis of brachymetatarsia is made clinically and radiographically. Clinical

presentation of brachymetatarsia becomes apparent with a shortened digit as the
foot develops (Fig. 1). However, a thorough history and physical exam is necessary
since some patients with brachymetatarsia may present with other skeletal condi-
tions seen with syndromes mentioned above and will require co-management with
Fig. 1 An AP image of a
female patient with
brachymetatarsia of the
fourth metatarsal
276 N. A. Siddiqui
other specialties. The patient may or may not complain of pain, but in both cases
one of the complaints is the appearance [4, 7, 9]. In the author’s experience, juvenile
patients do not complain of pain but present with a parent concerned of the appear-
ance and the long-term effect of the shortened digit. In many of these cases, the
parents may feel the cosmetic appearance will be concerning as the child transitions
to adolescence and adulthood. The meta-analysis by jones revealed that 93% of the
patients requiring surgical intervention have been female; thus cosmetic appearance
in open toe footwear can be a concern.
The severity of the shortening can be quantified in terms of length radiographi-
cally and has been described as a deviation of the original parabola defined by
Lelie’vre [3, 4, 11]. Other methods, such as the Maestro criteria, have been described,
in which, metatarsal length declines in a geometric pattern by a factor of two.
Deviation from this result is considered a shortening from the normal progression
[12]. However, the author uses a simple reproducible approach of connecting a line
from the metatarsal head of the second to the fifth metatarsal on a calibrated plain
anterior-posterior radiograph (Fig. 2). The distance from this line to the shortened
digit will be the amount of lengthening needed to restore a “patient normal” length.
This technique can be applied to all metatarsals even in cases of brachymetapodia,
acute or gradual correction, and a shortened first metatarsal by using a normal meta-
tarsal parabola angle [12].
Measure the distance from

the metatarsophalangeal
joint of the 4th toe to the
metatarsal parabola (14mm)
Osteotomy site
Fig. 2 A simple radiographic method to calculate the length needed for correction of brachymeta-
tarsia. (Modified with permission from Rubin Institute for Advanced Orthopedics, Sinai Hospital
of Baltimore, 2018)
4 Conservative Management
Brachymetatarsia can result in various forms of digital discomfort that can be allevi-
ated with nonoperative intervention. A contracted or overriding digit at the metatar-
sophalangeal joint will create callosities and hyperkeratotic lesions that are irritated
dorsally in shoe gear. Adjacent digits can deviate into the direction of the shortened
toe and can form hammer digit deformities, and even hallux valgus, that further cre-
ate difficulty with ambulation or shoes. Metatarsalgia of the adjacent metatarsals
can be painful and worsen the symptoms of the foot. Padding in the shoes with felt
or silicone padding can alleviate some of these painful symptoms. Additionally,
these various complaints can be managed with over the counter or custom foot
orthoses depending on the degree of deformity. Brachymetapodia can be managed
in a similar fashion, however, poses additional challenges due to the involvement of
multiple digits and metatarsals.
5 Surgical Planning/Treatment
Operative intervention of this condition requires a thorough exam of the foot. Noting
adequate perfusion to the foot is critical to prevent neurovascular compromise to the
digit during acute or gradual correction. Some key components to pay attention to
during the physical exam is the appearance of a hypoplastic digit that will often
accompany the shortened metatarsal. In some cases, despite achieving normal meta-
tarsal length, the hypoplastic digit may give the impression of inadequate correc-
tion. Evaluation of the range of motion of the digit and determining the flexible
versus a rigid contracture will be important to restoring normal metatarsophalangeal
joint (MTPJ) relationship. A Kelikian push-up test is an easy method to evaluate for
contracture of the MTPJ [13].
Radiological evaluation is the most important component in surgical interven-
tion. In bilateral cases, the author utilizes the method described earlier of connect-
ing a line from the second metatarsal head to the fifth metatarsal. When addressing
unilateral cases, one can obtain standard anterior posterior, oblique, and lateral
weight-bearing images. The author will obtain bilateral images despite unilateral
involvement to demonstrate to the patient certain radiographic features of this con-
dition. In many cases of brachymetatarsia, the associated digit phalanges will appear
hypoplastic when compared to the contralateral foot. This associated digital hypo-
plasia may give the digit a smaller appearance despite restoration of normal meta-
tarsal length, and this is discussed in the preoperative visit to prevent postsurgical
disappointment. An additional benefit of bilateral foot radiographs is the absolute
length of the normal and abnormal side metatarsal can be obtained. The differences
can be calculated, and the surgeon can have an anatomic blueprint to lengthen the
metatarsal of the affected side. However, if one chooses not to obtain bilateral films,
or has prior radiographs from the patient, then the method described above can be
278 N. A. Siddiqui
utilized. Surgical intervention can be performed by either acute or gradual methods

[14]. Acute lengthening is advised in cases of less than 1 cm [14]. However, in the
review offered by Jones et al., it revealed that the mean length gained by a variety of
interposition grafting methods was 13 mm. The author has had similar success and
has routinely performed acute lengthening in patients under <16 mm (Fig. 3).
The technique includes the following steps:
1. 5 cm incision made on the dorsum of the fourth metatarsal (can be centralized
over adjacent metatarsals if multiple require lengthening).
2. Blunt dissection is taken to the extensor tendon and a Z lengthening of the ten-
don is performed.
Fig. 3 An example of an
acute correction of 14 mm
of the fourth metatarsal
with iliac crest autograft
3. Under image intensification the appropriate metatarsal is confirmed, and mini-

mal/focal periosteal elevation.
4. Two 0.62 K-wires are inserted into the base and shaft of the metatarsal perpen-
dicular to its long axis.
5. A transverse osteotomy is completed at the met-diaphysis of the deformed
bone, and gradual correction is performed with a Hintermann distractor until
the desired lengthening is completed.
6. A 0.62 K-wire is antegraded through the medullary canal to the level of the
MTPJ. The dorsally displaced digit is reduced, and the pin is advanced through
the proximal phalanx until the proximal end of the wire is not visible at the
osteotomy (a dorsal capsulotomy and flexor tenotomy may be required to allow
manual reduction of the digit).
7. An iliac crest autograft is sized based of the desired lengthening and tamped
into the distraction osteotomy site. If autograft is not obtained, the author will
utilize fresh frozen iliac crest allograft that has soaked in bone marrow aspirate
concentrate.
8. While maintaining control of the graft, the medullary wire is retrograded into
the graft and traverses into the cuboid. (prior to final placement, the Hintermann
distractor can be manipulated to angulate the moving segment of the metatarsal
to align the direction of the metatarsal to avoid excessive adduction/abduction.
9. If the graft does not feel stable, an additional wire can be placed in a transverse
manner into the adjacent third or fifth metatarsals for stability.
10. The author has utilized placing a low-profile locking plate in cases where
patient compliance with remaining protected non weight-bearing is a concern
(Fig. 4).
The first described method of acute correction was by McGlamry and Cooper
utilizing a calcaneal autograft [15]. Additional methods have been authored, such as
an oblique osteotomy and interpositional grafting [16–20]. Myerson described
application of interpositional grafting for brachymetatarsia correction and reported
obtaining up to 18 mm of correction in a single stage without ischemia of the dig-
its [20].
One of the benefits of acute lengthening is it is accomplished in a single setting
without the need of external fixation. Lengthening of up to 15 mm can be per-
formed, and many patients on average are lengthened 13 mm [6, 17]. Patients can
return to activity sooner since healing is dependent on graft incorporation and not
regenerate consolidation, based on the mean healing index as analyzed by Jones et al.
Disadvantages of this method are donor site morbidity in cases of autograft har-
vest. Additionally, lengthening greater than 15 mm can risk vascular compromise
[17, 21]. Malunion, nonunion, hardware failure, MTPJ stiffness, and graft absorp-
tion are some of the reported concerns [6, 17, 21]. However, in a cohort of 41 feet,
Giannini reported 100% union with the use of a metatarsal allograft with K-wire
fixation with a follow-up of 3 years [17]. Patient AOFAS scores improved from 37
to 88, and none of the complications mentioned earlier were seen in this cohort. The
280 N. A. Siddiqui
a b
Fig. 4 (a/b) An acute correction with Iliac crest allograft soaked in bone marrow aspirate concen-
trate. (a) The graft was plated with a low-profile seven-hole locking plate. (b) Healed and well
incorporated union of allograft
author has seen similar outcomes with allograft and more recently has converted to
utilizing fresh frozen iliac crest allograft that is soaked intraoperatively in bone mar-
row aspirate concentrate (BMAC). Under correction is a possibility in the acute
setting and can create dissatisfaction for the patient. Therefore, it is critical to be
careful when selecting patients greater than 13–15 mm of length in one stage to
avoid disappointment.
The alternative to acute lengthening is gradual lengthening with a mini external
fixator via distraction osteogenesis. This method is utilized in cases of lengthening
greater than 1 cm (1, Scher). Multiple descriptions of this technique are available
and demonstrate an open approach to osteotomy and fixator application. The author
prefers a modified percutaneous method as described by Lamm [8]. Briefly, a sys-
tematic application of the external fixator is applied in the following steps (Fig. 5a–e):
a b
c d
Fig. 5 (a) An example of a young female with bilateral brachymetatarsia of the fourth metatarsal.
(b) A gradual correction with monolateral external fixator. The fourth MTPJ has been spanned
with a fixator to distract the MTPJ. (c) Correction achieved and consolidation noted of the regener-
ate. (d) Clinical presentation of the fourth digit preoperatively. Note the hypoplastic appearance
and dorsally contracted position of the digit. (e) The final corrected position of the fourth digit.
This patient was able to obtain excellent function of the fourth digit full dorsiflexion at the MTPJ
• All half-pins are inserted percutaneously, perpendicular to the metatarsal shaft in

a bicortical fashion, under fluoroscopic control. The key feature is to align the
proximal and distal half pins in a manner to ensure the vector of lengthening does
not create impingement against the adjacent metatarsal heads in the final position.
282 N. A. Siddiqui
• A percutaneous osteotomy is performed with a high torque low-speed burr as

close to the metatarsal metaphyseal-diaphysis.
• Acute distraction of 3–5 mm is performed (decreases time in frame).
• A 1-cm incision is made on the posterolateral aspect of the calcaneus and blunt
dissection is carried down to the lateral calcaneal wall.
• A small trephine is used to harvest a bone plug. Additional curettage and graft
can be obtained if needed, but a small trephine harvest provides plenty of graft in
most cases.
• The autograft is packed into the distracted osteotomy site to “supercharge” the
lengthening site during the 5–7 days latency period.
• Lengthening is initiated after 5–7 days at 0.5–0.75 mm/day until appropriate
radiographic position of the metatarsal head is obtained.
• The affected digit is pinned while reduced during the distraction to prevent
dislocation.
Once the patient obtains the length needed to correct the deformity, the digital
pin traversing the MTPJ is removed. The patient is given range of motion exercises
of the MTPJ in the sagittal plane to prevent stiffness. The external fixator is removed
once the regenerate bone achieves consolidation. Upon removal, the foot is pro-
tected in a flat postoperative shoe for 2–4 weeks. Full activity is allowed in support-
ive shoes at this stage.
One of the benefits of gradual lengthening is the patient can have a deformity
greater than 15 mm or <40% of the original length [1, 6, 8, 21, 22]. This expands
the opportunities for patients with significant deformity to undergo correction.
Another benefit is the ability to ambulate immediately compared to immobiliza-
tion for 6–8 weeks. The most common drawback with callus distraction is stiff-
ness of the MTPJ and infection of the pin site [6]. Pin site infections are most
often managed by oral antibiotics and have not been reported to lead to any deep
infections [6]. The stiffness of the MTPJ is concerning, and different methods
have discussed trans-articular pinning and early range of motion along with joint
spanning fixation [8, 23, 24]. However, no specific method has demonstrated
decreasing the potential of joint stiffness and arthrosis. The author has attempted
the various methods for joint ROM preservation, and none have shown to have
superiority in preserving function. Given this, the author recommends having
patients understand the limitations and the possibility of arthrosis and limited
range of motion.
6 Brachymetapodia
A less common yet challenging condition is brachymetapodia. In this scenario,

multiple metatarsals are shortened with respect to the normal metatarsal parabola.
Surgical corrections utilizing acute and gradual methods have been attempted.
Indications for acute and gradual correction are based on the length needed and
the ability to maintain vascularity to the digits. In the author’s experience, adja-
cent metatarsals with less than 15 mm of length required for correction can be
corrected in a single stage. However, it is critical to monitor the digit for blanch-
ing due to the stress on the distal digital vessels. Therefore, the author prefers
multiple monolateral fixators on the dorsum of the foot. The slow distraction rate
and the ability for the patient to ambulate immediately make this a desirable
method (Fig. 6a–c).
7 Lengthening Recommendations
When performing brachymetatarsia lengthening with gradual distraction, an

important aspect of the patient education is discussion of a timeline to full heal-
ing. As mentioned earlier the author prefers a distraction rate of 0.5–0.75 mm per
day. The rate is dependent on multiple factors such as age, general health, medi-
cal comorbidities, smoking status, the amount of lengthening, and the stage of
lengthening. Certain stages of lengthening require the rate to be decreased or
increased. For example, pediatric or juvenile patients have the capacity to dis-
tract at a faster rate versus adults due to the rapid healing seen in children.
Conversely, if the patient has slower forming regenerate or pain with lengthen-
ing, the rate can be decreased to allow for patient comfort and the regenerate to
improve radiographically.
8 Postoperative Protocol
The author prefers a 0.5 mm/day distraction rate, and the patient is given a general
timeline. The following can be utilized as a template for lengthening based of
0.5 mm of distraction daily for 15 mm of lengthening:
• Day 1: Osteotomy and frame application.
• Latency period 6 days.
• Day 7: Distraction initiated 0.5 mm daily (0.25 mm twice a day). This will be
performed for 30 days.
Fixator removal at 14–18 weeks [8].
The patient will be seen every 2 weeks to ensure proper alignment and signs
of regenerate formation. The patient is full weight-bearing in a protective flat
surgical shoe. The patient is allowed to resume daily showers and pin care after
the first postsurgical visit (day 7). Pin care is minimal, and emphasis is placed on
wrapping a single roll of gauze/Kling around the pin sites in a circular manner to
284 N. A. Siddiqui
a b
Fig. 6 (a) Brachymetapodia of the first and fourth metatarsals. (b) Abundant regenerate formation
with gradual correction. (c) Final outcome with restoration of alignment of the first and fourth
metatarsal
prevent soft tissue pistoning on the pin site, which can increase the likelihood of
a soft tissue infection. A broad-spectrum first-generation cephalosporin (cepha-
lexin) prescription is given prophylactically in the event of a perioperative pin
site infection. Instructions are also given regarding symptoms of pin site infec-
tions such as pain, redness, drainage, streaking, and inability to ambulate without
discomfort.
The fixator is maintained until signs of bony consolidation are noted on two
views via plain radiographs. As a general rule, the author will relate to the patient
the removal of the fixator will be three times the amount of the distraction phase.
Thus, based off our earlier example of 30 days, removal would be at 90 days post-
distraction or almost 16 weeks after the index operation. This general rule falls
within the time period that has been described by other surgeons [6, 8].
9 Pitfalls to External Fixation
One of the common concerns and complications is delayed union or lack of regener-
ate consolidation (Fig. 7). Various methods are available to manage this during
treatment. The first step is to rule out a metabolic or nutritional deficiency which can
inhibit bone formation. Bone stimulation via stimulators are an alternative nonsur-
gical option that can be helpful. For direct manipulation, the author has utilized
alternating reverse compression followed by distraction of the regenerate to stimu-
late healing. In some instances, the fixator itself needs to be gradually weakened to
allow the bone regenerate to progressively share the load. In cases the regenerate
fails to consolidate, the author’s preferred method of treatment is conversion to open
plating and autogenous or allograft bone grafting (Fig. 8a–e). If there is no active
pin infection, the patient is taken to the operating room for frame removal, and a
dowel-shaped bone graft is harvested from the ipsilateral calcaneus. The dowel is
placed within the regenerate sleeve, and a standard 1/3 tubular low-profile locking
plate is utilized that spans the metatarsal from the neck to the base to provide stabil-
ity to the bone. Alternatively, the author has utilized iliac crest allograft soaked in
BMAC to span the defect when there are no signs of regenerate formation. This is
plated with a low-profile locking plate to facilitate earlier weight-bearing during the
recovery. With these methods the author has not had any nonunions, and the appro-
priate length and alignment are secured. Lamm et al. described an alternative
approach of temporary medullary fixation for delayed healing to improve regener-
ate consolidation [24]. In this technique an Ilizarov wire is inserted into the medul-
lary canal from the dorsal aspect of the neck of the metatarsal and across the
regenerate until bony consolidation is noted. In the small cohort of patients, all
achieved bony consolidation.
286 N. A. Siddiqui
Fig. 7 A potential
complication of gradual
correction is lack of
regenerate formation
10 Final Thoughts
Brachymetatarsia is a challenging pathology, and acute and gradual correction

methods have been described. Acute and gradual corrections have both demon-
strated to be effective in resolving the limb length deficits in metatarsals. The fourth
metatarsal is the most common followed by the first metatarsal. Gradual correction
has demonstrated to be effective at obtaining greater amounts of correction, how-
ever, has a greater number of potential complications [6]. Acute correction has less
a b
Fig. 8 (a/b) In this example the patient had an overzealous tarsometatarsal arthrodesis with 1.8 cm
shortening. He underwent gradual correction and due to slow regenerate formation required graft-
ing and plating with iliac crest bone allograft and locked plating. (c) Lateral view of the foot with
appropriate axial distraction of the shortened metatarsal. (d) AP and (e) Lateral views of plating of
the consolidating regenerate, demonstrating maintenance of length and regenerate consolidation
288 N. A. Siddiqui
d e
Fig. 8 (continued)
potential for complications but has shown to have a limitation in the amount of cor-
rection that can be obtained in a single setting. Regardless of method the patient
needs to understand the benefits of improved cosmetic appearance, but not neces-
sarily improved function given the high degree of stiffness noted at the MTPJ post
correction [6]. In the author’s experience, both methods have their merits, when
applied appropriately, and patients report high levels of satisfaction.
Conflict of Interest Although none of the authors has received or will receive benefits for per-
sonal or professional use from a commercial party related directly or indirectly to the subject of
this article.
References
1. Davidson RS. Metatarsal lengthening. Foot Ankle Clin. 2001;6:499–518.

2. Kelikian AS, Sarrafian SK, eds. Sarrafian’s anatomy of the foot and ankle: descriptive, topo-
graphic, functional. 3rd edition. Philadelphia, PA: Wolters Kluwer; 2011.
3. Lelie‘vre J. Pathologie du pied [Pathology of the foot]. Paris: Masson; 1971.
4. Urano Y, Kobayashi A. Bone-lengthening for shortness of the fourth toe. J Bone Joint Surg
Am. 1978;60:91–3.
5. Concheiro Barreiro G, Gadañón García A, Giráldez Domínguez JM. Percutaneous foot sur-
gery for the treatment of brachymetatarsia: a case report. Foot Ankle Surg. 2017;23:e1–5.
6. Jones MD, Pinegar DM, Rincker SA. Callus distraction versus single-stage lengthening
with bone graft for treatment of brachymetatarsia: a systematic review. J Foot Ankle Surg.
2015;54(5):927–31.
7. Magnan B, Bragantini A, Regis D, Bartolozzi P. Metatarsal lengthening by callotasis during
the growth phase. J Bone Joint Surg Br. 1995;77:602–7.
8. Lamm BM. Percutaneous distraction osteogenesis for treatment of brachymetatarsia. J Foot
Ankle Surg. 2010;49(2):197–204.
9. Schimizzi A, Brage M. Brachymetatarsia. Foot Ankle Clin. 2004;9:555–70.
10. https://hpo.jax.org/app/browse/term/HP:0010743
11. Tachdjian MO. Pediatric orthopedics. 2nd ed. Philadelphia: WB Saunders; 1990. p. 2633–7.
12. Besse JL. Metatarsalgia. Orthop Traumatol Surg Res. 2017;103(1S):S29–39.
13. Rozbruch R, Hamdy R. Limb lengthening and reconstruction surgery case atlas. Foot and
ankle; metatarsal reconstruction case 79 Brachymetatarsia 563–570.
14. Shecaira AP, Fernandes RMP. Brachymetatarsia: one-stage versus two-stage procedures. Foot
Ankle Clin. 2019;24(4):677–87.
15. McGlamry ED, Cooper CT. Brachymetatarsia: a surgical treatment. J Am Podiatr Assoc.
1969;59:259–64.
16. Choudhury SN, Kitaoka HB, Peterson HA. Metatarsal lengthening: case report and review of
the literature. Foot Ankle Int. 1997;18:739–45.
17. Giannini S, Faldini C, Pagkrati S, et al. One- stage metatarsal lengthening by allograft-
interposition: a novel approach for congenital brachymetatarsia. Clin Orthop Relat Res.
2010;468:1933–42.
18. Kashuk KB, Hanft JR, Schabler JA, et al. Alternative autogenous bone graft donor sites in
brachymetatarsia reconstruction: a review of the literature with clinical presentations. J Foot
Surg. 1991;30:246–52.
19. Singh D, Dudkiewicz I. Lengthening of the shortened first metatarsal after Wilson’s osteotomy
for hallux valgus. J Bone Joint Surg Br. 2009;91(12):1583–6.
20. Myerson M. Management of metatarsalgia. In: Myerson M, Kadakia A, eds. Reconstructive
foot and ankle surgery: Management of complications. 2nd edition. Philadelphia, PA: WB
Saunders/Elsevier; 2010:123–33.
21. Kim HT, Lee SH, Yoo CI, et al. The management of brachymetatarsia. J Bone Joint Surg Br
2003;85-B:683–90.
22. Scher DM, Blyakher A, Krantzow M. A modified surgical technique for lengthening of a meta-
tarsal using an external fixator. HSS J. 2010;6(2):235–9.
23. Masada K, Fujita S, Fuji T. Complications following metatarsal lengthening by callus distrac-
tion for brachymetatarsia. J Pediatr Orthop. 1999;19:394–7.
24. Lamm BM, Moore KR, Knight JM, Pugh E, Baker JR, Gesheff MG. Intramedullary metatarsal
fixation for treatment of delayed regenerate bone in lengthening of brachymetatarsia. J Foot
Ankle Surg. 2018;57(5):987–94.
Lesser Toe Deformities
Carlos Pargas and Pablo Wagner Hitschfeld
Summary The most frequent deformities that affect the lesser toes in pediatric
population are called curly toes, hammer toes, overlapping toes, polydactyly, and
macrodactyly. The first three diagnoses are mainly due to tendons imbalance and,
therefore, are many times corrected through soft tissue procedures. The last two are
congenital abnormalities that include anatomical differences (soft tissue and bone
tissue) that need to be addressed more aggressively. It is important to follow these
patients given the deformity relapse risk.
1 Introduction
The growth and development of the lesser toes in children can present multiple
variations that need only observation and time to resolve or normalize. However,
there are certain congenital and developmental lesser toe abnormalities that can be
approached and managed in a straightforward and practical manner.
The most frequent deformities that affect the lesser toes in pediatric population
are called curly toes, hammer toes, overlapping toes, polydactyly, and macrodac-
tyly. The first three diagnoses are mainly due to tendons imbalance and, therefore,
are many times corrected through soft tissue procedures. The last two are congenital
abnormalities that include anatomical differences (soft tissue and bone tissue) that
need to be addressed more aggressively. It is important to follow these patients
given the deformity relapse risk.
C. Pargas (*)
Sinai Hospital of Baltimore, Baltimore, MD, USA
P. Wagner Hitschfeld
Orthopedic Surgery Department, Clínica Alemana de Santiago - Universidad del Desarrollo,
Hospital Militar de Santiago – Universidad de los Andes, Santiago, RM - Santiago, Chile

Switzerland AG 2022
292 C. Pargas and P. Wagner Hitschfeld
This chapter will include the diagnosis and management of curly toes, hammer
and claw toes, overlapping toes, polydactyly, and macrodactyly.
2 Curly Toes
This term refers to a flexion and adduction deformity of a lesser toe with concurrent
external rotation. This deformity is typically attributed to a congenital contracture
of the toe at the proximal and distal interphalangeal joints.
The pathophysiology is a contracture of the flexor digitorum longus and most
often concurrent contracture of the flexor digitorum brevis tendon. The tendons
subluxate to the tibial side of the toe resulting in adduction/varus of the toe with
external torsion along with the main flexion contracture (Figs. 1 and 5). The varus
occurs at the level of the PIP and DIP joints. Some authors state that this deformity
does not occur in the second toe; however, Turner [5] described a variant of curly
toe resulting in a flexion and valgus deformity of the second toe and overlapping
third toe.
The incidence of curly toes is noted to be 2.8% (84 toes per 1588 live births) in
a Canadian study [4] and 3.2% (38 toes per 1167 live births) in a South Korean
study [1]. No associated syndromes or chromosomal anomalies are associated with
this lesser toe deformity.
Unresolved curly toes can result in painful callosities on the end of the toe, nail
plate problems, and pressure issues on the adjacent toe. Turner cited 10% of patients
with curly toes complained of discomfort with shoe wear [5]. Studies differ on the
most commonly affected toe. Cho et al. stated the fourth toe is the most commonly
affected digit (68%) [1]. However, Hamer et al. [2] found an even distribution of the
Fig. 1 Fifth curly toe. The

toe is externally rotated in
90° degrees
Lesser Toe Deformities 293
involvement of the third and fourth digits (47.8%). Interestingly, most authors state
the second toe is not involved, but Turner reported a 25% incidence of second toe
involvement. Bilaterality is common (up to 80%) with the same toe effected on each
foot but with varying severity [5]. The flexion contracture is present at birth but can
go unnoticed unless it is moderate to severe. Most families present after the child
has started to stand and cruise. The parents complain of either the curled toe or the
cock-up appearance of the adjacent toe. Diagnosis is simply made with observation
of the contracted toe on standing and the incomplete full extension of the toe with
passive stretch. The toe that appears contracted but is able to be fully extended pas-
sively is a dynamic type or positional curly toe. This type of positional curly toes
either resolves spontaneously or responds to stretching and strapping treatments in
the author’s experience. Ross and Menelaus [3] state the importance of delineating
a true curly toe from other causes of a fixed flexion deformity of the toe. A curly toe
by definition is a deformity caused by the foreshortening or contracture of the flexor
tendons. Menelaus stated that observing full extension of the PIP and DIP joints
with MTP joint flexion confirms the contracture of the flexor tendons [3]. This type
of toe deformity will resolve with elongation of the flexor tendons. The severity of
the deformity can be graded by the following:
Grade 0 No deformity
Grade 1 Mild curl with no concurrent adduction or external rotation
Grade 2 Grade 1 + adduction with overlapping of adjacent toe
Grade 3 Grade 2 + increased flexion where the toenail cannot be seen when looking down on
the dorsum of the foot
Conservative management of curly toes consist of observation, stretching, and

strapping/taping the contracted digit. It should be noted that reports have cited spon-
taneous resolution of the curly toe in 25–50% of patients [4]. Many authors refer-
ence Sweetnam’s study who stated in 1958 that strapping and taping methods did
not alter the natural history of this congenital deformity. Other authors have demon-
strated 68% [5] to 94% [4] success rate with strapping methods. However, after the
strapping was discontinued, an incidence of 62.5% loss of improvement was noted.
The other limitations on the success of the strapping/taping method appears to be
the initiation of the treatment within the first few weeks of life. The prolonged time
of strapping (3–12 months) and skin irritation were other problems noted with this
treatment method.
Definitive surgical treatment has been recommended for unresolved curly toes
[2, 3]. The incidence of true long-term problems with unresolved curly toes has not
been completely elucidated. Cho et al. reported symptoms in adults with unresolved
curly toe deformity [1]. The most common symptom was the sensation of “stepping
on the toe” and callosity formation on the interphalangeal joint. The author has
noted painful callosities on the tip of the contracted toe in adolescent patients. The
two most common surgical techniques for correction of curly toe deformity are
simple flexor tenotomy and flexor tendon transfer to the extensor tendon. Initially,
the curly toe deformity was believed to be caused by a paresis of the flexor muscles
creating an imbalance between the flexor structures and the extensor structures.
Intuitively, a flexor release and transfer to the extensor mechanism was the surgical
technique recommended. However, there has been no definitive evidence of paresis
or other neurological causes of the typical curly toe deformity. Also, Hamer et al.
demonstrated no significant difference in success between the two techniques in a
randomized, double-blinded study [2]. Ross and Menelaus demonstrated a success
rate of 95% with simple flexor tenotomy of both the long and short flexor tendons.
The 5% poor results were due to postoperative contracture of longitudinal incisions
that crossed the flexor crease or a missed slip of the flexor tendon. The recommen-
dations are an open release with a transverse incision [3].
2.1 Author’s Preferred Approach to Curly Toe
Observation and gentle stretching are the simplest forms of treatment in the first few
months of life. If the child is under 1 year of age, I encourage the family to stretch
the curly toe and strap the toe at night. Most mild or dynamic forms of curly toe will
resolve. If the deformity persists or presents after the child is walking, then I recom-
mend a simple flexor tenotomy as an outpatient procedure. I wait until the child is
walking and the foot is large enough to safely perform an open tenotomy. Since one
of the most common complications of curly toe release is recurrent scar formation
with recurrent contracture, I perform the tenotomy with a V to Y skinplasty. This
allows lengthening of both the tendon and skin structures with excellent healing and
minimal scar formation.
The incision is a V shape with the apex pointing distal and just proximal to the
flexion crease of the MTP joint. After the incision is created, the soft tissues are
spread in line with the neurovascular bundle and retracted exposing the tendon
sheath. The tendon sheath is incised longitudinally, and the three tendon strips are
lifted with a micro hemostat and sharply released. The toe should maintain an
extended position. With the toe extended, the V incision is converted into a Y and
closed with simple absorbable sutures. A typical sling dressing of gauze is placed
holding the toe in an extended position. A short leg semirigid walking cast is
placed on patients between 2 and 4 years of age, and a simple soft dressing is
applied to patients 5 and older. The dressing is maintained for 7–10 days and
removed at the follow-up appointment. The incision site is covered with a simple
band aid if needed, and the patient is allowed to advance to full activities as toler-
ated. In older patients (adolescent), tenotomy will not be enough to correct this
rotational deformity. A Butler’s procedure is the recommended technique for these
cases (Fig. 2).
Fig. 2 Fifth curly toe.

Planning of a Butler
procedure
3 Hammer and Claw Toes
These are common deformities of the lesser toes although rarely studied in children.
Epidemiology, physiopathology, and clinical features of these deformities in pediat-
ric patient have been barely reported with details.
Each deformity has a particular combination of joint affectation. Hammer toe is
characterized by excessive flexion of proximal interphalangeal (PIP) joint accompa-
nied by extension of distal interphalangeal (DIP) joint. The metatarsophalangeal
(MTP) joint used to be normal, however, depending of the severity of the deformity
could show some levels of subluxation by hyperextension [6]. The hammer toe is
most common between the second and fourth toe with significant predilection for
the second [8]. Otherwise, claw toe is characterized by flexion of PIP and DIP joint
as well as hyperextension at the MTP joint (Figs. 3 and 4).
These deformities are subject of loss of balance between extrinsic and intrinsic
muscles flexors and extensors. Also, insufficient plantar capsule and extensions of
the plantar aponeurosis to keep the dynamic balance of the joint. Adherences may
develop that subsequently exacerbate the deformities [11].
3.1 Treatment
The nonsurgical management of hammer and claw toes is very similar. The only
purpose is relief the pressure and subsequent pain of the involved areas. In hammer
toes the dorsal aspect of PIP is the most affected and should be the most padded
area. In children that already use shoes, we recommend high and wide toe box of the
shoes. In cases where the deformity is severe and compromise the MTP joint, high
pressure could be appreciated with a callus in the plantar area of the metatarsal
head. In this case we recommend metatarsal pads placed proximal to the metatarsal
Fig. 3 Preoperative
hammer toes on second
and fourth. Flexible
deformity
Fig. 4 Postoperative flexor

tenotomies hammer toes
on second and fourth.
Flexible deformity
head. In claw toes in addition to dorsal PIP padding, we also recommend nail pad-
ding protection to avoid irreversible nail deformities.
Surgical options go from release, lengthening, or transfer of soft tissue to bone
procedures that include joint resection, arthrodesis, or even bone shortening
(Gonzalez-Rincon). However, before moving on with surgical management, some
variables should be considered such as age of the patient, severity, associated dis-
ease, flexible, or fixed deformity [10]. The deformity is considered flexible when it
is corrected during plantar flexion movement of the ankle, while fixed deformity
does not correct with any change of position. Flexor digitorum longus (FDL) tenot-
omy or transfer is recommended in flexible deformities. Otherwise, fixed deformity
requires PIP resection or fusion. Patients with severe deformity, without remnant
growth, and associated disease as neurologic problems could benefit from perform-
ing bone procedures if the soft tissue does not allow complete correction.
Ross and Menelaus reported FDL tenotomy for hammer and curly toes was suc-
cessful with only 5% of poor results, and it was more related with scar problems. In
addition, they claimed that the open flexor tenotomy was preferred because it allows
you to identify appropriately the flexor tendon [3]. Jacobs also concluded that open
flexor tendon lengthening in hammer toes is a safe and reliable procedure. They
recommend a transverse skin incision and Z-lengthening of the flexor digitorum
longus [7].
If bone shortening is going to be performed in a fixed deformity, just consider
that some issues related to excessive bone resection (shortening) have been reported
and it is recommended to start with less bone resection (only resection of the head
of proximal phalangeal) [9].
3.2 Complications
Complications may be present in any surgery, and these deformity corrections are
not the exceptions. Some of the most feared complication involved the vascular
insufficiency resulting the tension placed in the vessels during acute correction or
collapse of vessel during shortening. Close monitoring of toe irrigation should be
considered after correction [6]. Otherwise, scar contraction with recurrence of
deformity or partial restriction of movements also could happen, and it is one of the
most common [3]. On the other hand, general complications observed in others
surgery as infection, nerve injuries, no union, or malalignment are latent.
3.3 Summary
1. Determine if the deformity is flexible (nonsurgical or soft tissue procedure as

treatment) or fixed (soft and/or bone procedure).
2. The Hammer toe and claw toe share similar nonsurgical and surgical manage-
ment in pediatric patient.
3. Surgical treatment as first step is the soft tissue characterized by FDL tenotomy
or transfer.
4. Be careful with irreversible complication (neurovascular bundle damage).
5. Primary goal is to obtain toes without pain, fit into the shoe, and have acceptable
appearance.
4 Overlapping Toe
It is a congenital deformity represented by overriding of the fourth toe by the fifth

toe. This deformity has not gender predilection and usually bilateral although this
remain controversial. Previous studies reported 20–30% of bilateral overriding toes.
Low incidence of 1.8% was described in a population of 3100 children by
Gonzalez-Rincon.
The MTP joint is the apex of the tri-planar deformity. It is characterized by
adduction in the transverse plane, hyperextension in the sagittal, and external rota-
tion in the coronal plane developing a subluxation dorsal-medial of MTP joint; the
PIP and DIP usually are normal. The more acceptable cause of this pathology is the
retraction of soft tissues mainly shortening and adduction of extensor digitorum
longus with capsular adhesions at the metatarsal head [5, 6] (Fig. 5).
The most frequent complaint in this patient is pain, accompanied by formation of
callus in the dorsal area of the fifth toe due to wear of tied shoes. On the other hand,
cosmesis plays a relevant role in female patient. 50% of the patient could present
dysfunctional gait [6].
Fig. 5 Image showing a

combination of a fifth
overlapping toe and a
fourth curly toe
4.1 Treatment
The first treatment options in pediatric patient is nonsurgical. Stretching passive

exercises, use of corrective soft wrap, or orthosis is well tolerated in younger
patients. However, in adolescent wearing of orthosis is less tolerated. Indication of
wide and confortable shoes becomes a better option.
When the nonsurgical treatment fails, multiple surgical procedures take the
place. These range from skin to bone techniques. V or Y shape of fifth toe skin is
performed with poor results due to scar retraction, syndactyly of fourth and fifth
toes described by McFarland [17] with often unacceptable cosmetic results, and
EDL transfer from fifth toe to the neck of fifth metatarsal or abductor digiti quinti
tendon [15, 16].
Butler’s technique makes adjustment in different soft tissue (mainly rotational)
areas with good results reported by many authors [13, 14]. This requires a racquet
incision with a plantar handle inclined laterally and a dorsal handle following the
EDL tendon. Subsequent, EDL and dorsal medial and volar capsule release to allow
the deformity correction. No fixation is used (however, the author recommends a
temporal k-wire to hold the reduction), and skin flap from lateral to dorsal side of
the foot is sutured [12, 14]. Soft tissue surgery is less common, but arthroscopic
technique has been reported to have good results which stabilize the plantar plate
anchored to EDL tendon and reduce the MTP joint, release of dorsal-medial cap-
sule, and plication of lateral capsule [18].
On the other hand, bone surgeries have been described with partial success,
however are not common in pediatric population. These involve bone shortening
of metatarsal or proximal phalanges (diaphysis), distal metatarsal osteotomy
(Weil technique), or total resection of proximal phalanges. Gonzalez-Rincon
described good results in 82.9% of the patient in a report of proximal phalangeal
shortening.
4.2 Summary
1. The overriding toes is a complex multiplanar MTP joint deformity that is com-
mon bilaterally.
2. The goal of the treatment is to obtain a pain-free toe with acceptable appearance.
3. Try as first line of treatment passive stretching exercises and soft padding in
young patient; wide shoes are recommended.
4. The clue in the surgical treatment obtains a balance between the soft tissue previ-
ously contracted (EDL and capsule).
5 Polydactyly
Foot polydactyly is the most common malformation of the forefoot that results
from defective development during pre- or postaxial patterning of developing limb
[19]. This is categorized as excessive malformation and characterized by more than
five digits with a wide variation in its clinical presentation going from a minor pro-
tuberance to a complex malformation compromising midfoot/forefoot to duplicate
bone, sometimes, sharing the same bone, neurovascular bundle or just skin
(syndactyly).
This could be related to syndromic problems, new single isolated event, or other
body malformation, being the hand, the most common involved [20, 21]. Foot poly-
dactyly causes functional limitation (pain) and cosmesis problems [21, 22].
The incidence of foot polydactyly is a 1.7 per 1000 live births. Ethnicity rates are
highest in Afro-American population 3.6–13.9 per 1000 live births whereas in Caucasian
is around 0.3–1.3 per 1000 live births [20, 23]. According to gender, the reports are not
conclusive. There is an increased tendency to involve the left foot rather than the right
[19]. Considering the anatomy area, the lateral ray is more common (79%), while
medial column is 15–17% and central toes in just 4–6% of incidence [20, 21].
5.1 Etiology and Pathophysiology
Etiology has not been fully known. However, continuing efforts in researches have
achieved some progress. Genetic areas have been able to identify some responsible
gene of polydactyly such as GLI3 which is associated with Greig cephalopolysyn-
dactyly syndrome, sonic hedgehog gene (SHH), fibroblast growth factor (FGF),
homeobox protein aristaless-like 4 (ALX4), homeobox D (5′-HoxD), ZNF141,
MIPOL1, IQCE, and PITX1 [24].
The pathophysiology is not completely clear. One theory is related to disorder in
the programmed cell death during fetal limb development, and another is the genetic
mutations in some gene loci.
Some signals are responsible of promote development and growth of limbs. The
zone of polarizing activity (ZPA, posterior portion of mesenchyme) which is medi-
ates by the sonic hedgehog (SHH) molecule and the atypical ectodermal ridge
(AER, distal portion del ectoderm) that expresses fibroblast growth factors (FGF)
could lost the balance and induce the formation of extra digits [25].
5.2 Anatomy, Classification, and Diagnosis
Polydactyly mainly has been classified by multiples authors according to anatomy:

Temtamy and Mckunsick categorized these as preaxial (first ray or hallux), central
(middle rays, second, third, and fourth), and postaxial (fifth ray) [20]. Venn-Watson
Fig. 6 Left foot central polydactyly. Preoperative and postoperative clinical and radiological
images are shown. Operative sequence of a second ray excision
described a classification based in the anatomy configuration of the metatarsal: (1)

normal metatarsal with distal duplication, (2) block metatarsal, (3) Y-shaped meta-
tarsal, (4) T-shaped metatarsal, (5) normal metatarsal shaft with a wide head, and (6)
ray duplication [20, 23]). Also, Watanabe et al.’s classification was based in the seg-
ment involved: (1) tarsal type (with one subtype), (2) metatarsal type (with three
subtypes), (3) proximal phalangeal type (with five subtypes), and (4) distal phalan-
geal type (with six subtypes) (Fig. 6).
Although, this classification gives us an idea where the deformity is located, its
surgical planning is not clear enough. For that reason, Seok et al. classified the foot
polydactyly focused in practical surgical orientation to avoid the common compli-
cations as axis deviation, skin issues, or remaining lesion of the extra digit. They
divided this in three main variables (SAM): syndactylism, axis deviation, and meta-
tarsal extension (with three subtypes for each variable) [26].
The diagnosis starts with an accusative general physical examination. In these
patients, even if the extra digit is obvious, we should be alert due to syndromic asso-
ciation. On the other hand, the extra toe sometimes hides complex deformity beyond
the forefoot. Therefore, soft tissue (skin), axial deformities, and nail should be eval-
uated and considered for an appropriated diagnosis and plan.
Imaging evaluations are considered when bony connection is suspect; this nor-
mally is indicated around the first year of age to allow time for the bony ossification
nucleus to show up. Most of the time, radiographic AP and lateral are enough to
decide a plan. However, we do not rule out the use of CT scan or MRI [20, 23]) for
more complex associated deformities in mid-/hind foot (Fig. 6).
5.3 Management
Treatment of this condition is wide as well as its variability presentation. This could
be from no surgical in mild undeveloped extra toes where the patient does not refer
any discomfort or cosmesis problems to a surgical treatment in more complex
deformities or simply functional and cosmesis complaint. Surgical treatment is indi-
cated mainly around the first year of age to avoid any walk developmental delay due
to use of cast, orthosis, or any psychological issue related to cosmesis [23]. However,
Ozren and Darko did not find any significant differences related to age of foot poly-
dactyly surgery (Ozren).
The main goal of surgery treatment in foot polydactyly should be create a better
shape of the foot to fit well into a shoe, comfortable and with acceptable appearance
that allows the patient to feel good about themselves. In order to get this, the sur-
geon must make excision of extra digit(s), consider making an osteotomy of associ-
ated bone duplication and an appropriated skin coverage without forgetting to
maintain alignment, joint stability, and soft tissue balance [23].
The tendency in surgical treatment is saving the most dominant ray and/or digit.
Though, in some cases the dominant extra toe(s) could have some associated defor-
mity, hypertrophic condition, or related skin problems which lead you to think about
making an excision of this. The debate shows up when both digits are very similar.
In this case, it is relevant to consider the risks of vascularity, foot stability, and soft
tissue coverage.
In simple case, when the extra digit is attached to a thin soft tissue, suture liga-
tion (occlusion of artery) is an option. However, some complications related to neu-
roma formation or remnant of skin could become symptomatic requiring a second
procedure. In patient with extra digit attached to a dense soft tissue, racquet-type
excision is recommended with neurovascular bundle visualization to decrease the
possibility of a neuroma formation.
On the other hand, when the extra lateral digit (postaxial) is attached with the
metatarsal and had created a real articulation, a disarticulation of lateral digit is
required. Careful collateral ligament dissection and reattachment are essential to
avoid joint instability. Sometimes temporal k-wire fixation could be necessary.
When the metatarsal head is wide or with Y or T shape, cartilage remodeling (phys-
iolysis) or osteotomies could be necessary to obtain an appropriated alignment. The
recommendation always is focused toward removing the most lateral toe.
The complex preaxial foot deformities have worse outcomes than postaxial
deformities. Poor outcomes are mainly secondary to hallux varus (incidence
40–87%) [20, 21] caused by inadequate bone resection, soft tissue reattachment, or
presence of epiphyseal – physis deformation (bracket). Adequate treatment should
include removing the extra medial rudimentary toe, lateral metatarsophalangeal
ligament repair and a first metatarsal osteotomy [20, 21, 23].
Central polydactyly has some additional challenges such as requiring a dorsal
and plantar approach. However, we do not recommend the plantar approach to
avoid painful scars. Longitudinal approach could be used during central excision of
one toe and Z-plasty when it is going to be more than one. The most relevant con-
sideration during central toe excision is the width of the foot; for that reason central
cuneiform bone resection is sometimes necessary. Also reconstruction of inter-
metatarsal ligaments using suture, wire, or cerclage helps create a narrow foot
(Fig. 6).
In addition, periosteum or cartilage of extra digit should be removed completely
to avoid recurrence.
5.4 Summary
1. Foot polydactyly is the most common forefoot deformity than could be associ-
ated with other syndromes.
2. Careful physical examination should be performed. The diagnosis is usually
easy normally requiring foot X-rays.
3. The most used classification is preaxial, central, and postaxial. However, the
developing of SAM gave us more surgical planning orientation.
4. The trend is excision of medial of lateral toes in preaxial or postaxial, respec-
tively. Saving the dominant toe.
5. Preaxial has more complications than post-axial deformities.
6. Be careful with remaining foot width in cases of central polydactyly.
Appropiate intermetatarsal ligament reconstruction and cuneiform excision
are necessary.
7. During the surgery remember excision, soft tissue balance, and joint alignment.
8. The final goals of treatment are pain-free foot and an acceptable foot appearance.
6 Macrodactyly
Macrodactyly is a rare condition characterized by enlargement of every part of the

toe(s) [27]; it involves an extensive variety of clinical features which in some cases
even the metatarsal could be compromised [28]. This condition could cause many
problems as pain, difficulty with shoe wear, psychological and cosmetic problems
and diffculty with gait development, between others. If there is an asymmetric bone
growth, secondary deformities as flexion/extension contraction or valgus/varus
deviation appear. Macrodactyly sometimes could be associated with syndactyly
(23%) and polydactyly (4%) [29].
Incidence is 1 in 18,000 live births with no clear gender difference [29, 30].
Multiple digits are more affected than isolated toes (2:1) with preference for mid-
line digits.
Macrodactyly can be classified in: Primary which is characterized by congenital
overgrowth no related to syndrome, usually involving soft and bony tissue and sec-
ondary or syndromic which is associated with external conditions as overgrowth
secondary to tumors (neurofibromatosis, lymphangioma, hemangioma, etc.) or as
part of disorders (Proteus, Klippel-Trenaunay syndrome). In this secondary group,
the soft tissues are mainly affected. Also, macrodactily can be classified as static
when there is only an initial toe(s) overgrowth (evident at birth) followed by a nor-
mal growth in the following years, and as progressive if there is an increased toe
growth during childhood [29, 30].
6.1 Etiology
The etiology remains to be elucidated. It is believed not related to inheritance. Some

theories have been mentioned in isolated macrodactyly such as abnormal nerve stimu-
lator signals to the affected digit causing thickening of the nerve, whereas others believe
that it is more related to increased blood supply in the area [31]. On the other hand,
some theories related to PIK3CA mutations have been mentioned; however, this muta-
tion is also related to some tumors [29].
6.2 Management
In most cases, surgical treatment is preferred by orthopedic surgeons. The main goal
is to develop a functional shoeable foot. Cosmesis is considered especially in female
foot. Surgical management often involves bone and soft tissues. Due to wide vari-
ability, the orthopedic surgeon should prepare different techniques that include skin/
subcutaneous resection/reconstruction, neurolysis, epiphysiodesis, osteotomies,
arthrodesis, and/or amputations.
Treatment options depend on the degree of compromise of soft tissue and/
or bone.
Some reports with isolated soft tissue surgeries have had poor results due to sub-
sequent secondary procedures [28, 32, 33]. For that reason, we just recommend soft
tissue procedures in patients with mild macrodactily an age close to skeletal
maturity.
In cases where isolated phalange(s) affectation is present, techniques such as
amputation of phalanges, epiphysiodesis, and shortening have been described. All
of them are accompanied by soft tissue debulking. Chang et al. [28] referred skin
problems in cases of amputation. Epiphysiodesis has a shortening risk given that it
is not possible to calculate the exact timing for that procedure.
Epiphysiodesis also could be applied when metatarsal bone is affected. There is
risk of over shortening; however, with the development of new devices, temporal
epiphysiodesis decreased that risk. Also, acute diaphysis shortening of the metatar-
sal bone with internal fixation can achieve good correction, but in immature patient,
secondary shortening could be required. The most important disadvantage with
these techniques is the limitation to decrease the width of the foot. For that reason,
some authors have inclination for ray resection accompanied by soft tissue debulk-
ing. Dedrick and Kling [33] recommended ray resection when the foot is wider than
two standard deviation of a normal foot. Chang et al. [28] recommended ray resec-
tion when intermetatarsal angle exceeds the normal side by >10 degrees. In mild
cases, shortening and repeat debulking may be an option. In central toes macrodac-
tyly, the recommendation is central ray amputation which decreases the intermeta-
tarsal angle. Plantar and dorsal approach is recommended to help with appropriated
bone and soft tissue resection.
Same indications are recommended when the great toe is involved except for ray
amputation. The first metatarsal has an important role in weight-bearing and gait.
Exceptional cases could be considered.
Treatment algorithm can be summarized as follows:
If there is only soft tissue compromise: soft tissue debulking vs amputation (if
severe compromise). If there is a combination of soft tissue and bone: soft and bone
tissue debulking (shortening osteotomy, ostectomy, partial resection) vs amputa-
tion (if severe compromise). Epiphysiodesis is a treatment option with mild correc-
tion power. If chosen, always associate it with debulking (Figs. 7, 8, 9, 10, 11,
and 12).
Fig. 7 Second toe

macrodactyly. Clinical
image
Fig. 8 Second toe

macrodactyly. Preop
planning
6.3 Summary
1. Macrodactyly is a rare condition characterized by enlargement of every part of

the toe sometimes involving all ray(s).
2. Can be classified as static or progressive being central toes the most common
affected.
3. Unknown etiology with stronger theory related to abnormal nerve stimulator
signal. Overgrowth related to nerve territory distribution.
4. Multiple treatment options from soft tissue resection to amputations, with some
other options as epiphysiodesis or shortening.
5. Final treatment goals are to reduce the foot size, cosmesis and be able to fit shoes.
Fig. 9 Second toe

macrodactyly. Preop X-ray
Fig. 10 Second toe

macrodactyly after bone
and soft tissue debulking
Fig. 11 Second toe

macrodactyly. Postop
clinical image
Fig. 12 Second toe

macrodactyly. Postop
X-ray
Acknowledgments Thank you to Dr. Shawn Standard, MD, for his help with images and text
edition.
References
1. Cho JY, Park JH, Kim JH, Lee YH. Congenital curly toe of the fetus. Ultrasound Obstet
Gynecol. 2004;24(4):417–20. https://doi.org/10.1002/uog.1087. PMID: 15343596.
2. Hamer AJ, Stanley D, Smith TW. Surgery for curly toe deformity: a double-blind, randomised,
prospective trial. J Bone Joint Surg Br. 1993;75(4):662–3. https://doi.org/10.1302/0301-620
X.75B4.8331129. PMID: 8331129.
3. Ross ER, Menelaus MB. Open flexor tenotomy for hammer toes and curly toes in childhood.
J Bone Joint Surg Br. 1984;66(5):770–1. https://doi.org/10.1302/0301-620X.66B5.6501376.
PMID: 6501376.
4. Smith WG, Seki J, Smith RW. Prospective study of a noninvasive treatment for two common
congenital toe abnormalities (curly/varus/underlapping toes and overlapping toes). Paediatr
Child Health. 2007;12(9):755–9. https://doi.org/10.1093/pch/12.9.755. PMID: 19030460;
PMCID: PMC2532862.
5. Turner PL. Strapping of curly toes in children. Aust N Z J Surg. 1987;57(7):467–70. https://
doi.org/10.1111/j.1445-2197.1987.tb01399.x. PMID: 3475061.
6. Shirzad K, Kiesau CD, DeOrio JK, Parekh SG. Lesser toe deformities. Am Acad Orthop Surg.
2011;19(8):505–14.
7. Jacobs R, Vandeputte G. Flexor tendon lengthening for hammer toes and curly toes in paediat-
ric patients. Acta Orthop Belg. 2007;73(3):373–6. PMID: 17715729.
8. González-Rincón JA, Valle-de Lascurain G, Oribio-Gallegos JA. Diafisectomía de la falange
proximal en el quinto dedo supraducto y dedo en martillo en niños [Diaphysectomy of the
proximal phalanx in quintus varus supraductus and hammer toe in children]. Acta Ortop Mex
2013;27(2):103–8. Spanish. PMID: 24701761.
9. Janecki CJ, Wilde AH. Results of phalangectomy of the fifth toe for hammertoe. The Ruiz-
Mora procedure. J Bone Joint Surg Am. 1976;58(7):1005–7. PMID: 977609.
10. Angirasa AK, Augoyard M, Coughlin MJ, Fridman R, Ruch J, Weil L. Hammer toe, mallet toe,
and claw toe. Foot Ankle Spec. 2011;4(3):182–7. https://doi.org/10.1177/1938640011409010.
11. Scheck M. Etiology of acquired hammertoe deformity. Clin Orthop Relat Res. 1977;123:63–9.
PMID: 856521.
12. Simões R, Alves C, Tavares L, Balacó I, Sá Cardoso P, Pu Ling T, Matos G. Treatment of the
overriding fifth toe: Butler’s arthroplasty is a good option. J Child Orthop. 2018;12:36–41.
https://doi.org/10.1302/1863-2548.12.170099.
13. De Boeck H. Butler’s operation for congenital overriding of the fifth toe: retrospec-
tive 1–7-year study of 23 cases. Acta Orthop Scand. 1993;64(3):343–4. https://doi.
org/10.3109/17453679308993641.
14. Cockin J. Butler’s operation for an over-riding fifth toe. J Bone Joint Surg Br. 1968;50(1):78–81.
PMID: 4868030.
15. Lantzounis LA. Congenital subluxation of the fifth toe and its correction by a periosteocapsu-
loplasty and tendon transplantation. J Bone Joint Surg. 1940;22(I):147–50.
16. Lapidus PW. Transplantation of the extensor tendon for correction of the overlapping fifth toe.
J Bone Joint Surg. 1942;2(4):555–9.
17. McFarland B. Congenital deformities of the spine and limbs. In: Platt H, editor. Modem trends
in orthopedics. New York: P B Hoeber; 1950. p. 107–8.
18. Lui TH. Arthroscopic-assisted correction of claw toe or overriding toe deformity: plan-
tar plate tenodesis. Arch Orthop Trauma Surg. 2006;127(9):823–6. https://doi.org/10.1007/
s00402-006-0224-4.
19. Al Amin ASM, Carter KR. Polydactyly. In: StatPearls [Internet]. Treasure Island: StatPearls
Publishing; 2021; 2021 Jan–. PMID: 32965966.
20. Turra S, Gigante C, Bisinella G. Polydactyly of the foot. J Pediatr Orthop B. 2007;16(3):216–20.
https://doi.org/10.1097/01.bpb.0000192055.60435.31. PMID: 17414786.
21. Phelps DA, Grogan DP. Polydactyly of the foot. J Pediatr Orthop. 1985;5(4):446–51. https://
doi.org/10.1097/01241398-198507000-00012. PMID: 4019759.
22. Kubat O, Antičević D. Does timing of surgery influence the long-term results of foot polydac-
tyly treatment? Foot Ankle Surg. 2018;24(4):353–8. https://doi.org/10.1016/j.fas.2017.04.001.
Epub 2017 Apr 13. PMID: 29409237.
23. Kelly DM, Mahmoud K, Mauck BM. Polydactyly of the foot: a review. J Am Acad Orthop
Surg. 2021;29(9):361–9. https://doi.org/10.5435/JAAOS-D-20-00983. PMID: 33443388.
24. Umair M, Ahmad F, Bilal M, Ahmad W, Alfadhel M. Clinical genetics of polydactyly: an
updated review. Front Genet. 2018;9:447. https://doi.org/10.3389/fgene.2018.00447. PMID:
30459804; PMCID: PMC6232527.
25. Bouldin CM, Harfe BD. Aberrant FGF signaling, independent of ectopic hedgehog signaling,
initiates preaxial polydactyly in Dorking chickens. Dev Biol. 2009;334(1):133–41. https://doi.
org/10.1016/j.ydbio.2009.07.009. Epub 2009 Jul 17. PMID: 19616534.
26. Seok HH, Park JU, Kwon ST. New classification of polydactyly of the foot on the basis
of syndactylism, axis deviation, and metatarsal extent of extra digit. Arch Plast Surg.
2013;40(3):232–7. https://doi.org/10.5999/aps.2013.40.3.232. Epub 2013 May 16. PMID:
23730599; PMCID: PMC3665867.
27. Khanna N, Gupta S, Khanna S, Tripathi F. Macrodactyly. Hand. 1975;7(3):215–22. https://doi.
org/10.1016/0072-968x(75)90056-x. PMID: 1205357.
28. Chang CH, Kumar SJ, Riddle EC, Glutting J. Macrodactyly of the foot. J Bone Joint Surg Am.
2002;84(7):1189–94. https://doi.org/10.2106/00004623-200207000-00015. PMID: 12107320.
29. Chen W, Tian X, Chen L, Huang W. Clinical characteristics of 93 cases of isolated macro-
dactyly of the foot in children. J Orthop Surg Res. 2021;16(1):121. https://doi.org/10.1186/
s13018-020-02196-2. PMID: 33557883; PMCID: PMC7869226.
30. Hardwicke J, Khan MA, Richards H, Warner RM, Lester R. Macrodactyly – options and out-
comes. J Hand Surg Eur. 2013;38(3):297–303. https://doi.org/10.1177/1753193412451232.
Epub 2012 Jun 26. PMID: 22736742.
31. Dennyson WG, Bear JN, Bhoola KD. Macrodactyly in the foot. J Bone Joint Surg Br.
1977;59(3):355–9. https://doi.org/10.1302/0301-620X.59B3.893515. PMID: 893515.
32. Megalodactylism RK. Report of 7 cases. Acta Orthop Scand. 1967;38(1):57–66. https://doi.
org/10.3109/17453676708989619. PMID: 6035453.
33. Dedrick D, Kling TF, jr. Ray resection in the treatment of macrodactyly of the foot in children.
Orthop Trans. 1985;12:40–6.
Neurologic Foot
Gino Martínez and Gonzalo Chorbadjian
1 Introduction
The neuromuscular diseases of childhood frequently compromise the locomotive

system and its development, among which infant cerebral palsy, peripheral neuropa-
thies, and myopathies stand out [1, 2]. The foot is frequently affected in its normal
function as well as in its structural development during the skeletal growth, deterio-
rating in diverse magnitude the capacity of standing, walking, and performance in
recreational and sport activities. The eventual concomitant deterioration of other
anatomical segments further aggravate the patient global motor function [3, 4].
In this chapter, the main neuromuscular diseases of childhood that impact the
locomotor system, specifically the foot and ankle, will be analyzed. The physiopa-
thology of each disease, its natural history, and current treatments available will be
detailed. In addition, the main morphological and functional alterations of the foot
derived from these diseases will be analyzed with the options of orthopedic and
surgical treatment, detailing the most used techniques depending on each particu-
lar case.
G. Martínez (*)
Clínica Universidad de Los Andes, Santiago, Chile
Instituto Teletón, Santiago, Chile
G. Chorbadjian
Clínica Alemana – Universidad del Desarrollo, Santiago, Chile

Switzerland AG 2022
314 G. Martínez and G. Chorbadjian
1.1 Neuromuscular Diseases in Childhood
Numerous neuromuscular diseases can affect the development of the child and
especially his or her locomotive system. These conditions can have a congenital or
acquired origin. They can globally compromise the psychosensory and/or motor
faculties of the child. The motor involvement can have an increased or decreased
muscle tone, depending on the primary condition. Both conditions have a very dif-
ferent therapeutic strategy [5, 6].
The main neurological diseases affecting the locomotor system in children are:
• Infant cerebral palsy
• Charcot-Marie-Tooth peripheral neuropathy
• Spinal dysraphia
• Muscular dystrophies
1.2 Infant Cerebral Palsy (ICP)
It is the most important cause of disability in childhood, affecting 2–2.5 /1000 live
births. It corresponds to a set of clinical syndromes derived from damage to the
central nervous system during its development, characterized by various patterns of
motor and posture abnormalities. By definition, it is a nonprogressive encephalopa-
thy resulting from a damage in the immature brain but whose clinical manifestations
and on the locomotive system are evolving as the central nervous system and loco-
motive system develop. Its etiology is varied and sometimes multifactorial, being
associated mainly to preterm births and low birth weight, which makes newborns
more susceptible to damage on the central nervous system (CNS). The injuries can
be ischemic, hemorrhagic, infectious, or of unknown etiology in a significant per-
centage of children. The motor disorders of cerebral palsy are often associated with
alterations in sensitivity, perception, cognitive ability and communication, epilepsy,
and motor swallowing disorders.
According to the type of motor disorder, it can be classified as spastic, ataxic,
dystonic, athetotic, and mixed, depending on the area of CNS damaged. The most
frequent is spastic, in which the damage is produced at the level of the first motor
neuron, where hypertonia is developing as a mechanism of self-regulation and pro-
tection of the motor area involved, which generates an increase in muscle tone fun-
damentally triggered by muscle-tendon stretching [7].
According to the topographic area involved, it can be classified as:
• Quadriplegia: Compromise of the four extremities, usually by severe and diffuse
damage of the CNS, usually with important cognitive-sensorial affection.
• Diplegia: Mainly affects the lower limbs (LL) and in a lesser grade the upper
limbs (UL). Usually due to internal capsule involvement by periventricular leu-
komalacia, consequence of intraventricular hemorrhage. The motor involvement
Neurologic Foot 315
is usually moderate to severe, with different degrees of cognitive impairment,

and there may be self-sufficient patients in adult life.
• Hemiplegia: Damage of the motor area of a cerebral hemisphere, usually due to
ischemic or punctual hemorrhagic lesions. The motor disorder is unilateral, with
different degrees of functional compromise depending on the extension of the
lesion. The patients usually do not present cognitive compromise and are self-
sufficient [7].
Spasticity has important effects on the locomotor system development. In addi-
tion to causing movement disorders and limbs dysfunction, it causes anatomical
changes in the muscles, joints, and bones. These changes can be primary, secondary,
or tertiary. Primary changes refer to the direct effect of spasticity on muscle length
and trophism, which generates a relative muscle shortening and decreases the joint
range of the affected segments; this causes abnormal postures, gait disorders and a
low functional performance of the UL, between others. Secondary changes origi-
nate in the persistence of muscle shortening that becomes structural and irrevers-
ible, which causes irreducible joint contractures and a greater degree of functional
compromise. In turn, the muscle contractures generate bone deformities as the skel-
eton grows, which further aggravates the situation by causing joint dislocations and
disorders of the lever arms necessary for efficient walking. Tertiary changes are
adaptive disorders of the articular segments adjacent to the affected one, as compen-
sation for primary and secondary alterations, which can lead to other deformities
that are not originally the result of spasticity [8, 9].
The foot and ankle are frequently affected in ICP. In ambulatory children it can
compromise the efficiency of walking and a lower performance in sports activities,
along with difficulties in normal footwear. In nonambulatory children foot deformi-
ties can generate problems for the adequate use of orthoses and footwear, also caus-
ing skin injuries and local hygiene problems [10, 11].
For an efficient gait the foot must be plantigrade, painless, and with a rotational
profile as close as possible to neutral (forward). In the stance phase, there should be
an initial contact with the heel and then a stable monopodal support, with the rear-
foot aligned and with the gastro-soleous complex with sufficient strength and length
to stop the advance of the tibia and passively extend the knee (plantiflexor knee
extension couple). Gastrocnemius should have enough power for the subsequent
takeoff of the heel. For all these stages, a mobile ankle and a stable and aligned
forefoot are essential.
In the swing phase, the foot must be in adequate dorsiflexion to avoid the toes
touching the ground and tripping.
Foot disorders may involve different stages of walking or all of them, depending
on anatomical and functional involvement. The clinical analysis then includes the
clinical history (degree of functional impairment, use of orthoses, spasticity man-
agement, previous treatments, etc.), observational analysis of the gait, general and
specific physical orthopedic examination of the foot, radiological study, and labora-
tory analysis of gait if necessary [12–14].
The observational analysis of the gait is fundamental, to evaluate the dynamics

of the foot in all its phases and the alterations in other segments of the LL. The foot
is analyzed by segments, determining if there are deformities of the hindfoot, mid-
foot, or forefoot. In standing we can observe two main patterns of deformity: plano-
valgus and cavus-varus. We must analyze the articular ranges, especially the ankle
and subtalar (the ankle is usually affected in PC by spasticity and/or gastro-soleus
shortening, generating equinus). We also must look for evidence of skin lesions by
pressure or abnormal contact with the ground. Finally, we have to evaluate if the
deformities of the foot are flexible or rigid (degree of manual correction) and to
evaluate the extrinsic muscular power and degree of spasticity [15].
The radiographic study allows us to evidence the structured deformities of the
foot, in the PA and LAT plane with load, and also of the hindfoot by means of the
Saltzman view. This is fundamental for making decisions about the most appropri-
ate treatment for the different deformities [16].
If necessary and there are larger segments involved that require correction, the
laboratory gait analysis can provide us with the elements of judgment to decide
which procedures to carry out on the foot and lower limbs [17].
Below we will describe the main alterations:
1.3 Equinus
Plantar flexion of the ankle due to spasticity and/or shortening of the sural triceps,
which may be the first detectable alteration on physical examination. It may initially
cause an abnormal initial contact on the ground, which alters the dynamics of the
walk, hyperextending the knee in early stages by the generation of a force vector in
front of the knee on contact with the ground. In later stages, a permanent equinus
with compensatory flexion of knees and hips is produced to maintain the center of
gravity in the sagittal plane, which increases energy requirements and pressure on
the patella and extensor apparatus. In the foot, injuries are produced by anterior
overload and metatarsalgia. It is important to differentiate if the equinus is only due
to the involvement of the soleus or of the whole triceps sural by means of the
Silfverskiöld test, which determines the treatment to follow: if the equinus is reduc-
ible with the knee flexed, the involvement is only of the gastrocnemius; if it is not,
it is because the soleus is also shortened (Achilles contracture) [15].
1.4 Equinus-Cavus-Varus
Deformity produced as a consequence of overactivity of plantar flexors (gastro-

soleus) and foot inverters (mainly posterior tibial). Initially a flexible dynamic
deformity is produced, with manually reducible equinus and varus of the
Neurologic Foot 317
Fig. 1 Deformity in equinus-cavus-varus: increased height of the longitudinal arch, equinus of the
ankle and varus of the hindfoot
hindfoot. With time the equinus and varus get stiff; in turn a cavus of the forefoot
is added as a result of the traction of the plantar structures and the long peroneal
tendon. The cavus added to a greater traction of the toes and hallux flexors generate
a claw toe and hallux cock-up deformities (proximal phalanx hyperextension and
interphalangeal flexion) (Fig. 1).
As mentioned above, initially this deformity is flexible, mainly due to the influ-
ence of the extrinsic muscles. In the swing phase, there may be an inversion of the
foot generated by overactivity of the tibialis anterior, causing an initial support of
the foot with the lateral border, which aggravates the hindfoot varus [18].
This deformity is frequent in patients with spastic hemiplegia and initial cases of
spastic diplegia (they can evolve to plano-valgus with skeletal growth).
In patients with quadriplegia, it is common to see precocious and severe develop-
ment of equinus-cavus-varus that makes standing and orthotic handling diffi-
cult [19].
1.5 Equinus-Plano-Valgus
Deformity produced as consequence of overactivity of the plantar flexors (gastro-

soleus) and evertors of the foot (peroneus). This deformity is caused initially by a
flexible valgus flat foot accompanied by equinus of the rearfoot, with elevation of
the calcaneus. It progresses to a midfoot collapse with talonavicular subluxation and
forefoot eversion (Fig. 2). The impossibility to generate an adequate take off (struc-
tured equinus and everted and unstable forefoot) leads to a “false dorsiflexion” at
Chopart’s joint level, which is known as “midfoot break” that aggravates the struc-
tural condition of the foot [20] (Fig. 3).
Initially, the deformities can be reduced manually, but with time they become
more severe and stiff, also evolving to degenerative changes at the subtalar and
talonavicular levels. Even a secondary ankle valgus can be a consequence. In the
most severe cases, the weakness and shortening of the gastro-soleus complex lead
to an anterior inclination of the tibia in the stance phase along with a knee
Fig. 2 Flatfoot valgus: collapse of the longitudinal arch + equinus of the calcaneus, abduction of
the midfoot + talonavicular subluxation and severe valgus of the hindfoot
Neurologic Foot 319
Fig. 3 Midfoot break:

collapse of the midfoot and
subluxation of the
Chopart’s joint, due to the
limitation of the
dorsiflexion of the ankle
and the absence of an
aligned and stable forefoot
extension deficit (plantiflexor-extensor coupling failure), which generates a

crouch gait.
This type of deformity is frequently seen in spastic diplegia, and usually
causes severe disorders in the lever arms necessary for the generation of an effi-
cient gait, in addition to other angular and torsional deformities of the lower
limbs bones [21].
1.6 Charcot-Marie-Tooth Neuropathy
It corresponds to a hereditary sensory-motor polyneuropathy, of which there is a

great variety of genetic subtypes and severities. It is the most frequent hereditary
neuropathy (1/2500 persons), being one of the most frequent causes of cavus-varus
foot in children and adults.
Within all the subtypes there are two main ones:
• Type 1: 2/3 of the patients, with abnormal axonal myelination and slowed con-
duction to electromyography (EMG). Its transmission is autosomal dominant.
• Type 2: about 1/3 of the patients, with abnormal axonal function and normal
myelinization, so EMG shows normal conduction velocity but with lower mag-
nitude of potentials. Its transmission is autosomal recessive.
Compromised nerves show progressive axonal degeneration. The involvement of
the peripheral motor branches generates atrophy and muscle weakness of the
extremities, mainly appendicular, where the feet are the most affected. Less fre-
quently, the sensory nerves are also affected, which aggravates the clinical condi-
tion [22].
The clinical history should emphasize the family history. In most cases there is a
known history of the disease, with varying degrees of penetrance and severity. The
great majority present cavus-varus foot, but others may have mild manifestations
such as repetitive ankle sprains or only claw toes.
In general, the disease is manifested by progressive distal involvement of the
lower extremities mainly involving the leg muscles and the intrinsic foot muscles.
Initial atrophy of the intrinsic foot musculature leads to the initial development of
claw toes and pes cavus. The weakness is initially greater in the muscles of the
anterior compartment of the leg (tibialis anterior, peroneus brevis, and toe extensor),
which contributes to generate a steppage gait and ankle instability. On the other
hand, the greater relative activity of the posterior tibial and peroneus longus (they
are compromised more slowly) generates a varus of the hindfoot and a descent of
the first metatarsal, aggravating the cavus. The gastro-soleus complex can be com-
promised late, generating equinus by atrophy and contracture.
As mentioned, the main deformity generated with the CMT is the cavus-varus
foot, accompanied by claw toes. Initially flexible, with the skeletal growth and pro-
gression of neuropathy, it becomes more severe and rigid, eventually generating
joint incongruencies and degenerative changes. The cavus is initially driven by a
pronated forefoot (first metatarsal descent), which generates a secondary varus of
the hindfoot, aggravated by the instability of the ankle due to muscle weakness. To
test whether the hindfoot varus is reducible, we use the Coleman test, which con-
sists of a block under the fifth metatarsal head. If the hindfoot varus aligns into
neutral or mild valgus, the rearfoot varus is driven by a pronated forefoot. With
time, the hindfoot varus becomes rigid, generating a secondary rigid hindfoot varus
deformity.
It is very important to examine the extrinsic muscular strength, mainly the capac-
ity to evert and dorsiflect the foot (peroneus brevis and tibialis anterior), that is fre-
quently severely compromised muscles.
Often there are associated skin injuries: lateral hyperkeratosis at the base of the
fifth metatarsal secondary to lateral overload, metatarsal head plantar hyperkera-
tosis (especially at the first and fifth metatarsals), and dorsal interphalangeal
hyperkeratosis secondary to claw toes. The eventual sensory involvement can
aggravate these lesions generating deep ulcers and infections.
Electrodiagnosis is fundamental to confirm the disease and define its prognosis,
together with the respective genetic study [5, 23].
1.7 Spinal Dysraphia
Concept that groups congenital defects of the neural tube closure, which can involve
only a hidden spina bifida by defects of the posterior arch closure and herniation of
the peridural fat (lipomeningocele), of the duramadre (meningocele), or of the roots
of the spinal cord together with all the anterior structures (myelomeningocele).
Myelomeningocele is the most common of the neural tube closure defects, being a
major cause of disability as it is compatible with life. The incidence is 1/1000 live
Neurologic Foot 321
births, being the most frequent location in the lumbosacral region. The herniation
of the lower spinal roots leads to a series of disorders by peripheral denervation,
causing sensory-motor paralysis and bladder and intestinal dysfunction. In addi-
tion, it is frequently associated with hydrocephalus and other neural tube malforma-
tions such as diastematomyelia or syringomyelia, which further aggravate the
neurological deficit.
Its etiology is strongly associated with the deficit of folic acid intake during the
first trimester of pregnancy, so its incidence has decreased significantly in countries
where regular supplementation of this compound has been implemented in pregnant
women. It is also associated with genetic factors and exposure to chemical sub-
stances, among which valproic acid stands out, commonly used as an antiepileptic.
On the other hand, the prenatal diagnosis of neural tube anomalies has led to the
elective interruption of pregnancies, as well as to the development of intrauterine
surgery for the closure of these defects, which has made it possible to partially
improve the motor function of these patients [24].
They are classified according to the motor level involved, with the lower levels
being less affected and having a better functional prognosis:
1. High thoracic-lumbar: lack of activation of quadriceps (only hips flexion)
2. Low lumbar: lack of activation of the gluteus medius and maximum. Partial
quadriceps and hamstring activity (knee extension)
3. Sacrum: complete activation of quadriceps and gluteus medius (knee extension
and flection)
• High sacrum: lack of gastro-soleus activation (dorsiflect ankles)
• Lower sacrum: gastro-soleus activation (active ankle flexion)
• The prognosis of independent walking depends on the motor level, com-
monly achieving walking with the assistance of orthotics and canes if there is
active knee extension capacity (low lumbar level). The lower the level, the
less external support is required for walking. The low lumbar and sacral levels
are the most frequent, so the great majority of these patients have a great
potential for independent walking with adequate orthotic support.
• The foot is compromised in all cases. Denervation produces muscular atrophy
and progressive fibrous retraction, which causes early skeletal deformities
accompanied by local sensory deficits, which facilitates the appearance of
skin lesions due to pressure, ulcers, local infections, and osteomyelitis [25,
26] (Fig. 4).
The most frequent deformities are:
• Clubfoot: equinus-cavus-varus: 44% (low lumbar level). It can often present as a
severe “clubfoot” in the newborn, difficult to manage (usually associated with
other lesions of the spine).
• Calcaneal varus and cavus foot: 25% (low lumbar and sacral level). Cavus and
adductus of the forefoot plus varus of the hindfoot without significant equinus.
• Calcaneal foot: 12% (sacral level). Vertical calcaneus and ankle dorsiflexion.
Elongated Achilles.
Fig. 4 Foot equinus-cavus-varus in patient with myelomeningocele, low lumbar level, with
important cutaneous injury secondary to lateral hyperpressure, painless by local insensibility
Less frequent:
• Vertical talus (high levels). Total sensory and motor paresis below the knee
• Plano-valgus (low sacral level)
Isolated equinus (when there are lesions of the spine)
The deformity of the feet is added to the rest of the lower extremity depending
on the level affected. In levels above L3, there are often contractures in knee flexion,
significant rotational disorders of the lower extremities, and hip instability [27].
1.8 Muscular Dystrophies
They correspond to a heterogeneous group of genetic diseases that cause degenera-

tion and muscle weakness. The genetic defect causes some muscle protein to be
defective or not to be produced in the amount needed for normal function. This
causes the muscle tissue to degenerate and be replaced by nonfunctional fibrous tis-
sue, causing lack of strength and muscle atrophy, resulting in joint retractions and
skeletal deformities of varying magnitude, depending on the severity of the
condition.
In some, other tissues are also affected, such as the heart or brain. The vast major-
ity of genetic defects are identified, and the pattern of inheritance is known. The
prognosis varies according to the type of dystrophy and the speed of progression.
Some are mild and evolve slowly, allowing a relatively normal life expectancy,
while others are more severe and cause severe functional disability. All worsen as
the muscles degenerate and become progressively weaker. Most patients eventually
Neurologic Foot 323
lose the ability to walk. Life expectancy depends on the degree of muscle weakness
and respiratory or cardiac involvement.
Its most common forms in boys, Duchenne and Becker muscular dystrophies,
affect about 1 in 3500–5000 boys [28].
Duchenne dystrophy is the most common; it is due to the alteration of the dystro-
phin protein gene resulting in the absence of the protein. Linked to the X chromo-
some, females are carriers, and only males manifest the disease. It is rapidly
progressive, causing the loss of the gait around the age of 12–14 years, and then they
present cardiopathy and respiratory failure. Usually, they do not exceed 20
years of age.
Muscle involvement initially generates proximal weakness, so patients lose
strength in the trunk and large muscle groups around the hips and shoulder girdle.
At this stage, the sign of Gowers is characteristic, in which children have great dif-
ficulty in standing up when sitting on the floor, helping themselves with their four
extremities to be able to stand up. Over time, the muscles are affected distally, and
muscular atrophy and fibrosis begin to occur. This causes the patient to lose his gait
and deformities appear in knee flexion and equinus-varus feet, due to the retraction
of the gastro-soleus and tibialis posterior. The muscles of the extremities are infil-
trated with fat, especially in the posterior region of the leg, which gives the impres-
sion that they are larger (pseudohypertrophy) [29].
Becker’s dystrophy is the second most frequent. It is a milder variant than
Duchenne, because of the partial but poor function of the dystrophin protein. The
manifestations start around 10–11 years and then progress slowly. The deterioration
of the gait is slow and variable, and not all patients lose the ability to walk com-
pletely. The cardiac and respiratory deterioration is also milder, so that the life
expectancy is much higher, exceeding 40 years for the vast majority [30].
Among the other less frequent dystrophies, it is worth mentioning Emery-
Dreyfus Dystrophy, the scapulohumeral fascia, and the congenital one; the latter can
be very severe with early mortality.
The diagnosis is made by clinical suspicion, compatible electromyographic
study, elevated blood levels of creatine phosphokinase, muscle biopsy, and corre-
sponding genetic study.
For the correct approach, we must first evaluate the foot in its global aspect, as well
as clearly differentiate each one of the segments that compose it. The interrelation-
ship between rearfoot, midfoot and forefoot, and the way in which they develop the
compensations must be analyzed in detail. Hand in hand with the above should be a
thorough knowledge of the anatomy of the foot and the various structures that
compose it.
In addition, in the context of a foot with neurological affectation, we must con-

sider all those variables that will condition the result, not only anatomical factors
but also a correct classification of the functional level and of the biopsychosocial
determinants [31], as well as an adequate control of variables such as spasticity and
dystonia, among others.
On the other hand, the different alterations can be grouped by levels of deformity,
as proposed by Davis according to the degree of flexibility or rigidity of the foot,
and whether their appearance is primary (effect of the base pathology), secondary
(as a response to the primary), or tertiary (as a compensation to the secondary). This
guides the decision-making process in a comprehensive manner [10].
The use of orthotic elements is useful in those deformities that are flexible, where
their use will prevent the progression and/or structuring of these deformities. In
those cases in which the deformities are structured, their use is contraindicated,
since they will not contribute to the correction of the deformities.
Among the orthotic alternatives available on the market, the most widely used is
the ankle-foot orthosis or AFO. It consists of a plastic splint made to measure for the
patient and respecting his anatomy, which covers from the infrapatellar area includ-
ing the foot in its entirety. It is possible to add diverse complements that block the
normal tendency of the foot toward the deformity, as well as elements of padding
that avoid the appearance of pressure ulcers [32–34] (Fig. 5).
Other conservative measures such as pharmacological (botulinum toxin,
baclofen) and physical therapies (physiotherapy, acupuncture, among others) con-
tribute to modify the primary variables in order to avoid the appearance of subse-
quent deformities [35].
Fig. 5 Types of ankle-foot orthosis: simple or AFO (only to maintain aligned and stable position
of the foot and ankle). Ground force reaction or GRAFO (to avoid anterior translation of the tibia
in mid support, helping the knee to extend). Dynamic (articulated, to allow active mobilization of
the ankle)
Neurologic Foot 325
2.1 Equinus Foot
It is probably the deformity that we will find most often in patients with CP.
It must be certified in detail if the equinus origin is at the ankle or midfoot. In the
first case, we must evaluate the contribution of gastrocnemius and soleus to the
deformity, as well as if it is flexible or structured (Silfverskiöld test).
The initial approach includes physical therapy as a method of stretching in flex-
ible/reducible cases prior to structuring. In spastic patients, infiltration with botuli-
num toxin prior to rehabilitation is useful. In addition to infiltration, some patients
benefit from the placement of corrective casts; in this way a greater amount of cor-
rection is achieved [36–38]. If normal range of motion cannot be restored, the next
step involves surgical lengthening.
In order to consider a conservative management, we must value its flexibility as well

as other factors that could influence the anomalous position of the foot, like the
external tibial torsion. It should be borne in mind that the correction of equinus in
certain patients will condition their loss of gait (form equinus gait will end up in a
crouch gait).
The use of corrective braces (insoles, plantar inserts, or similar) is useful as a first
option. Although some components of the valgus plane are susceptible to contain-
ment by orthosis, the equinus will necessarily require correction to ensure a planti-
grade and efficient footprint and thus avoid the appearance of cascading deformities.
However, there is no evidence that conservative treatment has a proven role in pre-
venting the natural evolution of the deformity; there are even detractors based on the
lack of development of the various muscle groups with the use of orthosis.
Identified muscular imbalances due to “hyperactivity,” these muscle groups are
susceptible to local pharmacological management (botulinum toxin).
It is probably one of the most complex deformities, due to the multiplicity of ele-
ments involved and by the appearance of compensations.
We must consider each of the elements separately, as well as the respective com-
pensations. In the clinical assessment, it is necessary to determine and differentiate
those components of the deformity that are reducible and those that are structured.
Once this level of deformity has been reached, it is very likely that the different
components have some degree of irreducibility, which will mean that conservative
Fig. 6 Serial casts for correction of clubfoot, after local infiltration with botulinum toxin
treatment will only succeed in preventing the progression of the deformities. At an

early age, these deformities can be totally or partially be corrected by the use of
serial casts, to allow an adequate fit of orthosis or to lessen the magnitude of an
future surgical interventions [39] (Fig. 6).
The equinus is frequently the initial deformity, and at this stage it is already
structured, so a conservative approach will not correct it. The varus of the hindfoot
must be assessed for its flexibility by means of the Coleman test, according to which
it must be defined if it will be susceptible to conservative management or if it will
require a corrective hindfoot osteotomy. For cases where standing is difficult or the
patient is uncooperative, unloading assessment methods have been described.
Forefoot pronation is often a secondary compensation of the deformity. It can be
exacerbated by increased activity of the peroneus longus tendon. Assessing its con-
tribution is crucial when planning treatment. If this is the case and the deformity is
reducible, we should consider elongation by means of physical therapy or comple-
mentary management with botulinum toxin injection [5, 40].
3 Surgical Treatment
It should be borne in mind that the ideal time to perform any foot surgery is one in
which it is possible to avoid the appearance of secondary and tertiary deformities,
being a timely treatment that achieves the best result and avoids such compensation.
Neurologic Foot 327
This is not always possible in clinical practice, and we are often faced with complex
and progressive deformities. If more radical procedures such as arthrodesis are nec-
essary, it is desirable that they be performed after the age of 8, considering that the
important thing is to achieve correct alignment. This last one is the fundamental
condition for the maintenance of the result in the long term.
Depending on the underlying pathology, it is relevant to consider the overall
management of certain conditions such as dystonia or spasticity, as a fundamental
pillar of treatment. A global mismanagement could affect the effectiveness or dura-
bility of the result achieved after a surgical intervention.
A useful way of dividing the procedures is to group them into procedures aimed
at correction and procedures aimed at maintaining the correction. Within the first
group, we have all those procedures that are necessary to obtain an anatomical res-
toration of all the segments of the ankle-foot (usually tenotomies, joint releases,
osteotomies, arthrodesis), while in the second group, we find those procedures that
seek in a static or dynamic way the maintenance of this correction (mostly muscle
balance) [41].
On the other hand, some patient’s foot deformities may be associated with other
alterations of the lower extremities that must be identified and treated in the same
surgical act in order to optimize functional results (multilevel surgery) [42].
3.1 Clubfoot
Once the structuring of the deformity is achieved, it is necessary to correct it to

avoid the appearance of secondary deformities. The equine as a unique deformity
has different alternatives for surgical treatment depending on the level of alteration
and structure involved.
The posterior region of the leg is divided into three zones, which define the type
of lengthening procedure and the structures on which they act.
We must divide the deformities in those in which the equinus remains both in
flexion and extension of the knee (gastrocnemius and soleus involvement, Achilles
involvement), from the equinus only happening in extension of the knee (Silfverskiöld
+ gastrocnemius involvement). In the first scenario, the correction should be made
at the Achilles tendon level (zone 3) if the equinus is severe (equinus >15°) or at the
myo-tendinous junction (zone 2) if the equinus is maintained around 5–10°; while
in the second scenario, we should perform procedures that maintain the soleus
indemnity according to the reducibility in the clinical evaluation.
Among the alternatives to be performed, we have the disinsertion of the medial
to proximal gastrocnemius muscle head (Barouk’s procedure), Bauman’s surgery
(muscular aponeurotic recession of medial gastrocnemius), Strayer or similar (distal
myo-aponeurotic recession of gastrocnemius), and to lengthen the Achilles tendon
the open Z-tenotomy as the percutaneous triple hemitenotomy (Hoke) [43, 44]
(Fig. 7).
Fig. 7 Strayer’s technique for equinus foot: aponeurotic elongation of the gastrocnemius (intact
soleus under the sectioned aponeurosis), gaining 30° of dorsiflexion without losing muscular
strength and allowing mobilization after a few weeks
In any of the techniques used, it is recommended that a cast be kept on for the
first 3 weeks (with indication for discharge), followed by another 3 weeks with
partial immobilization, allowing weight bearing and begining a program of progres-
sive muscle strengthening.
Special mention should be made at this point to the deformity called “apparent
equinus.” In advanced stages of certain neurological alterations, a pseudoequinus
appears as a functional response to a knee and hip flexion. In this scenario, a surgi-
cal elongation of the gastro-soleus complex would be contraindicated. Achilles
lengthening for these cases would end up in crouch gait, with absolute loss of
independent gait.
There is consensus that the moment to recommend foot surgery is when the defor-
mity alters its role as a stable base of support or when pain appears. Each one of the
components of the deformity must be individualized, and then the origin of each one
of them must be determined. We must also assess whether there is instability of the
ankle or of the midfoot (especially talonavicular).
The approach then will be to make a sequential correction of each deformity,
using the principles of stage therapy. For the release of the equinus component, the
same guidelines detailed in the previous sections should be followed.
The correction of the plano-valgus component seeks to restore correct tripod sup-
port of the foot, trying to preserve the mobility of adjacent joints (especially in
patients with adequate functional demand). For this, it must be identified if any of the
components is flexible or due to compensation for another deformity (which could
aggravate it by correcting the original alteration). The lengthening of the lateral col-
umn, whose classic procedure is the Evans osteotomy (later modified by V. Mosca),
seeks to restore the alignment of the osseous structures, without sacrificing articular
mobility [45, 46]. It is indicated in patients with moderate functional demand and
Neurologic Foot 329
Fig. 8 Evans osteotomy: lateral column lengthening for the treatment of severe flexible flatfoot.
Note the simultaneous correction of the planus and abductus (interposed structured bone graft, in
red) with the subsequent reduction of the talonavicular joint
relatively good motor control (Fig. 8). A talonavicular arthrodesis can be added if
this joint is very unstable or presents degenerative changes, especially in adolescents
[47]. Subtalar arthrodesis will anatomically correct the alignment of the hindfoot,
having the inconvenience of overloading the neighboring joints; therefore, it would
be indicated only in patients with low functional demand or severe deformities.
Once the hindfoot has been corrected, the persistent deformity in the midfoot
should be assessed, as well as areas of hypermobility. This is how shortening oste-
otomies of the internal column (subtractive wedges of the medial cuneiform), talo-
navicular arthrodesis could be indicated in the case of an abducted forefoot. In cases
of pathological midfoot instability, a plantar midfoot wedge could help with mid-
foot collapse and regain sagittal plane stability [4].
The triple arthrodesis should be reserved as the last therapeutic option, by trans-
ferring all the biomechanics of the hindfoot to the ankle and forefoot. Although
there are reports of good long-term results, we do not recommend it as a first line
treatment except for patients nearing preadolescence and with low or no functional
demand [21].
This deformity is very demanding from a functional point of view, since it usually
occurs in patients who are ambulatory. This is how we will find feet that have vari-
ous areas of hyperpressure, which will guide areas where anatomical restoration
will be essential.
In the correction algorithm, we must begin by releasing the equinus to correctly

assess the effect on other deformities. Due to the structuring of the equinus, a Z
lengthening of the Achilles tendon may be necessary.
Then, and depending on what was obtained in the Coleman test, we proceed to cor-
rect the hindfoot, by means of a calcaneous valgus osteotomy [48]. Here, diverse alter-
natives exist (wedge resection or sliding osteotomies) according to the type of
necessary correction. In this point it is possible to make special mention to those cases
in which the equinus is slight, which could be corrected together with the hindfoot
varus through an osteotomy of lateral and superior slide of the posterior calcaneal
tuberosity. It is necessary to evaluate the role of the posterior tibialis tendon in the
deformity. A decision has to be made to carry out a tibialis posterior lengthening or a
transfer (as procedure of maintenance). As a useful parameter, we must assess in
radioscopy the correct talocalcaneal divergence, an adequate talonavicular coverage,
and the restoration of the Meary’s angle in the frontal and lateral projection.
The midfoot cavus is usually associated with a forefoot adduction and pronation.
The need for correction will depend on the reducibility once the primary deformi-
ties are corrected. Among the therapeutic alternatives are superficial medial and
deep talonavicular release and osteotomies of the medial column [23].
For the forefoot correction, it should be evaluated if pure pronation exists (which
increases the cavus) and/or if an adductus exists. For the first case, the subtractive
dorsal wedge osteotomy of the first metatarsal or medial cuneiform is useful. A
plantar additive wedge osteotomy of the medial cuneiform is an option as well. If
there is a residual forefoot adductus, it should be addressed before the pronation
Fig. 9 Severe equinus-cavus-varus feet in adolescent with spastic quadriplegia, treated with mid
and hindfoot osteotomies plus arthrodesis and soft tissue release (flexor tendons, tibialis posterior,
and Achilles), achieving a plantigrade foot to recover orthotic-assisted standing
Neurologic Foot 331
correction. Midfoot osteotomies that shorten the external column (cuboid subtrac-
tive osteotomy) are useful here. In adolescent patients with low functional capacity
and complex structured deformities, “a la carte” osteotomies and arthrodesis are an
alternative to obtain a plantigrade foot that allows standing [49] (Fig. 9).
References
1. Dobbe A, Gibbons P. Common paediatric conditions of the lower limb. J Paediatr Child Health.
2017;53(11):1077–85.
2. Lovell W, Winter R. In: Morrissy R, Weinstein S, editors. Pediatric orthopaedics. 6th ed.
Philadelphia: Lippincott Williams & Wilkins; 2006.
3. Tachdjian M. The child’s foot. Philadelphia: W B Saunders Co; 1985.
4. SEOP. Parálisis cerebral infantil. In: Martínez I, Abad J, editors. Manejo de las alteraciones
músculo-esqueléticas asociadas. Madrid: Ergon; 2015.
5. Neumann J, Nickisch F. Neurologic disorders and cavovarus deformity. Foot Ankle Clin.
2019;24(2):195–203.
6. Butterworth M, Marcoux J, editors. The pediatric foot and ankle. Diagnosis and management.
Springer; 2020.
7. Patel D, Neelakantan M, Pandher K, Merrick J. Cerebral palsy in children: a clinical overview.
Transl Pediatr. 2020;9(suppl1):s125–35.
8. Miller F, editor. Cerebral palsy. Springer; 2005.
9. Graham K, Selber P. Musculoskeletal aspects of cerebral palsy. J Bone Joint Surg (Br).
2003;85-B:155–66.
10. Davids JR. The foot and ankle in cerebral palsy. Orthop Clin North Am. 2010;41(4):579–93.
11. Bennet G, Rang M, Jones D. Varus and valgus deformities of the foot in cerebral palsy. Dev
Med Child Neurol. 1982;24:499–503.
12. Gage J, Schwartz M, Koop S, Novacheck T. In: Hart H, editor. The identification and treatment
of gait problems in cerebral palsy. 2nd ed. London: Mac Keith Press; 2009.
13. Keenan W, Rodda J, Wolfe R, Roberts S, Borton D, Graham K. The static examination of
children and young adults with cerebral palsy in the gait analysis laboratory: technique and
observer agreement. J Pediatr Orthop B. 2004;13(1):1–8.
14. Chang F, Rhodes J, Flynn K, Carollo J. The role of gait analysis in treating gait abnormalities
in cerebral palsy. Orthop Clin N Am. 2010;41:489–506.
15. Devinney S, Prieskorn D. Neuromuscular examination of the foot and ankle. Foot Ankle Clin.
2000;5(2):213–33.
16. Lamm B, Stasko P, Gesheff M. Normal foot and ankle radiographic angles, measurements, and
reference points. J Foot Ankle Surg. 2016;55(5):991–8.
17. Davids J, Bagley A. Identification of common gait disruption patterns in children with cerebral
palsy. J Am Acad Orthop Surg. 2014;22:782–90.
18. Michlitsch M, Rethlefsen S, Kay R. The contributions of anterior and posterior tibia-
lis dysfunction to varus foot deformity in patients with cerebral palsy. J Bone Joint Surg.
2006;88-A:1764–8.
19. Ziebarth K, Krause F. Updates in pediatric cavovarus deformity. Foot Ankle Clin N Am.
2019;24:205–17.
20. Dare D, Doswell E. Pediatric flatfoot: cause, epidemiology, assessment, and treatment. Curr
Opin Pediatr. 2014;26(1):93–100.
21. Kadhim M, Miller F. Pes planovalgus deformity in children with cerebral palsy: review article.
J Pediatr Orthop. 2014;23(5):400–5.
22. Jani-Acsadi A, Ounpuu S, Pierz K, Acsadi G. Pediatric Charcot-Marie-Tooth disease. Pediatr
Clin N Am. 2015;62(3):767–86.
23. Lin T, Gibbons P, Mudge A, Cornett K, Menezes M, Burns J. Surgical outcomes of cav-
ovarus foot deformity in children with Charcot-Marie-Tooth disease. Neuromuscul Disord.
2019;29:427–36.
24. Swaroop V, Dias L. Orthopedic management of spina bifida. Part I: hip, knee and rotational
deformities. J Child Orthop. 2009;3:441–9.
25. Swaroop V, Dias L. Orthopedic management of spina bifida-part II: foot and ankle deformities.
J Child Orthop. 2011;5:403–14.
26. Akbar M, Bresch B, Seyler T, Wenz W, Bruckner T, Abel R, et al. Management of orthopaedic
sequelae of congenital spinal disorders. J Bone Joint Surg Am. 2009;91:87–100.
27. Gunay H, Celal Sozbilen M, Gurbuz Y, Altinisik M, Buyukata B. Incidence and type of
foot deformities in patients with spina bifida according to level of lesion. Childs Nerv Syst.
2016;32(2):315–9.
28. Mercuri E, Bönnemann C, Muntoni F. Muscular dystrophies. Lancet. 2019;394(10213):
2025–38.
29. Apkon S, Alman B, Birnkrant D, Fitch R, Lark R, Mackenzie W, et al. Orthopedic and surgical
management of the patient with Duchenne muscular dystrophy. Pediatrics. 2018;142(Suppl
2):s82–9.
30. Flanigan K. Duchenne and Becker muscular dystrophies. Neurol Clin. 2014;32(3):671–88.
31. Martínez Caballero I, Chorbadjian Alonso G, Egea Gámez R, et al. Evaluación funcional y de
factores limitantes del tratamiento de los trastornos de la marcha en la parálisis cerebral infan-
til: desarrollo del sistema de clasificación de niveles de deambulación funcional. Rev Neurol.
2020;71(7):246–52.
32. Aboutorabi A, Arazpour M, Ahmadi Bani M, Saeedi H, Head JS. Efficacy of ankle foot ortho-
ses types on walking in children with cerebral palsy: a systematic review. Ann Phys Rehabil
Med. 2017;60(6):393–402.
33. Bjornson K, Zhou C, Fatone S, Orendurff M, Stevenson R, Rashid S. The effect of ankle-foot
orthoses on community-based walking in cerebral palsy: a clinical pilot study. Pediatr Phys
Ther. 2016;28(2):179–86.
34. Degelaen M. Effect of ankle-foot orthoses on motor performance in cerebral palsy. Dev Med
Child Neurol. 2019;61(2):119–20.
35. Sees J, Miller F. Overview of foot deformity management in children with cerebral palsy. J
Child Orthop. 2013;7:373–7.
36. Dursun N, Gokbel T, Akarsu M, Dursun E. Randomized controlled trial on effectiveness of
intermittent serial casting on spastic equinus foot in children with cerebral palsy after botuli-
num toxin – a treatment. Am J Phys Med Rehabil. 2017;96(4):221–5.
37. Park E, Rha D, Yoo J, Kim S, Chang W, Song S. Short-term effects of combined serial casting
and botulinum toxin injection for spastic equinus in ambulatory children with cerebral palsy.
Yonsei Med J. 2010;51(4):579–84.
38. Blackmore A, Boettcher-Hunt E, Jordan M, Chan M. A systematic review of the effects of
casting on equinus in children with cerebral palsy: an evidence report of the AACPDM. Dev
Med Child Neurol. 2007;49:781–90.
39. Janicki J, Narayanan U, Harvey B, Roy A, Ramseier L, Wright J. Treatment of neuromuscular
and syndrome-associated (nonidiopathic) clubfeet using the Ponseti method. J Pediatr Orthop.
2009;29(4):393–7.
40. Kedem P, Scher D. Foot deformities in children with cerebral palsy. Curr Opin Pediatr.
2015;27(1):67–74.
41. Rehbein I, Teske V, Pagano I, Cúneo A, Pérez ME, Von Heideken J. Analysis of orthopedic
surgical procedures in children with cerebral palsy. World J Orthop. 2020;11(4):222–31.
42. Martínez I, Lerma S, Ramírez A, Ferullo M, Castillo A. Multilevel surgery for gait disorders
in cerebral palsy. Quantitative, functional and satisfaction outcomes measurement. Trauma.
2013;24(4):224–9.
Neurologic Foot 333
43. Dreher T, Buccoliero T, Wolf S. Long-term results after gastrocnemius-soleus intramuscular

aponeurotic recession as a part of multilevel surgery in spastic diplegic cerebral palsy. J Bone
Joint Surg Am. 2012;94(7):627–37.
44. Shore B, White N, Graham K. Surgical correction of equinus deformity in children with cere-
bral palsy: a systematic review. J Child Orthop. 2010;4(4):277–90.
45. Andreacchio A, Orellana C, Miller F, Bowen T. Lateral column lengthening as treatment
for planovalgus foot deformity in ambulatory children with spastic cerebral palsy. J Pediatr
Orthop. 2000;20:501–5.
46. Kadhim M, Holmes L, Church C, Henley J, Miller F. Pes planovalgus deformity surgical cor-
rection in ambulatory children with cerebral palsy. J Child Orthop. 2012;6:217–27.
47. Turriago C, Arbelaez M, Becerra L. Talonavicular joint arthrodesis for the treatment of
pes plano valgus in older children and adolescents with cerebral palsy. J Child Orthop.
2009;3:179–83.
48. Dwyer F. Osteotomy of the calcaneus for pes cavus. J Bone Joint Sur [Br]. 1959;41-B:80–6.
49. Mubarak S, Van Valin S. Osteotomies of the foot for cavus deformities in children. J Pediatr
Orthop. 2009;29(3):294–9.
Pediatric Diaphyseal Tibia and Distal Tibia
Fractures
Cristian Olmedo Gárate and Cristian Artigas Preller
1 Introduction
Tibial diaphysis fractures are the third most common long bone fracture in the pedi-
atric patient [1, 2]. In the diaphysis of the tibia, 40% of the fractures occur [1], and
the anatomical distribution within the same diaphysis varies, being more frequent
those of the distal third with approximately 50% of the total diaphyseal fractures.
This is followed by mid-diaphyseal fractures with 39% and finally by fractures of
the proximal third of the tibia with 11% [2, 3]. In the context of the polytraumatized
patient, it is the third most frequent fracture after femur and humerus fractures. Up
to 10% of diaphyseal tibia fractures are exposed.
On the other hand, metaphyseal fractures of the distal tibia are infrequent; their
incidence varies in the different series from 0.35% to 0.45% [4].
C. Olmedo Gárate (*)

Clinica Alemana de Santiago, Santiago, Chile
Hospital Padre Hurtado, Santiago, Chile
C. Artigas Preller
Universidad de Chile, Santiago, Chile
Hospital de Niños Roberto del Río, Santiago, Chile

Switzerland AG 2022
336 C. Olmedo Gárate and C. Artigas Preller
2 Etiology: Pathophysiology
Due to its anatomical location, the leg is constantly exposed to various traumas.
Sports and traffic accidents are the main cause of tibia fractures in patients between
4 and 14 years of age [5, 6]. Torsional forces are the cause of approximately 80% of
fractures with an intact fibula, producing a characteristically oblique or spiral
feature [7].
Most isolated tibia fractures occur from direct blows, while more than 50% of
ipsilateral tibia and fibula fractures are caused by traffic accidents [8, 9].
Finally, unfortunately, the tibia is the second most frequent long bone fracture in
the child with non-accidental injuries, varying between 11% and 26% depending on
the series [10].
3 Anatomy
The tibia is a bone of subcutaneous location in its medial part, which makes it very
susceptible to exposed fractures, being the most frequent exposed fracture in the
pediatric population [11]. The tibia has a triangular shape, but its endomedullary
canal remains round which makes it a long bone susceptible to interlocking.
Tibia and fibula are joined by the interosseous membrane; as the child grows, the
fibula takes a more posterior position in relation to the tibia. The indemnity or pres-
ence of fibular fracture will determine the tendency to deviation of the fracture by
the insertions of the muscles of the anterior and lateral compartments of the leg. It
is relevant to know the muscular compartments of the leg; there are four of these,
the anterior, lateral, and the two posterior (superficial and deep), since the fractures
of this segment can present in their evolution an acute compartment syndrome
[1, 3, 9].
4 Diagnosis
These patients present clinically with pain, inability to bear weight, and in severe
cases segmental deformity. In preschool children, they may present only with gait
claudication. Remember that in the context of polytraumatized children, it is a fre-
quent fracture, so in these scenarios we must perform thorough primary and second-
ary evaluations according to the protocols of Advanced Vital Trauma [12, 13].
It is oriented by the mechanism of trauma, either direct or indirect. Special con-
sideration should be given to the presence of skin injury and soft tissue damage to
the leg, using the Gustilo and Anderson classifications and/or the AO classification
[14, 15].
Pediatric Diaphyseal Tibia and Distal Tibia Fractures 337
Making a clinical diagnosis of neurovascular indemnity is relevant, in addition to

having a high index of suspicion of compartment syndrome, with disproportionate
pain being a cardinal symptom in the pediatric population [16].
Consider in the initial diagnosis simple radiography with anteroposterior and
lateral orthogonal projections of the leg including the knee and ankle, being relevant
to consider ipsilateral ankle involvement, there being an association with triplanar
fractures, so we should add projections of the ankle and eventual evaluation of the
ankle with computed axial tomography (CT) [17]. Remember the study of other
segments in polytraumatized patients according to our primary and secondary eval-
uation [18].
In order to determine which type of treatment is the most appropriate for a patient,
it is necessary to study and assess the necessary to study and evaluate the different
variables of the case:
(a). Of the patient: age and size, remaining growth potential, quality of the bone
involved (pathological bone metabolic diseases), activity level (e.g., high-
performance athlete), and functional capacity (e.g., neurological diseases).
(b). Fracture: affected area, stability, and comminution.
(c). Trauma: amount of energy involved, involvement of adjacent soft tissues, neu-
rovascular involvement, and involvement of other systems or associated
injuries.
In general, these are contraindications for orthopedic treatment:
–– Polytraumatized
–– Floating knee
–– Neurological and/or vascular compromise
–– Significant soft tissue involvement, suspected compartment syndrome.
Relative contraindications for orthopedic treatment:
–– Large, obese patients
–– Segmental fractures
–– Exposed fractures
–– Features difficult to control with a cast, e.g., varus greater than 10° with intact
fibula [19]
Conservative treatment of tibial fractures using an in situ cast or closed reduction
and a cast has proven to be a useful and cost effective tool [6, 9]. Sarmiento laid the
foundation for defining the parameters and limits of orthopedic management of
diaphyseal tibial fractures in the adult patient [20, 21]. Based on this and subsequent
studies, the parameters and limits for the management of these fractures in pediatric
patients are detailed in Table 1 [1, 22].
Table 1 Acceptable Age < 8 y/o > 8 y/o

alignment of diaphyseal
Varus 10° 5°
fractures of the tibia in the
pediatric patient according Valgus 5° 5°
to Henrich and Apex anterior angulation 10° 5°
Mooney [1] Apex posterior angulation 5° 0°
Shortening 10° 5°
Rotation 5° 5°
In distal tibia fractures, angulation tends to occur mainly in recurvatum, so it is

important to leave the foot in plantar flexion for 3–4 weeks. The criteria for tolerable
angulation are similar and applicable to distal tibial fractures.
Embarking on orthopedic treatment implies assuming continuous and direct care
of the patient’s evolution, with successive weekly controls initially and then more
sporadic until the end of skeletal growth. The casting technique must be precise and
the molding established according to the fracture pattern.
Once the diagnosis has been made and the decision made to perform orthopedic
management, this can be done in three different ways:
1. Cast in emergency box, consultation or procedure room – reserved for low-
energy fractures, with little soft tissue involvement, and acceptable alignment
according to described parameters that do not require reduction maneuvers.
Patients usually cooperate effectively and may be accompanied by their parents.
2. Reduction and cast under sedation – for fractures that require some reduction
gesture to achieve acceptable alignment parameters and thus will require maneu-
vering and casting of the cast which may cause significant pain to the patient.
This directly influences the casting technique. It is a sine qua non condition to
have an adequate procedure room to perform these procedures, with institutional
protocols and personnel trained in sedation and cast placement assistance.
3. Reduction and cast under general anesthesia – involves hospitalization of the
patient and use of the ward. Reserved for fractures that require more intense
reduction and traction maneuvers or for patients in whom the installation of the
cast and molding is technically more difficult (obese).
It is very important to have trained personnel. The assistance of a second trauma-
tologist and/or a cast technician is key to the success of the reduction and cast instal-
lation. There are several factors to take into account during the procedure, e.g.,
control of rotation and axes, adequate three-point support, cast bandage tension, and
soft tissue care. If only one person tries to cover all this, it is highly probable that he/
she will be distracted from some of the aspects, and this could have a direct impact
on the final result of the treatment (Images 1 and 2).
Images 1 and 2 Long boot cast in initial treatment of leg fracture. Includes bar to prevent rotation
Some recommendations to keep in mind for orthopedic treatment are:

–– The patient’s position is of vital importance for a good result. We recommend
leaving the leg hanging on the edge of the stretcher during the reduction and
installation of the cast; in this way the same force of gravity helps in the traction
and alignment of the segments.
–– It is necessary to protect adequately with synthetic padded bandage the skin and
soft parts of injuries that can produce the cast, especially in areas where there are
bony prominences.
–– Casting should be performed according to the pattern and deformity of the injury,
with three-point support and taking care of the position of the foot. We strongly
recommend using the palms of the hands without the fingers during casting to
avoid protrusions that could injure the skin.
–– Once the first half of a long boot (which is a short boot) is installed and com-
pleted, three or four 1–2 cm unloading incisions should be made with a plaster
scissors on the proximal edge to avoid a constriction ring in this area.
–– In patients younger than 2 years, the cast may slip, so a knee flexion at 90 degrees
plus an ankle flexion at 90 degrees achieves an effective locking of the cast pre-
venting it from coming out.
–– During the installation of the second half (thigh), it is important to make a good
molding in the supracondylar area of the femur. The idea of this molding is to
avoid slippage of the cast, especially in younger children.
–– We recommend a leg X-ray after cast installation to have a starting point for
follow-up and effective comparison with future images during follow-up.
5.1 Yesotomies
Yesotomy is a technique that allows for minor corrections in orthopedically man-

aged fractures that have partially lost reduction during control. It is useful for angu-
lar corrections in the coronal and/or sagittal plane. The plaster cast is limited to a
correction of 15° and requires the patient’s cooperation, since the manipulation can
cause discomfort and pain. Corrections greater than this could generate soft tissue
injuries or even compartment syndrome. We reiterate that the idea of a plaster cast is
not to achieve an anatomical reduction but to recover an acceptable axis of the limb.
It is necessary to carry out a thorough planning prior to the plaster cast with radio-
graphs in strict anteroposterior and lateral projections, more oblique as needed. See
Fig. 1. It is necessary to take into account in the design of the plaster cast that the
wedge can be of opening or closing, which will influence the length of the segment.
Once the wedge is designed, a cut is made between ½ and ¾ of the circumference.
Once the wedge is made, a smooth and controlled reduction is performed until the
desired correction is achieved. When the wedge is open, it is kept open with wooden
plugs cut to size, and then it is stabilized with one or two more plaster bandages [23].
5.2 Postreduction Handling
Once the cast is installed, the long boot should be maintained for 3–4 weeks. Then
a short boot should be changed to a short boot for a total of 6–8 weeks. Depending
on the stability of the feature, loading may be initiated by moving to a short boot in
Fig. 1 5-year-old patient who suffers blunt force trauma to the leg. Fracture of the tibia and frac-
ture of the fibula. Orthopedic reduction that evolves with valgus dislocation. It was decided to
perform a lateral opening wedge plaster cast. Final result with good alignment
stable fractures or eventually deferred until a more generous callus is obtained at

around 6 weeks in more unstable fractures. Loading in older patients, able to use
canes, is initiated with progressive partial loading, whereas in younger children who
cannot use canes, it is initiated with the short boot cast. It is also possible in stable
fractures to switch from a long boot cast to a walking boot, which is usually more
comfortable for the patient, allowing skin care and grooming.
5.3 Rehabilitation
Rehabilitation is usually not necessary in healthy younger patients. There are a

small number of patients who benefit from physical therapy. Gait, muscle trophism,
and joint range are restored with the return to activities of daily living.
In older patients and adolescents, targeted physical therapy is necessary for reedu-
cation of gait, joint range, lower extremity strengthening, balance, and equilibrium.
Surgical management will be chosen depending on the age of the patient and the
initial displacement or subsequent displacement to perform an adequate orthopedic
reduction with an appropriate casting technique, especially during the first 3 weeks
of evolution.
There are multiple osteosynthesis to be used, ideally trying to achieve a closed
reduction. Among the surgical techniques, we can use elastic endomedullary nails,
rigid endomedullary nails, plates with traditional or minimally invasive technique,
external fixators in their multiple forms (monolateral, hybrid or circular), Kirschner
wires, or even mixtures of these.
The final choice will depend on the surgeon’s experience, the patient’s age, if the
fracture is open or closed, the fracture comminution and its location.
Strict indications for surgical management are considered to be the concomi-
tance of a compartment syndrome of the leg, the presence of vascular lesions, and
the presence of floating knee or in the context of polytraumatized patients. When we
are faced with open fractures, it is important to first perform an extensive cleaning
and debridement; it should be noted that in recent years good results has been shown
in open fractures treated with cleaning and debridement in the emergency room
through minimal exposure in addition to antibiotic treatment initiated during the
first 3 hours of the fracture [11, 24]. See Fig. 2.
In polytraumatized patients, the systemic compromise and the need for emer-
gency surgery (abdominal, thoracic, cerebral, etc.) should be the first problems to
solve [13]. For open fractures, acute management with surgical cleaning during the
first 24 hours and the early indication of antibiotics according to known protocols
can be accompanied by definitive osteosynthesis with any of the techniques already
Fig. 2 Exposed fracture of the tibia and fibula Gustilo II with oblique feature and comminution
due to run over in an 11-year-old patient. After surgical cleaning, osteosynthesis is performed with
closed reduction of the focus. Final result after removal of the endomedullary nails with good
alignment
mentioned. It is possible to perform treatment with molded casts and cast windows
(in cases of minimal exposures to perform wound care through the cast) for stable
fractures.
The tibia is a long bone that is susceptible to interlocking. The stable elastic
interlocking technique is the most widely used for the management of tibial
diaphyseal fractures in children and was popularized by Metaizeau [25]. The ade-
quate placements of these nails, with prestressing and three-point support, are the
most relevant points for them to be successful and achieve the expected result.
See Fig. 3.
The surgical technique begins with the patient in the supine position, the proxi-
mal physis of the tibia is marked with fluoroscopy, and distal to it an anteromedial
Fig. 3 Fracture of the distal third of the leg associated with fracture of both malleoli in a 14-year-
old patient due to a traffic accident as a passenger. Closed reduction with flexible titanium endo-
medullary nails (TEN) and osteosynthesis of both malleoli were performed
and anterolateral incision is made. Two proximal holes are created as entry points
for the elastic nails. The diameter of each nail should be 40% of the width of the
endomedullary canal, so that 80% of the width of the canal is occupied when two
elastic nails are used. The nails should be prebend in a C shape prior to insertion, in
order to achieve greater cortical contact at the height of the fracture, thus achieving
optimal three-point support. The prebend nails are inserted at the entry points, the
fracture is reduced, into the distal fragment, after the fracture is reduced. They
should be left 1-2 cm proximl to the distal tibial physis. After obtaining an adequate
reduction, the nails are cut proximally, not leaving too short in order to be able to
remove them when the fracture is healed. Finally, postoperative immobilization
with a cast is used.
If the technique is used correctly, it can be used in the great majority of diaphy-
seal fractures, especially if we are faced with simpler and not complex fracture
patterns [26, 27].
The use of rigid endomedullary nails is reserved for adolescents close to skeletal
maturity, being able to use some radiological parameters of the proximal tibia to
consider their use [28]. See Fig. 4.
Fig. 4 15-year-old patient who is kicked during a soccer game. He evolves with a displaced leg
fracture. Due to age it was decided to treat with a solid tibia nail. She evolves with satisfactory
shafts and consolidation
The use of an external fixator is considered in the treatment of open fractures and
in polytraumatized patients due to the rapidity of its installation [29, 30].
Plates, mainly locked, are preferred in very comminuted features, or affecting
very distal or very proximal segments, ideally with minimally invasive techniques
in order to preserve the biology of these fractures [31, 32] (Fig. 5).
6.1 Surgical Treatment of Distal Tibial Fractures
More distal fractures pose a significant surgical challenge, and there are modifica-
tions to the classic technique (Metaizeau) of stable elastic endomedullary nailing,
with the use of divergent nailing [33], nail rolling (placement of nails in the opposite
direction to the initial deformity), or more than two nails [34].
Likewise, it is a segment in which in children older than 12 years, we could use
locked LCP plates with minimally invasive technique or in younger children the use
of crossed Kirchner wires [35].
Fig. 5 Patient 13 years old. Fall from height. Distal metaphyseal fracture of the leg with medial
exposure of 1 cm. Deep and superficial peroneal hypoesthesia associated with pale foot, no capil-
lary refill and no foot pulse. Urgent reduction was performed plus cleaning and osteosynthesis with
LCP plates. It evolves satisfactorily with good axes, adequate consolidation and function
6.2 Postoperative Protocol
Depending on the stability achieved with our osteosynthesis and the type used, we
can perform early weight bearing (from the first weeks). At least three cortices must
be healed to allow full weight bearing [36].
Passive mobility of the ankle and knee can be initiated very early if we achieve
stable osteosynthesis, even from the first postoperative week.
Gait reeducation and more intense exercises under physical therapy supervision
will be performed when an advanced bone callus is achieved. Intense and risky
sports activities should be avoided during the first 6 months postoperatively, espe-
cially in adolescents. Children under 10 years of age will probably not require reha-
bilitation, since the usual demand of children’s games at this age allow patients to
quickly recover their muscular trophism and motor skills.
During the first 4–6 postoperative weeks, clinical and imaging controls should be
performed biweekly to analyze radiological parameters and be alert to loss of reduc-
tion (especially when a stable construct was not achieved surgically).
7 Treatment Complications
We have divided the complications according to the treatment option.

A. Conservative treatment (cast)
(a) Compartment syndrome
(b) Pressure ulcers
(c) Neuropraxias
(d) Joint stiffness
(e) Malunion
I. Angular malalignment
1. Varus-valgus
2. Pro-recurvatum
II. Rotation
III. Length discrepancy
B. Surgical treatment
(a) Compartment syndrome
(b) Infection
(c) Delayed consolidation/nonunion
(d) Symptomatic osteosynthesis
(e) Malunion
I. Angular malalignment
1. Varus-valgus
2. Pro-recurvatum
II. Rotation
III. Length discrepancy
Acute compartment syndrome can have devastating long-term sequelae, so early
diagnosis and a high index of suspicion are relevant; risk factors such as age older
than 14 years, exposed fractures with significant soft tissue involvement, and the use
of endomedullary nailing are described. Increased anxiety and increased analgesia
requirements are relevant symptoms in the pediatric population; the measurement
of intracompartmental pressure is cumbersome in practice, and there are no clear
values in the pediatric population [37, 38].
Emergency fasciotomy is the treatment of choice and can be performed through
two approaches to open the four compartments of the affected leg; the closure of
this fasciotomy can be performed 5–7 days after it is performed if the skin allows
it [39].
Malunions should be detected early in the postoperative period. If a malunion is
detected, the deformity apex should be identified by using appropiate xrays (long
leg xrays) to determine the correction site and surgical method. We must remember
that axial malunions (malrotations) do not remodel with time. The surgeon must
stay alert to this deformity in the postoperative period [3, 27, 40, 41].
Acute and chronic bone and soft tissue infections should be treated aggressively
with surgical cleanings and/or bone resection until infection-free edges are obtained.
In addition, adequate antibiotic treatment (according to bone cultures) with duration
according to the context and under the supervision of a infectious disease specialist
is mandatory. Soft tissue coverage is of utmost importance, so early coverage helps
prevent or treat bone infections [42, 43].
Delayed or non unions are not common in the pediatric population. If they occur,
mechanical and/or biological causes must be identified to address all of them during
treatment [27]. Overgrowth is not as frequent in tibia fractures as in femur fractures,
but it is important to monitor this situation especially in children under 10 years of
age [44].
Osteosynthesis can be symptomatic, proximally with elastic nails, anteriorly at
the knee with rigid nails, and medially at the ankle with distal tibia plates. In these
cases, removal is recommended when complete bone healing is achieved. Hopefully
hardware removal should be performed before 1 year postoperative, since bone
growth can make this removal very difficult if performed after 1 year [40, 45]. This
can be even faster with titanium material.
References
1. Mooney J, Hennrikus W. Fractures of the shaft of the tibia and fibula. In: Flynn JM, Skaggs
DL, Waters PM, editors. Rockwood and Wilkins fractures in children. 8th ed. Philadelphia:
Wolters Kluwer Health; 2014. p. 1874–932.
2. Larsen P, Elsoe R, Hansen SH, Graven-Nielsen T, Laessoe U, Rasmussen S. Incidence and
epidemiology of tibial shaft fractures. Injury. 2015;46(4):746–50. Epub 2015 Jan 16.
3. Raducha JE, Swarup I, Schachne JM, Cruz AI Jr, Fabricant PD. Tibial shaft fractures in chil-
dren and adolescents. JBJS Rev. 2019;7(2):e4. https://doi.org/10.2106/JBJS.RVW.18.00047.
4. Cravino M, Canavese F, De Rosa V, et al. Outcome of displaced distal tibial metaphyseal frac-
tures in children between 6 and 15 years of age treated by elastic stable intramedullary nails.
Eur J Orthop Surg Traumatol. 2014;24(8):1603–8.
5. Mellick LB, Reesor K, Demers D, et al. Tibial fractures of young children. Pediatr Emerg
Care. 1988;4:97–101.
6. Shannak AO. Tibial fractures in children: follow-up study. J Pediatr Orthop. 1988;8:306–10.
7. Cheng JCY, Shen WY. Limb fracture pattern in different pediatric age groups: a study of 3350
children. J Orthop Trauma. 1993;7:15–22.
8. Hansen BA, Greiff S, Bergmann F. Fractures of the tibia in children. Acta Orthop Scand.
1976;47:448–53.
9. Hogue GD, Wilkins KE, Kim IS. Management of pediatric tibial shaft fractures. J Am Acad
Orthop Surg. 2019;27(20):769–78.
10. Pandya NK, Baldwin K, Wolfgruber H, et al. Child abuse and orthopaedic injury patterns:
analysis at a level I pediatric trauma center. J Pediatr Orthop. 2009;29(6):618–25.
11. Nandra RS, Wu F, Gaffey A, Bache CE. The management of open tibial fractures in children: a
retrospective case series of eight years' experience of 61 cases at a paediatric specialist centre.
Bone Joint J. 2017;99-B(4):544–53.
12. Advanced Trauma Life Support for Doctors. ATLS student manual. 8th ed. American College
of Surgeons; 2008. p. 225–57.
13. Kay RM, Skaggs DL. Pediatric polytrauma management. J Pediatr Orthop. 2006;26(2):268–77.
14. Gustilo RB, Anderson JT. Prevention of infection in the treatment of one thousand and twenty-
five open fractures of long bones: retrospective and prospective analyses. J Bone Joint Surg
Am. 1976;58(4):453–8.
15. Volgas DA, Harder Y. Preoperative assessment and classification of soft-tissue injuries. In:
Manual of soft-tissue management in orthopaedic trauma. Stuttgart, New York: Georg Thieme
Verlag; 2011. p. 54–77.
16. Lin JS, Samora JB. Pediatric acute compartment syndrome: a systematic review and meta-
analysis. J Pediatr Orthop B. 2020;29(1):90–6.
17. Sheffer BW, Villarreal ED, Ochsner MG 3rd, Sawyer JR, Spence DD, Kelly DM. Concurrent
ipsilateral tibial shaft and distal tibial fractures in pediatric patients: risk factors, frequency,
and risk of missed diagnosis. J Pediatr Orthop. 2020;40(1):e1–5.
18. Miele V, Di Giampietro I, Ianniello S, Pinto F, Trinci M. Diagnostic imaging in pediatric poly-
trauma management. Radiol Med. 2015;120(1):33–49.
19. Sarmiento A, Sharpe FE, Ebramzadeh E, et al. Factors influencing the outcome of closed tibial
fractures treated with functional bracing. Clin Orthop Relat Res. 1995;315:8–24.
20. Sarmiento A. On the behavior of closed tibial fractures: clinical/radiological correlations. J
Orthop Trauma. 2000;14:199–205.
21. Sarmiento A, Gersten LM, Sobol PA, et al. Tibial shaft fractures treated with functional braces.
Experience with 780 fractures. J Bone Joint Surg Br. 1989;71:602–9.
22. Mashru RP, Herman MJ, Pizzutillo PD. Tibial shaft fractures in children and adolescents. J Am
Acad Orthop Surg. 2005;13:345–52.
23. Böhler L. Verbandlehre für Schwestern, Helfer, Studenten und Ärzte. Wien: Wilhelm
Maudrich; 1943. German.
24. Godfrey J, Choi PD, Shabtai L, Nossov SB, Williams A, Lindberg AW, Silva S, Caird MS,
Schur MD, Arkader A. Management of pediatric Type I open fractures in the emergency
department or operating room: a multicenter perspective. J Pediatr Orthop. 2019;39(7):372–6.
25. Ligier JN, Metaizeau JP, Prévot J. L'embrochage élastique stable à foyer fermé en trauma-
tologie infantile [Closed flexible medullary nailing in pediatric traumatology]. Chir Pediatr.
1983;24(6):383–5.
26. Goodbody CM, Lee RJ, Flynn JM, Sankar WN. Titanium elastic nailing for pediatric tibia
fractures: do older, heavier kids do worse? J Pediatr Orthop. 2016;36(5):472–7.
27. Pennock AT, Bastrom TP, Upasani VV. Elastic intramedullary nailing versus open reduction
internal fixation of pediatric tibial shaft fractures. J Pediatr Orthop. 2017;37(7):e403–8.
28. O'Connor JE, Bogue C, Spence LD, Last J. A method to establish the relationship between
chronological age and stage of union from radiographic assessment of epiphyseal fusion at the
knee: an Irish population study. J Anat. 2008;212(2):198–209.
29. Myers SH, Spiegel D, Flynn JM. External fixation of high-energy tibia fractures. J Pediatr
Orthop. 2007;27(5):537–9.
30. Iobst CA. Hexapod external fixation of tibia fractures in children. J Pediatr Orthop.
2016;36(Suppl 1):S24–8.
31. Özkul E, Gem M, Arslan H, Alemdar C, Azboy I, Arslan SG. Minimally invasive plate osteo-
synthesis in open pediatric tibial fractures. J Pediatr Orthop. 2016;36(4):416–22.
32. Radhakrishna VN, Madhuri V. Management of pediatric open tibia fractures with supracutane-
ous locked plates. J Pediatr Orthop B. 2018;27(1):13–6.
33. Harly E, Angelliaume A, Lalioui A, Pfirrmann C, Harper L, Lefèvre Y. Divergent intramedul-
lary nailing (DIN): a modified intramedullary nailing technique to treat paediatric distal tibial
fractures. J Pediatr Orthop. 2019;39(10):e773–6.
34. Shen K, Cai H, Wang Z, Xu Y. Elastic stable intramedullary nailing for severely displaced
distal tibial fractures in children. Medicine (Baltimore). 2016;95(39):e4980.
35. Brantley J, Majumdar A, Jobe JT, Kallur A, Salas C. A biomechanical comparison of pin
configurations used for percutaneous pinning of distal tibia fractures in children. Iowa Orthop
J. 2016;36:133–7.
36. Jenkins MD, Jones DL, Billings AA, Ackerman ES, France JC, Jones ET. Early weight bearing
after complete tibial shaft fractures in children. J Pediatr Orthop B. 2009;18:341–6.
37. Livingston KS, Glotzbecker MP, Shore BJ. Pediatric acute compartment syndrome. J Am Acad
Orthop Surg. 2017;25(5):358–64.
38. Flynn JM, Bashyal RK, Yeger-McKeever M, Garner MR, Launay F, Sponseller PD. Acute
traumatic compartment syndrome of the leg in children: diagnosis and outcome. J Bone Joint
Surg Am. 2011;93(10):937–41.
39. Herman MJ, Martinek MA, Abzug JM. Complications of tibial eminence and diaphyseal frac-
tures in children: prevention and treatment. J Am Acad Orthop Surg. 2014;22(11):730–41.
40. Gordon JE, Gregush RV, Schoenecker PL, Dobbs MB, Luhmann SJ. Complications after tita-
nium elastic nailing of pediatric tibial fractures. J Pediatr Orthop. 2007;27(4):442–6.
41. Dwyer AJ, John B, Krishen M, Hora R. Remodeling of tibial fractures in children younger than
12 years. Orthopedics. 2007;30:393–6.
42. Glass GE, Pearse M, Nanchahal J. The orthoplastic management of Gustilo grade IIIB frac-
tures of the tibia in children: a systematic review of the literature. Injury. 2009;40(8):876–9.
Epub 2009 May 5.
43. Berkes M, Obremskey WT, Scannell B, Ellington JK, Hymes RA, Bosse M, Southeast Fracture
Consortium. Maintenance of hardware after early postoperative infection following fracture
internal fixation. J Bone Joint Surg Am. 2010;92(4):823–8.
44. Lee SH, Hong JY, Bae JH, Park JW, Park JH. Factors related to leg length discrepancy after
flexible intramedullary nail fixation in pediatric lower-extremity fractures. J Pediatr Orthop
B. 2015;24(3):246–50.
45. Bakhsh WR, Cherney SM, McAndrew CM, Ricci WM, Gardner MJ. Surgical approaches to
intramedullary nailing of the tibia: comparative analysis of knee pain and functional outcomes.
Injury. 2016;47(4):958–61. Epub 2016 Jan 18.
Ankle Transitional Fractures
Matias Sepulveda and Estefania Birrer
1 Introduction
Fractures of the distal tibia constitute the third most frequent site of physeal frac-
tures, approximately 11% of them, with this physis being the most frequently
injured in the lower extremities [1]. The complex growth of the distal tibia predis-
poses the presentation of specific fracture patterns for certain age groups. Thus,
during the last years of development of the distal tibia segment, there are two unique
fracture patterns of adolescence that are called “transitional fractures,” since they
occur during the transition process from adolescence to adulthood. These corre-
spond to intra-articular and transphyseal fractures of the distal tibia. They occur
immediately prior to the end of growth in this segment, usually between 12 and
15 years of age in girls and between 13 and 18 years of age in boys [2]. Two types
of transitional fractures are described: the juvenile Tillaux and the triplanar fracture.
The juvenile Tillaux usually presents as a Salter-Harris III fracture, while the tripla-
nar fracture corresponds to a Salter-Harris III fracture in anterior-posterior view and
Salter-Harris II fracture in lateral view. The pattern of these fractures will be deter-
mined by the size of the physeal closure at the time of injury and the force vectors
M. Sepulveda (*)
AO Foundation, PAEG Expert Group, Davos, Switzerland
E. Birrer

Switzerland AG 2022
352 M. Sepulveda and E. Birrer
associated with the trauma. Proper diagnosis and management of these injuries will
seek to restore joint congruence, reducing the risk of early osteoarthritis.
2 Physiology and Physeal Anatomy
Initially, the distal physis of the tibia is a transverse, linear structure (Fig. 1). As it
develops, ripples begin to appear in the tibia from the age of 12 months. Within the
first year of life, the secondary ossification center appears, with a central presenta-
tion, which is distributed homogeneously until it gives shape to the tibial plafond,
like a wedge toward the lateral face (Fig. 2). Between the ages of 6 and 7 years,
ossification advances toward the medial malleolus, which is completed at the end of
adolescence (Fig. 3) [3]. Both ossification of the distal tibia and its physeal closure
begin from the anteromedial area, progressing toward the posterior and lateral areas
a b
Fig. 1 Anteroposterior (a) and lateral (b) X-ray views of the right ankle of a 1-day-old girl. The
presence of the physis is observed in a horizontal linear fashion. Secondary ossification nucleus
has not yet appeared
Ankle Transitional Fractures 353
a b
Fig. 2 Anteroposterior (a) and lateral (b) X-ray views of the left ankle of a 9-month-old girl. The
secondary ossification nucleus can be seen in the distal tibial epiphysis, central, with a wedge
shape (medial base)
a b c
Fig. 3 Anteroposterior (a), mortise (b), and lateral (c) X-ray views of the left ankle of a 6-year-old
child. The beginning of ossification of the medial malleolus and the presence of a distal tibial
“wavy” physis are visualized
(Fig. 4). The distal fibula physis continues its growth after tibial physis closure.
Prior to the tibial physeal closure, there is a ripple in the distal tibial physis, in the
anteromedial area, called “Poland hump” or “Kump’s hump” (Fig. 5), from where
closure progresses to medial and then to posterior and lateral [4]. This growth pat-
tern has been confirmed by magnetic resonance imaging [5], which shows that phy-
seal closure begins in girls between 11 and 12 years of age and in boys between
a b c d
12 ½ y.o. 13 y.o. 13 ½ y.o. 14 y.o.
Fig. 4 Physeal closure sequence for the distal tibial physis. Starts with the closure of the “Poland
hump” at the anteromedial area (a), from where it progresses to medial (b), then to lateral (c), to
complete the closure (d)
a b c
Fig. 5 Anteroposterior (a), mortise (b), and lateral (c) X-ray views of the right ankle of a 12-year-
old boy, showing the beginning of the physeal closure at the level of the “hump of Poland” (arrow),
and the complete ossification of the medial malleolus
a b c
Fig. 6 Anteroposterior (a), mortise (b), and lateral (c) X-ray views of the left ankle of a 14-year-
old girl. The physiological closure has been completed, achieving the adult ankle anatomy
12 and 13 years of age. The growth given by the distal physis will correspond to
approximately 45% of the length of the tibia [6].
The process of physeal closure can last up to 17 years in girls (average 14 years)
and 20 years in boys (average 16 years), in a process that usually takes 18 months
(Fig. 6) [7]. The distal tibia physis is the first of the lower extremity to close. Given
the long period that elapses during this physeal closure, the distal tibia is susceptible
to this type of fractures [8].
3 Juvenile Tillaux Fracture Pathophysiology
Paul Jules Tillaux (1834–1904) described in a cadaver specimen in 1892 the iso-
lated avulsion of the lateral margin of the distal tibia by means of a forced abduction
mechanism, without mentioning the presence of physis and demonstrating a differ-
ent triangular lateral fragment than that found in adolescents [9]. From this descrip-
tion, the term juvenile Tillaux was born, to refer to the fracture of the distal anterior
tubercle of the tibia in adolescents, without being exactly the same as what is today
known as Juvenile TIllaux. However, Cooper in 1822, was the first to describe the
fracture pattern [10].
This fracture is secondary to a foot abduction and external rotation mechanism
or internal rotation of the tibia with the foot fixed on the ground. In this way the
fibula is moved posteriorly, causing tension of the anterior tibiofibular ligament and
avulsion of the distal anterolateral tibial tubercle, which is susceptible to fracture
because it is narrower in the anteroposterior plane (Fig. 7).
Fig. 7 Juvenile Tillaux

fracture. The square-
shaped fragment
corresponds to the distal
anterior tubercle of the
tibia. With external rotation
of the ankle (or internal
rotation of the tibia with
the foot fixed to the
ground), the fibula moves
posteriorly, pulling the
distal anterior tibial tuber
through the anterior
tibiofibular ligament
Juvenile Tillaux occurs in adolescents when the medial portion of the distal phy-
sis of the tibia has closed but laterally is still open. It usually consists of a Salter-
Harris III type pattern, with a horizontal component through the physis and a vertical
one in the epiphysis, creating a square bone fragment (Fig. 8). In cases closer to the
growth end, a Salter-Harris IV type pattern may occur, with a small lateral triangu-
lar metaphyseal fragment, similar to the adult Tillaux lesion [2].
There are no specific classifications for this type of fracture, since the anatomical
description is enough, and they are usually specified as a group of independent
fractures [11, 12].
a b c
Fig. 8 Computerized tomography (CT) scan of the right ankle of a 15-year-old boy, showing a
juvenile Tillaux. The square-shaped fragment is observed in the axial (a) and coronal (b) views and
the coronal line in the sagittal view (c)
They correspond to 3–5% of all ankle fractures in children [13]. The usual age of
presentation is between 11 and 15 years of age, with an average of 13 years. It
occurs more frequently in girls, in a ratio of 2:1 [2].
4 Triplanar Fracture Pathophysiology
The triplanar fracture occurs in three planes: coronal, transverse, and sagittal. In the
transverse plane, it corresponds to a physeal fracture, in the coronal plane a metaph-
yseal fracture, and in the sagittal plane an epiphyseal fracture [14].
These injuries were described in 1957 by Johnson and Fahl in their classification
of ankle fractures in children [15], while the term “triplanar fracture” was developed
by Lynn in 1972 [16].
The triplanar fracture is secondary to a twisting mechanism of the ankle in which
the “hump of Poland” is present. This hump stabilizes the medial portion of the
physis causing a sagittal fracture at the epiphyseal level, which can be medial (only
some published cases) or lateral to it (most cases). Physeal closure does not need to
be started; nevertheless, the hump (of Poland) must be present.
Its classic presentation consists of an epiphyseal sagittal fracture, lateral to the
“hump of Poland,” accompanied by a posterolateral metaphyseal coronal fracture
line. Both are connected by a transverse fracture through the physis. This would
correspond to a Salter-Harris IV type pattern but is usually described as a Salter-
Harris III pattern in the anteroposterior view and a Salter-Harris II pattern in the
lateral projection (Fig. 9). This pattern is very variable, determining different
a b c
Fig. 9 CT scan of the right ankle of a 12-year-old girl, with a triplanar fracture, showing a metaph-
yseal coronal plane fracture line in the axial view (a), a physeal and sagittal epiphyseal fracture line
in the coronal view (b), and a physeal and coronal metaphyseal fracture line in the sagittal view (c)
a b c d
Fig. 10 A schematic of the main patterns of triplanar fractures with joint involvement: lateral
epiphyseal in two parts (a), lateral epiphyseal in three parts (b), lateral epiphyseal in four parts (c),
medial epiphyseal in three parts (d)
presentations in relation to the epiphyseal fragment [17]: lateral epiphyseal in two

parts, three parts, and in four parts and medial epiphyseal in three parts (Fig. 10).
Extra-articular epiphyseal patterns are also described (Fig. 11), in which the frac-
ture line is directed to the medial malleolus [18] (Fig. 12).
Triplanar fractures correspond to 4–10% of ankle fractures in children and
7–20% of fractures of the distal physis of the tibia [14]. The usual age of
Fig. 11 Schematic of an
extra-articular triplanar
fracture presentation
pattern
presentation in girls is 11–12 years and in boys 13–14 years. This age corre-
sponds to the beginning of pubertal growth spurt and the beginning of the distal
tibial physis closure. The younger the patient, the more medial the epiphyseal
fracture line.
a b c
Fig. 12 CT scan of the left ankle of a 13-year-old girl with an extra-articular triplanar fracture.
The sagittal fracture line involving the medial malleolus is seen in the axial (a) and coronal (b)
views. The sagittal view (c) shows the metaphyseal-physeal fracture line
5 Diagnosis
For the diagnosis of transitional fractures, we must have the suspicion of this type
of injury in adolescent patients, when the injury mechanism is present.
In the juvenile Tillaux type, a moderate extremity edema will appear in the
anterolateral ankle, with pain on compression and dorsiflexion limitation. The phys-
ical examination of a triplanar fracture will be variable, depending on the mecha-
nism and force of the traumatic injury. In high-energy injuries, the presence of soft
tissue involvement can be found, including a compartment syndrome [13].
The study with simple X-ray should include the anteroposterior, mortise, and
lateral projections [13]. In these projections, a widening of the medial clear space
can be seen in 86% of cases, depending on the separation of the fracture segments
[19], as well as a widening of the affected physis (Fig. 13).
In the juvenile Tillaux, the lateral projection may show an incongruity in the
anterior aspect of the distal tibia, or even no alteration at all. The mortise projection
is essential in order to see the juvenile Tillaux lesions that are occasionally hidden
behind the fibula in the anteroposterior (AP) view [8]. In the AP projection, a verti-
cal fracture line from the physis to the joint will be evident in most cases (Fig. 14).
The fracture location will depend on the amount of medial physeal closure that
a b c
Fig. 13 X-ray views of the right ankle of a 12-year-old girl, with a juvenile Tillaux. The fracture
line is evident in the anteroposterior (a) and mortise (b) views. In the lateral view (c), a subtle
incongruence is observed on the anterior aspect of the distal tibia
a b c
Fig. 14 X-ray views of the left ankle of a 14-year-old boy, with a juvenile Tillaux. The fracture
line is subtle in the anteroposterior view (a) but is more clearly seen in the mortise view (b). No
evidence of a fracture in the lateral plane (c) due to slight displacement
a b c
Fig. 15 X-ray views of the right ankle of a 13-year-old boy with a triplanar fracture (blue dotted
line). In the anteroposterior view (a), the metaphyseal fracture is evident as a “Gothic arch.” In the
mortise view (b) the epiphyseal fragment is observed. In the lateral view (c), the metaphyseal
feature is more clearly seen
occurred at the time of the injury. The greater the closure, the more lateral the loca-
tion of the fracture line. Usually the study with simple X-rays is enough to evaluate
these injuries, detecting lesions greater than 1 mm; however, their displacement can
be better evaluated with computed tomography (CT) [20].
For triplanar fractures, the three fracture lines can be seen in the AP view, if the
displacement of the fragments is significant. The epiphyseal sagittal line can be
intra-articular or deviated to the medial malleolus as an extra-articular fracture [21,
22]. The coronal metaphyseal line can be evidenced as a “Gothic arch” in this
image. Occasionally the sagittal fracture line is oblique, being better evaluated in
the mortise projection. In the lateral projection we can better visualize the coronal
metaphyseal line and see if it reaches the joint, which would condition a fracture in
three parts (Fig. 15).
The study with CT is recommended for all triplanar fractures diagnosis and treat-
ment planning, especially to precisely analyze the axial plane [14, 23]. A classic
description of this axial view is a three-pointed star sign, “Mercedes-Benz sign”
(Fig. 16). Computed tomography allows to specify the number and size of frag-
ments and their displacement and to plan the appropriate treatment [24, 25]. CT
assessment influences the surgical indication [26]. The use of magnetic resonance
imaging has been described to support the diagnosis and characterization of these
lesions; however, the higher cost, dubious value in treatment, and time of acquisi-
tion limit its use [13, 14].
a b c
Fig. 16 CT scan of the left ankle of a 14-year-old boy. The “Mercedes-Benz” sign can be seen on
the axial view (a). He has a triplanar fracture in three parts, with an intra-articular fracture line
visible in the coronal (b) and sagittal (c) views
6 Treatment
The main goal of treatment is the restoration of joint congruence in order to pre-
serve the functionality of the ankle joint.
The patient presenting with a transitional ankle fracture will be at the beginning
of the physeal closure, so the risk of growth arrest secondary to physeal damage is
minimal, especially in the case of a juvenile Tillaux. Most authors define a joint line
displacement of up to 2 mm as acceptable [18] and can be treated conservatively,
i.e., non-weight-bearing in a walking boot for 4 weeks followed with progressive
weight-bearing for 2–4 weeks. Displacements greater than 2 mm are not consistent
with good long-term results [27], associated with arthritic changes, usually asymp-
tomatic, between 6 and 9 years after the injury [28]. Conservative treatment can also
be performed on extra-articular triplanar fractures with small displacement [14],
with excellent results (Fig. 17).
If the fracture is a juvenile Tillaux with a displacement greater than 2 mm, it is
necessary to reduce and stabilize this fragment. This is achieved by internal rotation
of the foot. If the reduction is achieved, verified in a mortise image, definitive stabi-
lization can be carried out with a cannulated compressive screw, through a percuta-
neous approach. If reduction is not achieved, an ankle arthroscopy or an anterolateral
approach should be performed to allow adequate visualization of the joint surface
(Fig. 18). During the surgical approach, the joint capsule must be minimally opened
a b c
Fig. 17 Radiological images of the right ankle of a 13-year-old girl with a triplanar fracture.
Initial X-ray AP view (a) demonstrates the intra-articular fracture line. CT scan of the ankle (b)
confirms a triplanar fracture, displaced less than 2 mm. Conservative treatment is decided.
Radiographic control at 3 months shows bone healing without joint gap (c)
a b c
Fig. 18 Radiological images of the right ankle of a 14-year-old girl. Anteroposterior and lateral
X-ray views (a) demonstrate a displaced juvenile Tillaux. CT scan (b) shows significant articular
compromise. Surgical management is performed by open reduction and stabilization with cannu-
lated screw (c)
avoiding injuring the tibiofibular ligament. Interposition of tissue or periosteum is

rare, since in this type of fracture the metaphysis is usually not affected. Once frac-
ture anatomic reduction has been achieved, it is stabilized with a compression screw.
The decision on surgical treatment should in the first week, given that healing pro-
cess will be advanced by 7–10 days [13].
In the case of triplanar fractures, adequate understanding of the number and size
of the bone fragments, the direction of the fracture lines, and their displacement is
required for treatment decision and planning. We recommend the evaluation with
CT for all triplanar fractures. Surgical management is usually indicated for fractures
with more than 2 mm of articular line displacement. Some authors recommend a
stricter limit of 1 mm. In addition, it is fundamental to evaluate the congruence of
the syndesmosis that could be unstable if there is an associated fibular fracture,
which occurs in approximately 50% of cases [29]. Significant displacements of the
fibula or shortenings greater than 2 mm should be reduced and anatomically stabi-
lized [30]. Some authors recommend surgical treatment only after the reduction
maneuver has been performed (under sedation or general anesthesia) [31], broaden-
ing the indication for conservative treatment if adequate reduction of the fragments
is achieved.
If surgical treatment is decided for a triplanar fracture, the goal of therapy will be
an anatomic reduction of all articular fracture lines. Extra-articular fractures do not
require anatomical reduction [32]. The reduction maneuver is performed starting
with sustained traction of the foot in plantar flexion and internal rotation for lateral
fractures or external rotation for medial fractures. Afterward, anterior translation
and maximum dorsiflexion of the ankle should be performed [14]. If the reduction
is achieved in a closed manner with this maneuver, the stabilization of the fragments
can be done with percutaneous compression screws (Fig. 19). If open reduction is to
be considered, the surgical approach will depend on multiple considerations, includ-
ing the fracture pattern and the soft tissue condition [1]. Typically, medially dis-
placed triplanar fractures will be approached anteromedially, while laterally
displaced fractures are approached anterolaterally [14]. To achieve adequate joint
a b c
Fig. 19 Radiological images of the right ankle of a 13-year-old child. Anteroposterior and lateral
X-ray views (a) demonstrate a triplanar, with Gothic arch sign and joint involvement. CT scan (b)
shows a joint step greater than 2 mm. Surgical treatment is performed by closed reduction and
percutaneous fixation with screws (c)
congruence, reduction of the anterolateral fragments should be carried out first, fol-
lowed by the posteromedial fragments. There are no long-term differences in sec-
ondary joint deformities between open fixation treatment and percutaneous
fixation [33].
Using ankle arthroscopy for fracture visualization and reduction has been
described with good results [14, 34]. This technique limits the aggressiveness of the
approach and the soft tissue injury, obtaining a direct visualization of the joint.
However, it is a technique that requires a learning curve in order to obtain its maxi-
mum benefit.
Postoperative period consists of non-weight-bearing in a removable walking
boot for 3–4 weeks, followed by rehabilitation therapy for 3–6 weeks. Return to
sport is indicated at 9–12 weeks.
7 Complications
In juvenile Tillaux there are no complications related to growth alterations, angular

deformities, or avascular necrosis of bone. Residual joint incongruence can lead to
joint stiffness, pain, and early onset osteoarthritis and should therefore be avoided
[19, 35]. Occasionally, there may be discomfort associated with symptomatic osteo-
synthesis. If osteosynthesis is to be removed, it should be done early since implants
that remain in the area for more than a year are difficult to remove [36]. As for tri-
planar fractures, their prognosis will be determined by the age of presentation, the
type of injury, and the treatment performed. The earlier the presentation, the more
likely it is that there will be growth alterations due to physeal damage. A compart-
ment syndrome should be sought directly both preoperatively and postoperatively
[37]. Without doubt the most frequent complication of triplanar fractures is persis-
tent pain, due to edema and degenerative changes, which have been described in up
to one out of three cases, associated with a noncongruent reduction of the joint
surface [1, 29]. For this reason, anatomic reduction of these fractures is of para-
mount importance.
8 Summary
Transitional fractures are common traumatic injuries to the ankle in adolescents at

the end of growth, usually between 12 to 15 years in girls and 13 to 18 years in boys.
Given its characteristics, they require an early diagnosis, adequate radiological
study including the use of computerized tomography in triplanar fractures, and sur-
gical treatment for joint defects greater than 2 mm. An anatomic reduction is
required to obtain good clinical results.
References
1. Peterson HA. Chapter 11: Distal tibia. In: Peterson HA, editor. Epiphyseal growth plate frac-
tures. Berlín Heidelberg: Springer; 2007. p. 273–388.
2. Olgun ZD, Maestre S. Management of pediatric ankle fractures. Curr Rev Musculoskelet Med.
2018;11:475–84.
3. Ogden JA, McCarthy SM. Radiology of postnatal skeletal development VIII. Distal tibia and
fibula. Skelet Radiol. 1983;10:209–20.
4. Mac Nealy GA, Rogers LF, Hernandez R, Poznanski AK. Injuries of the distal tibial epiphysis:
systematic radiograph evaluation. AJR Am J Rad Roentgenol. 1982;138:683–9.
5. Chung T, Jaramillo D. Normal maturing distal tibia and fibula: changes with age at MR imag-
ing. Radiology. 1995;194:227–32.
6. Birch JG. Growth and development. In: Herring J, Tachdjian MO, editors. Tachdjian’s pediat-
ric orthopaedics. 4th ed. Philadelphia: Saunders; 2008. p. 3–22.
7. Hansman CF. Appearance and fusion of ossification centers in the human skeleton. Am J
Roentgenol. 1962;88:476–82.
8. Mosca VS. Techniques of operative reduction and fixation of triplane and juvenile Tillaux
fractures in adolescents. Oper Tech Orthop. 1995;5:171–7.
9. Tillaux P. Traité d’Anatomie Topographique avec Applications à la Chirurgie, 7th edn [French].
Paris: Asselin et Houzeau; 1892.
10. Ogden JA. Chapter 23: Tibia and fibula. In: Ogden JA, editor. Skeletal injury in the child. 3rd
ed. Nueva York: Springer-Verlag; 2001. p. 990–1090.
11. Dias LS, Giegerich CR. Fractures of the distal tibial epiphysis in adolescence. J Bone Joint
Surg. 1983;65A:438–44.
12. Tachdjian MO. Fractures and dislocations. In: Pediatric orthopaedics. 2nd ed. Philadelphia:
WB Saunders; 1990. p. 3013–373.
13. Wuerz TH, Gurd DP. Pediatric physeal ankle fracture. J Am Acad Orthop Surg.
2013;21(4):234–44.
14. Schnetzler KA, Hoernschemeyer D. The pediatric triplane ankle fracture. J Am Acad Orthop
Surg. 2007;15(12):738–47.
15. Johnson EW Jr, Fahl JC. Fractures involving the distal epiphysis of the tibia and fibula in chil-
dren. Am J Surg. 1957;93:778–81.
16. Lynn MD. The triplane distal tibial epiphyseal fracture. Clin Orthop. 1972;86:187–90.
17. Hadad M, Sullivan B, Sponseller P. Surgically relevant patterns in triplane fractures. A map-
ping study. J Bone Joint Surg Am. 2018;100:1039–46.
18. Shea K, Frick S. Chapter 32: Ankle fractures. In: Flynn J, Skaggs D, Waters P, editors.
Rockwood and Wilkins’ fractures in children. 8th ed. Philadelphia: Wolters Kluwer Health;
2015. p. 1173–224.
19. Gourineni P, Gupta A. Medial joint space widening of the ankle in displaced tillaux and tri-
plane fractures in children. J Orthop Trauma. 2011;25:608–11.
20. Horn BD, Crisci K, Krug M, Pizzutillo PD, MacEwen GD. Radiographic evaluation of juve-
nile Tillaux fractures of the distal tibia. J Pediatr Orthop. 2001;21:162–4.
21. Feldman DS, Otsuka NY, Hedden DM. Extra-articular triplane fracture of the distal tibial
epiphysis. J Pediatr Orthop. 1995;15(4):479–81.
22. Denton JR, Fischer SJ. The medial triplane fracture: report of an unusual injury. J Trauma.
1981;21:991–5.
23. Schneidmueller D, Sander A, Wertenbroek M, Wutzler S, Kraus R, Marzi I, Laurer H. Triplane
fractures: do we need cross-sectional imaging? Eur J Trauma Emerg Surg. 2014;40:37–43.
24. Eismann E, Stephan Z, Mehlman C, Denning J, Mehlman T, Parikh S, Tamai J, Zbojniewicz
A. Pediatric triplane ankle fractures: impact of radiographs and computed tomography on frac-
ture classification and treatment planning. J Bone Joint Surg Am. 2015;97:995–1002.
25. Kim JR, Song KH, Song KJ, Lee HS. Treatment outcomes of triplane and tillaux fractures of
the ankle in adolescence. Clin Orthop Surg. 2010;2:34–8.
26. Liporace FA, Yoon RS, Kubiak EN. Does adding computed tomography change the diagnosis
and treatment of Tillaux and triplane pediatric ankle fractures? Orthopedics. 2012;35:e208–12.
27. Rapariz JM, Ocete G, Gonzalez-Herranz P, et al. Distal tibial triplane fractures: long-term
follow-up. J Pediatr Orthop. 1996;16:113–8.
28. Crawford A. Triplane and tillaux fractures: is a 2 mm residual gap acceptable? J Pediatr
Orthop. 2012;32:S69–73.
29. Ertl JP, Barrack RL, Alexander AH, VanBuecken K. Triplane fracture of the distal tibial epiph-
ysis: long-term follow-up. J Bone Joint Surg Am. 1988;70:967–76.
30. Thordarson DB, Motamed S, Hedman T, et al. The effect of fibular malreduction on contact
pressures in an ankle fracture malunion model. J Bone Joint Surg Am. 1997;79:1809–15.
31. Manderson EL, Ollivierre CO. Closed anatomic reduction of a juvenile Tillaux fracture by
dorsiflexion of the ankle. A case report. Clin Orthop Relat Res. 1992;276:262–6.
32. Tan ACB, Chong R, Mahadev A. Triplane fractures of the distal tibia in children. J Orthop
Surg. 2013;21(1):55–9.
33. Zelentya W, Yoonb RS, Shabtaid L, Choid P, Martine B, Hornf D, Feldmang DS, Otsukac
NY, Godfrieda DH. Percutaneous versus open reduction and fixation for Tillaux and triplane
fractures: a multicenter cohort comparison study. J Pediatr Orthop B. 2018;27:551–5.
34. McGillion S, Jackson M, Lahoti O. Arthroscopically assisted percutaneous fixation of triplane
fracture of the distal tibia. J Pediatr Orthop B. 2007;16:313–6.
35. Landln L, Danlelsson L, Jonsson K, Pettersson H. Late results in 65 physeal ankle fractures.
Acta Orthop Scand. 1986;57:530–4.
36. Peterson HA. Metallic implant removal in children. J Pediatr Orthop. 2005;25(1):107–15.
37. Patel S, Haddad F. Triplane fractures of the ankle. Br J Hosp Med. 2009;70(1):34–40.
Part III
Adult Orthopaedics: Forefoot
Hallux Valgus
Pablo Wagner Hitschfeld and Emilio Wagner Hitschfeld
1 Introduction
The hallux valgus (HV) or bunion is the valgus deviation of the great toe and a
medial deviation of the first metatarsal. This toe deviation is often associated with
pronation (internal rotation) of the first metatarsal [1]. This deformity is usually
progressive, evolving into a metatarsophalangeal subluxation. Occasionally, due to
the lateral pressure exerted by the hallux, secondary pathologies develop in lesser
toes and the sole of the foot. Among these are claw and mallet toes, metatarsalgia
(plantar pain in the head of the metatarsals), synovitis, and intermetatarsal
neuropathies.
About 90% of the patients are female, who have been carrying the deformity for a
long time and request medical evaluation when it begins to limit their daily functional
activity. A prevalence of 20–30% of hallux valgus is described [2, 3]. Historically, in
the nineteenth century, it was part of the general knowledge that bunions were pro-
duced by increased volume of soft tissue or bone [4]. Clinically, it manifests itself
with medial pain over the head of the first metatarsal as this area becomes more
prominent due to the valgus deviation of the great toe. The skin becomes erythema-
tous and sensitive due to the constant pressure that footwear exerts on it, and ulcers
may form. High-heel shoes are the ones that generate more pressure on the area of the
first metatarsophalangeal joint. This is why most patients with symptomatic hallux
valgus are women. The ratio of women to men is estimated at 3:1 [3].
P. Wagner Hitschfeld (*)

E. Wagner Hitschfeld
Orthopedic Surgery Department Clínica Alemana de Santiago - Universidad del Desarrollo,

Switzerland AG 2022
372 P. Wagner Hitschfeld and E. Wagner Hitschfeld
2 Normal Anatomy
Anatomy is fundamental to understand the elements involved in the deformity.

Regarding bones, the first metatarsal articulates with the base of the proximal pha-
lanx and proximally with the medial cuneiform (Figs. 1, 2, and 3). The metatarsal
head rests on two bones, medial and lateral sesamoids. These articulate with the
metatarsal head on two sesamoid facets that are separated from each other by the
Fig. 1 Diagram of
periarticular
a
metatarsosesamoid
ligaments: coronal cut. (a)
Non pronated metatarsal.
(b) Pronated first
metatarsal. 1. Second
metatarsal. 2.
Intermetatarsal ligament. 3.
Metatarsosesamoid
ligament. 4. Extensor
hallucis longus tendon. 5.
Flexor hallucis longus
tendon. 6. Medial
sesamoid. 7. First
metatarsal intersesamoid b
crista. 8. Intersesamoid
ligament. 9. Metatarsal
sesamoid facet. 10. Flexor
hallucis brevis medial head
(insertion in medial
sesamoid)
Fig. 2 Diagram of first

metatarsophalangeal
ligaments: sagittal cut. 1.
Extensor hallucis longus
tendon. 2. First metatarsal.
3. Flexor hallucis longus
tendon. 4.
Metatarsosesamoid
ligament. 5. Collateral
ligament. 6. Sesamoid. 7.
Extensor hood. 8. Proximal
phalanx. 9. Distal phalanx
Hallux Valgus 373
Fig. 3 Diagram of first

metatarsophalangeal soft
tissues: axial cut. 1.
Adductor hallucis tendon.
2. Adductor hallucis
oblique head. 3. Adductor
hallucis transverse head. 4.
Abductor hallucis tendon.
5. Flexor hallucis brevis
tendons inserting in
sesamoids. 6. Medial
sesamoid. 7. First
metatarsal. 8. Proximal
phalanx
intersesamoid crest or “crista.” The sesamoid bones can be bipartite in 20–30% of

cases. One or both may be congenitally absent. The sesamoids have various func-
tions, including flexor hallucis longus (FHL) tendon protection from weight load,
lever arm increase for flexor muscles (flexor hallucis brevis tendons), and load-
bearing surface (load up to 50% body weight and up to 300% body weight during
impulse), among others [5–8] (Fig. 1).
Regarding soft tissues surrounding the hallux metatarsophalangeal (MTP) joint,
multiple ligaments and tendon structures are present. Beginning with plantar struc-
tures, besides being weight-bearing loading bones, the sesamoids are accessory
ossicles in the path of the short flexor muscle tendons of the hallux (flexor hallucis
brevis, FHB). The FHB has a distal plantar insertion into the hallux proximal pha-
lanx. The flexor hallucis longus (FHL) tendon runs between the FHB tendons and
the respective sesamoids. The FHL inserts at the distal phalanx of the hallux. The
FHL is contained in a ligament sheath protected by the sesamoids. The adductor
hallucis muscle has two heads, the oblique and the transversal head. They are
inserted distally into the lateral sesamoid bone and in the lateral corner of the proxi-
mal phalanx. The hallux abductor muscle, on the other hand, is inserted medially
into the medial corner of the hallux proximal phalanx. It is the adductor antagonist.
Finally, the extensor hallucis brevis (EHB) and extensor hallucis longus (EHL) are
inserted dorsally at the toe. The EHB runs laterally to the EHL and inserts into the
dorsum of the proximal phalanx. The EHL is inserted into the dorsum of the distal
phalanx of the hallux. The EHL and EHB are kept centered and attached to the
proximal phalanx and distal metatarsal by the extensor hood. This sheath has both
medial and lateral insertions at the proximal phalanx and first metatarsal, as well as
metatarsophalangeal capsular insertions (Fig. 1).
The ligaments surrounding the metatarsophalangeal joint are multiple. Among
the most important are the medial and lateral metatarsophalangeal collateral liga-
ments, the suspensory or metatarsosesamoid, intersesamoid, intermetatarsal, and
sesamoid-phalangeal ligaments. These determine, together with the sesamoid bones
and flexor tendons, a “hammock” (e.g., plantar plate) or hanging surface that par-
ticipates in the stability and load capacity of the metatarsophalangeal joint [5–8]
(Fig. 2).
Irrigation of the first metatarsal originates from a nourishing artery that enters at
the lateral diaphysis of the metatarsal at the junction of the distal third and the two
proximal thirds. This artery divides endomedullary into a short distal branch and a
long proximal branch. The short distal branch anastomoses with short epiphyseal
vessels. This artery is at risk when performing a distal Chevron osteotomy eventu-
ally causing avascular necrosis of the metatarsal head, if the anastomosis of this
branch is insufficient. The proximal branch has an extensive anastomosis with a
large network of proximal epiphyseal vessels [8, 9] (Figs. 1, 2, and 3).
3 Etiology: Physiopathology
Identifying the cause of HV has not been without controversy. Multiple theories
have been postulated, but none has been unanimously accepted by the medical com-
munity. Among the intrinsic causes that would explain its development can be men-
tioned: cuneometatarsal instability, medial column malrotation with the consequent
metatarsophalangeal instability, and sesamoid complex malalignment causing devi-
ation of the hallux, insufficiency of the metatarsophalangeal ligament complex,
muscular imbalance around the hallux including long and short flexors and long and
short extensors of the hallux, and instability of the entire medial column, among
others [10, 11]. Genetics plays a clear role in HV, although an exact cause has not
yet been found. A prevalence of HV of up to 94% has been described in mothers of
children with HV [12]. There is no doubt that the most important extrinsic factor in
HV is the use of narrow shoes [13]. This became evident after World War II when
the incidence of HV in Japanese women increased as they began to wear pointed
and heeled shoes [14].
Hallux Valgus 375
There are important anatomical considerations in hallux valgus that determine

the occurrence of the deformity. Already mentioned and described in detail in Roger
Mann’s 1987 book Surgery of the Foot [7], they have shown validity over time in
subsequent studies. The shape of the metatarsophalangeal joint is one of them. The
square shape has less risk of hallux valgus than the rounded shape [15]. As previ-
ously mentioned, the initial trigger of the deformity is under discussion; however, a
combined instability of the medial foot column appears to be the most likely cause
for progressive deformity of the first metatarsal [11]. As the varus deviation of the
metatarsal progresses, the first metatarsal pronates, and the hallux deviates into val-
gus. The most likely theory of this process starts as follows: due to the strong liga-
mentous attachment of the sesamoid complex to the second metatarsal and the base
of the proximal phalanx of the hallux, a varus deviation of the first metatarsal does
not change the sesamoid complex position. The stability of the plantar plate is fur-
ther enhanced by the musculature of the adductor hallucis which functions as a
post-anchoring the sesamoids and proximal phalanx to the lesser metatarsals. The
sesamoid-plantar plate is attached to the metatarsal sesamoid facets through its
metatarsosesamoid ligaments, which attach at the plantar surface of the metatarsal.
Due to the strong attachment between the sesamoid-plantar plate and the rest of the
forefoot, a varus deviation of the first metatarsal derives in an inevitable pronation
of the metatarsal, given that its plantar half is fixed to the plantar plate, but not the
dorsal half. This rotational motion occurs not only in the metatarsal but also in the
medial cuneiform [10, 11] (pronation of the entire medial column). The tarsometa-
tarsal joint does not demonstrate rotational instability in the majority of hallux val-
gus patients (except in severe, advanced cases or patients with collagen disease).
The metatarsal continues to medialize and pronate as the severity of the deformity
increases. The rotational deformity is a factor that further contributes to a rapid
worsening of the bunion. Due to the progressive varus and rotation of the medial
column, the flexor tendons (FHB and FHL) trajectory is lateral to the center of the
metatarsal head; hence, the action of these muscles increases the valgus vector of
the great toe or the so-called dynamic deforming force [7, 16–18]. This progres-
sively positions the phalanx into more valgus and thus worsens the vicious circle of
hallux valgus deformity. This is why it is said that the muscles play a predominant
role in the progression of the deformity. In conclusion, not only the skeletal align-
ment should be considered of great importance when treating this pathology but
also the dynamic stability (Fig. 1).
There is a moment when the plantar plate and the suspensory ligaments loose
adhesion to the metatarsal. This is manifested by a real dislocation of the sesamoids
and plantar plate of the metatarsal, even with erosion or even total loss of the inters-
esamoid crest, with loss of the articular relationship of the sesamoid facets with the
sesamoids [1, 19]. When the metatarsosesamoid congruency is lost, the lateral teth-
ering effect the plantar plate has over the metatarsal is lost too, and a decrease in
pronation and an increase in metatarsal varus can be observed. Sometimes even a
complete correction of the pronation deformity can occur, with a concurrent increase
in metatarsal varization. The latter would occur because there is no longer a fixation
of the metatarsal to the lateral ligament structures. By dislocating the plantar plate
off the sesamoid facets, a significant relief can be observed from the pain coming
from pronation and metatarsosesamoid arthritis [19]. This is evident in patients
when they report that bunion pain has suddenly subsided, even though the deformity
increased considerably.
Hallux valgus has other consequences from a mechanical point of view. The hal-
lux itself is frequently pronated (internal rotation) as well. A keratosis will often be
observed at the plantar medial side of the hallux at the interphalangeal joint level.
This is secondary to the medial ray pronation. Inefficient flexion (secondary to a
rotated toe), valgus, and pronation of the hallux lead to an altered gait. This, together
with the insufficient medial column and the imbalance of the flexor-extensor mus-
cles, produces a relative increase in the load and impact on the lesser metatarsals
(which could end up in transfer metatarsalgia). Also, the hallux valgus will cause a
lateral deviation of the lesser toes, contributing even more, to the lesser MTP joints
instability. These mechanical consequences will be dealt with in the chapter on
metatarsalgia.
History and physical examination: It is important to find out the patient’s occupa-
tion, since this changes and determines to a great extent the treatment that will be
recommended. Frequently, patients need to be on their feet all day at work, wear
pointed and high-heel shoes, and walk constantly, among others. This must be eval-
uated very well before considering therapeutic options. Usually, the patient has not
fully perceived the limitations caused by HV, because the symptomatology is very
insidious and not disabling. Common limitations found in the patient’s history
include stopping to wear shoes of his own choice, avoiding certain social activities,
and stopping certain sports to avoid pain in the affected foot. Some people say that
the pain is not disabling, being their main reason for consulting that they are
ashamed of their feet. They say that they hide them when they are in public or at the
beach. As the reader can see, it can be a painful pathology, not only from a physio-
logical point of view but also from a psychological one.
The physical examination is a determining factor in the type of treatment the
patient will need. The most obvious is the medial protrusion at the level of the first
metatarsal head; however, it is probably the least important. Among other aspects,
flexibility of the hallux in flexoextension and the presence of pain in the midrange
of movement, both of which are important in order to rule out associated osteoar-
thritis, should be ascertained. The presence of metatarsalgia (2–5 MTP) (whether or
not associated with plantar keratosis, “corns”), pain and/or deformity of the lesser
toes (claw or mallet deformity), pain and deformity of the foot attributable to a flat
foot, or a short gastrocnemius-soleous complex should also be evaluated during
physical examination. We refer readers to the corresponding chapters on metatarsal-
gia or lesser toe deformities for further study regarding these pathologies.
Hallux Valgus 377
5 Diagnostic Imaging
Standing X-ray is the most widely used diagnosis method worldwide. It is essential
to measure the deformity in order to plan the best treatment. Lateral projection
X-rays are useful to detect any evidence of osteoarthritis or instability (step or
asymmetry) at the tarsometatarsal joint (TMT) that might change the surgical plan.
The standard sesamoid axial projection is not performed under load and does not
represent the physiological position of the components of the MTP joint [20].
Weight-bearing axial sesamoid view [17, 21, 22] is not comfortable for the patient
as it includes dorsiflexion of the toes in addition to an ankle equinus. In this projec-
tion it is possible to see the sesamoid-metatarsal relationship, evaluating whether
there is a dislocation of the sesamoids from their facets or a pronation of the meta-
tarsal with sesamoids still congruent [17, 21, 22]. The image obtained with weight-
bearing computerized tomography (WBCT) is the option that will provide the most
detail regarding the metatarsal varus, pronation of the medial column, degree of
existing arthrosis, the sesamoid-metatarsal congruence, and the metatarsophalan-
geal deviation, among others. The problem with WBCT is its poor availability
worldwide. There are still no published studies analyzing if the additional informa-
tion provided by the WBCT changes the treatment plan.
The most commonly used measurements or angles to quantify the deformity are
the following: intermetatarsal (IMA), metatarsophalangeal (MTF) [23], angle to be
corrected [24], sesamoid position [25], distal articular metatarsal angle (DMAA)
[26], and metatarsal pronation three-level estimation [27]. These angles are mea-
sured with the AP foot weight-bearing view (Figs. 3 and 4). For the IMA, the angle
between two lines drawn along the diaphysis of the first and second metatarsal is
measured, with normal values up to 9 degrees [23]. The metatarsophalangeal angle
is measured between the diaphyseal line representing the axis of the first metatarsal
and the line forming the axis of the proximal phalanx, with a normal value of up to
15 degrees. The authors recommend measuring this last angle between the first
metatarsal axis and a line drawn between the base of the proximal phalanx and the
tip of the distal phalanx. This line represents more precisely the alignment of the
entire hallux which is what should be corrected. The angle to be corrected [24] is
measured between a line that begins at the base of the first metatarsal and ends in
the midpoint between the sesamoids and another along the axis of the first metatar-
sal. This angle is based on the fact that the sesamoids do not change their position,
and it is the metatarsal that deviates in varus and moves away from its original posi-
tion. It has the limitation that the plantar plate with its sesamoids does undergo some
pronation, so that they can overlap in an AP X-ray, not being possible to draw the
aforementioned line. The sesamoid position [25] was separated into seven levels
according to Hardy and Clapham and evaluates the position of the medial sesamoid
with respect to the metatarsal axis in a standing AP X-ray. This classification cannot
assess whether the sesamoids are dislocated or only congruent but pronated along
with the metatarsal, although it is an aid in assessing the deformity severity [17, 25].
Fig. 4 Diagram of main

hallux valgus angle to be
measured. 1. Hallux valgus
angle (HVA): drawn
between a first metatarsal
line (mid-diaphysis) and a
great toe line (mid
proximal phalanx to mid
distal phalanx). 2. Distal
metatarsal articular angle
(DMAA): drawn between a
line along the first
metatarsal diaphysis and a
perpendicular to the distal
first metatarsal articular
surface. 3. Intermetatarsal
angle (IMA): drawn
between a first metatarsal
line (mid-diaphysis) and a
second metatarsal line
(mid-diaphysis)
The sesamoid position is one of the factors associated with relapse of an operated
bunion (factors to be treated later), so it is a valuable observation.
In a weight-bearing foot AP X-ray, it is also possible to estimate the pronation of
the medial column. This is done by analyzing the shape of the lateral contour of the
metatarsal head [27] (Fig. 5). The head takes on a progressively more rounded shape
as it pronates (external rotation). A mild pronation (<20 degrees), is manifested by
a rather “flat” or “square” lateral contour, where a mildly rounded contour proximal
Hallux Valgus 379
Fig. 5 First ray internal rotation stagesMild: shows a lateral metatarsal head shape that is angled
laterally at the joint edge (arrow). It has a round contour proximal to the joint lateral edge. This
shape can be seen when 10–20° of metatarsal pronation is present (measured with weight-bearing
computerized tomography, WBCT)Intermediate: shows a lateral metatarsal head shape that has no
angle or edge) but is completely round. It has a different curvature radius than the distal metatarsal
joint. This shape can be seen when 20–30° of metatarsal pronation is present (measured with
WBCT)Severe shows a lateral metatarsal head shape that is round. It has no difference in curvature
radius comparing it with the distal metatarsal joint shape. This shape can be seen when more than
30° of metatarsal pronation is present (measured with WBCT)Stage 0 (not shown in diagram)
shows a straight-flat lateral head contour. This shape can be seen when less than 10° of metatarsal
pronation is present (measured with WBCT). Please check Fig. 9
to the MTP lateral corner can be found. This rounded ridge appears proximal to the
metatarsophalangeal joint corner, corresponding anatomically to the lateral edge of
the lateral metatarsal condyle [19, 27, 28]. A moderate pronation (20–30 degrees) is
visible in the standing AP X-ray as a metatarsal head with a rounded lateral border
that is continuous laterally with the MTP joint (i.e., without any corners or steps in
between). Severe metatarsal pronation (>30 degrees) is manifested as a completely
circular lateral head contour, representing the complete profile of the lateral meta-
tarsal condyle as seen from a frontal view (Fig. 5). Metatarsal pronation can also be
accurately measured on a WBCT [1, 19, 29], using the loading surface as a refer-
ence (floor) and measuring the angle of this line to one running from the medial
edge of the medial sesamoid facet to the lateral edge of the lateral sesamoid facet
(Fig. 6). The advantage of using the sesamoid facets is that this is the working axis
of the metatarsal, which is determined by the plantar vectors (sesamoids and FHL),
being independent of anatomical variations of the metatarsal.
Published studies measuring first metatarsal pronation show approximately 10
degrees more pronation angle in the hallux valgus population vs. controls [30, 31].
The pronation of the first ray in feet without hallux valgus varies from 0 to 15
Fig. 6 Weight-bearing computerized tomography coronal cut at the metatarsosesamoid joint. First
metatarsal pronation angle is shown. It is measured between a line along the weight-bearing sur-
face and another along the metatarsosesamoid facet
Fig. 7 Bilateral AP foot

weight-bearing X-ray. The
dotted lines depict lateral
round contours at the each
first metatarsal head: they
represent the metatarsal
lateral condyle, which can
be seen on an AP foot
X-ray given the metatarsal
pronation. The distal solid
line follows the distal
metatarsal joint surface.
The joint surface is
dysplastic, showing an
increased DMAA
degrees [1, 30]. In cases of hallux valgus, the pronation angle shows an average of
22–29 degrees [31, 32]. Dayton et al. showed that to correct hallux valgus, it was
necessary to correct 22 degrees of pronation on average. The origin of this pronation
has not yet been accurately determined; however, available information shows that
it occurs along the entire medial column, including the naviculocuneiform, intercu-
neiform, cuneometatarsal, and metatarsophalangeal joints [10]. A recent cadaveric
study [11] confirmed the finding that the entire medial column pronates. Finally, the
DMAA represents the orientation of the metatarsophalangeal joint with respect to
the metatarsal axis. This measurement has been shown to be an essential factor in
juvenile hallux valgus [26], being also present in adults [33]. It is a recognized
deformity relapse factor. It is measured between a line that follows the axis of the
first metatarsal and another that is parallel to the MTP joint surface. DMAA should
not be confused with metatarsal pronation (Figs. 7 and 8).
Hallux Valgus 381
Fig. 8 Bilateral AP foot weight-bearing X-ray. Same feet shown in Fig. 7 with an operated hallux
valgus using the PROMO and Akin techniques. Please note that the dotted line representing the
pronation is now straight (stage 0), showing that pronation was fully corrected. Please note that the
distal metatarsal joint surface is still laterally deviated as the DMAA was not corrected with a
biplanar Chevron
Hypermobility of the medial column has been a topic of discussion for decades.
It has been described in some studies using special devices [34], the most recent
being Kimura’s work using weight-bearing CT [10]. Coughlin et al. [35] published
how this hypermobility of hallux valgus was corrected after corrective osteotomies
(and not arthrodesis). The authors consider that this hypermobility is a product of
skeletal malalignment and altered muscle balance (traction vector of FHL and EHL
off-axis of the metatarsal), not constituting a causative factor in every hallux valgus.
Once the skeleton and muscle traction are corrected, hypermobility disappears.
However, there are exceptions where pathological hypermobility is the cause of hal-
lux valgus [18], mainly in cases of undiagnosed hyperlaxity (idiopathic, Marfan,
Ehlers Danlos). This is observed in approximately 5% of operated cases, being an
intraoperative finding not identifiable in preoperative studies. In these cases, after
performing the corrective technique of choice, it is observed that the intermetatarsal
angle is not corrected as planned, evidencing a pathological midfoot hypermobility.
This occurs both after osteotomies and after tarsometatarsal arthrodesis (TMT)
techniques (modified Lapidus), because the hypermobility occurs along the entire
medial column and not only at the first cuneometatarsal joint. In these cases, you
should be prepared in surgery to add flexible (“suture button”) or rigid (screws) fixa-
tions from the medial to the intermediate column (intercuneiform, medial cunei-
form to second metatarsal or intermetatarsal 1–2). There are cases in which
hyperlaxity can be identified in X-rays at the TMT joint. An asymmetry or incon-
gruency at the TMT is the most frequent findings. In these cases, a fusion is recom-
mended including the TMT and intercuneiform joints.
Regarding conservative treatment, it is important to mention that there is no demon-

stration in the literature about its effectiveness in correcting the deformity; however,
it can be useful in relieving the patient’s pain. Conservative measures include adhe-
sive tapes, silicone bunion protections, metatarsal silicone pads (frequently indi-
cated for associated metatarsalgia), and night splints (sometimes painful and poorly
tolerated by patients), between others. The most relevant factor is to avoid direct
pressure on the bunion. This can be achieved mainly with square toe-box shoes,
wide last, and preferably using cloth or flexible material. New shoes are classically
more painful than old ones, because an already worn shoe is already partially
molded to the deformity, thus causing less pressure on the area. In the case of men,
it is frequent that changing shoes for a wider one is enough for pain relief. However,
in women who wear high-heel shoes for work, it is difficult (if not impossible) for
them to change their shoes. This is not accepted in today’s society, where the use of
fashionable shoes is required.
7 Surgical Treatment-Timing-Postoperative Protocol
Initial surgical treatments focused on resection of soft tissue (bursa) and/or promi-
nent bone. The first surgical bone treatment was described by Reverdin in 1881,
which consisted of a medial closing wedge at the metatarsal neck [4]. Today there
are more than 150 surgical techniques described to correct hallux valgus [36]. They
range from soft tissue procedures to amputations, fusions, and tendon transfers
among many other techniques. This great variety of techniques is proof that none is
appropriate for correcting all bunions. It is the consensus today that surgical treat-
ment should be based on osteotomies and all soft tissue procedures are secondary
[37–39]. All feet are different from each other, varying in factors intrinsic to hallux
valgus (severity of the deformity, for example) and extrinsic (e.g., obesity, collagen
disease). We see in practice patients who are dissatisfied with surgery, finding
among the most frequent reasons: recurrence of the deformity, remaining pain and
inability to return to sports activities, among others. It is of vital importance to men-
tion to patients that the pain may not completely subside after surgery, that there
may be some increased stiffness in their big toe, and that the possibility of a relapsed
deformity exists (to be discussed in the complications section). There are certain
groups of patients who should be specially advised before embarking on surgery.
These are patients with skeletal immaturity and patients who make a living from
sports. In the case of the infant-adolescent, the recommendation is to perform sur-
gery, if possible, after skeletal maturity (after 15 years) to decrease the risk of recur-
rence [40]. However, if it is very painful, it is possible to consider surgery, but
parents should be warned of the possibility of recurrence being higher than in adult-
hood, approximately 30% [26, 40–42].. In patients under 10 years of age, it is
Hallux Valgus 383
possible to perform a combined metatarsal and proximal phalangeal hemiepiphys-

iodesis [43, 44], which is an operation with minimal morbidity and demonstrated
effectiveness. If the patient is an adolescent (less than 15 years), the option is to
perform an osteotomy that must correct all the altered parameters with adequate
power. As it will be detailed later, altered DMAA is often present in adolescents and
must be corrected [26]. In the case of athletes, there must be a complete understand-
ing by the patient that the pain of the prominence is likely to improve; however, the
big toe joint will be somewhat less mobile, which should be evaluated by the athlete
if it could influence future performance. It is also important to consider the patient’s
psychological profile. People with depressive disorders have poorer functional out-
comes [45], so they should be evaluated and advised according to their expectations
of the surgery.
It is important for these reasons not to operate on every hallux valgus. They are
all different patients with different realities, and all feet are different from each
other, so if they are operated on, it is not appropriate to solve them all with the same
technique.
Objectives and considerations of hallux valgus surgery:
• To evaluate the patient’s suitability for surgery.
• Master various surgical techniques that can correct the deformity.
• To know treatment options in case of complications.
• Correct completely the metatarsal varus and pronation of the first metatarsal.
• Restore the load capacity of the first metatarsal to the rest of the foot.
• Restore the muscular balances around the hallux metatarsophalangeal
joint (MTTF).
7.1 Decision-Making
It is vital to have multiple options in the surgical technique cabinet to solve a hallux
valgus according to its specific type.
The variables to take into account when choosing a surgical technique are:
1. Degree of deformity in the frontal plane
It is important to make certain measurements in the radiograph (measurement
technique already mentioned previously) that include the IMA and the MTP
angles mainly. In cases of mild deformities, with IMA angles less than 14
degrees, a distal osteotomy (Chevron-type) would be indicated [46]. In cases of
moderate deformities, with an IMA between 15 and 19 degrees, an osteotomy
with greater corrective power would be recommended: long Chevron, Scarf,
PROMO or Bosch-PECA-MICA (MIS variant) [46–51]. Which one to choose
depends on the presence of metatarsal rotation, tarsometatarsal instability, and
metatarsus adductus, between others. In cases of IMA greater than 20°, a Lapidus
(tarsometatarsal fusion) is recommended [52, 53].
2. Degree of pronation of the medial column

This requires a measurement in the WBCT or in the weight-bearing AP foot
X-ray. By means of the three-level estimation, it is possible to estimate a mild,
moderate, or severe pronation. In cases of mild pronation (less than 20 degrees),
there is no need for pronation correction, as it falls within the normal pronation
range for feet without deformity. In this case, a Chevron-type translation oste-
otomy, Scarf, PECA, MICA, or Bosch [46–51] can be performed. In cases of
moderate (20–30°) or severe (>30°) pronation, it is advisable to perform a tech-
nique that corrects the malrotation. These include: PROMO, Lapidus, and dome
osteotomy [52–59]. This degree of pronation will not be corrected with pure
translation techniques such as Chevron, Scarf, PECA, etc.
3. Degree of joint surface inclination (DMAA)
This deformity is difficult to identify in cases with associated metatarsal pro-
nation. The pronation appearance is often mistaken for an increased DMAA and
vice versa (Figs. 7 and 8). It frequently happens that, once the pronation has been
corrected, the DMAA normalizes. In cases of an altered DMAA (>15 degrees),
a distal osteotomy should be added to the surgery to correct the joint inclination.
Currently the recommended technique is a biplanar Chevron [60].
4. Degree of metatarsus adductus
Metatarsus adductus is a deformity that prevents complete correction of the
metatarsal varus, due to the proximity of the minor metatarsals to the first meta-
tarsal. This deformity should be evaluated and discussed with the patient. If this
deformity is present and is >15 degrees [61] (Sgarlato angle), correction of the
metatarsus adductus is recommended. In cases where the metatarsus adductus is
not corrected, an undercorrection of the deformity may result. For cases in which
the metatarsus adductus is corrected, the recommendation is to calculate the
IMA with the metatarsal adductus corrected. This resulting angle is very fre-
quently >18, being necessary in most cases to perform a Lapidus technique due
to its great corrective power. The technique recommended by the authors to cor-
rect the metatarsus adductus consists of minimally invasive osteotomies (MIS
acronym) of the base of metatarsals 2, 3, and 4, with a lateral closing wedge
(4 mm diameter conical burr is used). Only the osteotomy of the second metatar-
sal is recommended to be fixed with a 2.5 mm cannulated compressive screw to
maintain its position. After the metatarsus adductus correction, the Lapidus pro-
cedure is performed (Figs. 9 and 10) [62].
5. Tarsometatarsal instability or arthrosis
Tarsometatarsal instability can be identified by a joint incongruency or by a
plantar gapping. In these cases, and in patients with symptomatic TMT osteoar-
thritis, a Lapidus technique should be considered [63, 64].
By taking all these factors into account when choosing a surgical technique, the
risk of recurrence will be minimized. An algorithm is attached that summarizes the
decision-making process (Fig. 11).
Surgery objective regarding skeletal alignment:
Approximately the following immediate postoperative angular values should be
obtained to have a low risk of deformity relapse:
Hallux Valgus 385
Fig. 9 Bilateral AP foot weight-bearing X-ray. Left foot shows no hallux valgus with no prona-
tion. Note the lateral head contour with a flat shape. Right foot shows a stage 3 pronation (dotted
line follows same curvature radius as distal articular solid line). Metatarsus adductus is evident on
right foot. Sgarlato measurement technique is used. Method: draw a medial tarsal line between the
medial first metatarsal base and proximal-medial navicular corner. The lateral tarsal line is drawn
between the lateral fourth metatarsal base and the cuboid proximal lateral corner. A third line (tar-
sal axis line) is drawn between the medial and lateral tarsal lines midpoints. A line is drawn per-
pendicular to the tarsal axis line. The metatarsus adductus angle (X in the figure) is measured
between the latter (line perpendicular to the tarsal axis) and a second metatarsal diaphyseal line
• Intermetatarsal angle 1–2 (IMA): < 7

• Hallux valgus angle (MTF): <5
• Mild Pronation: < 20, stage 1
• Sesamoid position <3
• Metatarsus adductus <15
7.2 Hallux Valgus Surgical Techniques
They are separated into the following types

• Exostectomy
• Soft tissue technique (McBride)
• Distal intracapsular: Chevron-Peico
• Distal extracapsular PECA-MICA
• Proximal osteotomies: PROMO, dome
• Tarsometatarsal and metatarsophalangeal arthrodesis
• Hallux phalanx osteotomy: Akin
• Postoperative dressing
Fig. 10 Right foot AP

X-ray. Same foot as from
Fig. 9. Note the corrected
metatarsus adductus
performed with a
minimally invasive second,
third, and fourth metatarsal
osteotomy. Only the
second metatarsal
osteotomy was fixed with a
cannulated compression
screw. After this correction,
a Lapidus technique was
performed, given the
increase (>20°) in
intermetatarsal angle after
the metatarsus adductus
correction. Note how the
first metatarsal had to be
shortened to be able to
correct the deformity. To
compensate for this
shortening, the surgeon
increased the plantar
flexion of the first
metatarsal to avoid transfer
metatarsalgia to the lesser
metatarsals
Rotational
>18º
lapidus*
Yes
IMA 12-17º Scarf or PECA
TMT instability or No
Hallux valgus
arthritis <11º Chevron*
No Pronation>20º
Yes
IMA <18º PROMO*
Rotational
>18º
lapidus*
Fig. 11 Hallux valgus treatment algorithm. See text for details. *:if DMAA >10°: add biplanar
Chevron. **: if metatarsus adductus >15°: correct needed (before Hallux Valgus surgery)
Hallux Valgus 387
7.2.1 Exostectomy
This technique is not recommended as an isolated treatment for a symptomatic bun-

ion. It is commonly associated with other corrective techniques when there is a
palpable and symptomatic prominence of the metatarsal head. There are rare occa-
sions when this treatment can be offered to patients with hallux valgus. These cases
can include very mild deformities and low functional demand patients with exclu-
sive symptoms of exostosis rubbing against shoes, with an X-ray with a great exos-
tosis. It should be explained to the patient that the origin of the deformity is not
being treated. It is certain that the deformity will recur in the short to medium term.
The advantage is the recovery that takes about 3–4 weeks compared to the rehabili-
tation of a formal bunion surgery that takes at least 3–4 months.
Technique: It can be done openly or minimally invasive (MIS). For the open
approach, a longitudinal medial approach is recommended at the metatarsal head,
approximately 2- to 3-cm long, starting 5 mm distal to the MTTP joint and advanc-
ing proximal up to the metatarsal neck. After passing through the subdermal fat, the
joint capsule is exposed. Care has to be taken to protect the dorsal and plantar digital
sensory branches. A straight medial longitudinal capsulotomy is then performed,
exposing the head exostosis medially. It is not necessary to expose more than the
medial prominence. There are different capsulotomy techniques; however, in prac-
tice they make no difference from the point of view of functionality. In theory,
inverted L capsulotomy would have greater corrective power when repaired than
other capsulotomies [65], but this does not seem important to the authors since its
aim is not to correct the deformity but only to resect the prominence. After exposing
the prominence, using an oscillating saw (which may also be an osteotome), the
medial eminence is resected following the medial edge of the diaphysis up to the
medial articular sulcus. Then the edges are softened with a rongeur. Capsulorrhaphy
is performed by three separate stitches using a resorbable suture. Skin closure is
performed using an intradermal technique.
In case of opting for the MIS approach, a 0.5 mm incision is made perpendicular
to the skin, in the proximal-inferomedial corner of the metatarsal head at the level
of the proximal pole of the medial sesamoid, preferably using a beaver blade. The
scalpel is then inserted aiming to the center of the head at an oblique angle until it
contacts the bone. Then, using a dissector or elevator, the capsule is separated from
the metatarsal head until a space or pocket is created around the metatarsal head.
Introduce the “Shannon” burr (usually 2 mm diameter and 12-mm-long), and using
a suitable motor (high torque, speeds 3000–5000 rpm), proceed to remove the exos-
tosis. After eminence resection, squeeze the area to help remove the resected bone
through the skin incision. Irrigate thoroughly the incision with the help of a syringe.
Close the skin portal with one single stitch.
It is important to note, that when the exostectomy (resection of medial head
prominence) is performed, the head is being freed from any medial capsule-liga-
ment attachment. This results in the sesamoid-plantar plate system losing its medial
attachment to the head and being pulled to the side. This is evident when performing
this procedure under X-rays, where it is evident how a lateral displacement of the
sesamoids occurs after the capsule elevation. This, however, is not important, given
that as soon as the patient activates muscles and starts to walk, sesamoids are relo-
cated in their facets. In the 2 weeks postoperative X-ray, sesamoids are already
centered under the metatarsal head [7, 8, 66].
7.2.2 Soft Tissue Techniques
The classical soft tissue technique was initially popularized by Silver and later mod-
ified by McBride and several other authors [7, 67, 68]. It consists of a dorsal
approach between the first and second metatarsals and a release of the adductor
tendon, the intermetatarsal ligament, and the lateral metatarsophalangeal capsule.
Only if the fibular sesamoid is arthritic could its resection be considered. A resec-
tion of the medial metatarsal exostosis (bunionectomy) and a plication of the medial
metatarsal capsule are then performed. The intermetatarsal space is sutured and
closed using sutures between the lateral metatarsal capsule and the adductor tendon
with the intermetatarsal and metatarsosesamoid ligament. This technique is cur-
rently not recommended as the sole treatment for bunion deformity [69]. It can be
used as an adjunct to an osteotomy but has no scientific basis for use as an isolated
technique.
Currently the recommended soft tissue release consists of a percutaneous release
of the adductor tendon that attaches to the lateral base of the proximal phalanx of
the hallux. This procedure can also be associated with the release of the lateral
metatarsosesamoid ligament at the lateral edge of the fibular sesamoid.
Technique: via MIS, under X-rays a scalpel (ideally Beaver-type) is positioned
1 cm proximal and 1 cm lateral to the proximal lateral corner of the proximal hal-
lux. It is introduced with an angulation of 45 degrees lateral to medial and 45
degrees proximal to distal. Checking under X-rays, the scalpel will enter the dorso-
lateral metatarsophalangeal capsule of the hallux. Once inside the joint, perform a
lateral movement with the scalpel to section the lateral metatarsophalangeal cap-
sule. Then follow the lateral corner of the proximal phalanx with the scalpel releas-
ing the adductor tendon and collateral ligament. This gesture should be performed
while applying varus force to the hallux. Normally, a click is felt when this release
is made [66, 69].
7.2.3 Metatarsal Osteotomies
Distal Intracapsular
Chevron: The best-known distal osteotomy is the Chevron-Austin osteotomy.

Described and designed by Austin in 1981 [70], this osteotomy consists of a meta-
tarsal head V-cut, with an apex at the center of the head rotation. It is a reliable
procedure, with a low complication rate and a predictable corrective power [46, 67,
69, 70]. The corrective power is approximately 5–7 degrees of IMA [46]. It should
Hallux Valgus 389
be borne in mind that this osteotomy, both in its open modality and MIS (Peico)
[71], cannot correct pronation. Since they are translational and uniplanar osteoto-
mies (like Scarf), it is geometrically impossible for them to achieve head rotation
correction.
Chevron Technique: Through the same medial approach described previously,
the metatarsal head is exposed up to the neck. A minimal exostectomy should be
performed, which only facilitates osteotomy planning but does not remove substan-
tial bone. The metatarsal head is exposed medially and dorsally. The center of rota-
tion of the head is drawn on the medial side with a marker pen. The center of the
osteotomy is located 3 mm proximal to the head rotation center. From this point, the
vertical branch of the osteotomy is drawn perpendicular to the foot weight-bearing
surface. On the dorsum of the metatarsal, the osteotomy should be perpendicular to
the second metatarsal, not perpendicular to the first metatarsal (this avoids lengthen-
ing the metatarsal once the osteotomy has been displaced, which would make cor-
rection of the deformity difficult). The second branch of the osteotomy starts at the
apex already described, extending proximally parallel to the foot bearing surface. It
will exit at the metatarsal neck. It is frequent that once the osteotomy is complete,
the lateral capsule remains attached to the head, preventing its adequate lateral dis-
placement. It must be released with the use of an elevator, either from the dorsolat-
eral aspect of the metatarsal or through the osteotomy. The head is then moved
laterally maintaining a minimum contact of 40–50% between the bone surfaces. It
is transiently fixed in the desired position with a 1.6 Kirschner wire, and the appro-
priate position is confirmed under X-rays. If an altered DMAA is detected, a medial
base wedge resection (biplanar Chevron) can be added in this step. If the position of
the metatarsal head is satisfactory, fixation is performed with a 2–3 mm diameter
screw. If fluoroscopy shows that the fibular sesamoid is not correctly positioned
under the metatarsal head, or that it prevents adequate displacement of the osteot-
omy, a soft tissue release including the adductor tendon and the metatarsosesamoid
ligament should be performed. In cases where there is associated osteoarthritis or
increased soft tissue tension, the metatarsal should be shortened by a 2–3 mm
through bone resection at the dorsal branch of the osteotomy (Fig. 12).
Reverdin-Isham: This osteotomy was the first osteotomy described for hallux
valgus. It was initially described by Dr. Reverdin in 1881 [4], as a medial base
wedge with lateral cortical indemnity. It has undergone some modifications, includ-
ing the approach. It is now best known for its modification called Reverdin-Isham,
which is performed via MIS. This osteotomy does not significantly correct the IMA
but is mainly indicated for alterations of the DMAA (joint orientation) and only
slight alterations of the IMA (corrects 1–2 degrees).
Technique: The MIS burr is inserted through the same incision described in the
exostectomy section. After medial eminence resection, at a 45-degree plantar-
proximal to dorsal-distal angulation at the metatarsal head, an incomplete osteot-
omy is performed initially advancing through the dorsal cortex and then terminating
at the plantar cortex. The lateral cortex should be left untouched. This technique is
performed so that the osteotomy is immediately proximal to the articular surface.
After the osteotomy is performed, the metatarsal head must be compressed
a b
Fig. 12 First metatarsal diagram. (a) Sagittal first metatarsal diagram, depicting the Scarf osteot-
omy (dotted line, 1) and the Chevron osteotomy (dashed line, 2). (b) Axial first metatarsal view,
showing the biplanar Chevron. Please note the medial base wedge, which after removal corrects
the DMAA
proximally in order to close the gap and achieve osteoclasia, thus angulating the
metatarsal head medially. Normally this technique does not require rigid fixation
due to its intrinsic stability [66].
Distal Extracapsular
These types of osteotomies were grouped together because of the anatomical area
where the osteotomy is performed. Extracapsular cervical osteotomies consist of
Bosch variants, PECA (percutaneous extracapsular Chevron-Akin) and MICA
(minimally invasive Chevron-Akin) [47, 48, 51, 72]. These are techniques per-
formed in MIS form on the metatarsal neck (proximal sesamoid pole). The differ-
ence between these types is the shape of the osteotomy. Bosch and PECA use a
single cut, straight, perpendicular to the metatarsal [47–49]. Different is the MICA
which is a Chevron osteotomy, with two bone cuts angled to each other in a “V”
shape [51]. The functional differences between these techniques lie in the shape of
the osteotomy. Bosch and PECA, being a straight cut, allow some head rotational
correction (they are able to correct mild metatarsal pronation (<20°). If there is
more pronation (>20°), this technique will not be able to correct it. The MICA oste-
otomy is more stable than the Bosch osteotomy due to the V-shape (Chevron cut vs.
single cut); however, it does not allow rotation correction due to the nature of the
bone cut. Like the open Chevron or Scarf, MICA is a purely translational osteot-
omy. These techniques are indicated for moderate deformities, 15–19° IMA.
Original Bosch technique [48]: MIS adductor release is performed, as previ-
ously explained. A 2.5 mm Kirschner wire is then inserted 5 mm medially to the
Hallux Valgus 391
medial base of the great toenail. The wire is then advanced medially, subperiosteal
to the proximal phalanx, and metatarsal head up to the metatarsal neck. Then,
using a Beaver-type scalpel, a sharp incision is made at the level of the metatarsal
neck (proximal sesamoid pole), located by means of radioscopy. Using a 2 mm
burr, 20-mm-long, between 3000 and 8000 rpm, the burr is inserted in the metatar-
sal neck midline, perpendicular to the second metatarsal. Then, applying small
oscillating back and forth movements, the upper half of the metatarsal is cut, tak-
ing care to maintain the perpendicularity of the metatarsal axis. This cut should not
take more than 5 seconds, thus avoiding thermal injury to soft tissue and bone.
Then, the osteotomy of the lower half of the metatarsal is completed. Again, this
cut should take no more than 5 seconds. It should be remembered that the move-
ment of the drill is pendulous, taking as its center of movement the skin where the
drill enters. After confirming that the osteotomy is complete, an elevator or
Hohmann retractor is inserted through the same approach. This instrument must
move the head laterally and then enter the endomedullary canal of the metatarsal
in a retrograde fashion. This will position the head over the sesamoids. Once the
head has been moved sideways, the Kirschner wire is advanced into the endomed-
ullary canal to the metatarsal base. The wire is cut 2 cm outside the skin (6 weeks
postoperatively, it must be removed). This technique is called second generation
MIS [71] (Fig. 13).
The technique recommended by the authors replaces the K-wire with screws.
This reduces the risk of infection, MTTF joint stiffness, and discomfort for the
patient during the period the wire is in position. The Bosch technique, where screws
are used instead of K-wires, is called PECA (percutaneous extracapsular Chevron-
Akin) [47, 71].
PECA [47, 49, 72] technique: Once the osteotomy has been completed, the meta-
tarsal head is moved laterally with the help of an elevator, Hohmann retractor, or
similar instrument that can be introduced into the metatarsal endomedullary canal.
The rotation of the hallux should be adjusted so that the metatarsal head has a
straight rather than a curved lateral edge under fluoroscopy (Fig. 5). Once the meta-
tarsal head is in the desired place and the rotation is corrected, it is fixed temporarily
with a 1.6 K-wire from the metatarsal to the head. Two cannulated screw wires are
then positioned from proximal medial to distal lateral. To facilitate the entry of the
wires into the medial cortex, it is recommended that an entry be made with the MIS
drill to facilitate the maneuverability of the wires. The first wire starts 1 cm distal to
the TMT and should ideally finish at the lateral cortex of the metatarsal head, cross-
ing the lateral diaphyseal cortex previously. This wire should then be replaced by a
4.0 cannulated screw. Then, a second wire starts 1 cm distal to the first and should
end in the middle of the metatarsal head. This is then replaced by a 3.0 or 3.5 mm
screw (Fig. 14). A modification of this technique consists in driving the wires prior
to the cervical osteotomy. This implies that once the osteotomy is performed and the
head is moved to the side, the wires should only be advanced, which quickly fixes
the head in the desired position. The disadvantage of this technique modification is
that the wires’ position is approximate. They frequently require repositioning if they
do not aim to the final head position.
Fig. 13 AP foot weight-

bearing X-ray showing a
Bosch technique. Please
note a transverse cervical
osteotomy was performed.
A wire is inserted starting
at the hallux
interphalangeal
dorsomedial crease,
passing adjacent to the
metatarsal head, entering
the metatarsal diaphysis
Fig. 14 Bilateral AP foot

weight-bearing X-ray.
Shows a bilateral PECA
osteotomy. Please note
how the most proximal
screw traverses the head
lateral cortex. This helps
with the osteotomy
stability
Hallux Valgus 393
MICA [51] technique: All steps are similar to those already described. The only
difference lies in the shape of the osteotomy. When entering the metatarsal neck
midline with the burr, the osteotomy in the top half of the head should be angled
proximally (approximately 30 degrees). Then, the plantar cut is made again angled
30 degrees proximally. The screws are then placed as previously described.
To perform this osteotomy, it is recommended that frequent radioscopic guidance be
used at least in the first ten cases operated on. MIS techniques with screws have a
low rate of infection but a high rate of OTS removal rate (24%) [71, 72].
Diaphyseal
Diaphyseal osteotomies are characterized by a moderate corrective power, similar

to the MIS cervical osteotomies already described. Scarf osteotomy is the most
widely used diaphyseal osteotomy. There are many others, including Ludloff, Mau,
Mitchell, etc., but they will not be detailed in this chapter. Scarf osteotomy is trans-
lational, i.e., the distal segment of the osteotomy is lateralized in one plane. Like
MICA or Chevron, it does not allow axial rotation. The indication for this technique
(similar to Bosch or MICA) is a moderate deformity, with an IMA of 10–15. The
shape of this osteotomy simulates an inverted “Z” that begins at the metatarsal neck
dorsum and ends at the proximal-plantar base (see Fig. 12). This shape has been
modified where the plantar and dorsal branches are as short as possible (5 mm), thus
avoiding fractures at the ends of the osteotomy. This osteotomy was initially
described as a purely lateral displacement one, but modifications have been pro-
posed where an angulation of the distal segment is added over the proximal in addi-
tion to the translation [46, 50, 73–75]. This effect increases the corrective power of
the IMA; however, when the distal segment is angulated, the DMAA (angulation of
the joint surface) also increases relatively. The main limitation of the Scarf is the
inability to add a biplanar Chevron in case the DMAA needs to be corrected. In
addition, there is a risk of a complication called the troughing effect. This refers to
what happens when two semicircular segments are placed one on top of the other;
they lack intrinsic stability and can collapse. After the Scarf osteotomy is performed,
two semicircular segments are produced, i.e., the plantar-proximal and dorsal-distal
segments of the metatarsal bone, which can collapse into each other producing an
elevation and pronation of the distal segment (Fig. 15). This is called troughing. To
decrease this risk, the distal and proximal osteotomy cuts should be made as distal
and proximal as possible, respectively, to have more bone density, which in turn
decreases the risk of troughing. In addition, it should be recommended not to bear
weight directly on the medial column in the postoperative period for approximately
1 month. This can be achieved by asking the patient to wander around carrying his
or her weight on the lateral edge of the foot or on the heel. The Scarf complication
rate can be as high as 50%, but with proper technique and postoperative manage-
ment, it is lower and not different from the complication rate of other techniques
[72–74, 76, 77].
Fig. 15 Coronal Scarf

osteotomy diagram a
(mid-diaphyseal cut). (a)
Shows the osteotomy in its
expected position. (b)
Shows the troughing effect.
The plantar metatarsal
segment impacts dorsally
into the dorsal segment.
This ends up in an elevated
and pronated metatarsal
head, which could lead to a
dorsal metatarsophalangeal
impingement and Hallux
valgus deformity relapse
Technique: A medial longitudinal approach is performed, starting at the metatar-

sal base and ending at the metatarsophalangeal joint. After skin incision, the bone is
exposed, maintaining adequate hemostasis. Distally, 1 cm proximal to the articular
surface, a 5-mm-thick dorsal-distal osteotomy is performed. Then, the osteotomy is
extended proximally along the metatarsal axis, with a slight angulation from distal-
dorsal to proximal-plantar. 1 cm distal to the tarsometatarsal joint, this longitudinal
branch of the osteotomy ends, and the plantar branch is performed. This plantar
branch should be a maximum of 5-mm-thick. Before finishing the osteotomy, it is
recommended to confirm that the plane of the osteotomy is being performed parallel
to the plantar foot. This is so that once the bone segments are displaced, they should
slide between them without elevating or descending. If the osteotomy is not made
parallel to the sole of the foot, by moving the distal segment laterally, it can elevate
or lower depending on the plane of the osteotomy. This can alter the loading pattern
on the lesser metatarsals producing transfer metatarsalgia. When displacing the
osteotomy, a minimum of 30–40% bone contact should be maintained between the
metatarsal segments. The recommended method of fixation is using two cannulated
screws 2–2.5 mm in diameter, orthogonal to the osteotomy.
Hallux Valgus 395
Proximal
The osteotomies that will be described in this section are the PROMO and the cupu-
liform or dome [7, 56, 57]. The PROMO osteotomy is a technique that consists of
an oblique osteotomy starting 1 cm from the base of the metatarsal. The bone is cut
obliquely from distal-dorsal to plantar-proximal. This obliqueness gives this tech-
nique the characteristic that, by rotating one bone segment with respect to the other,
the distal segment is also angled in its axis. In other words, this osteotomy is capable
of correcting the IMA and metatarsal pronation through a single osteotomy. A
wedge must not be resected to achieve this correction. The degree of obliqueness of
this osteotomy determines how many degrees of IMA and pronation it can correct.
The more transverse the osteotomy is to the metatarsal axis, the more pronation and
the less IMA it can correct. Conversely, the more longitudinal this osteotomy is
done in relation to the metatarsal, the more IMA it will correct, but the less prona-
tion it will correct. Thus, the obliqueness of this osteotomy can correct any combi-
nation of IMA and pronation. This obliquity is obtainable from published tables and
determined preoperatively. In addition, this osteotomy, being oblique, is stable
under load since it closes with weight-bearing [27, 54–56].
Technique: In the preoperative period, the IMA should be measured and metatar-
sal pronation (mild, moderate, severe) estimated. These parameters of the hallux
valgus deformity are entered into the PROMO osteotomy calculation table (Fig. 16),
which will provide the angle at which the osteotomy should be performed to correct
that particular foot. Through a 4-cm-long medial approach that starts at the metatar-
sal base and extends distally, the first metatarsal is exposed at its base and diaphysis
by dorsal and plantar. A guide wire is then placed 1 cm distal to the TMT joint,
parallel to the foot support surface, and perpendicular to the metatarsal. With the
help of the position guide, a second wire is positioned through the hole in the guide
that is marked with the metatarsal pronation measurement taken in that patient.
Then, with that second wire as a guide, the osteotomy is performed at the angulation
indicated by the table with the help of the osteotomy guide. Finally, once the oste-
otomy is completed, the rotation guide is used to mark the degrees of pronation to
Rotation angle
10–19-º 20–30-º >30 º-
8–10 º- 38 28 13
11–12º- 47 33 18
Intermetatarsal
angle 13–14 º- 55 38 23
15–17 º- 55 42 28
>17 º- 55 47 33
Fig. 16 Promo osteotomy calculation table. The osteotomy angulation is obtained by entering the
IMA and the rotation angle measured in AP foot X-ray. Note that if more rotation and less IMA is
present, the more transverse the osteotomy will need to be to correct the deformity parameters.
Vice versa, if more IMA and less rotation is present, the more longitudinal the osteotomy needs to
be to correct the first metatarsal deformity
be corrected. Both wires must be positioned parallel to each other so that the prona-
tion and IMA measured preoperatively will be corrected. Once the osteotomy has
been stabilized with two Kirschner wires, it is stabilized with a medial metatarsal
locking plate plus an interfragmentary screw (Fig. 17). For more details on the tech-
nique, it is recommended that the specific references be reviewed [55, 56]. For the
postop period, non-weight-bearing is recommended for 4 weeks.
The dome, crescentic, or cupuliform osteotomy is performed 2 cm from the tar-
sometatarsal joint. The disadvantage of this osteotomy is its intrinsic instability due
to the way it is performed. When applying weight load, this osteotomy, despite
being fixed, can easily lose congruence and malunite, producing an elevation of the
metatarsal. Malunion is one of the most frequent complications [7, 57–59] (13%).
Technique: Through a dorsomedial approach on the base of the metatarsal, the
diaphysis and base of the metatarsal are exposed. Using a curved saw blade, a
1.5 cm osteotomy distal to the TMT is marked dorsally on the metatarsal, drawing
a hemicylinder looking down on the metatarsal. This will create a semicircular

PROMO and Akin
osteotomy. Please note
how there is no rotation
present in that head (as
seen as a lateral curvature
at the metatarsal head)
Hallux Valgus 397
osteotomy perpendicular to the metatarsal. This allows a correction of the metatar-

sal varus. Originally described with a K-wire fixation, the authors recommend the
use of a medial locking plate in addition to a distal-dorsal to proximal-plantar inter-
fragmentary screw. In addition, because of the intrinsic instability of this osteotomy,
it should be protected from loading for 6 weeks postoperatively.
7.2.4 Tarsometatarsal (Lapidus) and Metatarsophalangeal Arthrodesis
These techniques are indicated for severe deformities, IMA >18, hallux valgus
angle >40°, TMT instability, and arthrosis.
The tarsometatarsal (TMT) arthrodesis or Lapidus technique [78–80] achieves
through a TMT fusion the first ray bone alignment. This technique achieves correc-
tion in a more proximal site than the previously described osteotomies, so it has
greater corrective power than them. In addition, it eliminates the risk of recurrence
of the deformity that could be caused by instability of the tarsometatarsal joint.
The other characteristic it has is its ability to rotate the metatarsal [31, 32, 52].
However, it has certain limitations. It can increase plantar pressure under the first
ray by up to 37% in mid-support phase (due to loss of flexibility) and by 22%
under the second metatarsal. The fifth metatarsal-cuboid and navicular-cuneiform
joints also suffer increased joint pressure (27% and 40%, respectively) [81]. Stress
fractures of minor metatarsals may also occur when the first metatarsal is short-
ened without sufficient plantar flexion to compensate for the shortening of the ray
[82]. Remember that all Lapidus are shortened by at least 5 mm. This shortening
can also have other consequences, such as metatarsalgia due to weight transfer,
plantar plate rupture, appearance of shortened hallux, etc. The rate of complica-
tions in Lapidus arthrodesis is approximately 16% [83]. The sports return rate is
around 30–80% [84]. The previously mentioned consequences together with the
fact that a generally healthy joint is being removed should be taken into consider-
ation when deciding to choose this procedure. For the authors, Lapidus arthrodesis
is indicated in cases of clearly unstable, arthritic joints or in cases of severe
deformities.
Furthermore, being an arthrodesis, its rate of fusion is lower than that of an oste-
otomy. Approximately the rate of nonunion is 3–10% [79, 80, 85, 86].
Technique: It can be done by open or minimally invasive technique. The open
technique consists of a medial incision that begins 2 cm proximal to the tarsometa-
tarsal and extends to the neck of the metatarsal. The TMT joint is exposed after
adequate hemostasis. 2 mm of cartilage is resected at the base of the metatarsal and
at the medial cuneiform using an osteotome or oscillating saw. Multiple holes
should be drilled in the subchondral plate allowing for pinpoint bleeding (Paprika’s
sign). Metatarsal alignment correction is achieved using a distal clamp between the
first and second metatarsals as a transient aid, fixing the TMT temporarily with
K-wires. Always remember to perform an external rotation (supination) and axial
compression of the metatarsal before positioning the transient wires (under fluoros-
copy evaluate the lateral metatarsal head silhouette, so that it has a straight edge,
and the sesamoids are relocated under the metatarsal head). The methods of fixation
are varied. Initially, two crossed screws were described. Biomechanical studies have
shown a greater stability of a medial plate [63, 87]. There is an option for fixation
even with an endomedullary nail type device [88], as well as cannulated screws. We
will describe the technique using a medial plate as fixation. After the bone segments
are aligned, a plate is placed medially. It is recommended to have two locking holes
distally and proximally, in addition to an oblong hole for the cortical screw. After
the plate is fixed distally to the metatarsal with a locking screw, the cortical hole is
used to place one cortical screw into the medial cuneiform. This should be placed at
the proximal end of the oblong hole to obtain compression with the plate. A 3.5 mm
compressive cannulated screw is then positioned outside the plate. This is normally
positioned from dorsal-distal to proximal-plantar. Before this screw is tightened
definitively, the plate cortical screw should be partially loosened, the cannulated
compressive screw is then tightened definitely, and then the cortical plate screw is
also retightened. Finally, position one more locking screw through the plate distally
(to the metatarsal) and two locking screws through the plate proximally (to the
medial cuneiform).
There are occasions where there is intercuneiform instability. After fixing the
TMT joint, an opening of the intermetatarsal angle is observed. In these cases, there
are two options. One is to add a distal Chevron (technique already described). The
other option is to add stability by integrating the intermediate column into the fixa-
tion. This corresponds to the original Lapidus technique, in which the base of the
one to two metatarsals are prepared and added to the arthrodesis. This can be done
with screws from the first metatarsal to the base of the second metatarsal or to the
intermediate cuneiform (Fig. 18).
Metatarsophalangeal fusion is a valid option in cases of very severe deformity
(>50 degrees of MTP angle) or advanced MTP osteoarthritis. In these cases, align-
ment through the metatarsophalangeal joint corrects the hallux valgus deformity.
Details of the technique will be described in the section on rheumatoid foot and
hallux rigidus.
7.2.5 Phalanx Osteotomy: Akin
Akin osteotomy is a technique that orients the toe itself, resecting a small medial
wedge and thus achieving a straight toe. Many times considered only a cosmetic
detail, it is really a very powerful realignment osteotomy. By orienting the hallux,
this osteotomy also orients the forces that balance the joint, mainly the FHL and
EHL. In any joint (see chapter on transfers), it is essential to have a balance
between agonists and antagonists. If this is not achieved, a deformity will cer-
tainly be created in the medium term. The same criteria apply to the hallux. This
osteotomy is vital for the final tendon balance. Even a suboptimal metatarsal
realignment can be compensated with an Akin, thus obtaining a satisfactory result.
Relapse rates have been shown to be lower in surgeries involving Akin vs. no Akin
(15% vs. 2%) [89].
Hallux Valgus 399

Lapidus arthrodesis. In this
case, a medial locking
plate and a compression
screw were used. In
addition, a one to two
metatarsal screws were
used (as in a classic
Lapidus). An Akin
osteotomy was performed
as well in these patients
together with a Weil
osteotomy to the second
metatarsal
Technique: This technique can be done minimally invasive or open. In MIS form,
it is performed by a percutaneous incision medial to the proximal phalanx, 5 mm
distal to the metatarsophalangeal joint, guided by X-rays. Then using the 2.0 x
12 mm burr (rpm 3000–7000), the osteotomy is performed. Start by entering with
the burr at the phalanx midline. The lateral cortex must be reached, but not crossed.
In this position (always maintaining small pendulum movements), the upper seg-
ment of the phalanx is cut. This should not take longer than 3–5 seconds to avoid
thermal injury. Then, using the same groove created, the osteotomy of the lower half
of the phalanx is completed. At the end, an incomplete osteotomy of the medial half
of the proximal phalanx is performed, keeping only the lateral cortex intact. With
manual axial pressure on the hallux, this osteotomy must be collapsed, thus varizat-
ing the hallux. It is then fixed with a cannulated oblique screw 2.0–2.5 mm in diam-
eter (Figs. 17 and 18).
The open technique is performed through a 3 cm medial approach starting at the

base of the proximal phalanx. The base of the proximal phalanx is exposed, protect-
ing the EHL and FHL dorsally and plantarly, respectively. Using a 1-cm-wide oscil-
lating saw, an incomplete osteotomy is carried out, maintaining the lateral cortex
unharmed, by resecting a 2 mm medial wedge. This osteotomy is then collapsed by
axial compression of the hallux. This technique can be fixed with a staple and a can-
nulated oblique screw or even left without osteosynthesis. In the latter case, it
depends on the postoperative dressing.
7.3 Postoperative Dressing
The postoperative dressing helps to control the edema and pain and can help main-
tain the alignment obtained. MIS techniques without osteosynthesis depend exclu-
sively on the postoperative dressing for their stabilization, so it is of vital importance
to master the technique. After hallux valgus surgery, regardless of the technique
used, a long gauze is applied between the hallux and second toe. In case you want
to increase the toe spread you can pass two bandages. These gauzes surround the
foot medially (protecting and covering the area of the medial surgical wounds. Then
pass another long gauze between the second and third toes, which also surrounds
the foot medially covering the wounds. A new gauze is then wrapped around the
forefoot, protecting the metatarsophalangeal joints of the hallux and the fifth toe.
Then, the last gauze covers the midfoot at the base of the fifth metatarsal, proximal
to the surgical wounds. Finally, the forefoot is wrapped with a protective bandage.
Care should be taken when applying the final bandage not to overtension it, so as not
to produce bullae or hyperpressure skin injury.
8 Complications
The main complications of hallux valgus surgery are recurrence of the deformity
and hallux varus. Less frequent complications are avascular necrosis of the first
metatarsal head, nonunion, malunion (metatarsus elevatus), and soft tissue compro-
mise secondary to surgery.
Deformity relapse is the most frequent complication (up to 70%) [90–92] in the
long term. There are multiple factors identified in the literature that increase the
probability of its occurrence [26, 33, 62, 92–95]. As a summary:
1. Identifiable in the preoperative period: metatarsophalangeal angle >40, inter-
metatarsal angle (the more deformity, the more risk of recurrence); metatarsal
adductus >23 degrees; pronation >20 degrees; DMAA >15 degrees; tarsometa-
tarsal instability, sesamoid position >3.
Hallux Valgus 401
2. Identifiable in the intraoperative period: DMAA >15; tarsometatarsal instability

(identified after fixation of the procedure, the first ray diverges from the second
metatarsal).
3. Identifiable in the early postoperative period (<1 month): sesamoid position >3;
hallux valgus >8°, pronation >20, gap, or tarsometatarsal step-off.
In the event of a relapse, defined as hallux valgus angle >15 degrees, it should be
assessed for associated symptoms. In general, it will depend on the personality and
expectations of the patient, what degree of recurrence will be symptomatic, and
whether it will eventually end in a reoperation.
As stated above, the published rate of recurrence of hallux valgus is 20–70%
[91]. This rate is extremely high, considering that there are factors identified that
when corrected can help lower that probability. Strict preoperative and intraopera-
tive care must be taken to identify and correct any factors that may increase the risk
of recurrence. When identifying a recurrence that needs to be treated, not only
should the angle of hallux valgus and intermetatarsal be corrected but also the factor
that was probably preponderant in the reappearance of the bunion. In case there is
an alteration in the DMAA, pronation, or metatarsus adductus, a new osteotomy
that can correct these factors should be considered. In case the factor is a tarsometa-
tarsal instability, a Lapidus arthrodesis should be used. If the cause of recurrence is
a nonunion of a Lapidus, the fusion should be revised. In case the medial ray has
been shortened due to repeated surgeries, an allograft or bone substitute should be
considered to recover medial column length, in order to avoid further shortening of
the ray and the consequent mechanical consequence for the foot. In selected cases
of Lapidus relapse, where bone angulation has not worsened in 1 year, an osteotomy
(e.g., Chevron) to correct the deformity may be considered without revising the
Lapidus (even if it has a nonunion).
Hallux varus is the second complication in frequency [96]. This is secondary to
techniques that overcorrect the deformity. It is defined by a negative hallux valgus
angle. From the treatment point of view, the analysis should be guided by symptoms
and X-ray. If it is asymptomatic, no treatment is required. In cases where it is symp-
tomatic (discomfort mainly due to medial rubbing of the hallux), X-rays should be
analyzed to evaluate the origin of the malalignment. In the case of hallux varus
secondary to metatarsal overcorrection, a reverse Chevron osteotomy is recom-
mended. The technique and methods of fixation are the same as for the Chevron
already described, only in this case the head movement is reversed (medial direc-
tion). If the varus deformity is caused by an overcorrection of an Akin, a reverse
Akin should be performed, using the same technique described previously, only
reverse. In case the correction of hallux varus is insufficient after the reverse
Chevron, it is recommended to add soft tissue techniques. The recommended ones
are EHB tenodesis and lateral synthetic ligament reconstruction. The first technique
consists of sectioning the EHB at its myotendinous junction, passing it from distal
to proximal under the intermetatarsal ligament and inserting it into a bone tunnel in
the first metatarsal, from lateral to medial. Another technique is to use a synthetic
suture reinforcement to the lateral metatarsophalangeal collateral ligament. This

can be done using a suture button that augments the lateral ligaments by attaching
medially at the proximal phalanx and metatarsal.
Other less frequent complications are Lapidus nonunion (3–10% of cases), meta-
tarsal head avascular necrosis (<1% of distal osteotomies), osteoarthritis, metatarso-
phalangeal stiffness, and osteotomy malunion. The latter usually occurs after
insufficient stabilization, early weight-bearing, poor bone quality, or incorrect tech-
nique [79, 80, 85, 86, 96, 97].
Complications of the MIS technique (13% on average) [98] include thermal
necrosis of the portals, infection (same rate as open technique, 2–3%), nonunion
and malunion, dysesthesia (nerve damage), aseptic nonunion due to thermone-
crosis, excessive shortening, joint stiffness, and heterotopic ossification [98–
102]. Most of these complications are avoidable with adequate training in MIS
surgery.
Finally, the overall dissatisfaction rate of hallux valgus surgery is approximately
10% [103]. This percentage is lower than the reported complications rate, which
shows that there are satisfied patients, even though their hallux valgus surgery had
some problems. This is probably because surgery is effective in controlling pain and
decreasing the functional limitation hallux valgus produces on patients.
9 Summary
Hallux valgus is a quite common condition, more frequently seen in women.

Surgical treatment must consider every factor of each individual foot to decide the
technique to be used, among others: severity of the deformity, presence of altered
DMAA, first ray malrotation (pronation), metatarsus adductus, etc. We must have
an adequate set of surgical techniques in order to choose one that can correct every
identified factor, and not rely on just one way to solve all deformities. This is the
only way to reduce the high relapse rate of hallux valgus.
References
1. Kim Y, Kim JS, Young KW, et al. A new measure of tibial sesamoid position in hallux val-
gus in relation to the coronal rotation of the first metatarsal in CT scans. Foot Ankle Int.
2015;36(8):944–52.
2. Nishimura A, Fukuda A, Nakazora S, et al. Prevalence of hallux valgus and risk factors
among Japanese community dwellers. J Orthop Sci. 2014;19(2):257–62.
3. Roddy E, Zhang W, Doherty M. Prevalence and associations of hallux valgus in a primary
care population. Arthritis Rheum. 2008;59(6):857–62.
4. Reverdin J. The deviation of hallux valgus and its treatment. De la deviation en dehors du
gros orl (hallux valgus) et son traitement chirurgical. Trans Int Med Cong. 1881;2:408–12.
5. Srinivasan R. The Hallucal-sesamoid complex: normal anatomy, imaging, and pathology.
Semin Musculoskelet Radiol. 2016;20(2):224–32.
Hallux Valgus 403
6. Dedmond BT, Cory JW, McBryde A Jr. The hallucal sesamoid complex. J Am Acad Orthop
Surg. 2006;14(13):745–53.
7. Capítulo 4: Hallux Valgus y sus complicaciones en “Cirugía del pie” de Roger Mann. Quinta
edición 1987. Editorial médica panamericana S.A.
8. Mark Myerson. Chapter 9: Hallux valgus. In Foot and ankle disorders. Vol. 1. Philadelphia,
Pennsylvania, USA: WB Saunders Company; 2000.
9. Tonogai I, Wada K, Higashino K, Fukui Y, Sairyo K. Location and direction of the nutri-
ent artery to the first metatarsal at risk in osteotomy for hallux valgus. Foot Ankle Surg.
2018;24(5):460–5.
10. Kimura T, Kubota M, Suzuki N, Hattori A, Marumo K. Comparison of intercuneiform 1-2
joint mobility between hallux valgus and Normal feet using weightbearing computed tomog-
raphy and 3-dimensional analysis. Foot Ankle Int. 2018;39(3):355–60.
11. Wagner E, Wagner P, Pacheco F, Villarroel C, Palma F, Guzman-Venegas R. Novel Hallux
Valgus cadaveric model: role of ligament damage and tendon pull in recreating the deformit,
eposter presentation at the 2020 AOFAS Annual Meeting.
12. Joseph TN, Mroczek KJ. Decision making in the treatment of hallux valgus. Bull NYU Hosp
Jt Dis. 2007;65(1):19–23.
13. Coughlin MJ, Thompson FM. The high price of high-fashion footwear. Instr Course Lect.
1995;44:371–7.
14. Kato T, Watanabe S. The etiology of hallux valgus in Japan. Clin Orthop Relat Res.
1981;157:78–81.
15. Piggott H. The natural history of hallux valgus in adolescence and early adult life.
JBJS. 1960;42:749–60.
16. Inman VT. Hallux valgus: a review of etiologic factors. Orthop Clin North Am. 1974;5:
59–66.
17. Saltzman CL, Brandser EA, Anderson CM, Berbaum KS, Brown TD. Coronal plane rotation
of the first metatarsal. Foot Ankle Int. 1996;17(3):157–61.
18. Perera AM, Mason L, Stephens MM. The pathogenesis of hallux valgus. J Bone Joint Surg
Am. 2011 7;93(17):1650–61.
19. Ono Y, Yamaguchi S, Sadamasu A, et al. The shape of the first metatarsal head and its
association with the presence of sesamoid-metatarsal joint osteoarthritis and the pro-
nation angle [published online ahead of print, 2019 Jul 17]. J Orthop Sci. 2019;
S0949–2658(19)30197–6.
20. Ota T, Nagura T, Yamada Y, et al. Effect of natural full weight-bearing during standing on the
rotation of the first metatarsal bone. Clin Anat. 2019;32(5):715–21.
21. Talbot KD, Saltzman CL. Assessing sesamoid subluxation: how good is the AP radiograph?
Foot Ankle Int. 1998;19(8):547–54.
22. Talbot KD, Saltzman CL. Hallucal rotation: a method of measurement and relationship to
bunion deformity. Foot Ankle Int. 1997;18(9):550–6.
23. Coughlin MJ, Saltzman CL, Nunley JA. Angular measurements in the evaluation of hallux
valgus deformities: a report of the Ad Hoc Committee of the American Orthopaedic Foot &
Ankle Society on Angular Measurements. Foot Ankle Int. 2002;23(1):68–74.
24. Ortiz C, Wagner P, Vela O, Fischman D, Cavada G, Wagner E. "Angle to Be Corrected" in
preoperative evaluation for hallux valgus surgery: analysis of a new angular measurement.
Foot Ankle Int. 2016;37(2):172–7.
25. Hardy RH, Clapham JC. Observations on hallux valgus; based on a controlled series. J Bone
Joint Surg Br. 1951;33:376–91.
26. Coughlin MJ, Roger A, Award M. Juvenile hallux valgus: etiology and treatment. Foot Ankle
Int. 1995;16(11):682–97.
27. Wagner P, Wagner E. Is the rotational deformity important in our decision-making process for
correction of hallux valgus deformity? Foot Ankle Clin. 2018;23(2):205–17.
28. Yamaguchi S, Sasho T, Endo J, et al. Shape of the lateral edge of the first metatarsal head
changes depending on the rotation and inclination of the first metatarsal: a study using digi-
tally reconstructed radiographs. J Orthop Sci. 2015;20(5):868–74.
29. Scheele CB, Christel ST, Fröhlich I, et al. A cone beam CT based 3D-assessment of bony
forefoot geometry after modified Lapidus arthrodesis [published online ahead of print, 2019
Dec 5]. Foot Ankle Surg. 2019;S1268–7731(19)30204–8.
30. Campbell B, Miller MC, Williams L, Conti SF. Pilot study of a 3-dimensional method
for analysis of pronation of the first metatarsal of hallux valgus patients. Foot Ankle Int.
2018;39:1449–56.
31. Conti MS, Willett JF, Garfinkel JH, et al. Effect of the modified lapidus procedure on prona-
tion of the first ray in hallux valgus. Foot Ankle Int. 2020;41:125–32.
32. Dayton P, Kauwe M, DiDomenico L, et al. Quantitative analysis of the degree of frontal rota-
tion required to anatomically align the first metatarsal phalangeal joint during modified tarsal-
metatarsal arthrodesis without capsular balancing. J Foot Ankle Surg. 2016;55(2):220–5.
33. Kaufmann G, Sinz S, Giesinger JM, Braito M, Biedermann R, Dammerer D. Loss of correc-
tion after Chevron osteotomy for hallux valgus as a function of preoperative deformity. Foot
Ankle Int. 2019;40(3):287–96.
34. Klaue K, Hansen ST, Masquelet AC. Clinical, quantitative assessment of first tarsometatar-
sal mobility in the sagittal plane and its relation to hallux valgus deformity. Foot Ankle Int.
1994;15(1):9–13.
35. Coughlin MJ, Jones CP, Viladot R, Golan’o P, Grebing BR, Kennedy MJ, Shurnas PS, Alvarez
F. Hallux valgus and first ray mobility: a cadaveric study. Foot Ankle Int. 2004;25(8):537–44.
36. Smyth NA, Aiyer AA. Introduction: why are there so many different surgeries for hallux
valgus? Foot Ankle Clin. 2018;23(2):171–82.
37. Trnka HJ. Osteotomies for hallux valgus correction. Foot Ankle Clin. 2005;10(1):15–33.
38. Pinney SJ, Song KR, Chou LB. Surgical treatment of severe hallux valgus: the state of prac-
tice among academic foot and ankle surgeons. Foot Ankle Int. 2006;27(12):1024–9.
39. Pinney S, Song K, Chou L. Surgical treatment of mild hallux valgus deformity: the state of
practice among academic foot and ankle surgeons. Foot Ankle Int. 2006;27(11):970–3.
40. Agrawal Y, Bajaj SK, Flowers MJ. Scarf-Akin osteotomy for hallux valgus in juvenile and
adolescent patients. J Pediatr Orthop B. 2015;24(6):535–40.
41. Gicquel T, Fraisse B, Marleix S, Chapuis M, Violas P. Percutaneous hallux valgus surgery in
children: short-term outcomes of 33 cases. Orthop Traumatol Surg Res. 2013;99(4):433–9.
42. Chell J, Dhar S. Pediatric hallux valgus. Foot Ankle Clin. 2014;19(2):235–43.
43. Schlickewei C, Ridderbusch K, Breyer S, Spiro A, Stücker R, Rupprecht M. Temporary
screw epiphysiodesis of the first metatarsal for correction of juvenile hallux valgus. J Child
Orthop. 2018;12(4):375–82.
44. Chiang MH, Wang TM, Kuo KN, Huang SC, Wu KW. Management of juvenile hallux
valgus deformity: the role of combined hemiepiphysiodesis. BMC Musculoskelet Disord.
2019;20(1):472. Published 2019 Oct 25.
45. Shakked R, McDonald E, Sutton R, Lynch MK, Nicholson K, Raikin SM. Influence of depres-
sive symptoms on hallux valgus surgical outcomes. Foot Ankle Int. 2018;39(7):795–800.
46. Wagner E, Ortiz C. Osteotomy considerations in hallux valgus treatment: improving the cor-
rection power. Foot Ankle Clin. 2012;17(3):481–98.
47. Robinson P, Lam P. Percutaneous surgery for mild to severe hallux valgus. [published online
ahead of print April 16, 2020]. Tech. foot ankle surg.
48. Bösch P, Wanke S, Legenstein R. Hallux valgus correction by the method of Bösch: a new
technique with a seven-to-ten-year follow-up. Foot Ankle Clin. 2000;5(3):485–vi.
49. Lam P, Lee M, Xing J, et al. Percutaneous surgery for mild to moderate hallux valgus. Foot
Ankle Clin. 2016;21:459–77.
50. Murawski CD, Egan CJ, Kennedy JG. A rotational scarf osteotomy decreases troughing
when treating hallux valgus. Clin Orthop Relat Res. 2011;469(3):847–53.
51. Vernois J, Redfern DJ. Percutaneous surgery for severe hallux valgus. Foot Ankle Clin.
2016;21(3):479–93.
52. Klemola T, Leppilahti J, Laine V, Pentikäinen I, Ojala R, Ohtonen P, Savola O. Effect of first
tarsometatarsal joint derotational arthrodesis on first ray dynamic stability compared to distal
Chevron osteotomy. Foot Ankle Int. 2017;38(8):847–54.
Hallux Valgus 405
53. Coetzee JC, Resig SG, Kuskowski M, Saleh KJ. The Lapidus procedure as salvage after failed
surgical treatment of hallux valgus. Surgical technique. J Bone Joint Surg Am. 2004;86-A
Suppl 1:30–6.
54. Wagner P, Ortiz C, Wagner E. Rotational osteotomy for hallux valgus. A new technique for
primary and revision cases. Tech Foot Ankle. 2017;16:3–10.
55. Wagner P, Wagner E. Proximal Rotational Metatarsal Osteotomy for Hallux Valgus
(PROMO): short-term prospective case series with a novel technique and topic review. Foot
Ankle Orthopaed. 2018;3(3):247301141879007.
56. Wagner P, Wagner E. The use of a triplanar metatarsal rotational osteotomy to correct hallux
valgus deformities. JBJS Essent Surg Tech. 2019;9(4):e43.
57. Yasuda T, Okuda R, Jotoku T, Shima H, Hida T, Neo M. Proximal supination osteotomy of
the first metatarsal for hallux valgus. Foot Ankle Int. 2015;36(6):696–704.
58. Dreeben S, Mann RA. Advanced hallux valgus deformity: long-term results utilizing the distal
soft tissue procedure and proximal metatarsal osteotomy. Foot Ankle Int. 1996;17(3):142–4.
59. Stith A, Dang D, Griffin M, Flint W, Hirose C, Coughlin M. Rigid internal fixation of
proximal crescentic metatarsal osteotomy in hallux valgus correction. Foot Ankle Int.
2019;40(7):778–89.
60. Corte-Real NM, Moreira RM. Modified biplanar chevron osteotomy. Foot Ankle Int.
2009;30(12):1149–53.
61. Dawoodi AI, Perera A. Reliability of metatarsus adductus angle and correlation with hallux
valgus. Foot Ankle Surg. 2012;18(3):180–6.
62. Aiyer A, Shub J, Shariff R, Ying L, Myerson M. Radiographic recurrence of defor-
mity after hallux valgus surgery in patients with metatarsus adductus. Foot Ankle Int.
2016;37(2):165–71.
63. DeVries JG, Granata JD, Hyer CF. Fixation of first tarsometatarsal arthrodesis: a retrospec-
tive comparative cohort of two techniques. Foot Ankle Int. 2011;32(2):158–62.
64. Lapidus PW. Operative correction of the metatarsus varus primus in hallux valgus. Surg
Gynecol Obstet. 1934;58:183–91.
65. Sever GB, Aykanat F, Cankuş C. Comparison of longitudinal and inverted L-type capsulor-
rhaphy in hallux valgus correction surgery. Medicine (Baltimore). 2019;98(24):e15969.
66. Mariano de Prado. Chapter 5: Hallux valgus. In: Minimally invasive foot surgery. About Your
Health publishers. 2009.
67. Johnson JE, Clanton TO, Baxter DE, Gottlieb MS. Comparison of Chevron osteotomy and
modified McBride bunionectomy for correction of mild to moderate hallux valgus deformity.
Foot Ankle. 1991;12(2):61–8.
68. Mann RA, Pfeffinger L. Hallux valgus repair. DuVries modified McBride procedure. Clin
69. Choi GW, Kim HJ, Kim TS, et al. Comparison of the modified McBride procedure and
the distal Chevron osteotomy for mild to moderate hallux valgus. J Foot Ankle Surg.
2016;55(4):808–11.
70. Austin DW, Leventen EO. A new osteotomy for hallux valgus: a horizontally directed “V”
displacement osteotomy of the metatarsal head for hallux valgus and primus varus. Clin
Orthop. 1981;157:25–3.
71. Del Vecchio JJ, Ghioldi ME. Evolution of minimally invasive surgery in hallux valgus. Foot
Ankle Clin. 2020;25(1):79–95.
72. Lee M, Walsh J, Smith MM, Ling J, Wines A, Lam P. Hallux valgus correction compar-
ing percutaneous chevron/akin (PECA) and open scarf/akin osteotomies. Foot Ankle Int.
2017;38(8):838–46.
73. John S, Weil L Jr, Weil LS Sr, Chase K. Scarf osteotomy for the correction of adolescent hal-
lux valgus. Foot Ankle Spec. 2010;3(1):10–4.
74. Coetzee JC. Scarf osteotomy for hallux valgus repair: the dark side. Foot Ankle Int.
2003;24(1):29–33.
75. Barouk LS. Scarf osteotomy for hallux valgus correction. Local anatomy, surgical technique,
and combination with other forefoot procedures. Foot Ankle Clin. 2000;5(3):525–58.
76. Bock P, Kluger R, Kristen KH, Mittlböck M, Schuh R, Trnka HJ. The scarf osteotomy with
minimally invasive lateral release for treatment of hallux valgus deformity: intermediate and
long-term results. J Bone Joint Surg Am. 2015;97(15):1238–45.
77. Lee SC, Hwang SH, Nam CH, Baek JH, Yoo SY, Ahn HS. Technique for preventing trough-
ing in scarf osteotomy. J Foot Ankle Surg. 2017;56(4):822–3.
78. Lapidus PW. The author's bunion operation from 1931 to 1959. Clin Orthop. 1960;16:19–135.
79. Myerson M. Metatarsocuneiform arthrodesis for treatment of hallux valgus and metatarsus
primus varus. Orthopaedics. 1990;13(9):1025–31.
80. Myerson M, Allon S, McGarvey W. Metatarsocuneiform arthrodesis for management of hal-
lux valgus and metatarsus primus varus. Foot Ankle. 1992;13(3):107–15.
81. Wang Y, Li Z, Zhang M. Biomechanical study of tarsometatarsal joint fusion using finite ele-
ment analysis. Med Eng Phys. 2014;36:1394–400.
82. Wong DW, Zhang M, Yu J, et al. Biomechanics of first ray hypermobility: an investigation on
joint force during walking using finite element analysis. Med Eng Phys. 2014;36:1388–93.
83. Willegger M, Holinka J, Ristl R, Wanivenhaus AH, Windhager R, Schuh R. Correction power
and complications of first tarsometatarsal joint arthrodesis for hallux valgus deformity. Int
Orthop. 2015;39(3):467–76.
84. Fournier M, Saxena A, Maffilli N. Hallux valgus surgery in the athlete: current evidence. J
Foot Ankle Surg. 2019;58(4):641–3.
85. Thompson IM, Bohay DR, Anderson JG. Fusion rate of first tarsometatarsal arthrodesis in the
modified Lapidus procedure and flatfoot reconstruction. Foot Ankle Int. 2005;26(9):698–703.
86. Mani SB, Lloyd EW, MacMahon A, Roberts MM, Levine DS, Ellis SJ. Modified lapidus
procedure with joint compression, meticulous surface preparation, and shear-strain-relieved
bone graft yields low nonunion rate. HSS J. 2015;11(3):243–8.
87. Klos K, Gueorguiev B, Mückley T, Fröber R, Hofmann GO, Schwieger K, Windolf
M. Stability of medial locking plate and compression screw versus two crossed screws for
lapidus arthrodesis. Foot Ankle Int. 2010;31(2):158–63.
88. Shofoluwe A, Fowler B, Marques L, Stewart GW, Badana ANS. The relationship of the
Phantom® lapidus intramedullary nail system to neurologic and tendinous structures in the
foot: An anatomic study. Foot Ankle Surg. 2021;27(2):231–4.
89. Kaufmann G, Hofmann M, Ulmer H, Putzer D, Hofer P, Dammerer D. Outcomes after
scarf osteotomy with and without Akin osteotomy a retrospective comparative study.
J Orthop Surg Res. 2019;14(1):193.
90. Pentikainen I, Ojala R, Ohtonen P, Piippo J, Leppilahti J. Preoperative radiological factors
correlated to long-term recurrence of hallux valgus following distal chevron osteotomy. Foot
Ankle Int. 2014;35(12):1262–7.
91. Jeuken RM, Schotanus MG, Kort NP, Deenik A, Jong B, Hendrickx RP. Long-term follow-up
of a randomized controlled trial comparing scarf to chevron osteotomy in hallux valgus cor-
rection. Foot Ankle Int. 2016;37(7):687–95.
92. Shibuya N, Kyprios EM, Panchani PN, Martin LR, Thorud JC, Jupiter DC. factors associated
with early loss of hallux valgus correction. J Foot Ankle Surg. 2018;57(2):236–40.
93. Park CH, Lee WC. Recurrence of hallux valgus can be predicted from immediate postopera-
tive non-weight-bearing radiographs. J Bone Joint Surg Am. 2017;99(14):1190–7.
94. Okuda R, Kinoshita M, Yasuda T, et al. The shape of the lateral edge of the first metatarsal
head as a risk factor for recurrence of hallux valgus. J Bone Joint Surg Am. 2007;89:2163–72.
95. Okuda R, Kinoshita M, Yasuda T, et al. Postoperative incomplete reduction of the sesamoids
as a risk factor for recurrence of hallux valgus. J Bone Joint Surg Am. 2009;91:1637–45.
96. Monteagudo M, Martínez-de-Albornoz P. Management of complications after hallux valgus
reconstruction. Foot Ankle Clin. 2020;25(1):151–67.
97. Filippi J, Briceno J. Complications after metatarsal osteotomies for hallux valgus: malunion,
nonunion, avascular necrosis, and metatarsophalangeal osteoarthritis. Foot Ankle Clin.
2020;25(1):169–82.
Hallux Valgus 407
98. Malagelada F, Sahirad C, Dalmau-Pastor M, Vega J, Bhumbra R, Manzanares-Céspedes MC,

Laffenêtre O. Minimally invasive surgery for hallux valgus: a systematic review of current
surgical techniques. Int Orthop. 2019;43(3):625–37.
99. McGann M, Langan TM, Brandão RA, Berlet G, Prissel M. Structures at risk during percuta-
neous extra-articular chevron osteotomy of the distal first metatarsal [published online ahead
of print, 2019 Dec 31]. Foot Ankle Spec. 2019;1938640019895917.
100. Arauz Y, Juan M. Treatment of minimally invasive hallux valgus surgery complications, tech-
niques. Foot Ankle Surg. 2017;16(1):11–9.
101. Iannò B, Familiari F, De Gori M, Galasso O, Ranuccio F, Gasparini G. Midterm results and
complications after minimally invasive distal metatarsal osteotomy for treatment of hallux
valgus. Foot Ankle Int. 2013;34(7):969–77.
102. Frigg A, Zaugg S, Maquieira G, Pellegrino A. Stiffness and range of motion after minimally
invasive Chevron-akin and open scarf-akin procedures. Foot Ankle Int. 2019;40(5):515–25.
103. Barg A, Harmer JR, Presson AP, Zhang C, Lackey M, Saltzman CL. Unfavorable outcomes
following surgical treatment of hallux valgus deformity: a systematic literature review. J
Bone Joint Surg Am. 2018;100(18):1563–73.
Hallux Rigidus: A Comprehensive Review
Gaston Slullitel and Valeria Lopez
1 Introduction
Hallux rigidus is a condition characterized by pain and restriction in motion of the

first metatarsophalangeal joint (MTPJ), especially in dorsiflexion. Symptoms com-
monly associated with degenerative arthritis of the first MTPJ were initially reported
by Davies-Colley in 1887, although Cotterill is credited with proposing the term
hallux rigidus. According to the etiology, hallux rigidus can be classified as primary
or secondary [1].
2 Etiology
Although various causes have been proposed for hallux rigidus, its exact etiology
has yet to be elucidated [1]. Trauma or osteochondritis dissecans may damage the
articular surfaces of the MTPJ. Several biomechanical and structural factors may
play a role in the development of hallux rigidus.
G. Slullitel · V. Lopez (*)

Instituto de Ortopedia y Traumatología Dr. Jaime Slullitel, Rosario, Santa Fe, Argentina

Switzerland AG 2022
410 G. Slullitel and V. Lopez
2.1 Functional Hallux Limitus or the Role

of the Dynamic Factor
Functional hallux limitus is a clinical condition in which the first MTPJ motion is
impaired on weight-bearing conditions but not when unloaded. That means that the
joint moves in an open kinetic chain, but not in a closed chain [2]. Its etiology serves
as an explanation of the influence of the soft tissue structures in the genesis of the
first metatarsophalangeal degenerative arthritis.
The range of motion in a weight-bearing condition depends on structures that are
not within the joint itself. Among these structures, the so-called Achilles-calcaneal-
plantar system and the medial column of the foot are mainly responsible for opti-
mally setting the first MTPJ in order to provide anteromedial support of the foot
during the third rocker or propulsive phase of gait; this requires adequate passive
dorsiflexion of the joint while the hallux is purchasing the ground and the vertical-
ized first metatarsal is axially loading the hallux-sesamoid complex [2]. Failure to
achieve first metatarsal plantar flexion or an increase in tensile stress at the plantar
fascia will limit passive first MTPJ dorsiflexion in the transition from the second
rocker (plantigrade support) to the third one (forefoot support). These can impede
the ideal gliding contact pattern at the first MTPJ, producing rolling contact on the
dorsal margin of the joint [2].
During the second rocker, the tibia must glide forward on the ankle to allow the
body’s center of mass to progress from an initial position posterior to the supporting
foot to a final position anterior to it. A restriction to ankle passive dorsiflexion dur-
ing the second rocker (derived from a contractured gastrocnemius) will increase
dorsiflexing moments at the forefoot, thus increasing tensile stress at the plantar soft
tissues due to the truss and beam mechanism of the plantar vault support [2].
A cadaveric study conducted by Viehofer et al. [3] demonstrated that increased
tension of the plantar fascia results in a decrease of first MTPJ dorsiflexion, and this
also provides a plausible explanation for the development of functional hallux
limitus.
2.2 The Structural Factor
The anatomy of the first metatarsal is unique, and its shape has been proposed to
play a significant role in the development of hallux rigidus [4]. The first metatarsal
head is a large transversely flattened quadrilateral structure with dorsoplantar diam-
eter smaller than transverse [5]. The normal MTPJ has a range of motion of 110
degrees, with a plantar flexion of 35 degrees and dorsiflexion of 75 degrees. The
consistency and three-dimensional geometry of the articular surfaces confer stabil-
ity to the center of rotation of the joint [6].
In a normal foot, the centers of rotation are constant in motion and are on the
metatarsal head, but in hallux rigidus they are located eccentrically to the metatarsal
Hallux Rigidus: A Comprehensive Review 411
head [7]. The proximal phalanx moves gradually into a plantar position relative to
the metatarsal head, resulting in progressive displacement of the center of rotation
[7]. This displacement causes dorsal impingement of the joint during dorsiflexion.
Cartilage lesions occur on the dorsal aspect of the first metatarsal head because of
repeated compression under high stresses. This compression eventually leads to the
development of dorsal osteophytes and joint degeneration [6].
Although in most patients with hallux rigidus it may be possible to objectively
detect an elevation of the first metatarsal with respect to the second metatarsal in a
lateral weight-bearing radiograph, in others this is not possible. In some cases, there
is evidence of instability of the first metatarsocuneiform joint on the sagittal plane
during clinical examination, but this may not be evident radiographically [2].
The role of metatarsus primus elevatus (MPE) in the pathogenesis of hallux rigi-
dus has been debated since its first description by Lambrinudi in 1938, although a
recent study hypothesized that with a higher grade of hallux rigidus, the plantar
fascia windlass mechanism no longer works. The hallux plantar plate contracts, thus
limiting hallux dorsiflexion and forcing the first metatarsal into MPE as a secondary
phenomenon [8]. It has been widely debated whether the elevation of the head of the
first metatarsal (Fig. 1) is the primary mechanical anomaly or whether the increase
in tension in the plantar aponeurosis is the culprit [2, 9]. In the presence of either
alteration, the other may end up occurring: an elevation of the head of first metatar-
sal will increase the tension in the plantar aponeurosis by reducing the vault’s anti-
collapse moment arm, while an abnormal increase in the tension of the fascia will
impede the gliding motion in the first MP joint, increasing the dorsal compressive
forces in the joint [2]. It changes the first MP joint motion from a gliding to a hing-
ing type.
Flat foot as a cause of hallux rigidus has been implicated in several studies, but
no demographic data were reported in any of these studies to substantiate the notion.
This concept may arise from a 1948 study that reported on 3619 normal military
recruits and noted that 15% of the patients had an asymptomatic depression of the
Fig. 1 Picture and radiograph depicting the elevated first metatarsal in advanced hallux rigi-
dus patient
longitudinal arch [10]. In a case series evaluated by Coughlin et al., 11% of 140
patients had pes planus and/or excess heel valgus.
The exact role of a long first metatarsal as an associated factor in this particular
entity is still controversial. Coughlin and Shurnas [10] found that a long first meta-
tarsal was no more common in patients with hallux rigidus than in the general popu-
lation. The author’s perspective has been that those flat or chevron-shaped first
MTPJs will be exposed to an axial overload during gait that might be the trigger
factor of the degenerative process. We believe this is far more significant than the
metatarsal length [11].
An increased hallux valgus interphalangeus angle has been evaluated as an asso-
ciated radiographic and clinical finding of hallux rigidus [12]. This association was
seen 90% of the time in the series by Coughlin and Shurnas [5, 10].
Development of degenerative changes can also be secondary to repetitive stress
or inflammatory or metabolic conditions such as gout, rheumatoid arthritis [13].
Coughlin and Shurnas [10] found in their study on etiology that adolescent patients
with unilateral disease are likely to have reported acute trauma. They also found in
the same study that if trauma was reported, the disease was unilateral in 78% of
patients regardless of age [5]. A hyperextension injury to the plantar plate and sesa-
moid complex (so-called turf toe) and a hyperplantar flexion injury may create com-
pression or shear forces that then lead to chondral or osteochondral injury, capsular
damage, synovitis, and adhesions and thus have been linked to the development of
hallux rigidus [6].
3 Anatomy and Radiological Findings
In 1988 Hattrup and Johnson published the most common classification system
used in orthopedic literature. It is based on radiographic changes of the first MTPJ
on standing anteroposterior and lateral radiographic examination of the foot. Grade
1 changes consist of mild to moderate osteophyte formation with preservation of
joint space. Grade 2 changes exist if there is less than 50% narrowing of joint space,
subchondral sclerosis, and moderate osteophyte formation. Grade 3 changes result
when there is marked osteophyte formation and more than 50% loss of visible joint
space, with or without subchondral cyst formation [1]. Lately Coughlin and Shurnas
have introduced a new classification method, adding a grade 4 stage, using clinical
information to classify the pathology. This classification includes the assessment of
pain patterns. According to this, late stages are characterized for pain in the mid-
range of motion of the 1 MTPJ [10] (Table 1).
Beeson et al. [14] conducted a systematic review to critically evaluate the various
classification systems for hallux rigidus. The authors criticized hallux rigidus grad-
ing systems because none had undergone independent testing to assess reliability
and validity. Despite this, the Coughlin and Shurnas grading scale for hallux rigidus
is the most commonly used and cited. It has been suggested to be prognostic of the
severity of great toe arthritis and used to guide treatment [15–17].
Table 1 Coughlin and Shurnas classification scheme

Dorsiflexion
Grade (degrees) Radiograph Clinical
0 40°–60 Normal No pain.
Stiffness and some loss of motion
1 30°–40° Dorsal osteophytes Mild/intermittent pain
Minimal joint narrowing Stiffness at maximal dorsiflexión/
Flattening of MTT head plantar flexion
Periarticular sclerosis
2 10°–30° Periarticular osteophytes Moderate/severe pain and stiffness
Mild to moderate joint more frequently
narrowing Pain appears near end ROM
3 < 10° Cystic changes Constant pain and stiffness
subchondrally Pain appears at end ROM
Sesamoid irregularities
4 < 10° Same as grade 3 Pain appears at midrange of ROM
Baumhauer et al. studied the relationship among the clinical factors making up
this most commonly used hallux rigidus grading scale, in patients with hallux rigi-
dus, and to explore the correlation of these factors to grade selection [15]. They
failed to find a positive correlation between active dorsiflexion ROM and VAS pain
scales at baseline with the Coughlin grade. More important, the Coughlin grade was
only weakly correlated with the presence of remaining cartilage as observed within
the joint and did not predict the success or failure of clinical treatment.
4 Diagnosis
4.1 Clinical Findings
Physical examination reveals a painful swollen MTP joint (Fig. 2) with restriction
of dorsiflexion. The patient usually reports a history of pain and stiffness that wors-
ens with activities involving an MTP dorsiflexion, such as stairs or running. Pain
during walking occurs above all in lift-off phase of the gait [18]. Moreover, the
patient can report numbness on the medial border of the great toe for the impinge-
ment of the medial branch of the superficial peroneal nerve from the dorsal osteo-
phytes [17].
At this point it is particularly important to determine if pain occurs at the mid-
range of motion or in maximum dorsiflexion. Pain at midrange of passive motion
refers to pain that is elicited not only at the extremes of passive dorsiflexion and
plantar flexion of the metatarsophalangeal joint but also in between [10].
This aspect must be considered to determine the appropriate surgical technique
for the patient. Osteophytes around the joint may cause a superficial bursitis, neuri-
tis, or skin ulceration. It is possible to observe an interphalangeal joint
Fig. 2 Clinical picture

demonstrating the
swollen MTPJ
hyperextension as compensation of restricted MTPJ dorsiflexion [1]. This could

eventually lead to nail disorders due to the continuous trauma with the toe box of the
shoe. Pain at the tarsometatarsal joint may also occur because of this same mechani-
cal compensation.
The inability to effectively dorsiflex the hallux during the swing phase, transfer
the load to the second and probably third metatarsal. In that case complaints that
lead to seek medical advice could be those of transfer metatarsalgia. When this
phenomenon takes place in a load transfer could even take place in the fifth metatar-
sal head, producing a mixed second and third rocker hyperkeratosis. This phenom-
enon can also be observed when the patient adopts an antalgic supinated gait due to
overpulling of the anterior tibial tendon.
Conservative care is the first indication for patients with hallux rigidus, depending
on the extent of arthritis and symptoms. The measures commonly used include foot
orthoses, modification in shoe-wear, limitations in activity, physical therapy, and
injections with corticosteroid or sodium hyaluronate [1].
Foot orthoses and modified shoe-wear are used to reduced motion and impinge-
ment at maximum dorsiflexion [19]. One clinical study found that 47% of patients
responded to custom orthoses alone, while another 10% responded to simple shoe
modifications [20] (Level IV evidence).
Shoe modifications include using low-heeled shoes and toe boxes that allow for
accommodation of the first MTPJ.
Injections with corticosteroid or sodium hyaluronate may provide temporary
relief of symptoms. Pons and colleagues [21] prospectively compared the effects of
injections with either corticosteroid or sodium hyaluronate. Clinical improvement

was observed in both groups at 3 months.
The results of these studies suggest that conservative treatment relieves pain
associated with daily activities and constitute fair evidence (grade B
recommendation).
An insole with a Morton extension [22] is commonly used in the management of
hallux rigidus. Made of either spring steel or carbon graphite composite, these
extensions are embedded between the layers of the sole, extending from the heel to
the toe. They can be placed in nearly any type of shoe and can be used together with
a rocker sole to enhance its function. The Morton extension also acts as a splint,
preventing the shoe from bending and in the process limiting dorsiflexion of the big
toe during gait and decreasing the forces acting through the midfoot and forefoot.
The rocker sole is one of the most prevalent modifications, the main function of
which is to rock the foot from heel strike to toe-off without requiring the shoe or
foot to bend. A high toe box can also be used to prevent direct contact between the
dorsal osteophyte and shoe [23].
Functional orthoses have been designed to reverse the windlass mechanism,
allowing the first metatarsal to achieve sufficient plantar flexion in preparation for
propulsion. First-ray cutouts, designed to allow plantar flexion of the first ray and
pronate the forefoot and forefoot postings are other functional orthotic modifica-
tions that have been used to improve first-ray function and reduce pain [6]. In con-
trast, accommodative orthoses are adopted for the immobilization and for the
alteration of the magnitude and temporal loading patterns of the first
MTPJ. Accommodative orthoses include custom orthoses with a navicular pad and
Morton extensions [6].
Physical therapy involves joint mobilization, manipulation, improving range of
motion, muscle reeducation, and strengthening of the flexor hallucis longus muscles
as well as the plantar intrinsic muscles of the feet to improve the stability of the first
MTPJ. Gait training, together with rest, ice, compression, and elevation, has also
been advocated in the reduction of pain and inflammation [6].
Surgical correction of hallux rigidus is indicated when conservative treatment fails

to relieve pain. At the most basic level, the surgical options involve either preserva-
tion or destruction of the articular surfaces, and the decision to pursue one option
over the other hinges on the degree of articular cartilage degeneration. At moderate
stages, joint-preserving procedures constitute a more rational approach. Different
techniques have been proposed, but the optimal surgical procedure has yet to be
defined [11].
6.1 Joint-Preserving Procedures
6.1.1 Cheilectomy
Dorsal cheilectomy can be performed for patients in early stages of hallux rigidus.
This can result in good relief of their symptoms provided that it mainly consist of
impingement pain and stiffness in the absence of mid-range pain and a negative
grind test. It is popular as an initial treatment for hallux rigidus as it improves pain,
preserves joint movement, maintains joint stability, and keeps future secondary
options open [24, 25]. The traditional open dorsal cheilectomy involves removing
dorsal osteophytes from both the metatarsal and phalangeal side of the joint and up
to 30% of the joint surface, in order to achieve dorsiflexion of greater than 45
degrees [26].
In Coughlin and Shurnas’s landmark series of 93 feet undergoing cheilectomy
with a mean follow-up of 9.6 years, they noted a 92% success rate in terms of pain
relief and function [10]. In a more recent investigation, Sidon et al. reported a 69%
rate of patient satisfaction with a 29% of failure rate [27].
The main difficulty is selecting the correct patient suitable for dorsal cheilec-
tomy. Most authors agree that mid-range pain with passive motion (Coughlin and
Shurnas grade 4) is a contraindication for dorsal cheilectomy [25]. Easley et al. [28]
reported in their series that 90% of the patients were satisfied with increased range,
and there was a 40-point improvement in American Orthopaedic Foot and Ankle
Society (AOFAS) score following cheilectomy at mean follow-up of 63 months. Of
the 58 patients in the series of Nicolosi et al. [29], 51 (87.9%) experienced no limi-
tations in their daily activities at an average follow-up of 7.1 years, with two patients
(3.3%) subsequently requiring an arthrodesis. Teoh et al. [25] reported on a cohort
of 89 patients (98 feet) which underwent minimally invasive cheilectomy followed
for a mean of 50 months, with considerable improvement of VAS and self-reported
outcome scores. Authors reported a 10% of grades 2 and 3 patients went onto an
arthrodesis at a mean of 15 (range, 8–30) months after initial surgery, and this could
be due to the fact that they offer MIS cheilectomy to a series of grade 3 patients.
6.1.2 Osteotomies
Metatarsal Osteotomies
Watermann was the first to report in 1927 a dorsal closing wedge trapezoidal oste-
otomy of the distal first metatarsal bone [13]. It was designed to relocate the viable
plantar cartilage to a more dorsal location, allowing more dorsiflexion of the hallux.
This was a relatively unstable osteotomy due to its perpendicular orientation and the
resulting difficult fixation.
Decompressive osteotomy would theoretically be able to alleviate pain and
improve function. A modification of this technique is the Green-Watermann, which
involves decompression and offers a more stable configuration of the osteotomy.
Finally, the long-arm decompression osteotomy was proposed by Robinson and

Frank as an intermediate to the distal decompression osteotomies and more proxi-
mal plantarflexory osteotomies. They reported that it offered the possibility of
greater shortening and greater plantar flexion than its more distal counterparts and
was also more stable than the proximal osteotomies [11].
Although it was initially conceived for a long first metatarsal, Youngswick oste-
otomy (Figs. 3 and 4) showed good results in both harmonic and nonharmonic for-
mulas, at alleviating pain and improving function over the short and intermediate
Fig. 3 Youngswick
osteotomy. Placed in order
to obtain a longitudinal
decompression of the joint
by proximal translation of
the metatarsal head and
plantarflexing it by moving
the apex of the osteotomy
plantarly
Fig. 4 Youngswick osteotomy. Placed in order to obtain a longitudinal decompression of the joint
by proximal translation of the metatarsal head and plantarflexing it by moving the apex of the
osteotomy plantarly
terms [30]. Its rationale is to obtain a longitudinal decompression of the joint by

proximal translation of the metatarsal head and plantarflexing it as desired by mov-
ing the apex of the osteotomy plantarly, allowing the surrounding soft tissues to
relax and remodel. Concerns may arise about survival of this joint-preserving pro-
cedures although Slulitell et al. published in 2019 a report zero cases of progression
to MTPJ arthrodesis despite of progressive worsening (recurrence of dorsal osteo-
phyte and joint space narrowing) of the radiographic appearance in a cohort of 61
patients followed through a mean of 54.8 months [30].
Phalangeal Osteotomies
Dorsiflexion phalangeal osteotomy, as first described by Kessel and Bonnie in 1958,

is an effective procedure for remodeling an arthritic first MTPJ, restoring pain-free
movement to the joint, and alleviating the pain associated with footwear irritation of
dorsal and medial osteophytes of the metatarsal head [31].
Roukis conducted a systematic review of 11 studies of cheilectomy and phalangeal
dorsiflexion osteotomy, with a mean follow-up period of 12 months. In 374 proce-
dures, pain was relieved in 89%, and 77% of the patients were satisfied or very satis-
fied with their outcomes. Just under 5% of the patients required revision surgery [32].
This osteotomy intends to gaining dorsiflexion at the expense of plantar flexion
[33] by changing the orientation of the hallux in relation to the first metatarsal for a
given angle between the metatarsal and proximal phalanx and may therefore change
the direction or distribution of forces at the joint [33]. In a cadaveric study by Kim
et al. [33], Moberg osteotomy proved to shift the center of contact pressure plantar
an average of 0.7 mm, but did not decrease the peak pressure therefore offloading
the diseased cartilage of the dorsal aspect of the joint. The Moberg osteotomy has
been studied in patients with advanced hallux rigidus, showing a reduction in pain
and improved range of motion 2–4 years after surgery [34]. Probably the main rea-
son for the good results obtained with this technique is that less dorsiflexion is
needed at the metatarsophalangeal joint, thus not producing any dorsal metatarsal
impingement.
6.2 Joint-Sacrificing Techniques
6.2.1 Metatarsophalangeal Arthroplasty
Arthroplasty has been proposed as an alternative surgical option. The main advan-
tage of arthroplasty over arthrodesis is the preservation of movement without the
risk of malunion or nonunion.
Cook and Carpenter et al. [35, 36] divided the prosthetic implants of the first
MTP joint into four categories:
• First generation: silicone implants.

• Second generation: silicone implants with grommets.
• Third generation: metal implants with press-fit fixation.
• Fourth generation: metal implants with threaded stem fixation.
Silastic implants using a silicone and plastic hybrid were introduced in the 1960s,
to improve the outcome of the Keller’s arthroplasty [37]. They were originally
single-stemmed hemi-implants. Initial studies in the 1980s, however, reported
extremely high rates of complications and failure, including synovitis, migration,
osteolysis, granulomas, and lymphadenopathy [38]. However those studies evalu-
ated single-stemmed Silastic implants which are no longer commercially available.
Biomechanically, the Silastic implant is designed to act as a sloppy hinged
dynamic spacer but has no inbuilt ability to correct deformity or maintain correc-
tion. It is not directly attached to the bone, allowing self-alignment in the axis of the
joint. This, combined with its low modulus of elasticity, reduces stress-shielding
and promotes bone loading, preventing bone reabsorption and fractures. It has vis-
coelastic properties and high resistance to fatigue. It is a single component; hence
once encapsulation occurs, backside wear is not seen [37]. Cautions and contraindi-
cations for Silastic implants should be the same as for any arthroplasty. We would
not recommend its use when there is a sizeable associated deformity such as valgus
or in rheumatoid disease where the bone may be soft and/or cystic [39].
A recent systematic review suggested that arthroplasty leads to similar outcomes,
satisfaction, rate of complications, and reoperation as arthrodesis [38, 39]. Despite
several subsequent studies in the 1990s reporting good outcomes with the new
implant with high satisfaction rates (80–90%), low rates of complication, failure,
and revision [39, 40], it continues to be rarely used and remains a controversial
surgical option for patients with end-stage HR [41].
There are several Silastic implants, with different stems length and angulation.
A 2020 study [39] on double stemmed Silastic implants reported a 97.2% implant
survivorship at a mean 5.3 years follow-up in a 108 hallux rigidus patient popula-
tion, with high satisfaction rates and considerable improvement in self-reported out-
come measures. Three patients require revision (one infection and two implant
fractures). A total of 25 patients (23.1%) had a complication, most were minor,
responding to simple treatment, and authors stated that this did not affect the out-
come. In the same scenario Van Duijvenbode et al. [42] described the results of 43
implants in 36 patients at a mean follow-up of 19 years. There was a 4% revision/
reoperation rate, with one revision to a further Silastic implant at 9 years and two
revisions to a Keller’s procedure at 13 and 17 years. They report good to excellent
patient-reported outcome measures (PROM) scores and a median satisfaction
rate of 10.
There are other possibilities when replacing the first MTPJ surface. A metallic
proximal phalangeal resurfacing was evaluated in a recent review which included a
total of 97 implants reported survival rates of 85.6% and rates of satisfaction of 75%
at a median follow-up of 5.4 years. Causes of failure included osteolysis and deep
infection but most commonly persistent pain. The authors concluded that this
implant should be used with caution in younger patients due to the high revision
rate [43].
Some three-component implants are available. There are studies showing good
early results for these implants [44]. Titchener et al., however, reported alarming
results in a series of 86 Toefit-Plus implants in 73 patients with a 9.3% intraopera-
tive fracture rate and 24% revision rate at a mean follow-up of 33 months (2–72)
[45]. Gupta and Masud [46] reported the results of 47 Toefit-Plus implants with a
21% (10/47) revision rate and a further 23% (11/47) complaining of ongoing pain
at a mean follow-up of 11.1 years. This field is still of ongoing investigation although
some results are promising in terms of preserving first MTPJ motion for those
patients with severe HR.
6.2.2 Metatarsophalangeal Hemiarthroplasty
Hemiarthroplasty consists of a unipolar implant designed to replace the articular

surface of the head of the metatarsal or the proximal phalanx base. This procedure
requires less bone resection and maintains the length of the first ray. Moreover, if a
conversion to arthrodesis becomes necessary, it should be technically easier. Meriç
et al. [47], with a mean follow-up of 24.2 ± 7.2 months, reported an improvement
from a preoperative AOFAS score of 33.9 ± 9.8 points to a final follow-up score of
81.6 ± 10.1 points, VAS diminished from 8.4 ± 0.9 to 1.21 ± 1.2 and first MTPJ
ROM improved from 22.8° to 69.6°. There was no implant loosening at follow-up
and only one case of revision in arthrodesis due to pain and immobility.
Mermerkaya and Adli [48] have retrospectively compared outcomes of total joint
arthroplasty and hemiarthroplasty of the metatarsal component to a mean follow-up
of 27.1 ± 7.5 months and 29.9 ± 5.2 months, respectively. Authors have observed
significant improvement in AOFAS scores and significant decreases in VAS in both
groups at follow-up, with no significant between-group difference, at last, follow-
up. No implant loosening, radiolucency, or subsidence was found in the cases
treated.
6.2.3 Polyvinyl Alcohol Implant
Historically, the most commonly performed procedure in patients with moderate to

severe HR is arthrodesis; however, this procedure leaves the patient with no motion
through the first MTPJ [49]. Newer techniques have focused on procedures that
maintain range of motion (ROM) and allow patients to weight-bear immediately
following surgery [50].
A novel polyvinyl alcohol (PVA) hydrogel implant has recently been developed
[51]. This synthetic material has water content comparable to healthy cartilage and
a compressive modulus and tensile strength similar to human articular cartilage.
Therefore it can withstand shear and axial load forces beyond those experienced in
the great toe, without fragmentation. These biomechanical features make it an ideal
material for use in hemiarthroplasty of the first MTPJ [50].
The efficacy and safety of this small PVA hydrogel implant in comparison to first
MTPJ arthrodesis was recently evaluated in a prospective, randomized, clinical trial
conducted at 12 centers in Canada and the United Kingdom. At the 2-year follow-
up, the implant hemiarthroplasty demonstrated equivalent pain relief and functional
outcomes to first MTPJ arthrodesis, with no cases of implant fragmentation, wear,
or bone loss [52].
An additional study evaluated the 5-year outcome of 27 grade 2, 3, and 4 HR
patients treated in 3 different centers, which were assigned to the PVA implant in a
random manner and reported clinically and statistically significant improvements in
patient-reported outcome measures (VAS, SF-36 FAAM-ADL) and 65% of patients
rating their overall function level as normal, with a 96% implant survivorship [50].
Interestingly, range of motion through the MTP joint improved following hemiar-
throplasty with the PVA hydrogel implant compared with baseline, which repre-
sents an additional benefit to these patients.
Cassinelli et al. [53], in a non-designer study, reported less favorable results in a
series of 64 implants in 60 patients with 38% (24/64) being “unsatisfied” or “very
unsatisfied,” a 20% (13/64) reoperation rate, and an 8% (5/64) rate of conversion to
arthrodesis, at a mean follow-up of 18.5 months (12–30).
6.2.4 Metatarsophalangeal Arthrodesis
First MTPJ fusion today represents the mainstay of surgical care for high-grade,
advanced hallux rigidus [54]. Improvement of pain is achieved by eliminating resid-
ual degenerated cartilage layer, overstepping the subchondral bone and sacrificing
the joint motion. Preparation of the surfaces may lead to the creation of complemen-
tary bone interfaces, through flat or conical molding of the metatarsal and phalan-
geal portions [54].
Fusion rates have been observed between 53% and 100%, depending on the type
of fixation and type of pathoanatomy [55]. Chraim et al. [56] reported the long-term
outcome of first MTPJ fusion using a transarticular screw and dorsal non-locked
plate, with 93.3% of fusion rate and 6.7% of painless nonunion with no needed
additional surgery.
Arthrodesis is particularly indicated in younger patients, with mid- or high-
performance requests or more active patients, in severe pathologies, such as salvage
procedure in recurrences or failed motion-sparing procedures (Fig. 5a–c). Recommended
fixation of the hallux is 10°–15° of dorsiflexion and 10°–15° of valgus [57, 58].
Different fixation techniques have been described to achieve fusion [59]. Recent
plating techniques yielded significant improvements in fixation stability and union
rates. While plating techniques are highly successful, they necessitate a relatively
large dorsal incision, which can lead to postoperative complications. The plates can
also be bulky, creating subsequent symptoms during activities and showing wear
over time. In contrast, arthroscopic fusion requires smaller incisions, which may
a b
Fig. 5 First MTPJ arthrodesis as a procedure to save a failed hemiarthroplasty that was in an unac-
ceptable hyperextension. (a) Radiograph depicting the hemiarthroplasty implant in position. Note
the osteolysis around the implant stem. (b) Photograph demostrating the hyperextension of the
MTPJ tha caused pain with shoe wearing. (c) Correct aligmnent after MTPJ arthrodesis
result in less swelling, less pain, and fewer complications. The evolution of mini-
mally invasive techniques and instruments has enabled the arthroscopic preparation
of an arthritic hallux MTPJ for arthrodesis. Fixation for arthroscopic MTPJ fusion
can be achieved by crossing compression lag screw [60].
Compression lag screws were previously compared with standard dorsal plates,
and standard plates were shown to be mechanically superior. Fully threaded head-
less screws may provide superior stability when compared with compression lag
screws because the threads engage the cortex in three places, the outer cortex at the
site of insertion and both cortices at the MTPJ. Standard compression lag screw
threads, however, do not always engage cortical bone, depending on surgeon tech-
nique. Fully threaded screws may provide a more stable construct to allow early
weight-bearing, particularly if the subchondral plate is preserved.
In a cadaveric study which compared the mechanical stability of the current gen-
eration of locking plates used in conjunction with a single compression lag screw to
fully threaded headless compression screws, there was a significant difference in

mean stiffness in favor of the plate plus lag screw construct; however, no significant
difference was found when examining mean load to failure [60].
6.2.5 Resection and Interposition Arthroplasty
A simple resection technique of the first phalangeal base has been described in 1904
by Keller and Menger [61], for treatment of hallux valgus associated with osteoar-
thritis of the first metatarsophalangeal joint, without replacement of the joint space
with non-tissue implants. Actually, this technique is used for decompression and
restoration of range of motion of high-grade hallux rigidus, especially in those
patients that refuse arthrodesis. Complications described include first MTPJ insta-
bility, cock-up deformity and transfer metatarsalgia [54]. This procedure is usually
reserved for older and low demand patients.
When a traditional resection arthroplasty is combined with the insertion of a
biologic spacer into the joint, it is called interposition arthroplasty. Its rationale is
given by the reduction in bone loss from the proximal phalangeal base, the mainte-
nance of length, and improving joint stability and motion. Various tissues have been
utilized and described: capsular autograft, meniscus allograft, regenerative tissue
matrix, and tendon autograft [62, 63].
7 Summary
Hallux rigidus is still a complex entity in which optimal treatment has yet to be
defined. New developments and techniques should be in the direction of joint and
motion preservation, especially in high demand or younger patients.
References
1. Migues A, Slullitel G. Joint-preserving procedure for moderate hallux rigidus. Foot Ankle
Clin. 2012;17(3):459–71. https://doi.org/10.1016/j.fcl.2012.06.006.
2. Maceira E, Monteagudo M. Functional hallux rigidus and the Achilles-calcaneus-plantar sys-
tem. Foot Ankle Clin. 2014;19(4):669–99. https://doi.org/10.1016/j.fcl.2014.08.006.
3. Viehöfer AF, Vich M, Wirth SH, Espinosa N, Camenzind RS. The role of plantar fascia tight-
ness in hallux limitus: a biomechanical analysis. J Foot Ankle Surg. 2019;58(3):465–9. https://
doi.org/10.1053/j.jfas.2018.09.019.
4. Coughlin MJ, Shurnas PS. Hallux rigidus: grading and long term results of operative treat-
ment. J Bone Joint Surg Am. 2003;85:2072–88.
5. Lucas DE, Hunt KJ. Hallux rigidus: relevant anatomy and pathophysiology. Foot Ankle Clin.
2015;20(3):381–9. https://doi.org/10.1016/j.fcl.2015.04.001.
6. Kunnasegaran R, Thevendran G. Hallux rigidus: nonoperative treatment and orthotics. Foot
Ankle Clin. 2015;20(3):401–12. https://doi.org/10.1016/j.fcl.2015.04.003.
7. Flavin R, Halpin T, O’Sullivan R, et al. A finite-element analysis study of the metatarsophalan-

geal joint of the hallux rigidus. J Bone Joint Surg Br. 2008;90(10):1334–40.
8. Cheung ZB, Myerson MS, Tracey J, Vulcano E. Weightbearing CT scan assessment of
foot alignment in patients with hallux rigidus. Foot Ankle Int. 2018;39:67–74. https://doi.
org/10.1177/1071100717732549.
9. Roukis TS. Metatarsus primus elevatus in hallux rigidus. Fact or fiction? J Am Podiatr Med
Assoc. 2005;95(3):221–8.
10. Coughlin MJ, Shurnas PS. Hallux rigidus: demographics, etiology, and radiographic assess-
ment. Foot Ankle Int. 2003;24(10):731–43. https://doi.org/10.1177/107110070302401002.
11. Slullitel G, López V, Seletti M, Calvi JP, Bartolucci C, Pinton G. Joint preserving procedure
for moderate hallux rigidus: does the metatarsal index really matter? J Foot Ankle Surg.
2016;55(6):1143–7. https://doi.org/10.1053/j.jfas.2016.06.003.
12. Hunt K, Anderson R. Biplanar proximal phalanx closing wedge osteotomy for hallux rigidus.
Foot Ankle Int. 2012;33(12):1043–50.
13. Galois L, Hemmer J, Ray V, Sirveaux F. Surgical options for hallux rigidus: state of the art
and review of the literature. Eur J Orthop Surg Traumatol. 2020;30(1):57–65. https://doi.
org/10.1007/s00590-019-02528-x.
14. Beeson P, Phillips C, Corr S, Ribbans W. Classification systems for hallux rigidus: a review of
the literature. Foot Ankle Int. 2008;29(4):407–14.
15. Baumhauer JF, Singh D, Glazebrook M, et al. Prospective, randomized, multi-centered clinical
trial assessing safety and efficacy of a synthetic cartilage implant versus first metatarsopha-
langeal arthrodesis in advanced hallux rigidus. Foot Ankle Int. 2016;37(5):457–69. https://doi.
org/10.1177/1071100716635560.
16. Deland JT, Williams BR. Surgical management of hallux rigidus. J Am Acad Orthop Surg.
2012;20(6):347–58.
17. Hamid KS, Parekh SG. Clinical presentation and management of hallux rigidus. Foot Ankle
Clin. 2015;20(3):391–9.
18. Ho B, Baumhauer J. Hallux rigidus. EFORT Open Rev. 2017;2:13–20. https://doi.
org/10.1302/2058-5241.2.160031.
19. Smith RW, Katchis SD, Ayson LC. Outcomes in hallux rigidus patients treated nonoperatively:
a long-term follow-up study. Foot Ankle Int. 2000;21(11):906–13.
20. Horton GA, Parks YW, Myerson MS. Role of metatarsus primus elevatus in the pathogenesis
of hallux rigidus. Foot Ankle Int. 1999;20(12):777–80.
21. Pons M, Alvarez F, Solana J, et al. Sodium hyaluronate in the treatment of hallux rigidus. A
single-blind, randomized study. Foot Ankle Int. 2007;28(1):38–42.
22. Sammarco VJ, Nichols R. Orthotic management for disorders of the hallux. Foot Ankle Clin.
2005;10(1):191–209.
23. Janisse DJ, Janisse E. Shoe modification and the use of orthoses in the treatment of foot and
ankle pathology. J Am Acad Orthop Surg. 2008;16(3):152–8.
24. Walter R, Perera A. Open, arthroscopic, and percutaneous cheilectomy for hallux rigidus. Foot
Ankle Clin. 2015;20(3):421–31.
25. Teoh KH, Tan WT, Atiyah Z, Ahmad A, Tanaka H, Hariharan K. Clinical outcomes following
minimally invasive dorsal cheilectomy for hallux rigidus. Foot Ankle Int. 2019;40(2):195–201.
https://doi.org/10.1177/1071100718803131.
26. Stevens R, Bursnall M, Chadwick C, Davies H, Flowers M, Blundell C, Davies
M. Comparison of complication and reoperation rates for minimally invasive versus open
cheilectomy of the first metatarsophalangeal joint. Foot Ankle Int. 2020;41(1):31–6. https://
doi.org/10.1177/1071100719873846.
27. Sidon E, Rogero R, Bell T, McDonald E, Shakked RJ, Fuchs D, Daniel JN, Pedowitz DI,
Raikin SM. Long-term follow-up of cheilectomy for treatment of hallux Rigidus. Foot Ankle
Int. 2019;40(10):1114–21. https://doi.org/10.1177/1071100719859236.
28. Easley ME, Davis WH, Anderson RB. Intermediate to long-term follow-up of medial-
approach dorsal cheilectomy for hallux rigidus. Foot Ankle Int. 1999;20(3):147–52. https://
doi.org/10.1177/107110079902000302.
29. Nicolosi N, Hehemann C, Connors J, Boike A. Long-term follow-up of the cheilectomy

for degenerative joint disease of the first metatarsophalangeal joint. J Foot Ankle Surg.
2015;54(6):1010–20.
30. Slullitel G, López V, Calvi JP, D'Ambrosi R, Usuelli FG. Youngswick osteotomy for treat-
ment of moderate hallux rigidus: thirteen years without arthrodesis. Foot Ankle Surg.
2019:S1268-7731(19)30208-5. https://doi.org/10.1016/j.fas.2019.11.008.
31. Coutts A, Kilmartin TE. Dorsiflexory phalangeal osteotomy for grade II hallux rigidus: patient-
focused outcomes at eleven-year follow-up. J Foot Ankle Surg. 2019;58(1):17–22. https://doi.
org/10.1053/j.jfas.2018.06.004.
32. RoukisTS. Outcomes after cheilectomy with phalangeal dorsiflexory osteotomy for hallux
rigidus:a systematic review. J Foot Ankle Surg. 2010;49:479–87.
33. Kim PH, Chen X, Hillstrom H, Ellis SJ, Baxter JR, Deland JT. Moberg osteotomy shifts con-
tact pressure plantarly in the first metatarsophalangeal joint in a biomechanical model. Foot
Ankle Int. 2016;37(1):96–101. https://doi.org/10.1177/1071100715603513.
34. O’Malley MJ, Basran HS, Gu Y, et al. Treatment of advanced stages of hallux rigidus with
cheilectomy and phalangeal osteotomy. J Bone Joint Surg Am. 2013;95:606–5. https://doi.
org/10.2106/JBJS.K.00904.
35. Cook KD. Capsular interposition for the Keller bunionectomy with the use of soft-tissue
anchors. J Am Podiatr Med Assoc. 2005;95(2):180–2. https://doi.org/10.7547/0950180.
36. Carpenter B, Smith J, Motley T, Garrett A. Surgical treatment of hallux rigidus using a meta-
tarsal head resurfacing implant: mid-term follow-up. J Foot Ankle Surg. 2010;49:321–5.
https://doi.org/10.1053/j.jfas.2010.04.007.
37. Swanson AB, Lumsden RM, Swanson GD. Silicone implant arthroplasty of the great toe. A
review of single stem and flexible hinge implants. Clin Orthop Relat Res. 1979;142:30–43.
38. Clough TM, Ring J. Silastic first metatarsophalangeal joint arthroplasty for the treat-
ment of end-stage hallux rigidus. Bone Joint J. 2020;102-B(2):220–6. https://doi.
org/10.1302/0301-620X.102B2.BJJ-2019-0518.R2.
39. Park YH, Jung JH, Kang SH, Choi GW, Kim HJ. Implant arthroplasty versus arthrodesis for
the treatment of advanced hallux rigidus: a meta-analysis of comparative studies. J Foot Ankle
Surg. 2019;58(1):137–43.
40. Ter Keurs EW, Wassink S, Burger BJ, Hubach PC. First metatarsophalangeal joint replace-
ment: long-term results of a double stemmed flexible silicone prosthesis. Foot Ankle Surg.
2011;17(4):224–7.
41. Majeed H. Silastic replacement of the first metatarsophalangeal joint:historical evolution, mod-
ern concepts and a systematic review of the literature. EFORT Open Rev. 2019;4(3):77–84.
42. van Duijvenbode DC, Bulstra GH, Nijsse BA. Nineteen-year follow-up of the silastic
double stemmed hinge prosthesis of the first metatarsophalangeal joint. Foot Ankle Surg.
2013;19(1):27–30.
43. Clement ND, MacDonald D, Dall GF, et al. Metallic hemiarthroplasty for the treatment of end-
stage hallux rigidus: mid-term implant survival, functional outcome and cost analysis. Bone
Joint J. 2016;98-B(7):945–51.
44. Tunstall C, Laing P, Limaye R, et al. 1st metatarso-phalangeal joint arthroplasty with ROTO-
glide implant. Foot Ankle Surg. 2017;23(3):153–6.
45. Titchener AG, Duncan NS, Rajan RA. Outcome following first metatarsophalangeal joint
replacement using TOEFIT-PLUS™: a midterm alert. Foot Ankle Surg. 2015;21(2):119–24.
46. Gupta S, Masud S. Long term results of the Toefit-Plus replacement for first metatarsophalan-
geal joint arthritis. The Foot (Edinb). 2017;31:67–71.
47. Meriç G, Erduran M, Atik A, Köse Ö, Ulusal AE, Akseki D. Short-term clinical outcomes after
first metatarsal head resurfacing hemiarthroplasty for late stage hallux rigidus. J Foot Ankle
Surg. 2015;54(2):173–8. https://doi.org/10.1053/j.jfas.2014.10.016.
48. Mermerkaya MU. Adli H.a comparison between metatarsal head-resurfacing hemiarthroplasty
and total metatarsophalangeal joint arthroplasty as surgical treatments for hallux rigidus: a
retrospective study with short- to midterm follow-up. Clin Interv Aging. 2016;11:1805–13.
https://doi.org/10.2147/CIA.S110865.
49. Yee G, Lau J. Current concepts review: hallux rigidus. Foot Ankle Int. 2008;29(6):637–46.
https://doi.org/10.3113/FAI.2008.0637.
50. Daniels TR, Younger AS, Penner MJ, et al. Midterm outcomes of polyvinyl alcohol hydrogel
hemiarthroplasty of the first metatarsophalangeal joint in advanced hallux rigidus. Foot Ankle
51. Younger ASE, Baumhauer JF. Polyvinyl alcohol hydrogel hemiarthroplasty of the great toe:
technique and indications. Techn Foot Ankle Surg. 2013;12(3):164–9.
52. Baumhauer JF, Singh D, Glazebrook M, et al. Correlation of hallux rigidus grade with motion,
VAS pain, intraoperative cartilage loss, and treatment success for first MTP joint arthrod-
esis and synthetic cartilage implant. Foot Ankle Int. 2017;38(11):1175–82. https://doi.
org/10.1177/1071100717735289.
53. Cassinelli SJ, Chen S, Charlton TP, Thordarson DB. Early outcomes and complications of
synthetic cartilage implant for treatment of hallux rigidus in the United States. Foot Ankle Int.
2019;40(10):1140–8.
54. Massimi S, Caravelli S, Fuiano M, Pungetti C, Mosca M, Zaffagnini S. Management of high-
grade hallux rigidus: a narrative review of the literature. Musculoskelet Surg. 2020; https://doi.
org/10.1007/s12306-020-00646-y.
55. Raikin SM, Ahmad J. Comparison of arthrodesis and metallic hemiarthroplasty of the hal-
lux metatarsophalangeal joint: surgical technique. J Bone Joint Surg Am. 2008; https://doi.
org/10.2106/JBJS.H.00368.
56. Chraim M, Bock P, Alrabai HM, Trnka HJ. Long-term outcome of first metatarsophalangeal
joint fusion in the treatment of severe hallux rigidus. Int Orthop. 2016; https://doi.org/10.1007/
s00264-016-3277-1.
57. Kelikian AS. Technical considerations in hallux metatarsophalangeal arthrodesis. Foot Ankle
Clin. 2005;10(1):167–90.
58. McNeil DS, Baumhauer JF, Glazebrook MA. Evidence-based analysis of the efficacy
for operative treatment of hallux rigidus. Foot Ankle Int. 2013;34(1):15–32. https://doi.
org/10.1177/1071100712460220.
59. Migues A, Calvi J, Sotelano P, Carrasco M, Slullitel G, Conti L. Endomedullary screw fixa-
tion for first metatarsophalangeal arthrodesis. Foot Ankle Int. 2013;34(8):1152–7. https://doi.
org/10.1177/1071100713483113.
60. Fuld RS 3rd, Kumparatana P, Kelley J, Anderson N, Baldini T, Younger ASE, Hunt
KJ. Biomechanical comparison of low-profile contoured locking plate with single
compression screw to fully threaded compression screws for first MTP fusion. Foot Ankle Int.
2019;40(7):836–44. https://doi.org/10.1177/1071100719837524.
61. Konkel KF, Menger AG. Mid-term results of titanium hemi-great toe implants. Foot Ankle Int.
2006;27(11):922–9.
62. Clews CNL, Kingsford AC, Samaras DJ. Autogenous capsular interpositional arthroplasty sur-
gery for painful hallux rigidus: assessing changes in range of motion and postoperative foot
health. J Foot Ankle Surg. 2015;54(1):29–36. https://doi.org/10.1053/j.jfas.2014.09.004.
63. Delacruz EL, Johnson AR, Clair BL. First metatarsophalangeal joint interpositional arthro-
plasty using a meniscus allograft for the treatment of advanced hallux rigidus: surgi-
cal technique and short-term results. Foot Ankle Spec. 2011;4(3):157–64. https://doi.
org/10.1177/1938640011402821.
Sesamoiditis
Florencia Pacheco Martinez and Eduardo Fuentes Morales
1 Introduction
The term “sesamoid” was originally coined by Galen in 180 BC, due to the similar-
ity in shape of this bone with sesame seeds. The function of each sesamoid varies
according to its location in the skeleton. The sesamoids of the foot are contained in
the plantar plates of the interphalangeal and metatarsophalangeal joints [1].
Specifically, the sesamoids of the first metatarsophalangeal joint play an impor-
tant role in the function of the hallux. The sesamoid complex acts as a pulley to
enhance the movement and flexor force of the metatarsophalangeal joint during
walking. “Sesamoiditis” is a pathology that describes a wide spectrum of patholo-
gies that have as a common factor the pain of the sesamoids under the head of the
first metatarsal and can be due to diverse causes which we will analyze in this chapter.
2 Anatomy
The sesamoids begin their development in the fetus during the third month.
Ossification begins at age 8 in women and 12 in men, starting with the lateral and
then the medial sesamoid. There is up to 30% of the population in which the sesa-
moids will not complete the ossification process, giving rise to bipartite or multipar-
tite sesamoids. This is more frequent to see in the medial sesamoid (10%) than in
the lateral one, appearing bilaterally in 25% [1, 2].
The joint of the first metatarsal, in relation to the sesamoids, is compared with the
patellofemoral joint. The crista divides the trochlear plantar surface from the
F. Pacheco Martinez · E. Fuentes Morales (*)

Instituto de Seguridad del Trabajo Viña del Mar, Clínica Ciudad del Mar, Viña del Mar, Chile

Switzerland AG 2022
428 F. Pacheco Martinez and E. Fuentes Morales
metatarsal head. The medial and lateral sesamoids articulate their dorsal surface
covered in hyaline cartilage with the corresponding facet of the metatarsal head [2].
The sesamoids are stabilized by the intersesamoid ligament, which runs between
the medial and lateral collateral ligaments, plus two accessory ligaments of the
metatarsal head, called the medial and lateral metatarsal-sesamoid ligaments.
However, in 13% of cases, the sesamoid can be located at the interphalangeal joint,
contained within the flexor hallucis longus tendon.
The sesamoid complex is a resistant capsuloligamentous structure, in which the
medial and lateral sesamoids are incorporated into the plantar plate and are joined
proximally to the proximal phalanx by the medial and lateral insertion of the heads
of the flexor hallucis brevis. In general, the medial sesamoid is slightly more distal
than the lateral one. The latter has connections with the transverse and oblique com-
ponent of the long hallux adductor, in addition to the intermetatarsal ligament which
is attached to the neck of the second metatarsal and the lateral sesamoid ligament.
The medial sesamoid has the insertion of the long hallux adductor and the medial
sesamoid ligament (Fig. 1).
The shape of the sesamoids is variable. The medial sesamoid is longer, ovoid,
and elongated compared to the lateral sesamoid which is smaller. The average size
of the medial sesamoid is 13.4 mm in length and 10 mm in width, while the side
measures 9 mm by 8 mm. Within the variations in size present, the medial sesamoid
is longer than the lateral by 80%, similar by 15% and smaller by 5% [1].
Fig. 1 Plantar vision of

the hallux anatomy. (1a)
Adductor hallucis brevis:
transverse belly. (1b)
Adductor hallucis brevis:
oblique belly. (2a) Flexor
hallucis brevis: lateral
belly. (2b) Flexor hallucis
brevis: medial belly. (3)
Intersesamoid ligament.
(4) Medial sesamoid. (5)
Sesamoid lateral. (6)
Medial metatarsal-
sesamoid ligament. (7)
lateral metatarsal-sesamoid
ligament. (8) Medial
phalangeal-sesamoid
ligament. (9) Lateral
phalangeal-sesamoid
ligament. (10) Flexor
hallucis longus tendon
Sesamoiditis 429
3 Circulation
The irrigation of the sesamoids is complex, and it has been seen that this is mainly
extraosseous [3].
The extraosseous circulation of the sesamoids has been evaluated by several
authors. Pretterklieber et al., in an arteriographic study on 29 corpses, divided the
patterns into three types. The most common anatomical distribution was a branch
of both the medial plantar artery and the plantar arch and was present in 52% of
the specimens. 24% had an isolated branch of the plantar arch, and a similar
percentage had an isolated branch of the medial plantar artery [4]. Sobel et al.
found that extraosseous circulation was provided by two major vessels (proximal
and plantar) and one minor vessel (distal). The proximal pole was irrigated by a
branch of the first plantar metatarsal artery that entered through the insertion of
the flexor hallucis brevis and irrigated the proximal 50–60% of the sesamoid [5].
The plantar vessels irrigate the distal aspect and to a lesser extent the circulation
at the capsular level. This acquires importance in the presentation of pathologies
like the osteonecrosis and the nonunion. The only intraosseous contribution is
from proximal to dorsal. In conclusion, the main source of irrigation of the sesa-
moids is the plantar vessels; therefore, in case of surgical resection, these can be
approached at intra or extra-articular level through medial and lateral incisions of
the capsule, which seems to be a safe avascular zone, reason why the knowledge
of the bony irrigation is of vital importance to avoid damaging it during the plan-
tar approaches.
4 Biomechanics
It is speculated that the biomechanical function of sesamoids is as follows:

1. Mechanical protection for the flexor hallucis longus tendon, which moves in the
intersesamoid space
2. As a pulley that promotes plantar flexion in an intrinsic way, increasing the lever
arm of the intrinsic muscles of the foot
3. To dissipate forces from the metatarsal head by elevating it
The metatarsal-sesamoid complex transmits 50% of the body weight and can
increase up to 300% in the take-off phase of the gait [1].
Cadaveric studies of the biomechanical effect of sesamoidectomy have reported
the importance of the hallucis longus flexor as the main hallux metatarsophalangeal
flexor. Aper et al. showed a significant reduction in the tendon lever arm when
resecting the medial or lateral sesamoid or both [6].
Normally, there is 60–80° of dorsiflexion in this joint. The hallux supports more
than two times the load of the lesser toes, which is equivalent to 40–50% of the body
weight. At full extension, the sliding action gives way to compression on the dorsal
surface of this joint. The stability of the joint is greater in the plantar aspect, as well
as in the medial and lateral sides.
The plantar support comes from the plantar plate reinforced by the medial and
lateral sesamoids and the collateral ligaments.
5 Etiology-Pathology
The pathology of the sesamoids covers 9% of ankle and foot injuries. Within the
etiologies, we find stress fractures (40%), acute fractures (10%), synovitis, chondro-
malacia, sesamoiditis (30%), arthritis (5%), and bursitis (5%) among others.
Although sesamoiditis can be seen as a separate entity from the rest of the patholo-
gies mentioned, the definition in the literature is ambiguous and can lead to encom-
passing up to 50% of the sesamoid conditions depending on the classification
used [1, 2].
If we base ourselves on the definition of “sesamoiditis” as any pain in the sesa-
moids under the head of the first metatarsal, we can differentiate this pathology
according to the following division: capsuloligamentous (turf toe), soft tissues
(synovitis, tenosynovitis, bursitis, nerve compression), acute fractures, stress inju-
ries (chondromalacia, osteochondritis, osteonecrosis, stress fracture), anatomical
alteration (asymmetry in size, rotational misalignment, condylar malformation),
and infections (cellulitis, osteomyelitis).
The sesamoid region experiences multiple forces during jumps or runs, which in
situations of excess or repetitive stress can result in an inflammation of one or both
sesamoids. This repetitive trauma may be secondary to increased activity, problems
with footwear, or anatomical variations that generate stress under the head of the
first metatarsal, such as pes cavus, hindfoot varus, or equinus. Sesamoiditis can also
occur due to other conditions such as infection, inflammatory pathology, and arthro-
sis in the absence of repeated trauma [7].
In general, there is no history of direct trauma. An insidious onset of weeks is
frequently described, with gradual progression of pain, focused edema, and discom-
fort to mobility, mainly to dorsiflexion. Athletes often report increased symptoms
when running, jumping, or facing changes in direction. Walking on the side edge of
the foot can minimize your discomfort. Claw deformity following a traumatic event
may raise the suspicion of a plantar plate injury.
The physical examination begins by looking for increased focal volume in the
plantar aspect of the foot. On palpation, the patient may report tenderness in rela-
tion to the involved sesamoid. In cases where there is a pes cavus associated with
Sesamoiditis 431
a first metatarsal in flexion, it may show an inflamed bursa under the head of the
metatarsal.
Dermatological causes of plantar pain may be related to a painful plantar kera-
toma, also called untreatable plantar keratosis. Part of the physical examination
includes passive and active assessment of the range of motion of the first metatarso-
phalangeal joint. The patient may refer increased pain to dorsiflexion in cases of
sesamoid stress fractures. Secondary to chronic repetitive trauma and medial inci-
sions secondary to hallux valgus surgical procedures, the medial plantar nerve may
be compromised. We can find the positive Tinel sign just above the medial sesamoid
or lateral to the fibular sesamoid.
We must differentiate tenosynovitis of the flexor hallucis longus (FHL) from
sesamoid pathology. Pain at plantar flexion against resistance of the hallux interpha-
langeal joint leads to tendon pathology.
It is important to document the alignment of the hallux, mainly after some epi-
sode of trauma or excision of one or both sesamoids. There may be some change in
alignment secondary to a muscle imbalance.
Upon examination, the position of the sesamoid can be deduced from the degree
of hallux pronation. We should examine the degree of contracture of the lateral
structures (adductor, lateral sesamoid ligament, and lateral capsular) and examine
the range of motion in dorsiflexion and plantar flexion with the corrected position of
the hallux.
Allen et al. in 2001 published a clinical test that allows isolating the dynamic
components associated to the sesamoids by means of the passive axial compression
maneuver (PAC test) (Fig. 2). With the patient in supine position with the leg
extended, the sesamoids are located by manual palpation. Then the hallux is brought
into dorsiflexion, and compression is generated just proximal to the sesamoid area.
Finally, the hallux is positioned in passive plantar flexion maintaining the compres-
sion, which generates pain associated with the bony compression of the sesamoids
against the base of the phalanx or head of the metatarsal, while the surrounding
structures are in relaxation [8].
a b c d
Fig. 2 Passive axial compression test. (a) The sesamoids are under the head of the first metatarsal.
(b) The maximum dorsiflexion of the hallux generates distal migration of the sesamoids. (c)
Generating compression proximal to the sesamoids stabilizes them in their more distal position.
(d) The test is positive if passive plantar flexion generates pain
7 Imaging
Within the imaging study, we must evaluate the patient with bilateral feet weight
bearing radiographs, both in the anteroposterior, lateral, and oblique planes. For a
more specific evaluation of the sesamoids, we request an axial projection of the
sesamoids visualizing the joint, in addition to the lateral and medial oblique projec-
tion at 40°, specific for each sesamoid separately. The axial projection of the sesa-
moids allows us to identify the adequate congruence of these in relation to the head
of the first metatarsal, besides evidencing possible degenerative compromises of the
metatarsal-sesamoid joint. However, the initial X-rays in the confrontation of sesa-
moiditis can be negative in up to 85% of the cases [9]. In case further imaging is
required, bone scintigraphy has been classically used as a support in the diagnosis
of sesamoiditis. The use of computed axial tomography (CT) allows us to better
evaluate the morphology of the sesamoid bone and joint complex, while MRI guides
us to the soft tissue pathology associated with the complex, in addition to evidenc-
ing bone edema as a secondary inflammatory sign. Capsuloligamentous lesions,
such as turf toe, are identifiable in sagittal sections, where we can visualize the pres-
ence of discontinuity of the plantar plate or changes in the signal, both in its union
with the sesamoids and in the base of the proximal phalanx. MRI also helps to dif-
ferentiate between bipartite sesamoids and nonunion [10]. Currently, the use of
SPECT-CT has acquired relevance in the differential diagnosis.
8 Diagnosis
The differential diagnosis of sesamoiditis is primarily clinical, identifying the area

of pain under the head of the first metatarsal. However, the specification based on
the etiology is necessarily associated with the imaging that provides the visualiza-
tion and differentiation of the great variety of structures present in the same region
[3, 11, 12].
9 Differential Diagnosis of Plantar First Metatarsal Pain
9.1 Capsuloligamentous Lesion (Turf Toe)
There must be a high index of suspicion in the capsuloligamentous lesions of the

first metatarsophalangeal (MTP) joint, and we can see from a slight sprain to a com-
plete lesion of these structures. The patient can present ecchymosis, increase in
volume, and pain during loading, mainly in the take-off phase. We must palpate the
Sesamoiditis 433
collateral ligaments and the dorsal capsular area in search of pain and instability. In
general, the referred pain proximal to the sesamoids suggests a low-intensity lesion,
while the located distal to these can orient to a greater severity and instability [11].
Based on the extent of the involvement, Clanton in 1994 described a classification
later modified by Anderson, which divides this injury into three degrees. Grade I
corresponds to damage to the joint capsule without loss of continuity, without alter-
ation of the range of motion or pain on walking. X-rays are negative for the lesion,
and magnetic resonance imaging (MRI) shows soft tissue edema. Grade II shows a
partial rupture of the plantar and capsular plate, associated with edema and ecchy-
mosis. The patient presents difficulty in walking and pain when moving the hallux,
and while the X-ray does not suggest injury, the MRI shows soft tissue edema and
alteration of the signal in the plantar plate that does not involve the whole of it.
Finally, a grade III lesion corresponds to a complete rupture of the plantar plate and
capsule, with secondary findings, such as sesamoid fracture (Table 1).
9.2 Acute or Stress Fracture
The history of an acute pain episode secondary to trauma should raise suspicions of
acute injury. We can differentiate it from a bipartite sesamoid by the characteristics
of the feature, and at the imaging level, we can support it with scans or MRIs. The
sesamoid frequently involved in fractures is the tibial, with a usually transverse
trait [12].
In the case of stress fractures, this diagnosis can be suspected according to the
patient’s history, as a result of an alteration in his or her usual training. The pain and
inflammation are related to the activity, and the X-rays are usually negative for the
injury, so the MRI study is very useful [9].
Table 1 Turf toe grade description

Hyperextension (turf toe)
I. Stretching of the plantar capsular ligamentous complex. Localized tenderness, minimal
swelling, and ecchymosis
II. Partial tear of plantar capsular ligamentous complex. Diffuse tenderness, moderate
swelling, and ecchymosis. Restricted movement with pain
III. Frank tear of plantar capsular ligamentous complex
Severe tenderness, marked swelling, and ecchymosis. Limited movement with pain,
and vertical Lachman’s test.
Possible associated injuries: medial/lateral injury. Sesamoid fracture or bipartite
diastasis. Articular cartilage/subchondral bone bruise
Classification system of capsuloligamentous lesions by hyperextension (turf toe) of the first pha-
langeal metatarsal joint. (Anderson RB)
9.3 Infection
Infection is a rare diagnosis in this area. A puncture wound that results in a direct
doorway or a major skin injury could result in sesamoid involvement.
9.4 Metatarsal-Sesamoid Arthritis
It can be seen associated with hallux rigidus or the isolated metatarsal-sesamoid

zone. It can be secondary to trauma or chondromalacia.
9.5 Intractable Plantar Keratosis (IPK)
This pathology is generated under the head of the metatarsal. This is related to
repetitive abrasion in a load zone. It is important to differentiate a IPK from a plan-
tar wart. The X-ray imaging study allows the detection of bone that explains the
increase in pressure under a certain area.
9.6 Bursitis
The intermetatarsal or adventitious bursa may be affected. Imaging can be per-

formed as MRI for diagnostic support and location of origin.
9.7 Nerve Compression
The digital medial and lateral plantar nerves run in relation to the sesamoids, and
their irritation or compression can cause neurological symptoms.
10 Treatment
In general, the treatment of all plantar MTP and sesamoid disorders begin with
general measures, which consist of unloading the first metatarso-phalangeal joint,
relative joint immobilization with rocker-soled shoes or insoles with carbon fiber
extension at the MTP, MTP taping, orthosis with or without first metatarsal head
Sesamoiditis 435
unloading, modifications of the patient’s physical activity, anti-inflammatory mea-

sures, and decreasing load at the first MTP (avoid use of high heel shoes).
Once conservative treatment fails, surgical treatment should be considered,
which will vary depending on each specific pathology. The techniques have changed
over the years. In the first place, any underlying cause should be looked for, like
shortening of the gastrocnemius-soleus complex or the plantar inclination of the
first metatarsal that can be observed in the patients with cavo-varus feet.
Among the surgical alternatives to be considered are percutaneous fixation (in
case of acute fractures) and partial or total medial or lateral sesamoidectomy.
Sesamoidectomy should be considered in those cases in which there are no altera-
tions in the alignment of the first metatarso-phalangeal joint [13].
10.1 Capsular Ligament Injuries: Turf Toe
10.1.1 Conservative Treatment
The treatment of capsuloligamentous lesions will depend on the degree of involve-

ment of the lesions. In all of them the first line of the treatment consists of rest, local
cold, elevation, and anti-inflammatory for a limited time. The conservative handling
is usually sufficient for those injuries of low degree.
A gradual return to sports activity is recommended after 2–6 weeks, until dorsi-
flexion between 50° and 60° of the metatarsophalangeal joint of the hallux can be
achieved and free of pain [12].
In moderate injuries, it is recommended that the first metatarsophalangeal joint
be immobilized in plantar flexion in order to allow healing of the plantar structures
(Fig. 3). Insoles do help with gradual sports return (Fig. 4). Joint infiltration with
corticosteroids is not recommended since they can mask other types of injuries.
Fig. 3 Hallux phalangeal

metatarsal plantar flexion
a b
immobilization systems
with bandage and plaster
(a) or functional taping (b)
Fig. 4 Orthosis with

carbon fiber extension to
decrease the mobility of
the hallux MTP
10.1.2 Surgical Treatment
In grade III injuries, with complete rupture of the capsuloligamentous apparatus,

surgical treatment is recommended, with direct repair of the compromised struc-
tures, which reports good results in the literature [2, 12].
Indications for surgical treatment:
1. Large capsular avulsions with joint instability
2. Sesamoid or bipartite sesamoid fracture with diastasis or retraction
3. Vertical instability at physical examination (mini Lachman test)
4. Post-traumatic hallux valgus
5. Intra-articular free body articular cartilage injuries
6. Failure of conservative treatment
10.1.3 Types of Approach
The approach that is generally used in the surgical management of these lesions is
the medial one, which can be angulated at 90° in the metatarsophalangeal fold, to
increase exposure and subsequently carry out the direct repair intrasubstance with
the use of anchors if there is tearing of the base of the proximal phalanx (Fig. 6).
10.1.4 Postoperative Handling
Immobilization in a plaster cast that maintains the plantar flexion of the hallux MTP
between 10° and 20° or a short orthopedic boot is recommended. Start of mobiliza-
tion a week after surgery to avoid arthrofibrosis, avoiding passive dorsiflexion and
plantar flexion against resistance so as not to damage the repair. Maintain the
Sesamoiditis 437
discharge of the operated foot for 4 weeks in an orthopedic boot. Start the load pro-
gressively from 4 weeks with a boot, which should be discontinued at 8 weeks, and
then using a rigid-soled shoe with a rigid forefoot insole in order to limit the dorsi-
flexion of the hallux MTP (Fig. 4).
Start kinesiotherapy to recover the joint range of hallux MTP from 8 weeks,
waiting for the return to sports activity from 12 to 16 weeks.
Patient expectations should be tempered in the sense that full recovery can take
up to a year and that residual pain and joint stiffness are common.
10.2 Acute and Stress Fracture of the Sesamoids
While displaced fractures suggest a break in the plantar plate and sesamoid complex
requiring surgical repair, in most cases, the abundant soft tissue connections keep
the fragments in relative apposition. In non-displaced or minimally displaced frac-
tures, conservative treatment is the first line of treatment. The typical protocol
involves 4–6 weeks of rigid immobilization with the hallux in plantar flexion with
an additional period of protected loading and gradual return to normal activity.
It should be taken into consideration that non-displaced sesamoid fractures are
difficult to differentiate from bipartite sesamoids in the radiographic study, as we
have already mentioned in this chapter.
Open surgery with meticulous reconstruction of the flexor hallucis brevis tendon
is mandatory to achieve good results. An alternative to open surgery is percutaneous
fixation with a cannulated screw, which is placed in a retrograde fashion. Pagenstert
G. and Hintermann B. [14] performed percutaneous screw fixation on eight athletes,
all patients returned to their pre-injury level of sports and occupational activity
within 12 weeks after surgery (Fig. 5).
Sesamoidectomy has been described in cases of persistent pain after conserva-
tive management, particularly in complex fracture patterns, comminuted fractures,
failure to use bone grafting, degenerative joint disease, or avascular necrosis [12].
The risks of this procedure include the development of hallux valgus following
medial sesamoid resection and hallux varus following fibular resection, claw defor-
mity secondary to hallucis brevis flexor involvement, transfer metatarsalgia, and
problems with operative wound or nerve injury. In order to avoid future deformities,
sesamoid resection should be performed as localized as possible (“shelling out”),
repairing the defect created including the involvement of the plantar plate and the
intersesamoid ligament.
Regarding the development of hallux valgus or varus after medial or lateral sesa-
moidectomy, respectively (10–20% of cases), Kane et al. [15], in a study of 46
patients, observed that those with lateral sesamoid fracture had low MTP and inter-
metatarsal angles, which tend to decrease after fibular sesamoidectomy. Patients with
medial sesamoid fractures, on the other hand, had higher than normal MTP and inter-
metatarsal angles preoperatively and both increased post-resection. In both cases this
situation did not determine that the measurements were clinically significant.
Fig. 5 Percutaneous
fixation with cannulated
screw described by
Pagenstert G. and
Hintermann B. Use of
anchors for fixation in the
hallux F1
10.3 Avascular Necrosis and Bone Edema

(Proper Sesamoiditis)
For patients with avascular necrosis (AVN) as well as sesamoiditis with bone edema
who do not respond to conservative treatment, resolution of the disease is less likely
to be achieved with correction of the underlying anatomical causes, and sesamoid-
ectomy (partial or total) may be indicated with or without further correction of the
malalignment or anatomical abnormalities.
Medial sesamoidectomy should be partial in cases of involvement of only part of
the sesamoid or in cases of mild sesamoiditis. In these cases, the plantar shaving of
the medial sesamoid can be considered, preferably using a direct approach. In this
case, there is a low risk of MTP valgus deformity, but, if symptoms persist, a risk of
a secondary surgery to perform a total sesamoidectomy exists.
In relation to total sesamoidectomy, there is consensus in the literature on the use
of the medial approach, with which most orthopedic surgeons are very familiar. To
perform fibular sesamoidectomy, which is a rare procedure, there are some authors
in favor of dorsal [16], lateral plantar [16, 17], or medial plantar [18] (Figs. 6 and 7).
10.4 Infections
If the course of osteomyelitis of the sesamoids is proven, the indicated treatment is

resection of the affected sesamoid. In neuropathic patients, with the presence of a
plantar ulcer, exposure to perform sesamoidectomy can be extended. Once the
resection and surgical cleaning of the area have been carried out with the corre-
sponding taking of cultures for the diagnosis of certainty, the repair of any tendon
Sesamoiditis 439
a b
Fig. 6 The image shows the medial approach for performing tibial sesamoidectomy. (a)
Demarcation of the medial approach to MTP from dorsal hallux to plantar skin. (b) Longitudinal
capsulotomy and release of the tibial sesamoid. (c) Extraction of the sesamoid
damage present is carried out in order to avoid subsequent deformities. The removal
of both sesamoids can cause the descent of the metatarsal head which alters the
position of the center of rotation of the head and can lead to the development of a
cock-up or intrinsic minus of the hallux [19].
10.5 Metatarso-Sesamoid Arthritis
In cases of hallux valgus-associated sesamoid subluxation showing signs of joint

degeneration of the metatarso-sesamoid joint, the realignment of the head of the
first metatarsal over the sesamoid apparatus in both the frontal and coronal planes
must be taken into account (treated in Hallux Valgus chapter). In case there is evi-
dent arthritis causing the patient’s symptoms, sesamoidectomy is the treatment
of choice.
a b
Fig. 7 The image shows the details of the lateral plantar approach for fibular sesamoidectomy. (a)
Longitudinal incision in relation to the lateral edge of the first metatarsal fat pad. (b) Identification
and isolation of the plantar digital branch (white arrow). (c) Resection of the fibular sesamoid
(black arrow)
Sesamoiditis 441
10.6 Intractable Plantar Keratosis (IPK)
Alternatives to conservative treatment include resection of the skin lesion, followed

by the use of insoles to avoid areas of overload, and also avoiding the use of high-
heeled shoes. For older patients with plantar fat atrophy, the use of total contact
insoles should also be considered.
In cases that do not respond to conservative treatment and in the absence of plan-
tar flexion of the first metatarsal, surgical alternatives such as sesamoid plantar
shaving of 30–50% can be considered [20]. In patients diagnosed with cavus foot
who present plantar flexion of the first metatarsal, elongation of the Achilles tendon
(Strayer or Hoke) should be considered and/or a first metatarsal elevation osteotomy
(oblique dorsal wedge resection) should be performed. This elevation osteotomy
with a dorsal wedge resection is performed at the base of the first metatarsal from
distal-dorsal to proximal-plantar, as appropriate [19].
11 Complications of Surgical Procedures
11.1 Turf Toe Surgery
Joint stiffness with loss of passive dorsiflexion, this can lead to joint compression,
chondrolysis, and osteoarthritis.
11.2 Medial Sesamoidectomy
Injury to the medial sensory branch and the common digital nerve during the
approach.
Injury of the medial tendon of the flexor hallucis brevis during sesamoid resec-
tion. Valgus and cock-up deformities are deformities associated with medial sesa-
moid resection, which can be avoided by reconstructing the medial soft tissues and
adequately balancing the intraoperative hallux MTP. Another complication associ-
ated with the resection of the tibial sesamoid is the decrease in plantar strength of
hallux MTP due to the decrease of the lever arm.
11.3 Fibular Sesamoidectomy
Injury to the lateral plantar digital branch of the hallux during the approach, painful
plantar scar. Other complications include varus deformity of hallux MTP and loss
of take-off force during the third rocker of the gait cycle.
11.4 Sesamoid Fracture
Complications of surgical treatment of fractures include osteoarthritis of the sesa-

moid metatarsal joint, avascular necrosis, and joint irritation from malposition of
the fixation screw.
References
1. Atiya S. Sesamoiditis of the metatarsophalangeal joint. OA Orthopaed. 2013;1(2):19.

2. Srinivasan R. The Hallucal-Sesamoid complex: normal anatomy, imaging, and pathology.
Semin Musculoskelet Radiol. 2016;20:224–32.
3. Cohen B. Hallux sesamoid disorders. Foot Ankle Clin N Am. 2009;14:91–104.
4. Pretterkleiber ML, Wanivenhaus A. The arterial supply of the sesamoid bones of the hallux.
Foot Ankle. 1992;13(1):27–31.
5. Sobel M, Hashimoto J, Arnoczky SP, et al. The microvasculature of the sesamoid complex.
Foot Ankle. 1992;13(6):359–63.
6. Aper RL, Saltzman CL, Brown TD. The effect of hallux sesamoid excision on the flexor hal-
lucis longus moment arm. Clin Orthop Relat Res. 1996;325:209–17.
7. Sims A. Painful sesamoid of the great toe. World J Orthop. 2014;5(2):146–50.
8. Allen M. The passive axial compression (PAC) test: a new adjunctive provocative maneuver
for the clinical diagnosis of hallucal sesamoiditis. Foot Ankle Int. 2001;22(4):345–6.
9. Greaser M. Foot and ankle stress fractures in athletes. Orthop Clin N Am. 2016;47(4):809–22.
10. Boric I. Hallux Sesamoiditis - radiological diagnostics and conservative management. RAD
540. Med Sci. 2019;48–49:27–32.
11. Clough T. Turf toe injury – current concepts and an updated review of literature. Foot Ankle
Clin N Am. 2018;23(4):693–701.
12. York P. Injuries to the great toe. Curr Rev Musculoskelet Med. 2017; https://doi.org/10.1007/
s12178-017-9390-y.
13. Boike A, Schnirring-Judge M, McMillin S. Sesamoid disorders of the first metatarsophalan-
geal joint. Clin Podiatr Med Surg. 2011;28(2):269–85.
14. Pagenstert G, Hintermann. Percutaneous fixation of hallux sesamoid fractures. Tech Foot
Ankle Surg. 2008;7(2):107–14.
15. Kane J. Radiographic results and return to activity after sesamoidectomy for fracture. Foot
Ankle Int. 2017;38(10);1100–106.
16. Kurian J. Dorsolateral excision of the fibular sesamoid: technique and results. Tech Foot
Ankle. 2014;13:226–35.
17. Efficacy FS. Outcomes, and alignment following isolated fibular sesamoidectomy via a plantar
approach. Foot Ankle Int. 2019;40(12):1375–81.
18. Harris T. Medial approach to lateral sesamoid removal and presentation of case series. Tech
Foot Ankle Surg. 2018; https://doi.org/10.1097/BTF.0000000000000193.
19. Myerson MS. Foot and ankles disorders, vol. 1. Philadelphia: Saunders; 2000.
20. Loretta B. Chou. Orthopaedic knowledge update: foot and ankle, Disorders of Hallucal
Sesamoids. Saul G. Trivino: Intractable Plantar Keratoma (Partial Medial Sesamoidectomy),
2018;1:393.
Metatarsalgia
Pilar Martinez de Albornoz and Manuel Monteagudo
1 Introduction
Metatarsalgia is defined as a symptom of excess pressure in the plantar region of the

forefoot that causes pain and inflammation. The most frequent cause is due to
mechanical alterations, while rheumatic diseases are becoming less prevalent thanks
to new pharmacological therapies. In metatarsalgia there will always be an inflam-
matory process, but the recognition of the mechanical factor that causes it will be
the key to understanding, diagnosing, and treating it correctly. There are feet with a
greater susceptibility to develop metatarsalgia. The anatomical and functional fac-
tors of the leg and foot during the gait cycle can cause a patient to develop metatar-
salgia. Even if a foot has a mechanically nonideal metatarsal formula (index plus
minus is associated with a lower risk of developing metatarsalgia), we cannot con-
sider it pathological as long as it is not painful.
A forefoot with a “pathological” structure can remain painless for years
thanks to the biological mechanisms of adaptation and load transfer, until one
day when the compensation mechanisms fail and pain appear. The “reading” of
the sole of the foot allows us to identify keratoses that “speak” of their mechani-
cal origin during the walking cycle. The visual analysis of the gait, the explora-
tion of the Achilles-calcaneal-plantar system, the identification of the keratoses,
the location of the pain within the forefoot, and the interpretation of weight-
bearing X-rays of both feet allow us to know what type of metatarsalgia the
patient has and to be able to indicate the most appropriate conservative and sur-
gical treatment.
In this chapter we will give some guidelines to the reader to identify the main
mechanical alterations present in the different types of metatarsalgia, and we will
P. Martinez de Albornoz (*) · M. Monteagudo


Switzerland AG 2022
444 P. Martinez de Albornoz and M. Monteagudo
study their consequences on the structures and tissues of the foot. We intend to
establish a clear link between clinical and radiological findings with the diagnosis
and the most appropriate treatment for each type of metatarsalgia.
2 Mechanics: Defining “Normal” and “Abnormal”
Not all metatarsals are the same. We can develop metatarsalgia because we walk,
and if we don’t understand how we walk, we can’t understand how we hurt our-
selves. There are several ways to explain the movement of the human body, and the
theory of the walking cycle and the mechanism of the three rockers described by
Perry [1], from our point of view, is the one that best explains the correlation
between the visual analysis of walking that we can do in consultation and the mech-
anism of generation of metatarsalgia. The nature of gait provides humans a perfect
mechanism to simultaneously achieve a continuous progression in movement as
well as a stable support.
The gait cycle is divided into three rockers or phases:
1. During the initial support phase, the initial contact of the foot is made at the heel,
over which the tibia rotates forward until the forefoot contacts the ground (first
rocker or heel rocker).
2. Once the foot is planted on the ground, the tibia rotates on the talus (second
rocker or ankle rocker); the supporting limb must be functionally longer to allow
the contralateral limb to perform the gait clearance.
3. When the body’s center of mass is anterior to the foot, the tibia rotates on the
metatarsophalangeal joints (third rocker or forefoot rocker) while at the same
time the foot push-off starts.
Metatarsalgia, as a mechanical disturbance, can develop during any of the three
rockers, although most metatarsalgia is generated during the third rocker of the gait.
3 Pathomechanics: How We Get Injured
A foot that has remained without pain for years can become symptomatic at any
moment of life. When the structure of the forefoot or the mechanical leg-ankle-foot
conditions is not harmonic or ideal, the mechanisms of adaptation and compensa-
tion end up failing and producing a mechanical overload in the metatarsal region.
Continuous mechanical overload produces tissue and bone stress, and this biologi-
cal damage can become symptomatic at a given time. Any forefoot tissue can suffer
the consequences of abnormal compression, tension, or shear forces that end up
injuring it [2]. The tissue will eventually develop signs (stigmas) of this overload
that will be visible to the scanner. Following the theory of the three rockers, we will
Metatarsalgia 445
explain the causes of metatarsalgia, its relationship with the gait cycle, its diagnosis,
and the solutions to be considered to improve the patient.
1. First rocker: Physiologically, during the first rocker, there is no contact between
the forefoot and the ground, so it would not be possible to generate first rocker
metatarsalgia. However, there are patients with pathological, neurological, or
post-traumatic equinus, who perform their first rocker on the forefoot instead of
on the heel.
2. Second rocker: During the second rocker of gait, the foot is plantigrade with
respect to the ground. Any mechanical overload on the metatarsal head during
the second rocker will increase the vertical and compressive forces to the soft
tissues located strictly plantar to the metatarsal head. The mechanical factors that
can potentially increase plantar pressure during the second rocker with the foot
planted on the ground are (i) a shortening of the gastrocnemius and/or (ii) an
excessive plantar tilt of a metatarsal. These factors can act in isolation or some-
times in combination to cause metatarsalgia.
(i) Shortening of the gastrocnemius: Under ideal mechanical conditions, in the
final milliseconds of the second rocker, the knee should achieve full exten-
sion and the ankle full dorsiflexion. When a patient has a short gastrocne-
mius, full dorsiflexion of the ankle cannot be executed with full extension of
the knee, and ground reaction forces will act on the metatarsal area causing
tissue damage. If the patient develops compensation mechanisms to avoid
this unfavorable mechanical situation – bouncy gait or tarsal pronation to
reach plantigrade – he or she can avoid metatarsal overload and not develop
second rocker metatarsalgia [3].
(ii) Excessive plantar tilt of a metatarsal (increased metatarsal incidence angle):
The anatomical and/or functional tilt of the metatarsals is crucial to ensure
adequate load distribution under each metatarsal head in the frontal plane
[4]. Excessive anatomical plantar flexion of one or more metatarsals (e.g.,
in a pes cavus), contiguous elevation of a metatarsal (such as iatrogenic
elevation following a fracture or osteotomy), or inadequate adaptation at
the Lisfranc joint may lead to the development of second rocker
metatarsalgia.
An example that we see in consultation with some frequency of second rocker
metatarsalgia is the case of painful keratosis located under the head of the 4th
MT. In the exploration of these patients, we found an excessive plantar flexion of the
fourth metatarsal, either constitutional or due to a lack of compensation in the sagit-
tal plane in the Lisfranc joint and a Silfverskiöld maneuver that indicates the exis-
tence of a gastrocnemius-dependent equinus. The relative length of the metatarsals
is not relevant in this phase of the gait, but it will be in the next one.
3. Third rocker: During the third rocker or propulsive phase, the ankle is subjected
to progressive flexion, and the longitudinal axis of the foot is placed vertically on
the ground. The body weight falls just on the front region of the plantar pad and
the structures that receive a greater load are those plantar-distal to the metatarsal
head (plantar plate, fat pad, skin). Keratoses in third rocker metatarsalgia are
plantar-distal to the metatarsal head and not strictly plantar as in second rocker.
The mechanical factors related to a third rocker scenario would be (i) the hallux:
an index minus or a hallux valgus could cause a loss of propulsive power in the
first radius generating a load transfer to the lesser metatarsals, and (ii) the rela-
tive length of the lesser metatarsals within the metatarsal parabola, with a non-
harmonic length causing an overload of certain metatarsal(s).
Although controversial, the metatarsal parabola described by Maestro is a good
model for explaining pathology in the third rocker and for treatment planning, pro-
vided that the sagittal plane does not present constitutional anomalies. The metatar-
sal formula that is associated with a smaller number of patients with metatarsalgia
is the index plus minus. The first metatarsal is equal to or slightly shorter than the
second, and the lesser metatarsals are in a decreasing parabola, all in a dorsal pro-
jection weight-bearing feet X-ray [5]. Ideally, and in order for the first radius to be
mechanically more competent, the head of the first metatarsal should be centered
over the sesamoids.
All metatarsal radiological variants are considered normal as long as the foot is
painless and functional. They will be considered pathological when symptoms
develop. Nonharmonic metatarsal formulas have a greater tendency to develop third
rocker metatarsalgia than harmonic formulas.
Depending on the phase of the gait in which the metatarsalgia is generated, we
can consider in a general way (excluding the atypical cases of first rocker) [4]:
(i) Metatarsalgia of 2nd rocker or non-rocker
(ii) Metatarsalgia of 3rd rocker or propulsive
Most of the metatarsals we treat in consultation are third rocker. Tissue stress, in
addition to pain, also produces deformities and histological changes such as kerato-
ses, soft tissue inflammation, bone adaptations, and bone stress reactions. The
knowledge of why and how metatarsalgias are generated will allow us to diagnose
and treat them. Some patients present mixed metatarsalgia, frequent in iatrogenic
cases, with signs and stigmas of second and third rocker in the same forefoot, and
require combined solutions of second and third rocker in the same forefoot.
4 Diagnosis of Metatarsalgia
As explained in the previous section, the orthopedic surgeon must know how to
“read” the sole of the foot, how to detect equinus, and how to “read” a bilateral feet
weight bearing X-ray.
Metatarsalgia 447
4.1 Physical Exploration
Examination (“reading”) of the sole of the foot, keratoses, limb alignment, and
visual analysis of the gait provide valuable information for understanding the
pathomechanics of metatarsalgia. With this information, even before having the
X-rays, the doctor must be able to recognize the main alterations and correlate the
metatarsalgia with one of the walking rockers. Plantar keratoses are key to suspect-
ing what type of mechanical stress is responsible for the clinical condition of each
patient. Increased pressure and/or shear forces are responsible for the development
of plantar calluses. The morphology and location of plantar keratoses reflect the
contact pattern between the foot and the ground.
The exploration of a metatarsalgia follows the reference of the previously men-
tioned rockers:
• Second rocker (non-propulsive metatarsalgia): Second rocker keratoses are strictly
located plantar to the metatarsal head and can be “drawn” only to the correspond-
ing metatarsal, without tendency to coalesce with neighboring lesions. In the sec-
ond rocker, the plantar plate is not damaged, and the progressive deformities that
can be associated in this phase are the digital claws with subluxation (never com-
plete dislocation) of the metatarsal-phalangeal joints. The elastic component of the
gastrocnemius can play an important role in the transition from the second to the
third rocker. An equinus will cause an increase in the reaction forces of the soil
against the metatarsal region. The “split-second effect” describes this mechanism
and its clinical consequences [3]. The Silfverskiöld test evaluates if the retraction
of the gastrocnemius is the only mechanism responsible for the equinus (positive
test) or if there is some other factor that causes the equinus (negative test: there is
not an increase of the dorsiflexion of the ankle with the knee bent and the forefoot
supinated to avoid the mediotarsial sagittal movement) [6].
Figure 1 shows sole of the foot with second rocker keratosis.
• Third rocker (propulsive metatarsalgia): During the third rocker, the foot rotates
externally on the ground, and this rotation produces a shearing of the plantar fat
pad located in a plantar-distal position to the lesser metatarsal heads. Keratoses
appear planto-distal to the bone plane. They often fuse with neighboring kerato-
ses, so that a single diffuse, rounded keratosis can appear, making it difficult to
recognize the metatarsal(s) involved in the lesion [4].
Figure 2 is sole of the foot with third rocker keratosis.
During this phase, the metatarsal is positioned vertically to the floor, transmitting
axial compressive forces on the plantar plate. The chronic overloading of the plantar
plate causes its rupture, allowing the base of the phalanx to be completely dislocated
dorsally, until the phalanx and metatarsal are placed parallel to each other. In addi-
tion, axial forces along the MT bone equally compress the compact/cortical and
cancellous bone. Since most of the MT head is made up of cancellous bone and its
modulus of elasticity is lower than the cortical bone, a transverse fracture could
occur in the MT head itself, deteriorating blood flow and producing secondary
Fig. 1 Foot sole with

second rocker keratosis.
Patient with second rocker
metatarsalgia and
circumscribed plantar
keratosis under the head of
the fourth metatarsal
osteonecrosis (Freiberg’s disease). This collapse of the metatarsal head sometimes

shortens the bone to the point necessary to achieve an ideal metatarsal parabola [7].
Many patients (especially after failed surgery) may present stigmas of both types
of mechanical metatarsalgia (mixed metatarsalgia), which makes the analysis and
management of these cases difficult. There are some “special” metatarsalgias that
we must correlate with the right gait rocker in order to plan the correct treatment.
Metatarsalgia with extensor recruitment (second rocker): When the tibialis ante-
rior does not mechanically assist the foot in the transition from the second to the
third rocker, either because of neurological dysfunction or because of a pes cavus,
the extensor digitorum longus is recruited to assist in propulsion. The problem is
that its activation occurs during the second rocker and is maintained during the third
rocker ending up in a claw toe that can be painful by rubbing against the footwear.
These claws never end up producing a complete dislocation but rather a subluxation
Metatarsalgia 449
Fig. 2 Foot sole with third

rocker keratosis. Patient
with bilateral third rocker
metatarsalgia and diffuse
plantar keratoses in lesser
metatarsals. The keratoses
are not limited to a single
radius
with sliding of the phalanx over the dorsal region of the head of its metatarsal. The
metatarsal pain is strictly plantar to the metatarsal head. The surgical treatment con-
sists in a extendor digitorum longus tenotomy and a secondary reinsertion into the
lateral cuneiform.
Figure 3 is extensor replacement case.
Metatarsalgia with second intermetatarsal space (third rocker) syndrome: The sec-
ond space syndrome is a group of signs and symptoms, including divergence of the
second and third toes in a weightbearing situation (they may not be divergent non-
weightbearing), with third rocker metatarsalgia. Sometimes there are neuritic symp-
toms similar to those produced by a third space Morton’s neuroma [8]. The second
space syndrome is accompanied by a third rocker keratosis. The cause is found in a
second and third metatarsal that is longer than the first and fourth, thus producing a
“pole effect” during the third rocker. The second and third toes diverge in an attempt
to gain a greater base of support and strength for propulsion and because of meta-
tarsophalangeal joint synovitis [9]. This is a third rocker metatarsalgia and the short-
ening of the second and third metatarsals until a harmonic metatarsal parabola is
achieved usually cures the metatarsal pain.
Figure 4 shows second space syndrome.
4.2 Radiological Examination: How to Read a

Weightbearing X-ray
The radiological study of the patient with metatarsalgia should include comparative
anteroposterior and lateral feet weightbearing X-rays. In order to estimate deformi-
ties, make measurements, and plan surgical correction, the projections of the loaded
a b
c d
Fig. 3 Extensor recruitment. The images show a typical case of extensor recruitment by a shorten-
ing of the medial gastrocnemius. (a–c) In the visual examination of the gait cycle, there is an exten-
sor substitution of the lesser toes that results in a flexible claw deformity of the toes. (d) In the right
foot sole, he presents some mixed painful keratoses under the heads of the 2nd–third metatarsals
and in the left foot some mixed keratoses under the head of the second metatarsal
radiographs must be technically accurate. The dorsal-plantar projection must be

centered and focused between both feet so that the examination is reproducible and
reliable. The second cuneometatarsal joint should be clearly seen (the joint should
show an orthogonal projection) [10]. There should be a geometric regression from
the first to the fifth metatarsal. In the ideal formula, the length of the first metatarsal
should be equal to or slightly shorter than the second metatarsal (index plus minus)
[5], and the head of the first metatarsal should cover both sesamoids. Maestro estab-
lished [5] that the center of the lateral sesamoid and the center of the head of the
fourth metatarsal should be at the same level in a dorsal-plantar projection. The
lateral projection must be able to show the tibia perpendicular to the floor. Figure 5
shows normal weightbearing feet X-rays.
Metatarsalgia 451
a b
Fig. 4 Second space syndrome. The images show the case of a patient with a “second space”
syndrome. (Image a) feet in standing position with divergence of second and third toes. (b) Image
of the diffuse plantar keratosis around the second metatarsal. (c) The dorsal-plantar projection of
the X-ray of the feet in load shows an index minus formula with an increased relative length of the
lesser rays and a complete dislocation of the third metatarsophalangeal joint in the right foot
Second rocker (non-propulsive metatarsalgia): In most second rocker metatarsal-

gia, the weightbearing radiographs reveal a correct metatarsal parabola in the dor-
sal-plantar projection, and the problem lies in the sagittal/coronal plane due to
increased plantar flexion of the metatarsal head. The surgeon must focus on the
lateral projection where the alignment of the first and second metatarsal can be
visualized. In an unoperated foot, the dorsal cortex of the diaphysis of both metatar-
sals should be (ideally) parallel. In this projection it is sometimes possible to iden-
tify a metatarsal with a different inclination to the neighbors (in dorsiflexion or
Fig. 5 Bilateral feet weightbearing X-ray and “normal” parameters. Dorsal-plantar foot projec-
tion under load. The X-ray is correctly centered and the second cuneometatarsal joint is visualized.
This would be a case of “ideal foot”: with index plus minus formula, in which there is a similar
length of the first and second metatarsals, the head of the first metatarsal covers both sesamoids,
there is a geometric regression of all rays and the center of the lateral sesamoid is centered or over
the head of the fourth metatarsal
plantar flexion). The axial sesamoid projection (Walter-Müller) can be helpful to

estimate the relative position of the metatarsal heads and the arthritic changes of a
dysplastic head.
Third rocker (propulsive metatarsalgia): The metatarsal parabola in weightbear-
ing X-rays, in dorsal-plant projection, is relevant in the diagnosis and management
of third rocker metatarsalgia. As previously mentioned, the problem may lie in:
(a) The hallux: when the head of the first metatarsal is not centered on both sesa-
moids (as in a hallux valgus), or the hallux is too short (index minus), there will
be a decrease in the efficiency of the mechanical work of the first radius, caus-
ing transfer metatarsalgia [11]. This scenario is especially evident when in
failed hallux valgus surgery there is a shortening and elevation of the first meta-
tarsal or its head.
(b) The length of the lesser metatarsals: The harmonic parabola with decreasing
lengths of the lesser metatarsals described by Maestro correlates well with the
diagnosis of third rocker metatarsalgia. In addition, we can use the same projec-
tion to measure the relative lengths of the metatarsals and perform correct pre-
operative planning. The amount (in millimeters) of shortening of the lesser
metatarsals and the correction/translation (in millimeters) of the hallux should
be calculated on weightbearing radiographs [7].
The physical examination together with weightbearing X-rays provide us with
enough information to be able to diagnose and manage 90% of all cases of metatar-
salgia. Rarely additional tests are required. Magnetic resonance imaging (MRI) can
Metatarsalgia 453
be helpful in assessing soft tissue, cartilage, and bone damage. MRI is useful for
diagnosing and quantifying the involvement in Freiberg’s disease, a stress fracture, a
ruptured plantar plate, or a soft tissue tumor. Computed tomography (CT) is used for
the evaluation of nonunions or malunions, loss of bone stock, subchondral cysts,
osteophytes, sclerosis, and alterations in the normal contour of the metatarsal heads.
The development of weightbearing CT can be helpful to accurately calculate meta-
tarsal lengths and angles of a metatarsal with respect to its neighbors. It is a great
tool in preoperative planning as well [12].
5 Treatment of Metatarsalgia
In any metatarsalgia, conservative treatment should always be attempted before sur-

gery is indicated. Being a mechanical problem, conservative treatment solutions
will also be mechanical.
5.1 Conservative
Generally, conservative treatments include pain medication, anti-inflammatory,

rehabilitation devices, physical therapy, stretching exercises, insoles, and footwear.
Nonmechanical treatments (other than insoles and footwear) have a very partial
and limited effect in time. But there are patients who improve with them. The expla-
nation may be due to the decrease in inflammation and the mechanisms of compen-
sation/transfer of the foot can once again function by entering a period of pain and
functional improvement.
Insoles are the cornerstone of treatment for metatarsalgia. Usually, and in order
to achieve symptomatic relief, a retrocapital pad/olive is formed (behind the meta-
tarsal heads) and with some medial longitudinal arch support, in EVA (ethylene-
vinyl-acetate)-type material [13]. In second rocker metatarsalgia, the point of
highest load is located under the metatarsal head, so the templates may incorporate
a fenestration (depression) under the affected metatarsal head. In third rocker meta-
tarsalgia, the insoles will focus on improving the function of the hallux and reliev-
ing the excess load on the planto-distal region of the metatarsal fat pad. To improve
hallux function, it may be helpful to incorporate a kinetic wedge under the head of
the first metatarsal to passively increase dorsiflexion of the first metatarsophalan-
geal joint [14]. To reduce the load on the central metatarsal region, insoles can be
fitted with an retrocapital pad. The increased surface area for load distribution
should decreae the metatarsal heads pressure and thus relieve metatarsalgia. The
retrocapital elevation also relaxes the transverse arch of the metatarsal area and
allows for pain relief by decompression of the interdigital spaces [14].
The metatarsal retrocapital bars unload all metatarsal heads. In some studies they
have shown greater efficacy than metatarsal retrocapital olives in reducing pain and
in forefoot function [15]. Figure 6 shows insoles.
Footwear can also help a patient with metatarsalgia. A wide toe-box can relieve
pain in patients with toe deformities like claw toe or Hallux Valgus. Reducing heel
height in women’s shoes reduces pain in propulsive metatarsalgia. Soft-soled shoes
usually relieve any type of metatarsalgia. Today, many brands are incorporating air
chambers in the soles or very soft materials such as memory foam, which allow
many patients to function with tolerable pain. Rocker-soled shoes improve the tran-
sition from the first to the third rocker gait phase and can alleviate metatarsalgia
symptoms. Those shoes may help as well in cases with reduced hallux range of
motion [16].
It usually takes about 4–6 months for insoles and appropriate footwear to reach
their maximum effect. If after that time the patient remains symptomatic and very
limited in his or her daily activities, surgery may be indicated.
5.2 Surgical
The goal of metatarsalgia surgery is the achievement of a painless, plantigrade,

functional foot.
Second rocker (non-propulsive metatarsalgia): Remembering the pathome-
chanics, a second rocker metatarsalgia can be due to two factors that can be found
isolated or combined – a shortening of the gastrocnemius and an excessive incli-
nation of a metatarsal – and solutions will go through modifying these two
scenarios.
Lengthening of the gastrocnemius: With the Silfverskiöld test, we can confirm if
the patient with second rocker metatarsalgia has a gastrocnemius-dependent
Fig. 6 Insoles. Test

template with retrocapital
bar for the treatment of
third rocker metatarsalgia.
Once its efficacy is
confirmed, the lining is
completed
Metatarsalgia 455
equinus. In these patients, tricep lengthening can be performed at different anatomi-

cal levels. The more distal (close to the calcaneus) is the release, more lengthening
is achieved, but also greater is the loss of muscle power in the gastrocnemius.
Numerous techniques – Baumann, Strayer, and Vulpius – have been described to
lengthen the triceps. Our experience indicates that it is not necessary to resort to
distal techniques and that most patients improve when the release of the gastrocne-
mius is limited to the medial gastrocnemius muscle head and is performed in the
most proximal region (popliteal zone of Silfverskiöld) [6]. Under local anesthesia
and through a small posterior and medial incision in the back of the knee, the sur-
geon easily accesses the superficial fascia in the popliteal region. After the fascia is
incised, the tendon of the medial gastrocnemius is individualized and cut. At this
level, the risk of excessive triceps surae elongation and neurovascular injury is
extremely low.
Figure 7 shows proximal gastrocnemius lengthening.
Proximal osteotomies: Traditionally, proximal osteotomies of the metatarsals
have been useful tools when it was necessary to elevate a metatarsal in the presence
of 2nd rocker metatarsalgia. A dorsal wedge osteotomy in the proximal metaphysis
of an excessively plantarized lesser metatarsal allowed relief of localized metatar-
salgia. The two models of osteotomy that allow the controlled elevation of a meta-
tarsal are the Goldfarb model and the BRT model (Barouk, Rippstein, Toullec) [17].
In the Goldfarb osteotomy, a dorsal closing wedge is performed in a chevron-shape.
Immediate weightbearing with a compliant patient is required to maintain the meta-
tarsal elevation until consolidation. But it was frustrating at times, if the patient was
in pain or afraid to perform loading, that the osteotomy would not lift the operated
metatarsal as much as it should. For this reason, the BRT osteotomy incorporated
synthesis with a screw. The BRT osteotomy is an oblique dorsal closing wedge
osteotomy. But what happens in the Goldfarb osteotomy depends on the patient’s
good work, in the BRT depends on the surgeon’s good work. And it is very compli-
cated to calculate (and execute) how much wedge to cut in order to raise the neces-
sary amount.
Fig. 7 Proximal medial

gastrocnemius lengthening.
Proximal lengthening in
the popliteal zone of the
medial gastrocnemius:
semi-circumferential
incision of the fibers of the
aponeurosis
And, again, it was frustrating to perform a BRT and elevate a metatarsal with the
clinical improvement of the metatarsalgia and the disappearance of the keratosis to,
a few months later, find the same situation in the neighboring metatarsal. The
appearance of transfer metatarsalgia is very common after a proximal elevation
osteotomy [7].
Distal osteotomies: The highly variable results of proximal osteotomies led to
the idea of a more reliable surgical procedure that would better control the elevation
of the lesser metatarsal without causing transfer metatarsalgia. The more distal the
osteotomy, the greater the control, but the lower the amount of elevation. The
Suppan-type osteotomy (“tilt-up” in the Anglo-Saxon literature) [18] consists of an
extra-articular cut preserving the cartilage, made in the neck of the metatarsal with
extraction of a dorsal wedge that will allow (as in a Freiberg) [19] the restoration of
the height of the metatarsal head and the relief of plantar pressure. If the collateral
ligaments are maintained, the osteotomy does not require internal fixation and
allows for immediate loading with very little discomfort to the patient, which usu-
ally makes them compliant with walking in postoperative shoes until the osteotomy
is healed. The results are more predictable, and the potential risk of producing trans-
fer metatarsalgia is much lower than with proximal osteotomies.
Figure 8 shows Suppan-type osteotomy.
There is no formula for deciding when to associate both surgeries – gastrocne-
mius lengthening and osteotomy – in the treatment of second rocker metatarsalgia,
but our threshold for performing a gastrocnemius lengthening is low if the patient
has a clear Silfverskiöld test or if he or she suffers or has suffered from other equine-
related pathologies (non-insertional Achilles tendinopathy, proximal plantar fasci-
itis). Our most common treatment for second rocker metatarsalgia combines
proximal lengthening of the medial gastrocnemius with a distal tilt-up osteotomy of
the problem metatarsal without internal fixation.
Third rocker (propulsive metatarsalgia): As previously mentioned, in third rocker
metatarsalgia, we can find two factors to be reconstructed in a surgery: a first radius
with a deformity (hallux valgus) or dysfunction (hallux limitus or rigidus) and lesser
metatarsals with a nonharmonic metatarsal parabola. The existence of an equinus
has no role in the generation of third rocker metatarsalgia, so it will not make any
sense to perform a gastrocnemius lengthening in these patients.
a b
Fig. 8 Suppan-type osteotomy. (a) An extra-articular cut is designed, preserving the cartilage,
performed on the metatarsal neck with extraction of a dorsal wedge. (b) The osteotomy allows
elevation and restoration of the height of the metatarsal head and relief of plantar pressure
Metatarsalgia 457
Hallux valgus treatment will not be treated in this chapter. This section will focus
on what type of intervention can be performed to improve the metatarsal formula
[5]. The controlled shortening of the lesser metatarsals, can be achieved through
shortening osteotomies. It is very important to avoid metatarsal elevation or descent
in order to avoid undesired a second rocker iatrogenic metatarsalgia. Although the
most popular osteotomy for third rocker metatarsalgia is Weil’s cervical-cephalic
and its variants, mini-invasive techniques have increased in popularity in recent years.
Cervicocephalic Weil and triple Weil osteotomy: Distal metatarsal osteotomies,
such as Weil and triple Weil osteotomies, are designed to produce a controlled short-
ening and allow the restoration of the ideal metatarsal parabola, with the secondary
forefoot load redistribution. Weil described a simple technique to shorten the lesser
metatarsals in a controlled manner [17]. In the distal area of the metatarsal, a single
cut in the transverse plane allows the proximal sliding of the metatarsal head. The
amount of shortening achieved can be calculated by measuring the length of the
upper distal end of the proximal fragment. The osteotomy starts around 2 mm distal
from the dorsal tip of the metatarsal head, and the inclination of the cut should be
made almost parallel to the floor in the second metatarsal and progressively increas-
ing the inclination of the cut as we progress toward the more lateral metatarsals. The
surgeon must be familiar with the anatomy of the bone to achieve a proper tilt plane
in each metatarsal. When planning shortening osteotomies, the surgeon should eval-
uate how many metatarsals should be shortened and how much shortening should
be achieved in each one. A weightbearing anteroposterior X-ray is required for sur-
gical planning. Barouk described the term “maximum shortening point” to assist in
the preoperative planning [17]. This corresponds to the point of greatest deformity
of the most affected metatarsal. This point is taken as a reference to calculate the
amount of shortening required on that radius. The base of the phalanx is usually the
location for the maximum shortening point. This spot is the reference point where
the metatarsal should be after shortening it. In many occasions it is necessary to
shorten more than one metatarsal. When we achieve a harmonic metatarsal parabola
in the dorsal plane, without causing iatrogeny in the sagittal plane, we can be sure
that the patient will achieve an improvement in pain and that the result will be very
durable. The results of Weil’s osteotomy have been well documented. Floating toes
and joint stiffness are the most common complications after Weil’s osteotomy [20].
These were especially evident in shortenings greater than 3 mm. In large shorten-
ings, the center of rotation of the metatarsal head would be below the center of
action of the interosseous muscles that would go from functioning as plantar flexors
to functioning as dorsiflexors. To avoid these complications, Maceira [21] popular-
ized the triple cut (triple Weil), achieving that the center of rotation of the metatarsal
head would be above the working axis of the interosseous muscles, which would
function as plantar flexors (avoiding floating toe). Furthermore, the postoperative
bandages with plantar flexor effect during the first 4 weeks facilitate a good soft tis-
sue healing and a better plantar motion of the lesser metatarsophalangeal joints. The
bandage provides rotational stability in the transverse plane and helps prevent dor-
sal and distal displacement of the metatarsal head, which justifies that the Weil
osteotomy without fixation can have similar results to the Weil with fixation,
although assuming a greater risk of displacement according to the degree of compli-
ance of the patient. Figure 9 shows triple Weil osteotomy.
When there is a degenerative metatarsophalangeal dislocation as a consequence
of long-lasting propulsive metatarsalgia, a degenerative rupture of the plantar plate
has occurred. In recent years, numerous techniques of reconstruction of the plantar
plate have been described in association with Weil’s osteotomy [22]. Most studies
of plantar plate repair have shown favorable results in terms of patient satisfaction,
pain, and AOFAS scores [23]. However, these results should be interpreted with
caution because of the inherent limitations of the studies (mostly case series without
a b
c d
Fig. 9 Triple Weil osteotomy. Weil and triple Weil osteotomy design. (a) Diagram of the metatar-
sal head and interosseous musculature located at the center of rotation. (b) Weil’s osteotomy with
cut in the transverse plane and proximal and plantar sliding of the metatarsal head. The center of
rotation remains plantar to the interosseous musculature. (c) Subtraction wedge design and double
cut parallel to the first one. (d) Final result of the triple Weil osteotomy in which the metatarsal
head is elevated and the center of rotation is restored. (e) Front view of the Weil metatarsal oste-
otomy ready to be fixed
Metatarsalgia 459
a control group) and because most of the patients included had undergone several
combined procedures (including Weil’s osteotomy) that could have skewed the
results [22, 23]. The authors are not in favor of the plantar plate repair in degenera-
tive cases because of the most frequent complication of its reconstruction – joint
stiffness. This complication is almost always symptomatic. In comparison, the most
common Weil osteotomy complication is floating toe, which is rarely symptomatic
and easy to repair. The Weil-type osteotomies and their variants are versatile and
also allow displacements toward medial or lateral of the metatarsal heads in case of
varus or valgus toe deviations. Figure 10 shows pre- and postoperative radiographs
of a complete realignment of the forefoot.
a b
Fig. 10 Pre- and postoperative radiographs of a complete realignment of the forefoot. Surgical
management of third rocker metatarsalgia. (Image a) Right foot with severe hallux valgus and
complete dislocation of the second metatarsal. (Image b) Surgical correction of the first metatarsal
with the head centered on the sesamoids and shortened to where the base of the proximal phalanx
was. Shortening of the second metatarsal to where the base of the proximal phalanx was to reduce
the dislocation. Shortening and regularization of the rest of the metatarsal parabola
Mini-invasive metatarsal osteotomies: Any surgical technique, open or mini-

mally invasive (MIS), is valid as long as it achieves the final purpose previously
indicated, to restore mechanical abnormalities and relieve pain. When a harmonic
restoration of the metatarsal parabola is achieved under load, it is indifferent whether
the result has been achieved with one or another osteotomy type or with an open or
mini-invasive technique. The most popular type of osteotomy within MIS surgery of
the forefoot is the distal metatarsal osteotomy (“distal metatarsal metaphyseal oste-
otomy,” DMMO). This is a percutaneous extra-articular osteotomy of the metatarsal
neck without any internal fixation. The amount of shortening in MIS osteotomies is
influenced by multiple factors including the release of soft tissue and the geometric
parameters of the osteotomy itself. Since no fixation is performed, the ground reac-
tion forces together with the immediate shortening forces will determine the final
position and orientation of the metatarsal heads. These mini-invasive techniques are
usually associated with less joint stiffness, but their results are potentially more
variable than open techniques because they depend on the patient’s compliance so
that the postoperative load is continuous and homogeneous and the osteotomies
consolidate without movements in the sagittal plane [24]. Figure 11 shows metatar-
sal realignment by minimally invasive surgery.
The authors usually perform triple open Weil osteotomies in third rocker meta-
tarsalgias. In the preoperative study, we calculate and draw on the radiography the
ideal metatarsal parabola. During the surgery we check with radioscopy the new
formula achieved. Once we reach the desired formula, we fix the osteotomies with
self-breaking twist-off screws.
Iatrogenic (mixed metatarsalgia): The safer, more reliable, and faster the surgical
procedures are, the more we increase the number of surgeries we do. The number of
surgical procedures on the forefoot has increased continuously in the last decades, but
with it the number of complications and new sequels has also increased. When the
surgeon does not correctly identify the type of metatarsalgia, it is easy to end up creat-
ing sequelae in the patient. A metatarsal elevation osteotomy (second rocker solution)
performed on a third rocker metatarsalgia will only succeed in creating a transfer
metatarsalgia on the neighboring metatarsal. A shortening osteotomy (third rocker
solution) performed on a patient with second rocker metatarsalgia will only change
the location of the keratosis and pain. Many iatrogenic metatarsalgias are mixed and
present a nonharmonic parabola in the dorsal and sagittal planes. These mixed pat-
terns are a new challenge for the foot surgeon. These mixed metatarsals often require
the combination, in the same operation, of shortening and elevation osteotomies in
the same or different metatarsals. The physical examination and weightbearing
X-rays allow to plan a “a la carte” treatment. When the joints are destroyed by previ-
ous surgical procedures, a frequently performed surgery for rheumatic forefeet is
recommended, as it is the first metatarsophalangeal arthrodesis in addition to a
lesser metatarsal heads resections (Hoffman procedure). The metatarsal head resec-
tion must also follow the formula of a harmonic parabola, with decreasing length
from the second to the fifth. Thee neoformation of fibrous joints usually gives a great
pain relief and a recovery of the plantar fat pad cushioning. Figure 12 shows iatro-
genic metatarsalgia.
Metatarsalgia 461
a b
Fig. 11 Metatarsal realignment through minimally invasive surgery (MIS). Surgical treatment of
third rocker metatarsalgia using minimally invasive techniques. (Image a) Severe bilateral hallux
valgus and third rocker metatarsalgia. (Image b) Right foot: radiography 3 months after surgery
with percutaneous correction of the first radius and percutaneous DMMO osteotomies without
fixation of second, third, and fourth rays. (Image c) Radiological control 12 months after surgery
of the right foot with healed osteotomies. Left foot with similar surgical management
Author’s treatment of choice in metatarsalgia:

1. Clinical exploration:
–– Static: Standing
–– Dynamic: Gait cycle
2. Weight-bearing feet X-rays
1 + 2: Provides 90% of the information needed to diagnose and discern
between second or third rocker metatarsalgia
Second rocker metatarsalgia: proximal medial gastrocnemius release in the pop-
liteal fosa and/or distal tilt-up metatarsal osteotomy
a b
c d
Fig. 12 Iatrogenic metatarsalgia. Case of a patient undergoing MIS surgery of the right foot.
Images (a–c) show the sequelae of severe deformities, mixed metatarsalgia, and non-plantable and
non-shoeable foot. Images (d, e) show surgical rescue using the Hoffmann technique. Figures (f,
g) show the images of the plantigrade, aligned, and painless foot
Metatarsalgia 463
e f
Fig. 12 (continued)
Third rocker metatarsalgia: approximately 90% of total cases of metatarsalgia.

Weil’s triple osteotomy used to shorten one or more metatarsals to achieve an ideal
metatarsal parabola.
The postoperative protocol include bandages that keep toes in plantar flexion for
4 weeks.
6 Conclusions
Metatarsalgia can develop in any of the three walking cycles. Second rocker or non-
propulsive metatarsalgia is less frequent than third rocker or propulsive
metatarsalgia.
Physical examination, including gait analysis, and weightbearing X-rays will
provide 90% of the most frequent metatarsalgia causes. That information will guide
the treating surgeon to the most appropiate treatment.
Adequate insoles improve most metatarsalgias. If they fail, surgery is indicated.
The surgical objective, regardless of the technique used, is to achieve a harmonic
metatarsal parabola. The authors prefer distal elevation osteotomies in second
rocker metatarsalgia assessing a proximal gastrocnemius lengthening if necessary
and triple Weil osteotomies in third rocker metatarsalgia assessing a hallux correc-
tion if necessary.
Table 1 Management of second rocker –non-propulsive- metatarsalgia

Examination features WB X-ray findings Surgical options
Keratoses Isolated keratosis Stress fracture located at the Goal: elevating the
pattern underneath the MT head neck of the MT affected MT ray
Keratoses located (Deutschländer fracture) Procedures:
strictly plantar to the Distal MT
MT head osteotomy: tilt-up
Proximal MT
osteotomy
Dislocations Claw toes Correct metatarsal formula in
the dorsoplantar view
Walking Extensor over
pattern recruitment
Silfverskiöld Most patients positive Proximal medial
test (gastrocnemius gastrocnemius
tightness) release
MT metatarsal, WB weight-bearing
Table 2 Management of third rocker-propulsive-metatarsalgia

Examination features WB X-ray findings Surgical options
Keratoses Diffuse keratosis that Stress fracture at the Goal: achieving a harmonic
pattern may span several head of the MT metatarsal formula.
heads (Freiberg disease) Procedure: realignment of
Keratosis located the MT parabola
planto-distal to the
MT head
Dislocations Rupture of the plantar Index minus MT formula Correction of the HV
plate Hallux valgus Weil osteotomy
MTPJ dislocations MTPJ dislocations Triple Weil osteotomy
Walking Worsen on heels
pattern
Silfverskiöld Variable No need to lengthen
test gastrocnemius in third rocker
metatarsalgia
MT metatarsal, WB weight-bearing, MTPJ metatarsophalangeal joint, HV Hallux valgus
Table 1 explains management of second rocker metatarsalgia.

Table 2 explains management of third rocker metatarsalgia.
References
1. Perry J. Gait analysis: normal and pathological function. Thorofare: Slack; 1992.
2. Espinosa N, Brodsky JW, Maceira E. Metatarsalgia. J Am Acad Orthop Surg. 2010;18:474–85.
3. Amis J. The split second effect: the mechanism of how equinus can damage the human foot
and ankle. Front Surg. 2016;27(3):38.
Metatarsalgia 465
4. Espinosa N, Maceira E, Myerson MS. Current concept review: metatarsalgia. Foot Ankle Int.
2008;29:871–9.
5. Maestro M, Besse JL, Ragusa M, et al. Forefoot morphotype study and planning method for
forefoot osteotomy. Foot Ankle Clin. 2003;8:695–710.
6. Barouk LS, Barouk P. Compte-rendu symposium gastrocnémien court. Toulouse Maitrise
Orthopédique. 2006;159:21–8.
7. Maceira E, Monteagudo M. Transfer metatarsalgia post hallux valgus surgery. Foot Ankle
Clin. 2014;19(2):285–307.
8. Viladot-Pericé A. Patología del antepié. Barcelona: Toray; 1974.
9. Maceira E, Monteagudo M. Mechanical basis of metatarsalgia. Foot Ankle Clin. 2019
Dec;24(4):571–84.
10. Ozonoff MB. Pediatric orthopedic radiology. Saunders; 1979. ISBN:0721670342.
11. David-West KS, Moir JS. Radiological assessment of tibial sesamoid position after scarf oste-
otomy for hallux valgus correction. Foot Ankle Surg. 2002;8:209–12.
12. Lintz F, de Cesar NC, Barg A, Burssens A, Richter M. Weight Bearing CT International Study
Group. Weight-bearing cone beam CT scans in the foot and ankle. EFORT Open Rev. 2018
May;3(5):278–86.
13. Arias-Martín I, Reina-Bueno M, Munuera-Martínez PV. Effectiveness of custom-made foot
orthoses for treating forefoot pain: a systematic review. Int Orthop. 2018;42(8):1865–75.
14. Park CH, Chang MC. Forefoot disorders and conservative treatment. Yeungnam Univ J Med.
2019;36(2):92–8.
15. Deshaies A, Roy P, Symeonidis PD, LaRue B, Murphy N, Anctil E. Metatarsal bars more effec-
tive than metatarsal pads in reducing impulse on the second metatarsal head. Foot (Edinb).
2011;21(4):172–5.
16. Hutchins S, Bowker P, Geary N, Richards J. The biomechanics and clinical efficacy of footwear
adapted with rocker profiles--evidence in the literature. Foot (Edinb). 2009;19(3):165–70.
17. Barouk LS. Forefoot reconstruction. 2nd ed. Berlin: Springer; 2005.
18. Suppan RJ. The cartilaginous articulation preservation principle and its surgical implementa-
tion for hallux abducto valgus. J Am Podiatry Assoc. 1974;64:635.
19. Gauthier G. Maladie de Freiberg ou 2me maladie de Kholer, position d’un traitement de
reconstruction au stade evolué de l’affection. 48e Réunion Annuelle de la SOFCOT. Rev Chir
Orthop. 1974;60(11):337–42.
20. Migues A, Slullitel G, Bilbao F, Carrasco M, Solari G. Floating-toe deformity as a complica-
tion of the Weil osteotomy. Foot Ankle Int. 2004;25(9):609–13.
21. Espinosa N, Myerson M, Fernandez de Retana P, Maceira E. A new approach for the treatment
of metatarsalgia: the triple Weil osteotomy. Tech. Foot Ankle Surg. 2007;6:254–63.
22. Elmajee M, Shen Z, A’Court J, Pillai A. A systematic review of plantar plate repair in the man-
agement of lesser metatarsophalangeal joint instability. J Foot Ankle Surg. 2017;56(6):1244–8.
23. Fleischer AE, Klein EE, Bowen M, McConn TP, Sorensen MD, Weil L Jr. Comparison of
combination Weil metatarsal osteotomy and direct plantar plate repair versus Weil metatarsal
osteotomy alone for forefoot metatarsalgia. J Foot Ankle Surg. 2020;59(2):303–6.
24. Biz C, Corradin M, Kuete Kanah WT, Dalmau-Pastor M, Zornetta A, Volpin A, Ruggieri
P. Medium-long-term clinical and radiographic outcomes of minimally invasive distal meta-
tarsal metaphyseal osteotomy (DMMO) for central primary metatarsalgia: do Maestro criteria
have a predictive value in the preoperative planning for this percutaneous technique? Biomed
Res Int. 2018;2018:1947024.
Deformity of the Lesser Toes
Pablo Sotelano and Daniel Sebastián Villena
1 Introduction
Pathology of the lesser toes is one of the most frequent reasons for consultation
with the ankle and foot specialist [9, 15]. Problems with shoewear and walking
have increased over the time. Patients seek quick and definitive solutions. The
problem is that surgical treatment of lesser toes deformities have a long postopera-
tive period. Another characteristic of these deformities is, that secondary to the
muscle imbalance between the intrinsic and extrinsic toe muscles, the deformity is
progressive.
Several nonsurgical treatments and toe devices have been described to reduce
pain and improve digital position, but with poor results. Therefore, when the defor-
mity is symptomatic and all the previous instances have been exhausted, surgical
treatment is indicated.
Many articles have been published with varying levels of evidence, but even
today, there is no consensus on the gold standard. With the development of percuta-
neous surgery or MIS (minimally invasive surgery), in the last decades it has been
possible to achieve results similar to those of open surgery, with less soft tissue
injury and better esthetic results.
In this chapter we are going to describe the different surgical options, both clas-
sic and MIS techniques.
P. Sotelano (*) · D. S. Villena

Hospital Italiano de Buenos Aires, Buenos Aires, Argentina

Switzerland AG 2022
468 P. Sotelano and D. S. Villena
2 Etiology
The deformity of the lesser toes frequently begins in the fourth decade of life and is
slowly progressive, giving the greatest symptoms between the fifth and seventh
decade [9]. But depending on the morphology of the foot, it may develop at an earlier
age (Fig. 1). The toe most frequently affected is the second one [1, 30, 18]. The type
of footwear is one of the most important external factors that generate deformity and
discomfort.
From an anthropological point of view, the changes that were generated in the
human species with respect to the lesser toes began three or four million years ago
[19]. The modification through the years due to bipedestation was the increase of
the MP dorsiflexion and morphological changes of the anatomical structures such as
the plantar plate.
Due to human habits such as footwear, there is an altered foot biomechanics,
with gastrosoleous and posterior tibial muscle hypotrophy. This limits the activa-
tion of the windlass mechanism, which is essential for a normal gait (Fig. 2).
Lesser toes deformities are underestimated by orthopedic surgeons and treated
with poor interest. This leads to frequent patient complains and poor surgical solutions.
In the last two decades, MIS has gained prominence mainly in the treatment of
forefoot pathology. Several surgical techniques have been developed for the lesser
toes which will be described in this chapter.
Fig. 1 Hammertoes in young patients
a b
Fig. 2 Windlass mechanism of the plantar fascia. (a) At rest. (b) Tightening the base of the proxi-
mal phalanx to assist toe-off force
Deformity of the Lesser Toes 469
3 Anatomy and Pathophysiology
The lesser toes are named numerically (second to fifth) from medial to lateral. They
are made up of three phalanges, with the exception of the fifth toe which in 15% of
cases has only two phalanges.
The phalanges have three zones: the base, diaphysis and the head or epiphysis.
The metatarsophalangeal (MP) and interphalangeal (IP) joints are joined by soft
tissues through dynamic and static stabilizers.
Dynamic stabilization is generated by extrinsic muscles (muscles that originate
in the leg) and intrinsic muscles (muscles that originate in the foot). The compo-
nents of static stabilization are the joint capsule, the plantar plate, and the collateral
ligaments.
3.1 Extrinsic Musculature
3.1.1 Extensor Digitorum Longus (EDL)
The EDL originates in the anterior compartment of the leg, passes under the
inferior extensor retinaculum, and divides into four tendons for the second
through the fifth toes; these are attached to the proximal phalanx dorsum by a
fibro-aponeurotic structure known as the extensor hood. After leaving this struc-
ture distally, the tendon divides into three parts: one central that inserts dorsally
at the base of the middle phalanx. The other two tendons continue on the sides
towards the distal phalanx (one medial and one lateral). After receiving contribu-
tions from the intrinsic muscles, the two side components run distally inserting
into the base of the distal phalanx through a single tendon known as the termi-
nal tendon.
Although the proximal phalanx does not receive a direct tendinous extensor
insertion, the extensor tendons generate an aponeurotic structure surrounding the
MP called the extensor hood. This structure fuses with the plantar plate [12]
(Fig. 3).
3.1.2 Flexor Digitorum Longus (FDL)
This muscle originates on the posterior aspect of the tibia. In the plantar region, the
flexor hallucis longus provides a communicating tendinous fascicle; then at its lat-
eral border, the quadratus plantar is inserted, followed by its division into four ter-
minal tendons. At the level of the MP joint, it penetrates fibrous sheaths and inserts
into the plantar base of the distal phalanx of the second, third, fourth, and fifth toes
(Fig. 3).
Fig. 3 Normal dorsal and plantar anatomy. (a) FDL, (b) FDB, (c) PP, (d) EDL, (e) EDB, (f) IO
(interosseous). (FDL flexor digitorum longus; FDB flexor digitorum brevis; PP plantar plate;
EDL extensor digitorum longus; EDB extensor digitorum brevis; IO interosseous)
3.2 Intrinsic Musculature
3.2.1 Extensor Digitorum Brevis (EDB)
The only muscle of the dorsum of the foot, also called the pedis muscle, originates
from the anterosuperior process of the calcaneus. It runs obliquely medially and
anteriorly before dividing into four fascicles, each of which ends in a flattened ten-
don. The tendons of the extensor digitorum brevis are generally thinner than those
of the extensor digitorum longus and attach laterally to it at the level of the MP joint,
contributing to the extensor apparatus from the first to the fourth toe.
3.2.2 Flexor Digitorum Brevis (FDB)
This muscle originates at the medial process of the calcaneal tuberosity. In the mid-
foot it divides into four fascicles that continue with four long flattened tendons on
the plantar aspect of the FDL. Upon reaching the level of the MP joint, it divides
into two portions to insert on the medial and lateral borders of the inferior aspect of
the middle phalanx (Fig. 3).
3.2.3 Lumbricals (L)
They originate from the FDL tendons. From their point of origin, the lumbrical
tendons run distally and diverge slightly to reach the medial side of the MP joints of
the second through the fifth toes. They can also insert to the base of the proximal
phalanx of the respective toe. Some authors report that the lumbrical muscles can
also insert through tendon fibers, at the base of the proximal phalanx [36].
3.2.4 Interosseous (IO)
The seven interosseous muscles (three plantar and four dorsal) originate on the
metatarsal shaft in the corresponding intermetatarsal space. The plantar muscles are
located in the second, third, and fourth intermetatarsal spaces and arise on the
medial and inferior aspect of these bones. The dorsal interosseous, which are thicker
than the plantar interosseous, are found in all the intermetatarsal spaces. The
tendons of the plantar and dorsal interosseous muscles run distally dorsal to the
deep transverse metatarsal ligament. They are closely associated with the capsule,
into which some fibers insert. The remaining fibers extend distally toward the base
of the proximal phalanx (Fig. 3).
Given their location plantarly to the center of rotation of the MP joint, the inter-
osseous muscles flex the proximal phalanx, opponent to the extensor function.
The second toe is anatomically different from the others because it has two dorsal
interosseous muscles and no plantar interosseous muscles. This would explain the
higher frequency of sagittal plane dislocation (MP dorsal dislocation).
3.3 Statics Stabilizers
3.3.1 Plantar Plate (PP)
The PP is a fibrocartilaginous structure, composed mainly of type I collagen (75%),

and is the main stabilizer of the MP joint. It is a thick, square structure, originating
proximally at the plantar fascia and metatarsal neck, inserting distally at the base of
the proximal phalanx. The strongest insertion of the PP is found at the proximal
phalanx base. The plate inserts into the bone through two bundles that derive directly
from the plantar fascia. Between these two bundles, a synovial recess can be found
and should not be confused with a tear. Proximally, the plantar plate attachment to
the metatarsal neck is through a loose and fragile synovial sheath and does not par-
ticipate in the joint stabilization. The plantar surface of the plate is covered with
Fig. 4 (a) Accessory

CL. (b) Phalangeal CL. (c)
FDB. (d) PP
collagen fibers that attach to the deep transverse intermetatarsal ligament [32]
(Fig. 4).
3.3.2 Collateral Ligaments (CLs)
The lateral and medial collateral ligaments are composed of two structures: the pha-
langeal collateral ligament, which inserts at the base of the proximal phalanx, and
the accessory collateral ligament, which sends an expansion toward the plantar plate.
These fan-shaped ligaments together with the plantar plate are the main stabiliz-
ers of the MP joint [8] (Fig. 4).
The pathophysiology of lesser toe deformities can occur gradually. Although
they may be caused by trauma, mechanical or inflammatory processes (hallux val-
gus, systemic inflammatory diseases, diabetes, neuromuscular abnormalities,
advanced age, improper footwear) [10]. During the toe-off phase, the forefoot may
experience up to 120% of the total body load, predisposing to transverse plantar
plate lesions at the MP joint. Some authors pointed out that these PP lesions are the
first step to develop lesser toe deformities.
The major adult sagittal plane deformities consist of claw toes, hammertoes, and
mallet toes. Axial plane deformities include crossover toes.
The position of the proximal phalanx in the MP joint is given by the powerful
action of the EDL through the extensor hood mechanism. The antagonists are the
intrinsic muscles (FDB, interosseous, and lumbrical) and the static stabilizers
formed by the plantar plate collateral ligaments and plantar aponeurosis.
The position of the middle and distal phalanx is subject to the action of the FDL
and FDB muscles, which are antagonized by the intrinsic extensor muscles (EDB).
In each of these joints, an imbalance between the intrinsic and extrinsic muscles
can occur, causing different deformities.
Fig. 5 Pathophysiology of the deformity. (a) EDL. (b) Extensor hood. (c) Center of rotation.
(d) Interosseous. (e) Lumbricals. (f) PP. (g) FDB. (h) FDL
Chronic hyperextension of the proximal phalanx maintained during walking

gradually weakens the static plantar structures until they become totally inefficient,
thus keeping the proximal phalanx in an abnormal position in dorsal flexion. In
addition, metatarsal overloads (originated in hallux valgus, pes cavus, flat foot, etc.)
generate slowly progressive and degenerative lesions of the PP structures, which
ends in its insufficiency to maintain the proximal phalanx flexion. The long and
short flexors of the toes flex the proximal interphalangeal (PIP) joint. The EDL loses
its tenodesis effect at the dorsum of the PIP joint, dislocating the two tendon bands
laterally, thus contributing to the flexed position of the middle phalanx. As the prox-
imal phalanx extends, the intrinsic flexors (interosseous and lumbrical) move dorsal
to the center of rotation of the metatarsal head. In this position, they further worsen
the MP extension deformity, not being mechanically able of flexing the proximal
phalanx (Fig. 5). This explains the deformities mainly in the sagittal plane. When
the imbalance between the extrinsic and intrinsic is combined with a lesion at the
level of the plantar plate, there may be concomitant MP subluxation and axial plane
misalignment.
The function of the plantar plate is to resist the dorsal displacement of the proxi-
mal phalanx during gait. The high functional demand on the plantar structures can
ultimately lead to dorsal subluxation of the MP joint. As PP damage worsens, an
imbalance between static and dynamic stabilizers leads to medial toe displacement
and cross-over deformity (supraducted toe). Ford et al. [20] note that dorsal instabil-
ity of the MP joint increases by 74% when the plantar plate is severed. Bhatia et al.
[4] demonstrated in their biomechanical study a 48% reduction in the force required
to dislocate the joint when both collateral ligaments were severed, compared to a
reduction in force of only 29% when only the PP was severed. The same observa-
tion was made by Barg et al. [2] reporting that sectioning of both accessory collat-
eral ligaments or both phalangeal collateral ligaments increased instability by
41.6% and 26.1% during dorsal subluxation of the MP joint, respectively. They
conclude that the accessory collateral ligament is more important than the phalan-
geal collateral ligament for joint stability due to of its insertion into the PP. The deep
transverse metatarsal ligament may also contribute to the dorsal stability of the MP
joint. When this joint is in a plantigrade position, the lumbrical and interosseous
muscles run plantar to the metatarsal head center of rotation. However, during the
toe-off phase of gait, hyperextension of the proximal phalanx leads the interossei to
run dorsal to the MP joint’s center of rotation. As already stated, this hinders its toe
flexion capabilities.
This dynamic imbalance can lead to a progressive MP dorsal displacement.
4 Diagnosis
Toe deformity can be congenital or acquired. The former is very rare, from 1% to
5% according to the literature (Fig. 6). And the acquired one can be primary, due to
rheumatoid arthritis, iatrogenic, traumatic, or neurological [10].
Numerous names have been attributed to digital deformities: “mallet toe,”
“claw toe,” “hammertoe,” “supraducted toe,” “infraducted toe,” “rigid,” and “flex-
ible,” but none of them define the complete deformity. The anatomy of the foot,
and more specifically that of the lesser toes, allows us to evaluate by observing and
quantifying the deformity in both the sagittal and axial planes without having to
perform complementary studies to reach a diagnosis. That is why we are going to
take the classification of Barbara Piclet-Legré, validated by the French Association
of Foot and Ankle Surgeons, for the sagittal plane [25], which is based mainly on
the simple visualization and morphology of the toes in the sagittal and axial planes,
allowing us with the physical examination to define whether it is rigid or flexible
and to make an accurate diagnosis and appropriate treatment for each pathology
(Table 1).
Fig. 6 Congenital second hammertoe
Table 1 French Association of Foot and Ankle Surgeons classification for toe deformities
Localization (proximal to distal) Deformation Reducibility Cause
MP = metatarsophalangeal joint f = flexion f = flexible rh = rheumatic
PIP = proximal interphalangeal e = extension sr = semi-rigid pt = posttraumatic
DIP = distal interphalangeal l = lateral deviation r = rigid nr = neurologic
m = medial deviation ic = iatrogenic
Fig. 7 Morphologic: second rigid claw and mallet
The cause of the deformity is placed after the toe number, while the deformity
and the degree of stiffness are placed after the deformity. The most frequent MP
deformity is in extension, so when it is in that position, the letter “e” is not added.
The same happens when the PIP and distal (DIP) joints are in flexion – the letter “f”
is not added. When any of the joints is dislocated, the sign “+” is added. The most
important thing about this classification is that it is reproducible (inter- and intra-
observer) and allows a treatment algorithm according to each subtype.
Example: a patient with rheumatoid arthritis (RA) and a subluxed or dislocated
second toe supraducted medially (Fig. 7). From a morphological point of view, 2
MP + m PIP DIP, where the second toe presents a MP in extension and dislocated
medially with the PIP and DIP in flexion. If we add the etiology (rheumatic [rh],
posttraumatic [pt], Iatrogenic [ic], neurologic [nr]) and the criteria of reducible or
not (rigid [r], semi-rigid [sr], flexible [f]), the above example would be 2 Ar MP + m
PIPsr DIPf, where 2 represents the second toe, “Ar” represents rheumatoid arthritis,
“MP+” is the MP in flexion and dislocated, “m” is the medial toe deviation, “PIPsr”
is the joint in semi-rigid flexion, and DIPf is the joint in flexible flexion (Fig. 7).
As complementary studies, weight-bearing AP and lateral view X-ray are suffi-
cient for prior diagnosis and evaluation of postoperative evolution. In the case of
having a diagnostic presumption of plantar plate lesion, it is suggested to comple-
ment with magnetic resonance imaging (MRI) or dynamic ultrasound (operator
dependent). Computed axial tomography (CT scan) is only reserved for osteoarticu-
lar alterations and deformities in the three planes.
5 Treatment
To evaluate the type of treatment to be performed, we must mainly take into account
the patient’s age and expectations. The alteration of gait in elderly patients, where
the lesser toes do not have an important role, will be very different from that of a
50-year-old patient, athlete, who needs the lesser toes to be able to perform his
physical activity.
Consequently, the same pathology, such as a second supraducted toe, can be
treated in an elderly patient and in an active patient in two different ways. The
elderly patient, with rigid second crossover toe, chronic ulceration, needs to return
quickly to his activity, and it is not advisable for him to rest for long periods of time.
Therefore, amputation of the second toe might be the method of choice. On the
other hand, the active patient, who needs the function of his second toe, is indicated
a metatarsal osteotomy, a PIP arthrodesis, and a transfer the flexor longus toward the
dorsal diaphysis of the proximal phalanx of the toe (Girdlestone-Taylor procedure),
and in this way he will be able to perform his activity. The postoperative time in the
latter case is much longer, but the functional result is better.
Another important point to make is the surgical result and the patient’s expecta-
tions. Within the surgical treatment, osteotomies, tendon transfers, arthrodesis, and
tendon elongation are performed. This implies that the operated toe will never have
the functionality of a normal toe. We will greatly improve the position and symp-
toms but limiting the function. This information should be provided to the patient in
a detailed and clear manner before surgery.
5.1 Nonsurgical
When the toe is reducible and flexible, the conservative treatment is based on
strengthening the intrinsic and extrinsic muscles and windlass mechanism of the
plantar fascia, which contributes to improve the MP plantar flexion. Strengthening
and stretching of the Achilles and tibialis posterior tendons, help improve gait and
decrease MP dorsiflexion deformity.
Fig. 8 Simple bandage. With correction in extension of the distal phalanx
Fig. 9 Serpentine bandage. To the previous bandage, we add the descent of the proximal phalanx
Bandages aim to reduce the dorsiflexion position of the MP joint by bringing the
toe into plantar flexion. They can be simple, in serpentine or in a tie shape (Figs. 8,
9, and 10).
Insoles is another good alternative. The insole can be partial size or full size
(Fig. 11). They aim to elevate the lesser metatarsals with a retrocapital pad, located
proximal to the metatarsal heads. This improves MP plantar flexion.
If the toe is rigid, conservative treatment will only be aimed at improving foot-
wear with a wide and high toe box, insoles in the case of associated deformities to
improve support, and biological silicone orthoses customized by specialists
(Fig. 12).
5.2 Surgical Treatment
Numerous surgical techniques have been described for the various deformities.
In our opinion, the clearest and most pedagogical way to list them is to evalu-
ate each joint deformity, indicating the appropriate treatment for each one
of them.
In a generic way, it is necessary to evaluate if the deformity is rigid or flexible. If
it is flexible, the correction options are through tenotomies and osteotomies. On the
other hand, if the deformity is rigid, the correction can be achieved through arthrod-
esis or joint arthroplasty.
Fig. 10 Tie bandage. For plantar flexion of the proximal phalanx
Fig. 11 Shoe insoles
Fig. 12 Customized silicone orthoses

Due to the importance that MIS has taken in the last two decades, it should be
noted that all the procedures mentioned have their adaptation to be performed with
MIS. At the end of the description of the classical techniques, we will describe the
MIS procedures and the author’s preferred treatment method.
5.2.1 Open Surgery
Distal interphalangeal (DIP) joint deformity, also called mallet toe. In this pathol-
ogy, the DIP joint is deformed in flexion and can be flexible or rigid.
Flexible DIP Flexion Deformity: Mallet Toe
The surgical objective is to release the FDL and perform a plantar DIP capsulotomy.
Through a longitudinal or transverse plantar incision at the distal skin fold, the
tenotomy and capsulotomy are performed. Those procedures can also be performed
through a dorsal transverse transarticular approach. The dorsal approach avoids soft
tissue complications (dehiscence), common in transverse plantar incisions for toe
flexion deformities.
Rigid DIP Flexion Deformity: Mallet Toe
The two gold standard open techniques are the DIP arthrodesis and the DuVries
[16] technique.
DIP arthrodesis: Dorsal fishmouth approach, tenotomy, and dorsal capsulotomy
releasing collateral ligaments. The joint is exposed, and the articular cartilage of
both articular surfaces is resected using a rongeur. Then a closure is made with deep
“U” or Donati skin stitches, which reach the articular capsule. If the deformity tends
to recur after skin and capsule closure, a 1.25 mm ⌀ intramedullary K-wire can be
used across the DIP joint.
The DuVries [16] technique uses the same approach but only resects the articular
cartilage of the middle phalanx epiphysis. In this way a fibrous union is obtained.
The authors refer that the toe remains in a more anatomical position than with the
arthrodesis.
If the deformity is in extension, tenotomy of the long extensor tendon is per-
formed by a dorsal approach for flexible deformity or eventually arthrodesis for
rigid deformity.
Flexible PIP flexion Deformity: Hammertoe or Claw Toe
The PIP flexion deformity, also called hammertoe or claw toe, occurs mainly in
flexion and rarely in extension. This deformity, like the previous one, can be flexible
or rigid.
Through a 2 cm longitudinal plantar approach at the level of the PIP toe crease,
perform a PIP plantar capuslotomy and a FDB tenotomy at the base of the middle
phalanx. If there is associated DIP joint deformity, perform a FDL and FDB tenot-
omy through the same approach. Use a postoperative K-wire for 3 weeks postopera-
tive until soft tissues healing is achieved.
Rigid PIP flexion deformity: Hammertoe or Claw Toe
The PIP joint deformity is frequently associated with a metatarsophalangeal (MP)

joint deformity. The joint deformity of PIP flexion and MP extension is called
claw toe.
In case of a rigid PIP joint deformity, the surgical options are resection arthro-
plasty as described by DuVries [16], or PIP arthrodesis [11, 24]. Most used fixations
are Kirschner wires or intramedullary devices (Fig. 13).
The surgical approach is similar for both techniques. Through a 20 mm dorsal
and longitudinal approach over the PIP joint, an extensor tendon tenotomy, dorsal
capsulotomy and collateral ligaments release are performed. If there is an associated
mallet toe deformity, a transarticular flexor tendon tenotomy and plantar capsulot-
omy are performed.
DuVries arthroplasty includes resection of the proximal phalanx head cartilage
and may or may not be fixed with a 1.5 Kirschner wire. PIP arthrodesis is performed
by resecting both articular surfaces (proximal phalanx head and middle phalax
base). It can be performed using a rongeur, oscillating microsaw, or burs [17, 37]
(Fig. 14). It can be fixed with transient K-wires (kept in place for 6 weeks), resorb-
able wires, or intramedullary devices (Fig. 13).
These deformities may be associated with a dorsal MP dislocation. In these
cases, metatarsal surgery is mandatory to reduce joint tension and thus reduce the
MP joint. This deformity is mainly due to static stabilizers insufficiency, such as the
PP and the collateral ligaments. In cases to acute PP or collateral ligaments injury,
direct repair is recommended (plantar plate repair). If these lesions are chronic,
indirect repair is recommended by performing a triple Weil osteotomy (discussed in
other chapter of this book).
Fig. 13 Intramedullary devices. Pre- and postoperative

a b
c d
Fig. 14 Reciprocal socket PIP arthrodesis. (a) Joint milling and endomedular fixation with 1.5
mm ⌀ K-wire. (b) Docking of proximal and middle phalanx. (c) Postoperative X-ray. (d) healed
arthrodesis
MP Extension Deformity
This deformity is generally flexible and reducible as long as the joint is not dislo-
cated or damaged by degenerative processes (such as Freiberg’s disease). Keeping
in mind that perfect reduction and position of this joint is not always achieved, many
times we must perform extra-articular surgical procedures in order to achieve a
good digital position, regardless of the joint reduction.
Through a 1 cm dorsal incision over the MP joint a “Z”- shaped tenotomy of the
extensor digitorum longus tendon is performed. If the toe position does not improve,
a dorsal capsulotomy is added. If further correction is needed, a Girdlestone-Taylor
(GT) tendon transfer can be added. GT is technically demanding and often result in
metatarsophalangeal stiffness. The objective of this technique is to change the inser-
tion position of the FDL from the distal phalanx to the proximal phalanx. Most
importantly, this transfer does not change the tendon traction vector; it is still a
flexor agonist, therefore, it has a great correction power. The alternative to the GT is
to perform a proximal phalanx tenotomy. This procedure is easily performed with
MIS using a shannon burr.
Girdlestone-Taylor technique (Fig. 15): plantar DIP 3 mm approach. Perform a
FDL tenotomy. Then perform a 5 mm plantar incision at the proximal phalanx
diaphysis. The FDL is pulled and divided into two halfs. After that, a 15 mm dor-
sal proximal phalanx incision is performed. The FDL halfs are transferred dor-
sally, one on each side of the phalanx. Then, both ends are sutured together giving
the necessary tension and balance to keep the proximal phalanx in neutral posi-
tion [31].
PP ruptures evolve to a claw toe deformity or MP dislocation. Chronic ruptures
progress to a PP degenerative lesion that ends in a rigid claw toe deformity. These
lesions can be repaired; however, it is only recommended when there is an acute
rupture in an athletic patient (to be discussed in the chapter on metatarsalgia). In
patients with chronic PP injury, the authors recommend not repairing it, but to
choose between the triple Weil and/or GT technique or proximal phalanx osteotomy
MIS technique.
If the claw toe is associated with metatarsalgia, a Weil-Maceira-type osteot-
omy [28] or DMMO with MIS technique [13] (Fig. 16) will be recommended as
metatarsalgia treatment. This will be discussed at length in the chapter on
metatarsalgia.
5.2.2 MIS (Minimally Invasive Surgery)
The goal of MIS is to perform the same procedures as in open surgery but with less
soft tissue injury, achieve a faster recovery of soft tissues, and reduce postoperative
pain. The postoperative bandage should be kept in place for 3 weeks being funda-
mental in this technique, so that the osteotomies form a fibrous callus and heal in a
good position [39].
a b
c d
Fig. 15 Girdlestone-Taylor technique. (a) Tenotomy of the FDL divided in two. (b) Dorsal trans-
fer. (c) Suture of the tendon to the dorsal. (d) Skin suture
For this surgery specific instruments are necessary such as a high-torque and
low-revolution drill, cutting drills (15 and 10 mm long) and reaming drills
depending on the brand (Shannon®, Arthrex®, Wright®, Vilex®), and Beaver
64, 64 MIS, and 67 blade scalpel for percutaneous surgery (Shannon®,
Aesculap®).
Fig. 16 Weil-Maceira osteotomy
Rigid and Flexible DIP Flexion Deformity
Perform a 2 mm plantar incision over the DIP joint. Proceed with a FDL tenot-
omy and plantar capsulotomy. If the joint is rigid, through the same plantar inci-
sion, introduce the short cutting reamer (10 mm) up to the joint and resect the
articular cartilage. It can then be transiently fixed with a 1.25 mm Kirschner
wire [27].
Rigid and Flexible PIP Flexion Deformity
Flexible: a 2 mm plantar incision is performed at the lateral or medial edge of the

middle phalanx base, depending on whether the surgeon operates with the right or
left hand. A FDB tenotomy is performed, followed by a plantar PIP capsulotomy. A
FDL tenotomy is added if necessary. If the deformity still persists, a dorsal exostec-
tomy of the proximal phalanx head and a middle phalanx dorsal closing wedge
osteotomy can be added.
Rigid: Perform a PIP arthrodesis with a short cutting reamer through the a plan-
tar incision. Fix it with a transient K-wire or a resorbable pin [3, 6].
Deformity in Extension of the MP Joint
Perform a 2mm dorsal incision at the level of the MP joint (Fig. 18). A EDL and
EDB tenotomy in addition to a dorsal capsulotomy are performed. More than half
of the MP deformities cannot be corrected with these procedures. In this case, we
must act on the proximal phalanx, performing a plantar wedge base osteotomy if the
deformity is only in the sagittal plane or a complete osteotomy if the deformity is in
two or three planes (Fig. 17). Bandaging for 4 weeks is used to achieve osteotomy
Fig. 17 MIS osteotomy at the base of the proximal phalanx
a b c
Fig. 18 (a) Extensor Tenotomy. (b, c) Minimally invasive distal metatarsal osteotomy
(DMMO) [35]
healing and thus, deformity correction. If the deformity continues and metatarsalgia
is present, a minimally invasive distal metatarsal osteotomy (DMMO) could be
added (Fig. 18) [35].
5.2.3 Preferred Author’s Treatment Method: PIP Arthrodesis

with Resorbable Pin
For severe rigid hammertoe the author’s preferred treatment method is a PIP arthrod-
esis with resorbable pins. The advantages of this technique are that it does not leave
any implant outside the skin and it is minimally invasive. In addition, is a persistent
deformity is evident after the PIP arthrodesis, a proximal phalanx osteotomy can
be added.
As described, through a 2 mm plantar incision at the PIP, a FDB tenotomy and
plantar capsulotomy are performed (Fig. 19). If there is distal deformity, tenotomy
of the FDL is added as well. Through this approach, the articular surfaces are pre-
pared with a 10 mm Shannon reamer. Under radioscopic control the intramedullary
canal is prepared. A 1.5 resorbable intramedullary pin [5, 22] is introduced from the
toe tip (Fig. 20).
If the toe is still extended after the PIP fixation, a minimally invasive proximal
phalanx osteotomy or a Girdlestone-Taylor tendon transfer can be added.
Fig. 19 (1) FDB tenotomy. (2) PIP arthrodesis. (a) FDB. (b) FDL. (c) Metatarsal. (d) Proximal
phalanx. (d, e) Middle phalanx. (f) Distal phalanx. (g) PIP
a b c d
e f g h i
Fig. 20 (a) Plantar incision; (b) PIP arthrodesis with drill; (c) skin incision for guide passage; (d)
guide placement; (e) fluoroscopy; (f) and (g) under fluoroscopy, measurement of the resorbable
pin, avoiding to invade the MP joint; (h) insert the implant with drill; (i) progression of the implant
with impactor leaving the DIP joint free
MIS techniques allow us to obtain similar results to open techniques with less
soft tissue damage, low complication rate and early rehabilitation. It is important to
note that when fixing the PIP joint, the FDL becomes a direct flexor of the MP joint
and not of the PIP and DIP joints, developing a good and permanent toe plantar
flexion moment.
6 Deformity of the Fifth Toe
Claw toes deformities of the fifth toe are treated the same way as mentioned above
including arthrodesis, tenotomies and osteotomies. In cases of severe deformities
associated with toe rotation, techniques that include EDL tendon transfer to the
abductor tendon have been described (Lapidus technique). Often, skin elongation
techniques must be added such as “V-Y” or “Z” plasty [14, 38].
7 Complications
The rate of complications range from 10% to 33% [7, 29, 33]. The complications
that will be discussed include: malalignment, joint deformities, infection, ischemia
and hardware related.
7.1 Malalignment: Many devices exist in the market that can maintain the position
obtained in the immediate postoperative period, Nevertheless, they will probably fail
in the long term if a DuVries resection arthroplasty (forms a fibrous union and not a
bone fusion) was performed and not an arthrodesis. In addition, it is the author’s
advice to shorten the toe in severe deformities (at the proximal phalanx or metatarsal
head). In this way soft tissue tension is reduced, and a better balance of the deforming
forces is achieved.
Another common complication is floating toe. It is found in 36% of cases after
the triple Weil - Maceira osteotomy is performed [21]. The incidence is even higher
if a PIP arthrodesis is performed at the same time [26] (Fig. 21).
7.2 Extension contracture of the MP, either with or without joint sublux-
ation, can be avoided by means of Girdlestone-Taylor tendon transfer and
repair of the plantar plate and eventually the collateral ligaments. These static
stabilizers are also responsible for deformities in the coronal plane. One way to
avoid this deformity is to perform a complete or incomplete MIS osteotomy at
the base of the proximal phalanx (to achieve flexion), as described in the MIS
section.
7.3 Infection: The rate of superficial and deep infections does not exceed 11%
(Fig. 22). Only 0.3% cause deep infections, often associated with the use of K-wires.
Most infections evolve favorably with adequate antibiotic treatment [34].
Fig. 21 Floating toe after

Weil-Maceira osteotomy
and PIP arthrodesis
Fig. 22 Superficial
infection after a DMMO of
the second metatarsal
a b c
Fig. 23 Ischemic toe after correction of a complex deformity with Z-plantar skin advancement.
(a) and (b) Immediate postoperative period. (c) Postoperative period at 1 year
7.4 Ischemia: Severe deformity corrections have a neurovascular risk. Kramer

et al. reported 0.4% of severe ischemic complications [23]. After large deformity
corrections, always evaluate the capillary filling at the end of the surgery. If any
decrease in circulation occurs, there are a few options to perform: start by moving
and partially removing the fixation wire. If this does not improve the ischemia,
apply warm saline and nitro paste (nitroglycerin) to the toe. If none of the previ-
ous procedures improve the ischemia, remove the osteodesis regardless of the
loss of correction (Fig. 23). Do not leave the operating room until ischemia is
resolved.
7.5 Hardware Related: The most frequent problem is K-wire failure. Screw
failure can happen as well if a screw or a metalic implant was used to stabilize the
toe. This failure usually occurs after the patient starts to walk [40]. This complica-
tion can be avoided using resorbable pins or by keeping the toe immobilized for
6 weeks.
8 Summary
The pathology of the lesser toes is still a challenge for any orthopedic surgeon,
due to its multiple deformities in a small segment of the anatomy. Many proce-
dures are necessary to completely correct the deformities, which is the reason for
its high recurrence rate. It is difficult after surgery to achieve normal function of
the toe. This is something that the patient should be aware of before undergoing
surgery.
Current percutaneous techniques have been able to correct deformities with less
soft tissue damage. Classic MIS techniques solely depend on postoperative ban-
dage. The evolution of some endomedullary devices help to achieve more predict-
able and reproducible results.
Although the lesser toes pathology is underestimated, surgical training and a
detailed study of the anatomy and pathophysiology are necessary to obtain good
results with a low complication rate.
References
1. Averous C, Leider F, Rocher H, Determe P, Guillo S, Cermolacce C, Diebold P. Interphalangeal

arthrodesis of the toe with a new radiolucent intramedullary implant (toegrip). Foot Ankle
Spec. 2015;8(6):520–4.
2. Barg A, Courville XF, Nickisch F, Bachus KN, Saltzman CL. Role of collateral ligaments in
metatarsophalangeal stability: a cadaver study. Foot Ankle Int. 2012;33(10):877–82.
3. Basile A, Albo F, Via A. Intramedullary fixation system for the treatment of hammertoe defor-
mity. J Foot Ankle Surg. 2015;54(5):910–6.
4. Bhatia D, Myerson MS, Curtis MJ, Cunningham BW, Jinnah RH. Anatomical restraints to
dislocation of the second metatarsophalangeal joint and assessment of a repair technique. J
5. Cicchinelli LD. Hammertoe surgery and the trim-it drill pin. Foot Ankle Spec.
2013;6(4):296–302. https://doi.org/10.1177/1938640013490123. Epub 2013 May 14. PMID:
23673417.
6. Coillard J, Petri G, van Damme G, et al. Stabilization of proximal interphalangeal joint in lesser
toe deformities with an angulated intramedullary implant. Foot Ankle Int. 2014;35(4):401–7.
7. Cordier G, Nunes GA. Minimally invasive advances. Foot Ankle Clin 2020. 2020;25(3):461–78.
8. Coughlin MJ, Baumfeld DS, Nery C. Second MTP joint instability: grading of the deformity and
description of surgical repair of capsular insufficiency. Phys Sportsmed. 2011;39(3):132–41.
9. Coughlin MJ, Saltzman CL, Mann RA. Mann’s surgery of the foot and ankle E-book: expert
consult – online. San Francisco, California: Elsevier Health Sciences; 2013.
10. Coughlin MJ. Lesser toe deformities. In: Coughlin MJSC, Anderson RB, editors. Mann’s sur-
gery of the foot and ankle. 9th ed. Elsevier; 2014. p. 322–424.
11. Coughlin MJ, Dorris J, Polk E. Operative repair of the fixed hammertoe deformity. Foot Ankle
Int. 2000;21(2):94–104.
12. Dalmau-Pastor M, Fargues B, Alcolea E, Martínez-Franco N, Ruiz-Escobar P, Vega J, Golanó
P. Extensor apparatus of the lesser toes: anatomy with clinical implications--topical review.
Foot Ankle Int. 2014;35(10):957–69.
13. De Prado M, Ripoll PL, Metatarsalgias GP, editors. Cirugía percutánea del pie. Barcelona:
Masson; 2003. p. 165–74.
14. Derhy Y, Binder JP, Mitrofanoff M, Haddad R, Pavy B. Quintus varus supraductus congénital:
technique chirurgicale [Congenital quintus varus supraductus: surgical procedure]. Ann Chir
Plast Esthet. 2004;49(4):373–7. French.
15. Doty JF, Coughlin MJ, Weil L, et al. Etiology and management of lesser toe metatarsophalan-
geal joint instability. Foot Ankle Clin. 2014;19(3):385–405.
16. DuVries HL. Dislocation of the toe. J Am Med Assoc. 1956;160:728.
17. Edwards WH, Beischer AD. Interphalangeal joint arthrodesis of the lesser toes. Foot Ankle
Clin. 2002;7(1):43–8.
18. Femino JE, Mueller K. Complications of lesser toe surgery. Clin Orthop Relat Res.
2001;391:72–88.
19. Fernández PJ, Mongle CS, Leakey L, Proctor DJ, Orr CM, Patel BA, Almécija S, Tocheri
MW, Jungers WL. Evolution and function of the hominin forefoot. Proc Natl Acad Sci U S
A. 2018;115(35):8746–51.
20. Ford LA, Collins KB, Christensen JC. Stabilization of the subluxed second metatarsophalan-
geal joint: flexor tendon transfer versus primary repair of the plantar plate. J Foot Ankle Surg.
1998;37(3):217–22.
21. Highlander P, VonHerbulis E, Gonzalez A, et al. Complications of the Weil osteotomy. Foot
Ankle Spec. 2011;4(3):165–70.
22. Konkel KF, Menger AG, Retzlaff SA. Hammer toe correction using an absorbable intramedul-
lary pin. Foot Ankle Int. 2007;28(8):916–20.
23. Kramer W, Parman M, Marks R. Hammertoe correction with K-wire fixation. Foot Ankle Int.
2015;36(5):494–502.
24. Lehman D, Smith R. Treatment of symptomatic hammertoe with a proximal interphalangeal
joint arthrodesis. Foot Ankle Int. 1995;16(9):535–41.
25. Lintz F, Beldame J, Kerhousse G, et al. Intra- and inter-observer reliability of the AFCP clas-
sification for sagittal plane deformities of the second toe. Foot Ankle Surg. 2020;26(6):650–6.
26. Migues A, Slullitel G, Bilbao F, et al. Floating-toe deformity as a complication of the Weil
osteotomy. Foot Ankle Int. 2004;25(9):609–13.
27. Migues A, Campaner G, Slullitel G, Sotelano P, Carrasco M, Solari G. Minimally invasive
surgery in hallux valgus and digital deformities. Orthopedics. 2007;30(7):523–6.
28. Monteagudo M, Maceira E. Evolution of the Weil osteotomy: the triple osteotomy. Foot Ankle
Clin. 2019;24(4):599–614.
29. Mueller CM, Boden SA, Boden AL, Maidman SD, Cutler A, Mignemi D, Bariteau
J. Complication rates and short-term outcomes after operative hammertoe correction in older
patients. Foot Ankle Int. 2018;39(6):681–8.
30. Myerson MS, Shereff MJ. The pathological anatomy of claw and hammer toes. J Bone Joint
Surg Am. 1989;71(1):45–9.
31. Nery C, Baumfeld D. Lesser metatarsophalangeal joint instability: treatment with tendon
transfers. Foot Ankle Clin. 2018;23(1):103–26.
32. Nery C, Coughlin MJ, Baumfeld D, Raduan FC, Catena F, Macedo BD, de Andrade MA. Lesser
metatarsal phalangeal joint arthroscopy: anatomic description and comparative dissection.
Arthroscopy. 2014;30(8):971–9.
33. Nieto-García E, Ferrer-Torregrosa J, Ramírez-Andrés L, Nieto-González E, Martinez-Nova
A, Barrios C. The impact of associated tenotomies on the outcome of incomplete phalangeal
osteotomies for lesser toe deformities. J Orthop Surg Res. 2019;14(1):308.
34. Phisitkul P. Managing complications of lesser toe and metatarsophalangeal joint surgery. Foot
Ankle Clin. 2018;23(1):145–56.
35. Redfern D, Vernois J. Percutaneous surgery for metatarsalgia and the lesser toes. Foot Ankle
Clin. 2016;21(3):527–50.
36. Sarrafian SK, Topouzian LK. Anatomy and physiology of the extensor apparatus of the toes. J
37. Ferna S, ́ndez C, Wagner E, Ortiz C. Lesser toes proximal interphalangeal joint fusion in rigid
claw toes. Foot Ankle Clin. 2012;17(3):473–80.
38. Tawil HJ, Pilliard D, Taussig G. Le quintus varus supraductus. Résultats du traitement chirur-
gical par plastie cutanée, capsulotomie interne et transfert externe de l'extenseur du 5e orteil
[Quintus varus supraductus. Results of the surgical treatment by cutaneous graft, internal cap-
sulotomy and external transfer of the extensor of the 5th toe]. Rev Chir Orthop Reparatrice
Appar Mot. 1992;78(2):107–11. French.
39. Yassin M, Garti A, Heller E, et al. Hammertoe correction with K-wire fixation compared with
percutaneous correction. Foot Ankle Spec. 2016;10(5):421–7.
40. Zingas C, Katcherian DA, Wu KK. Kirschner wire breakage after surgery of the lesser toes.
Foot Ankle Int. 1995;16(8):504–9.
Morton’s Neuroma
Rodrigo Melo Grollmus and Cristián Ortiz Mateluna
1 Introduction
Morton’s neuroma (also called Morton’s metatarsalgia, Morton’s disease, plantar

interdigital neuroma, interdigital neuritis, or plantar neuroma) is one of the common
causes of metatarsalgia. It corresponds to a painful syndrome of the forefoot pro-
duced by the pathology of one of the interdigital plantar nerves, most commonly
that of the third interosseous space and less frequently that of the second [1, 2].
The first anatomical report date back to 1835, in which Filippo Civinini, profes-
sor of anatomy at the University of Pisa (Italy), described an increase in volume of
the plantar interdigital nerve in the third interosseous space [3, 4]. Ten years later,
Lewis Durlacher [5] reported the first clinical case. But it was not until the clinical
series published in 1876 by Thomas Morton [6] that the lesion between the third and
fourth metatarsophalangeal joint was associated as a cause of metatarsalgia, which
in turn produced a neuralgia due to the involvement of the plantar nerve [3].
In 1893, Hoadley [7] was the first to report the resection of a small neuroma in
the area as a treatment of metatarsalgia, with good clinical results [8]. In 1940 Bett
[9] described Morton’s metatarsalgia as “neuritis of the fourth digital nerve,” and
Gauthier [10] in 1979 attributed it to nerve entrapment, supported by anatomical
studies. In addition, he was the first to describe his successful clinical results with
only release of the affected nerve.
R. Melo Grollmus (*)

Department of Orthopedic Surgery, Foot and Ankle Unit, Clinica Las Condes, Santiago, Chile
Department of Orthopedic Surgery, Foot and Ankle Unit, Hospital Militar de Santiago,
Santiago, Chile
C. Ortiz Mateluna
Department of Orthopedic Surgery, Foot and Ankle Unit, Clinica Universidad de los Andes,
Santiago, Chile

Switzerland AG 2022
494 R. Melo Grollmus and C. Ortiz Mateluna
2 Epidemiology
It is more frequent in the female sex (ratio 4:1) with an average age of presentation
between 40 and 55 years [1, 2, 11, 12]. It is usually unilateral, but in up to 15–21%
of cases, it is bilateral [11, 13, 14].
In the vast majority of patients, it affects the nerve in the third intermetatarsal
space (66% of cases) and less frequently in the second interosseous space.
Compromise of the first and fourth space is extremely rare and probably does not
exist as a clinical entity [12–14]. On the other hand, the involvement of simultane-
ous adjacent spaces is unusual (< 3% of cases) [11, 15].
3 Anatomy
The medial plantar nerve is divided into four digital branches: the most medial to
the hallux and the others to the first, second, and third interosseous spaces. The
lateral plantar nerve gives two digital branches: one to the fifth toe and the other to
the fourth interosseous space. This last branch, depending on the lateral plantar
nerve, can give a communicating branch to the third space that joins the branch of
the medial plantar nerve, which generates a thicker interdigital nerve (Fig. 1).
Different cadaveric studies have demonstrated the existence of this branch in up to
66% of the population [11, 16–18].
The interdigital nerve is in a small osteofibrous space, limited laterally and medi-
ally by the adjacent metatarsals, distally by the metatarsal heads and their respective
joints and periarticular structures (collateral ligaments, joint capsule, and flexor ten-
dons), dorsally by the transverse intermetatarsal ligament which is inserted into the
metatarsals slightly proximal to the heads, and plantarly by the plantar aponeurosis,
fat, and thick plantar metatarsal skin. This space also contains the interdigital artery
and veins [1]. The intermetatarsal bursa is located above the intermetatarsal trans-
verse ligament (Fig. 2) [11, 19]. Each nerve at the level of the intermetatarsal trans-
verse ligament normally measures about 1 mm in diameter. Distal to this and just
proximal to the heads of the metatarsals, it is divided into the two digital nerves [1].
4 Etiopathogenesis
Although its etiology remains unclear, there are multiple theories described in the
literature that attempt to explain its etiology, pathogenesis, and associated factors.
Probably, as well as a large number of entities in orthopedics, it is a multifactorial
condition in which each of the following factors collaborates to a greater or lesser
degree [11, 20–23]:
Morton’s Neuroma 495
Fig. 1 Anatomical
distribution of the plantar
nerves (Ntp posterior tibial
nerve, Npm medial plantar
nerve, Npl lateral plantar
nerve, Rc communicating
branch of the third space,
L transverse intermetatarsal
ligament)
Fig. 2 Cross-section
diagram of the
intermetatarsal anatomical
space. It is observed dorsal
to the transverse
intermetatarsal ligament
(L) and the intermetatarsal
bursa (B) and plantar to the
ligament, the interdigital
nerve (N), the artery (A),
and the vein (V)
4.1 Anatomical Factors
Various anatomical conditions, especially the innervation of the forefoot, would be

a fundamental etiopathogenic factor in the origin of Morton’s neuroma. As men-
tioned in the anatomical description, in a high percentage of the population it has
been demonstrated the existence of a communicating branch to the third space that
joins the branch of the medial plantar nerve. This co-joined nerve generates a thicker
interdigital nerve that it more exposed to trauma [16–18]. This branch can also pass
under the head of the metatarsal or under the metatarsophalangeal joint, which
increases its propensity for repetitive trauma [11, 16–18]. Another anatomical factor
is referred to the anatomical space itself, since both the third and the second interos-
seous spaces would be smaller, compared to the first and the fourth [11, 16]. A
widely discussed element is the difference in mobility and relative position of these
metatarsals with respect to the ground, which occurs at the level of the midfoot
joints between the medial and middle columns (rigid and inclined to the ground)
and the lateral column (mobile and parallel to the ground). This difference explains
that the third interosseous space is a more mobile transition area, which facilitates
nerve and bursa friction and trauma, generating neuropathy and shear bursitis [11,
17, 24]. This factor would not be present in cases of second interosseous space neu-
roma. This is the reason, why some authors think that neuromas, other than in the
third interosseous space, [25] do not exist and that symtoms are secondary to bursi-
tis and metatarsophalangeal synovitis.
4.2 Mechanical Factors
Different orthopedic conditions can cause alterations in the biomechanics of plantar

support, generating load transfer to the lesser metatarsals, which, added to some of the
anatomical factors described above, would favor repetitive trauma on the interdigital
nerve, generating neuropathy and symptomatology. These overload conditions can
occur at different stages of gait. During the second rocker, for example, the shortening
of the gastrocnemius favors a forefoot overload and the generation of an interdigital
neuritis. In the third rocker, multiple alterations can generate load transfer to the lateral
metatarsals, for example, hallux valgus, hallux rigidus, first ray insufficiency, long cen-
tral metatarsals, etc. [26]. The previously mentioned alterations exacerbate the trauma
on the plantar interdigital nerves during walking, especially when the metatarsophalan-
geal joints are in maximum dorsiflexion, which occurs, for example, with the use of
high-heeled shoes. Anatomically, this exposes the interdigital nerves at the metatarsal
level to trauma, which, associated with any of the anatomical predisposing factors
described above, would increase the risk of traumatic neuropathy. This situation could
explain the higher frequency of Morton’s neuroma in the female population [11].
Likewise, in the context of a patient with plantar fat atrophy, repetitive loads can make
the nerve more vulnerable to injury [8]. Watcher [27] and Franson [28] associate it to
the pes cavus, through the increase of the tension of the plantar fascia on the transverse
ligament, which would favor the microtrauma to the nerve. On the other hand, other
authors associate it to the pronation present in flat foot, which would produce traction
by neural stretching [29–33]. However, other authors [34] mention that there would be
no evidence that Morton’s neuroma is especially associated with any foot disorder.
4.3 Neural Compression Factor
The works of Lassman [21] and Graham [35] demonstrated a series of histological
changes in the interdigital nerve, exclusively distal to the transverse intermetatarsal
ligament. For this reason, Gautier in 1979 [10] and later other authors suggest that
the most important factor in the etiopathogenesis of Morton’s neuroma is a inter-
digital plantar nerve entrapment neuropathy at the level of the transverse intermeta-
tarsal ligament, which would be predisposed by the anatomical characteristics of the
osteofibrous space where the nerve is located [10, 11, 20, 21, 35–37].
4.4 Inflammatory Factor
Some authors have postulated that traumatic intermetatarsal bursitis, associated

with any of the mechanical factors described above, could produce irritation due to
nerve contiguity. Chronic perineural inflammation would secondarily produce
neurofibrosis. Thus, intermetatarsal bursitis would not produce pathology by true

compression, but secondarily by inflammation [11, 19, 38]. On the other hand, dif-
ferent pathologies of the metatarsophalangeal joints, especially those associated
with metatarsphalangeal joint bursitis (e.g. deformity of the lesser toes or a metatar-
sophalangeal dislocation secondary to rupture of the plantar plate), could end up
having neuropathy due to mechanical traction and inflammatory soft tissue changes
[8, 11]. Thus, it has been described that 10–15% of the patients with metatarsopha-
langeal deformities have neurological symptoms [11].
4.4.1 Ischemic Factor
Nissen [39] and Ringertz [40] suggest that the decrease in blood supply as a result
of degenerative changes in the lateral plantar artery would cause ischemia of the
peripheral nerves, which in turn would increase perineural fibrosis and interdigital
neuropathy. Although this etiopathogenic factor is not very considered today, mul-
tiple histopathological studies of Morton’s neuromas show the presence of arteriolar
vessels of diminished size [22, 23, 41].
4.4.2 Extrinsic Factors
The presence of extrinsic compressive and/or irritative lesions could also generate
neurological symptoms, such as tumor lesions (e.g., synovial cyst of the metatarso-
phalangeal joint, hypertrophic pseudoarthrosis of the metatarsal, rheumatoid nod-
ule, rupture of the plantar plate, etc.). The presence of a thickening of the
intermetatarsal transverse ligament of the second space has been described in some
patients, which would favor neural compression [11]. Also, direct trauma to the
nerve, such as a fall from a heavy object, or a previous foot lesion could generate a
traumatic neuropathy of the interdigital nerve [8].
5 Diagnosis
5.1 Clinical Presentation
The diagnosis of Morton’s neuroma is eminently clinical, and many authors con-
sider it the gold standard of diagnosis [1, 11, 41, 42]. The most common symptom
is neuritic pain (present in more than 90% of cases), described by the patient as
metatarsalgia in the third intermetatarsal space, usually radiated to one or both cor-
responding toes. Some patients refer to the sensation of “stepping on a foreign
body” or “having a wrinkled sock” [8]. There can also be neurological symptoms
with symptoms such as tingling, paresthesia, numbness or anesthesia of the corre-

sponding toe(s) [1, 2, 11]. Symptoms in the second intermetatarsal space can also
be present, frequently caused by bursitis secondary to a mechanical cause. This
bursitis can secondarily generates neuritis.
Usually, the patients refer that their symptoms are exacerbated with the use of
narrow anterior shoes and/or high heels and improve when retiring the footwear
[11]. It is hypothesized that this phenomenon would be caused by nerve trapping
between the metatarsal heads [11]. Less frequently, pain can migrate proximally to
the foot, ankle, and leg [1, 11].
The physical examination should be complete, like that of any patient who con-
sults for metatarsalgia. The whole affected extremity should be examined and com-
pared with the healthy one. Special care must be taken with the morphological
alterations of the forefoot, which favor the existence of mechanical factors or over-
loading of the lesser metatarsals, such as the presence of hallux valgus, rupture of
the plantar plate, deformities of the lesser toes, etc. [11]. Thus, the inspection
should focus on the areas of metatarsal support and the presence of hyperkeratosis
[2, 26].
On palpation, the pain is usually located in the affected intermetatarsal space,
mainly on plantar palpation. There is usually no dorsal or plantar pain of the
metatarsal heads and metatarsophalangeal joints. Palpation of the interosseous
space is initially performed locating the examiner’s thumb plantarly and the index
finger dorsally at the intermetatarsal space. This dorsal-plantar compressive
maneuver of the interosseous space, also called intermetatarsal sensitivity test,
reproduces the symptoms referred by the patient (pain, burning, paresthesia,
which can radiate distally to the affected toes, etc.) [11]. Sometimes a slight
increase in volume in the intermetatarsal space can be observed in the area of
sensitivity.
Another maneuver to be performed during the physical examination is the lat-
eral compression of the metatarsals or squeeze test (from the first and fifth metatar-
sals), which produces a decrease in the intermetatarsal space and thus generates a
palpable click-type sensation. This can occur in association with pain, which is
called “Mulder’s sign or click” (Fig. 3). This sign is associated with the existence
of Morton’s neuroma with a sensitivity described by some authors of up to 94–98%
[1, 43–45]. This sign is more usually seen in the third space than in the second
one [11].
The neurological examination should include a sensory-motor evaluation of the
entire limb, especially to rule out other proximal neurological etiologies with distal
symptoms. Palpation and percussion of the posterior tibial nerve should be per-
formed along its entire length. There is usually pain on percussion in the plantar
intermetatarsal space (or plantar percussion test) [2, 8]. From the point of view of
motor sensory evaluation, there are usually no specific alterations, except in some
cases that digital hypoesthesia can be identified.
Fig. 3 Dorsal-plantar
compression test of the
interosseous space (red
arrow) and lateral
compression test of the
metatarsals or squeeze test
(green arrows). If this
maneuver is associated
with a palpable click-and-
pain-type sensation, it is
called “Mulder’s sign or
click”
5.2 Imaging Study
Because the diagnosis of Morton’s neuroma is eminently clinical, many authors

consider that the use of imaging tests is controversial, especially after reports such
as Bencardino’s [46] and Symeonidis’ [47], where the presence of between 33%
and 54% of Morton’s neuromas in ultrasonography or magnetic resonance imaging
in asymptomatic patients is observed. Likewise, Raouf [48] described a statistical
correlation between clinical and histopathological findings. A sensitivity of 100%,
a positive predictive value of 100%, and a false-positive rate of 0% was found. This
calls into question the routine use of preoperative images, which in turn can repre-
sent a high economic cost.
For this reason, it is proposed that imaging studies should have the objective of
supporting the etiological diagnosis, within the extensive differential diagnosis of
metatarsalgia (see differential diagnosis of Morton’s neuroma) [26]. Thus, the study
begins with a weight-bearing X-ray of the affected foot (anteroposterior, oblique,
and lateral projections), which collaborates in the evaluation of osteoarticular anat-
omy [11].
The most commonly used imaging studies that seek the presence of a thickening
and/or increase in the size of the interdigital plantar nerve are ultrasonography (US)
and magnetic resonance imaging (MRI). The US has the advantage of being
dynamic, lower cost, being performed in less time, and presenting a high sensibility
(90%) and specificity (88%). Some specialists consider it the test of choice [8, 49–
52]. On the other hand, its limitations are that it is operator-dependent and does not
show bone pathology (e.g., bone edema, stress fractures, etc.) that can be part of the
Fig. 4 Ultrasound image showing a 6 mm nodule (N) in the third interosseous space compatible
with Morton’s neuroma
differential diagnosis of metatarsalgia [8, 50]. Morton’s neuroma is observed as an

ovoidal mass in the short axis, and as a fusiform and elongated mass in the long axis,
relatively hypoechogenic (Fig. 4). The lateral compression maneuver of the meta-
tarsals helps to extrude the content of the space to improve the visualization of an
eventual neuroma in the US [53].
Studies with MRI have shown a similarly high sensitivity as in the US (up to
93% in some series), however, with a lower specificity (reported as 68%) [49]. The
advantages of this method are that it provides static images that are reproducible and
not operator-dependent and can be interpreted by multiple clinicians. It allows an
evaluation of all anatomical structures of the forefoot [52]. Its disadvantages are a
lower specificity for Morton’s neuroma with respect to US, its higher economic
cost, and the longer time it requires to be performed [52].
In MRI, Morton’s neuroma is usually observed as a well-demarcated ovoidal
mass or a low-signal “dumbbell”- or “weight”-shaped mass in T1 and T2, which
contrasts with the hyperintense liquid of the intermetatarsal bursa [51, 53]. Coronal
cuts are usually the most useful (Fig. 5) [53]. With respect to the use of gadolinium,
there are dissimilar reports in the literature, about whether its use allows improving
the sensitivity of the exam with respect to the diagnosis of Morton’s neuroma
[51, 53].
The use of the lidocaine test (2 ml of lidocaine 2% in the affected intermetatar-
sal space, under the intermetatarsal ligament) with temporary cessation of pain can
be useful for diagnostic support, especially if it is performed under US guid-
ance [1].
Fig. 5 Magnetic nuclear images showing a dorsal hyperintense area in the third interosseous
space, compatible with bursitis (B), and plantar to it is a nodular image of about 7 mm compatible
with Morton’s neuroma (N)
Table 1 Differential diagnosis of Morton’s neuroma

Bone Mechanic metatarsalgia First ray insufficiency
Metatarsal length discrepancy
Iatrogenic (hallux valgus failed surgery, etc.)
Stress fracture
Freiberg disease
Joint Metatarsophalangeal synovitis Metabolic (gout)
Autoimmune (rheumatoid arthritis, psoriatic
arthritis, etc.)
Arthrosis/MTP osteochondral
lesion
Plantar plate rupture
Tumoral Benign Bone
Malignant Soft tissue
Neurologic Peripheral neuropathy
Tarsal tunnel syndrome
Radiculopathy
Others Gastrocnemius tightness
Foreign body
Electrodiagnostic studies are not useful, unless more proximal nerve compres-
sion or double crush syndrome is suspected [8, 11].
As already mentioned, because the diagnosis is eminently clinical and the prob-
lem to be solved with the imaging study is the differential diagnosis of metatarsal-
gia, we believe that the test that provides most information about the forefoot
anatomy is MRI.
6 Differential Diagnosis
It is extensive, since it must include all the pathologies that cause metatarsalgia (see
Table 1) [2, 26].
7 Pathological Anatomy
From the anatomopathological point of view, Morton’s neuroma does not corre-
spond to a true benign neoplasm and therefore does not correspond to a neuroma
[21, 42]. Moreover, its histology is not very different from biopsies of asymptomatic
interdigital nerves [2, 47, 54, 55].
Macroscopically, Morton’s neuroma is observed as a whitish-yellowish fusiform
volume increase, with a soft and smooth consistency in the nerve (Figs. 6 and 7),
Fig. 6 Dorsal longitudinal

approach, identifying the
interdigital nerve (blue
arrow), the thickened area
of Morton’s neuroma (red
arrow), and both digital
branches (white and black
arrows)
Fig. 7 Resected Morton’s

neuroma, with the neuroma
as an area increased in
volume (N), with its two
distal branches (D) and its
extensive proximal branch
of at least 3 cm (P)
just distal to the intermetatarsal transverse ligament and before the digital nerve
bifurcation [1].
Histologically, multiple reports characterize it by neural degeneration without
signs of Wallerian degeneration, epineural degeneration, sclerohyalinosis of the
interstitium, increase of elastic fibers in the stroma, endovascular hyalinization, and
peri- and intraneural fibrosis [21, 35, 37, 54].
8 Treatment
Treatment of Morton’s neuroma can be divided into conservative or surgical. The

initial management consists of footwear modification associated with an insole (that
includes a retrocapital insert). Corticoid infiltration at the site of the neuroma is
another option. Using this scheme, Bennett [56] reports satisfactory results in 70%
of the cases. Other types of infiltrations include the use of alcohol or botulinum
toxin. The success rate of treatment using the different methods of infiltration has
reached up to 85% [57]. The use of radiofrequency ablation and shock waves are
other treatment alternatives described [57–59]. The use of anti-inflammatories,
analgesics, and physical therapy is also included in the conservative treatment. In
case of conservative treatment failure and symptom persistence after 3–6 months,
surgical treatment is indicated, which consists of neuroma resection [56]. The suc-
cess rate for surgical treatment is 89% [57].
8.1 Conservative Treatment
8.1.1 Orthotics
Initially Morton’s neuroma is managed by placing a retrocapital insert associated

with a wide shoe (wide toe box). The orthosis aligns the head of the metatarsals and
relieves the pressure created by the neuroma on the forefoot, relieving the symp-
toms. There are retrocapital adhesive buttons that are options for narrower and
smaller shoes and summertime shoes (sandals). With regard to the use of insoles,
there is no difference in the final result by using alternatives for pronators or supina-
tors [60]. The use of orthoses alone provides an improvement in 48% of patients [57].
8.1.2 Infiltrations
Corticoid infiltration of the neuroma is one of the most frequently used techniques.
It is a method that serves both as a diagnostic and therapeutic alternative. There are
multiple types of infiltrations for the management of Morton’s neuroma, being the
use of steroids associated with local anesthetic (usually lidocaine) the most used
form in the treatment of the neuroma. A significant relief of symptoms is obtained

after the infiltration in 60–80% of the patients, which lasts at least 3 months [61,
62]. The corticoid generates a decrease in the inflammation around the neuroma,
which reduces the pressure of the anatomical space and therefore the pain. While
Lizano-Díez’s study [63] showed that for up to 6 months the isolated use of local
anesthetic is as effective in improving pain and function as combining them with
steroids, Thompson [61] found that the use of steroids was superior to the use of
local anesthetic alone. In addition, other studies have shown favorable results in a
wide spectrum of patients with the use of steroids [61, 64, 65]. When comparing
corticosteroid infiltration with the use of orthotics, infiltration showed better results
at 6 months [66]. The rate of recurrence of symptoms after steroid infiltration is
23% [57]. In addition, the greatest treatment success is achieved when the infiltra-
tion is carried out up to 1 year after the onset of symptoms [64]. Infiltration can be
performed using ultrasound guidance. However, Mahadevan [14] presented a ran-
domized double-blind study evaluating functional outcomes at 12 months after
infiltration with and without ultrasound support, showing no statistically significant
difference in functional outcomes between the two groups. Therefore, it is not rec-
ommended to routinely perform infiltration under ultrasound assistance. On the
other hand, a maximum number of three infiltrations is recommended, separated by
at least 3–4 weeks, with no other type of associated treatment. Caution should be
exercised when performing the infiltration, due to possible damage to the joint cap-
sule and collateral ligaments and/or atrophy of subcutaneous fat, when placing the
medication outside the intermetatarsal space.
Infiltration using alcohol has shown promising results. Alcohol would induce
chemical neurolysis, which helps with pain improvement. Studies with 1-year fol-
low-up have shown improvement in functional scales and decrease in the size of the
neuroma [67–69]. The treatment success rate is 71% [57], and it also generates a
volume decrease of 30% of the neuroma [70, 71]. However, there is a wide range of
alcohol concentrations used in the different studies. In Gurdezi’s study [67], after 5
years of follow-up, 36% of patients required surgical resolution. Espinosa [72]
reported improvement in only 20% of the patients. The use of alcohol generates an
extensive fibrosis in the surrounding tissues because it is not specific for the nervous
tissue. A secondary surgical resolution is more complex when required. That is why
some authors do not recommend its use. This type of infiltration is not currently
recommended as first-line treatment by this group of authors, being the infiltration
with corticoids the recommendation with better evidence.
8.1.3 Other Conservative Treatments
The use of botulinum toxin A has shown an improvement of 71% of patients at 3

months after an application, without adverse effects. However, 29% showed no
improvement [73]. The injection of hyaluronic acid by means of ultrasound support
achieved a significant improvement in AOFAS scores (>50 points) at 1 year of fol-
low-up [74]. Ultrasound-guided radiofrequency ablation is a method with
promising short-term results, with a success rate of up to 85% [58, 59]. Brooks [75]
demonstrated that performing three cycles of ablation obtained a high degree of
satisfaction and a low rate of adverse effects. However, studies with a better level of
evidence and greater follow-up and comparisons with different treatments are
required to define the real efficacy of these treatments.
There is little evidence on the use of shock waves for the treatment of Morton’s
neuroma. Positive results have been obtained when comparing this treatment with a
placebo control group [76]; however, it is not yet a recommended alternative, due to
the lack of conclusive literature.
Other options include the use of high-dose vitamin B6 (200 mg daily for 3
months and then 100 mg daily) [77], anti-neuritic drugs, serotonin inhibitors, non-
steroidal anti-inflammatory drugs, anti-epileptic drugs, and tricyclic antidepres-
sants, which may reduce patient symptoms.
In general, the improvements achieved with conservative treatments can be per-
manent or transitory, total, or partial. Some patients decide to manage their symp-
toms with wide shoes combined with inserts and occasional infiltrations.
If conservative measures fail, surgical treatment is recommended. Gaynor [78]

determined that patients benefit from surgical resolution by obtaining a better suc-
cess rate. In patients with symptoms lasting less than 6 months, conservative treat-
ment was successful in 38% versus 62% with surgical treatment. In patients with
symptoms lasting more than 6 months, 83% improved with surgical treatment. In
order to achieve an adequate success rate of surgery, the etiological diagnosis must
be adequately performed and the surgical technique carried out. Surgical resection
of the thickened neural area (neurectomy) is the most frequently performed surgical
treatment. Its success rate is between 51 and 85% in long-term follow-up studies
[25, 38, 79, 80]. Fifty percent of patients report no pain after surgery; 30% report
being better than before surgery, but with minimal residual pain; and only 10%
report worse pain than before surgery [38, 81, 82].
It has also been proposed to associate other surgical gestures with neurectomy:
intermuscular transposition to the intermetatarsal space, release of the transverse
intermetatarsal ligament (open or endoscopic), neurolysis, transposition of the
nerve, and/or osteotomy of the metatarsals. When comparing the results of patients
with and without section of the intermetatarsal transverse ligament, a slight improve-
ment was observed in the group where section was performed. In patients where no
ligament section was performed, worse results were obtained [81]. Although 83%
of good results were obtained with this technique, these were short term, and it
remains to be seen whether the results will be maintained with greater follow-
up [83].
Endoscopic decompression of the intermetatarsal transverse ligament has shown

promising results with a considerable decrease in pain and a low rate of complica-
tions [84]. A variant of this technique without endoscopic support was described by
Abdelaziz [85] obtaining complete resolution of pain at 26 months in 78% of the
patients [85].
The role of metatarsal osteotomy is to increase the space available between the
metatarsal heads, decreasing the compression and irritation of the surrounding tis-
sue, specifically the nerve, thus achieving pain reduction. Park [86] compared the
release of the transverse ligament versus osteotomies plus ligament release. The
functional outcomes were improved in the combined group. However, the authors
were unable to define the exact association between metatarsal shortening and neu-
roma decompression. Later Bauer [87] evaluated the efficacy of percutaneous distal
metaphyseal osteotomy and transverse intermetatarsal ligament release when com-
pared to neurectomy in the treatment of Morton’s neuroma. After 2 years of follow-
up, the patients with isolated neurectomy presented mechanical metatarsalgia,
requiring plantar orthoses; however, the group that was also managed with distal
metaphyseal osteotomies of the second, third, and fourth metatarsals did not require
them. The authors of the study suggest that both treatments are effective, but the
patients with osteotomy present better long-term evolution and a lower rate of resid-
ual metatarsalgia. The bias of this conclusion is that the study included patients with
pain of mechanical origin (not only by the neuroma) and not only in the third inter-
metatarsal space. That is why it cannot be extrapolated for all Morton’s neuroma
patients. Therefore, there is currently not enough evidence to show that the outcome
of the osteotomy is superior to neurectomy with release of the trans-metatarsal
ligament.
There are two types of approaches to perform neurectomy: the dorsal approach
and the plantar approach. The choice of approach depends on the surgeon’s training
and personal preference. No differences have been demonstrated in the functional
results of patients operated on for neuroma in relation to the type of approach used
[88]. However, the dorsal longitudinal approach would allow early loading and less
pathological scarring (formation of hyperkeratosis or keloid) with respect to the
plantar. Additionally, multiple authors have published successful results using the
dorsal approach. The review carried out by Coughlin [38] with a follow-up of more
than 5 years reported good and excellent results in 85% of the patients and pain-free
in 65% of them with the same follow-up. For these reasons, the dorsal longitudinal
approach is preferred by this group of authors.
In case there are two adjacent neuromas, it is advised the resection of the most
symptomatic neuroma and the release of the intermetatarsal transverse ligament of
the less symptomatic space, to avoid a significant hypoesthesia of the toe [15, 89].
The results are better when performing the resection of a single neuroma, compared
to the resection of multiple neuromas. There is no difference in functional outcomes
between patients who had resections of the second versus the third interdigital
space [81].
8.2.1 Dorsal Approach
The patient is placed in a supine position by placing a tourniquet on the limb to be

operated on. A longitudinal dorsal incision of 2–4 cm is made over the affected
intermetatarsal space. Meticulous dissection is performed on the tissue of the inter-
metatarsal space to find the intermetatarsal transverse ligament. The ligament is
sectioned parallel to the metatarsals. A lamina spreader is placed between the meta-
tarsals (to facilitate the vision of the content of the space), and pressure is applied
from plantar to dorsal, allowing observation of the thickened region of the nerve.
The common interdigital nerve will be observed proximal to the neuroma. A distal
dissection is performed until the bifurcation is observed, which will continue dis-
tally with two branches of the interdigital nerve (Fig. 6). The resection of the two
distal branches of the nerve is performed. The trunk of the common interdigital
nerve is identified, carrying out the resection at least 3 cm proximal to the bifurca-
tion of the interdigital nerve, making sure not to leave communicating plantar
branches. The sectioned plantar nerve is extracted, being bigger than 3 cm, and it is
sent to biopsy for the corresponding anatomopathological evaluation (Fig. 7). The
biopsy has to confirm that the nerve was resected and not only blood vessels that are
anatomically located on the neuroma and can induce error in the surgical technique.
Furthermore, it allows the occasional diagnosis of associated pathology such as
vasculitis of rheumatological origin. The proximal end of the severed nerve is hid-
den in the intrinsic musculature of the foot, reducing the possibility of recurrence by
inhibiting the growth of the amputation neuroma [90]. At this point the tourniquet is
released to perform hemostasis at the surgical site and to observe the vascular state
of the affected toes. In addition, this reduces the possibility of adhesions and the
formation of postoperative hematoma. The closure of the subcutaneous cellular tis-
sue uses 3.0 resorbable suture. The skin is closed with 4.0 monocryl using the con-
tinuous intradermal suture technique. The patient is placed in a compressive bandage
and postoperative shoes being authorized to bear weight as tolerated.
8.2.2 Plantar Approach
The plantar longitudinal approach described by Betts [9] can be used for the resec-
tion of Morton’s neuroma presenting similar functional results in the long term as
when performing the dorsal approach. The plantar approach presents better results
in the treatment of relapses [90, 91], since a better visualization of the nerve and its
residual plantar branches is obtained. The incomplete resection of the plantar
branches in the primary surgery is one of the most frequent causes of recurrence.
This approach is done in a longitudinal way, 1 cm proximal to the metatarsal heads,
to avoid the formation of scar that affects the load region of the forefoot. The incision
is made through the plantar adipose tissue, avoiding the excision of this tissue.
The plantar fascia is reached, and after separating the fascicles the neuroma is identi-
fied, resecting it in the same way as when performing the dorsal approach. The inter-
metatarsal ligament is preserved. The orientation of the incision could be transverse,
proximal to the flexion crease of the forefoot. In this way the loading area is avoided,
but it can lead to atrophy of the fatty tissue, and it is difficult to follow the interdigital
nerve proximally [92]. As mentioned, we reserve the plantar approach mainly for
relapses, since it is simpler to find the nerve amputation stump that is located closest
to the plantar area (Fig. 8).
a b c
d f
Fig. 8 (a) Dorsal approach previously performed. (b) Plantar approach for revision of recurrent
Morton’s neuroma. Longitudinal incision marking on the second plantar interdigital space, proxi-
mal to the metatarsal head. (c) Intraoperative picture using a plantar approach of recurrent Morton’s
neuroma with stump neuroma (red arrow). (d) Enlarged vision of neuroma in anatomical clamp.
(e) Resected area of 2 cm of nerve with stump neuroma. (f) Relocation of nerve to a more proximal
area, fixing it to the intermetatarsal muscles using fine suture (6-0)
8.2.3 Postoperative Management
Regardless of the approach used, the postoperative management consists of the

placement of a compressive bandage, foot elevation, oral analgesics, and authoriza-
tion to bear weight as tolerated using a postoperative shoe. Suture removal is after
14 days. The patient is warned that an area with hypoesthesia will be felt in the ter-
ritory of the resected nerve. This hypoesthesia tends to progressively decrease in
size, and finally the patient tends not to consciously perceive it despite its persis-
tence. Due to the physiological growth of the amputation neuroma, patients usually
experience an increase in local sensitivity around 10 weeks, which subsides after
2–3 weeks spontaneously. Physiotherapy can be prescribed to perform gait training
and massage at the incision site to prevent adhesions, area desensitization, and
edema management. High-impact activities such as jogging should be avoided until
the tenth week.
9 Complications
Among the complications, we find surgical wound infection, residual hematoma,

alterations in healing, or complex regional pain syndrome, among others. Akermark
[88] conducted a prospective study comparing the plantar and dorsal approaches,
obtaining good functional results in both groups. However, in spite of a low and
comparable number of complications between both groups, each one of the types of
approach has its own complications. The plantar approach presented hypertrophic
scar formation. In contrast, the dorsal approach presented erroneous resection of the
nerve (resected artery), operative wound dehiscence, operative wound infection,
and deep vein thrombosis. Therefore, the patient should be educated about the com-
plications according to the type of approach. It is important to note that the common
digital artery is found next to the nerve and is resected in 39% of cases. However,
this action does not generate major complications due to the presence of anasto-
motic communications, unless the arteries in adjacent spaces are resected as well
[93]. As previously mentioned, what should not happen is to remove only the artery
and leave the nerve in situ.
The failure rate for surgical treatment is 14–21% [94]. One of the usual causes of
failure of surgical treatment is incorrect etiological diagnosis of metatarsalgia. To
avoid this, it is essential to consider the entire differential diagnosis of Morton’s
neuroma (see Table 1). As it was already mentioned, the diagnosis is mainly clini-
cal, and the imaging methods allow ruling out associated pathologies. Figure 9
shows a patient in whom an erroneous diagnosis of Morton’s neuroma was made.
Finally, the patient evolves with erythema nodosum in the lower left extremity being
diagnosed with vasculitis. For this reason, the correct diagnosis is essentially with
the clinical history and physical examination [95]. In addition, the patient’s biome-
chanical alterations of the forefoot and comorbidities should also be considered.
Fig. 9 Erythema nodosum

of the lower left extremity,
consistent with the
diagnosis of vasculitis
9.1 Morton’s Neuroma Revision Surgery
The main causes of failure of primary surgical treatment are the presence of an
unidentified adjacent neuroma, incomplete resection of plantar branches, and recur-
rence of the neuroma, called amputation neuroma. The most common form of post-
surgical residual pain treatment is the use of steroid infiltration. Using this method,
adhesions and remaining scar tissue are released. If the symptoms persist, one
option is revision surgery (Fig. 8a–f).
The resection of the proximal neuroma is performed through a plantar approach

(Fig. 8b); after performing a dissection through the plantar fascia, the nerve is iden-
tified with its medial or lateral plantar branch (Fig. 8c and d). Afterwards, the neu-
roma is resected (Fig. 8e) with its plantar branches, and the remaining proximal
nerve is redirected to a more proximal location, fixing it within the intermetatarsal
muscles using a fine suture (6-0) (Fig. 8f). The nerve should be buried at least 1 cm
away from the skin [96].
The success rate for eliminating pain from primary surgery is 80% [90]; how-
ever, the success rate for revision surgery is less than that of primary neurectomy,
which should be discussed with the patient.
References
1. Di Caprio F, Meringolo R, Shehab Eddine M, Ponziani L. Morton’s interdigital neuroma of the

foot: a literature review. Foot Ankle Surg. 2018;24(2):92–8.
2. Gougoulias N, Lampridis V, Sakellariou A. Morton’s interdigital neuroma: instructional
review. EFORT Open Rev. 2019;4(1):14–24.
3. Larson EE, Barrett SL, Battiston B, Maloney CT Jr, Dellon AL. Accurate nomenclature for fore-
foot nerve entrapment: a historical perspective. J Am Podiatr Med Assoc. 2005;95(3):298–306.
4. Civinini F. Su di un gangliare rigonfiamento della pinata del plede. Mem Chir
Archiespedale. 1835;4
5. Durlacher L. A treatise on corns, bunions, the diseases of nails, and the general management
of the feet. Simpkin, Marshall, London, 1845, 52.
6. Morton TG. A peculiar and painful affection of the fourth metatarsophalangeal articulation.
Am J Med Sci. 1876;71:37.
7. Hoadley A. Six cases of metatarsalgia. Chicago Med Rec. 1893;5:32–7.
8. Peters PG, Adams SB Jr, Schon LC. Interdigital neuralgia. Foot Ankle Clin N Am.
2011;16:305–15.
9. Betts L. Morton’s metatarsalgia: neuritis of the fourth digital nerve. Med J Aust. 1940;1
10. Gauthier G. Thomas Morton’s disease: a nerve entrapment syndrome. Clin Orthop Relat Res.
1979;142:90–2.
11. Schon LC, Mann RA. Disease of the nerves. In: Surgery of the foot and ankle surgery, vol.
I. 8th ed. Mosby Elsevier. Philadelphia; 2007.
12. Bradley N, Miller WA, Evans JP. Plantar neuroma analysis of results following surgical exci-
sion in 145 patients. South Med J. 1976;69:853.
13. Mahadevan D, Salmasi M, Whybra N, Nanda A, Gaba S, Mangwani J. What factors predict
the need for further intervention following corticosteroid injection of Morton’s neuroma? Foot
Ankle Surg. 2016;22:9–11.
14. Mahadevan D, Attwal M, Bhatt R, Bhatia M. Corticosteroid injection for Morton’s neu-
roma with or without ultrasound guidance: a randomised controlled trial. J Bone Joint
J. 2016;98-B:498–503.
15. Thompson FM, Deland JT. Occurrence of two interdigital neuromas in one foot. Foot Ankle.
1993;14:15–7.
16. Levitsky KA, Alman BA, Jesevar DS, Morehead J. Digital nerves of the foot: anatomic varia-
tions and implications regarding the pathogenesis of the interdigital neuroma. Foot Ankle.
1993;14:208–14.
17. Govsa F, Bilge O, Ozer MA. Anatomical study of the communicating branches between the
medial and lateral plantar nerves. Surg Radiol Anat. 2005;27:377–81.
18. Frank PW, Bakkum BW, Darby SA. The communicating branch of the lateral plantar nerve: a
descriptive anatomic study. Clin Anat. 1996;9(4):237–43.
19. Bossley CJ, Cairney PC. The intermetatarsophalangeal bursa: its significance in Morton’s
metatarsalgia. J Bone Joint Surg Br. 1980;62:184–7.
20. Valero J, Salcini JL, Gallart J, Gonzalez L. Revisión de las teorías acerca de la etiología del
neuroma de morton. Revista Española de Podología. 2015;XXVI(2):42–9.
21. Lassmann G. Morton’s toe: clinical, light, and electron microscopic investigations in 133
cases. Clin Orthop Relat Res. 1979;142:73–84.
22. Valero J, Gallart J, Gonzalez D, Deus J, Lahoz M. Multiple interdigital neuromas. A retrospec-
tive study of 279 feet with 462 neuromas. J Foot Ankle Surg. 2015;54(3):320–2.
23. Volpe A. La sindrome di Morton. Lo Scalpello. 2011;25:60–73.
24. Wu KK. Morton's interdigital neuroma: a clinical review of its etiology, treatment and results.
J Foot Ankle Surg. 1996;35(2):112–9; discussion 187–8.
25. Mann RA, Reynolds JD. Interdigital neuroma: a critical clinical analysis. Foot Ankle.
1983;3:238.
26. Espinosa N, Brodsky JW, Maceira E. Metatarsalgia. J Am Acad Orthop Surg.
2010;18(8):474–85.
27. Wachter S, Nilson RZ, ThulJR. The relationship between foot structure and intermetatarsal
neuromas. J Foot Surg. 1984;23(6):436–9.
28. Franson J, Baravarian B. Intermetatarsal compression neuritis. Clin Podiatr Med Surg.
2006;23:569–78.
29. Sgarlatto T. Compendium of podiatric biomechanics. San Francisco: California College of
Podiatric Medicine; 1971. p. 31.
30. Levy M, Seelenfreund M, Maor P, Fried A. Post-traumatic Morton’s neuroma. Harefuah.
1972;83(5):202–33.
31. Shephard E. Intermetatarsophalangeal bursitis in the causation of Morton’s metatarsalgia. J
Bone Joint Surg. 1975;57B:115–33.
32. Carrier PA, Janigan JD, Weil LS, Smith SD. Morton’s neuroma: a possible contributing etiol-
ogy. J Am Podiatry Assoc. 1975;65(4):315–21.
33. Silvermann LJ. Morton’s toe or Morton’s neuralgia. J Am Podiatry Assoc. 1976;66:749.
34. Tate RO, Rusin JJ. Morton's neuroma: its ultrastructural anatomy and biomechanical etiology.
J Am Podiatry Assoc. 1978;68(12):797–807.
35. Graham CE, Graham DM. Morton’s neuroma: a microscopic evaluation. Foot Ankle.
1984;5:150–3.
36. Dellon AL, Aszmann OC. Treatment of superficial and deep peroneal neuromas by resec-
tion and translocation of the nerves into the anterolateral compartment. Foot Ankle Int.
1998;19(5):300–3.
37. Weinfeld SB, Myerson MS. Interdigital neuritis: diagnosis and treatment. J Am Acad Orthop
Surg. 1996;4(6):328–35.
38. Coughlin MJ, Pinsonneault T. Operative treatment of interdigital neuroma. A long-term fol-
low-up study. J Bone Joint Surg Am. 2002;84:1276–7.
39. Nissen KI. Plantar digital neuritis. Morton’s metatarsalgia. J Bone Joint Surg Br.
1948;30B(1):84–94.
40. Ringertz N, Unander-Scharin L. Morton’s disease: a clinical and pathoanatomical study. Acta
Orthop Scand. 1950;19:327.
41. Mulder JD. The causative mechanism in Morton’s metatarsalgia. J Bone Joint Surg Br.
1951;33:94–5.
42. Giannini S, Bacchini P, Ceccarelli F, Vanini F. Interdigital neuroma: clinical examination and
histopathologic results in 63 cases treated with excision. Foot Ankle Int. 2004;25(2):79–84.
43. Claassen L, Bock K, Ettinger M, Waizy H, Stukenborg-Colsman C, Plaass C. Role of MRI in
detection of Morton’s neuroma. Foot Ankle Int. 2014;35(10):1002–5.
44. Mahadevan D, Venkatesan M, Bhatt R, Bhatia M. Diagnostic accuracy of clinical tests for
Morton’s neuroma compared with ultrasonography. J Foot Ankle Surg. 2015;54(4):549–53.
45. Pastides P, El-Sallakh S, Charalambides C. Morton’s neuroma: A clinical versus radiological

diagnosis. Foot Ankle Surg. 2012;18(1):22–4.
46. Bencardino J, Rosenberg ZS, Beltran J, et al. Morton’s neuroma: is it always symptomatic?
AJR Am J Roentgenol. 2000;175(3):649–53.
47. Symeonidis PD, Iselin LD, Simmons N, Fowler S, Dracopoulos G, Stavrou P. Prevalence
of interdigital nerve enlargements in an asymptomatic population. Foot Ankle Int.
2012;33(7):543–7.
48. Raouf T, Rogero R, McDonald E, Fuchs D, Shakked RJ, Winters BS, Daniel JS, Pedowitz
DI, Raikin SM. Value of preoperative imaging and intraoperative histopathology in Morton’s
neuroma. Foot Ankle Int. 2019;40(9):1032–6.
49. Xu Z, Duan X, Yu X, Wang H, Dong X, Xiang Z. The accuracy of ultrasonography and mag-
netic resonance imaging for the diagnosis of Morton’s neuroma: a systematic review. Clin
Radiol. 2015;70(4):351–8.
50. Shapiro PP, Shapiro SL. Sonographic evaluation of interdigital neuromas. Foot Ankle Int.
1995;16(10):604–6.
51. Hulstaert T, Hulstaert T, Shahabpour M, Provyn S, Lenchik L, Simons P, Vanheste R, De
Maeseneer M. Forefoot pain in the lesser toes: anatomical considerations and magnetic reso-
nance imaging findings. Can Assoc Radiol J. 2019;70(4):408–15.
52. Bignotti B, Signori A, Sormani MP, Molfetta L, Martinoli C, Tagliafico A. Ultrasound versus
magnetic resonance imaging for Morton neuroma: systematic review and meta-analysis. Eur
Radiol. 2015;25(8):2254–62.
53. Ruiz F, Tomás P, Pryest P, Martínez A, Prados N. Role of imaging methods in diagnosis and
treatment of Morton’s neuroma. World J Radiol. 2018;10(9):91–9.
54. Morscher E, Ulrich J, Dick W. Morton’s intermetatarsale neuroma: morphology and histologi-
cal substrate. Foot Ankle Int. 2000;21(7):558–62.
55. Bourke G, Owen J, Machet D. Histological comparison of the third interdigital nerve in
patients with Morton’s metatarsalgia and control patients. Aust N Z J Surg. 1994;64(6):421–4.
56. Bennett GL, Graham CE, Mauldin DM. Morton’s interdigital neuroma: a comprehensive treat-
ment protocol. Foot Ankle Int. 1995;16(12):760–3.
57. Valisena S, Petri GJ, Ferrero A. Treatment of Morton’s neuroma: a systematic review. Foot
Ankle Surg. 2018;24(4):271–81.
58. Moore JI, Rosen R, Cohen J, Rosen B. Radiofrequency thermoneurolysis for the treatment of
Morton’s neuroma. J Foot Ankle Surg. 2012;51:20–2.
59. Chuter GS, Chua YP, Connell DA, Blackney MC. Ultrasound-guided radiofrequency ablation
in the management of interdigital (Morton’s) neuroma. Skelet Radiol. 2013;42:107–11.
60. Kilmartin TE, Wallace WA. Effect of pronation and supination orthosis on Morton’s neuroma
and lower extremity function. Foot Ankle Int. 1994;15(5):256–62.
61. Thomson CE, Beggs I, Martin DJ, McMillan D, Edwards RT, Russell D, Yeo ST, Russell IT,
Gibson JN. Methylprednisolone injections for the treatment of Morton neuroma. J Bone J Surg
Am. 2013;95(9):790–8.
62. Greenfield J, Rea J Jr, Ilfeld FW. Morton’s interdigital neuroma. Indications for treatment by
local injections versus surgery. Clin Orthop Relat Res. 1984;185:142–4.
63. Lizano-Díez X, Ginés-Cespedosa A, Alentorn-Geli E, Pérez-Prieto D, González-Lucena G,
Gamba C, De Zabala S, Solano-López A, Rigol-Ramón P. Corticosteroid injection for the treat-
ment of Morton’s neuroma: a prospective, double-blinded, randomized, placebo-controlled
trial. Foot Ankle Int. 2017;38:944–51.
64. Markovic M, Crichton K, Read JW, Lam P, Slater HK. Effectiveness of ultrasound-
guided corticosteroid injection in the treatment of Morton’s neuroma. Foot Ankle Int.
2008;29(5):483–7.
65. Thomson CE, Gibson JA, Martin D. Interventions for the treatment of Morton’s neuroma.
Cochrane Database Syst Rev. 2004; https://doi.org/10.1002/14651858.CD003118.pub2.
66. Saygi B, Yildirim Y, Saygi EK, Kara H, Esemenli T. Morton neuroma: comparative results of
two conservative methods. Foot Ankle Int. 2005;26(7):556–9.
67. Gurdezi S, White T, Ramesh P. Alcohol injection for Morton’s neuroma: a five- year follow-
up. Foot Ankle Int. 2013;34(8):1064–7.
68. Dockery GL. The treatment of intermetatarsal neuromas with 4% alcohol sclerosing injec-
tions. J Foot Ankle Surg. 1999;38(6):403–8.
69. Pasquali C, Vulcano E, Novario R, Varotto D, Montoli C, Volpe A. Ultrasound- guided alcohol
injection for Morton’s neuroma. Foot Ankle Int. 2015;36(1):55–9.
70. Musson RE, Sawhney JS, Lamb L, Wilkinson A, Obaid H. Ultrasound guided alcohol ablation
of Morton’s neuroma. Foot Ankle Int. 2012;33(3):196–201.
71. Fanucci E, Masala S, Fabiano S, Perugia D, Squillaci E, Varrucciu V, Simonettiet G. Treatment
of intermetatarsal Morton's neuroma with alcohol injection under US guide: 10-month follow-
up. Eur Radiol. 2004;14(3):514–8.
72. Espinosa N, Seybold JD, Jankauskas L, Erschbamer M. Alcohol sclerosing therapy is not
effective treatment for interdigital neuroma. Foot Ankle Int. 2011;32(6):576–80.
73. Climent JM, Mondéjar-Gómez F, Rodríguez-Ruiz C, Díaz-Llopis I, Gómez- Gallego D,
Martín-Medina P. Treatment of Morton neuroma with botulinum toxin A: a pilot study. Clin
Drug Investig. 2013;33(7):497–503.
74. Lee K, Hwang IY, Hyu Ryu C, Woo Lee J, Woo Kang S. Ultrasound guided hyaluronic acid
injection for management of Morton’s neuroma. Foot Ankle Int. 2018;39(2):201–4.
75. Brooks D, Parr A, Bryceson W. Three cycles of radiofrequency ablation are more efficacious
than two in the management of Morton’s neuroma. Foot Ankle Spec. 2018;11(2):107–11.
76. Fridman R, Cain JD, Weil L Jr. Extracorporeal shockwave therapy for interdigital neuroma: a
randomized, placebo-controlled, double-blind trial. J Am Podiatr Med Assoc. 2009;99:191–3.
77. Bae SY, Jung EY, Oh SC. Pyridoxine in the treatment of peripheral nerve related foot pain. J
Korean Foot Ankle Soc. 2013;17:203–8.
78. Gaynor R, Hake D, Spinner SM, Tomczak RL. A comparative analysis of conservative versus
surgical treatment of Morton’s neuroma. J Am Podiatr Med Assoc. 1989;79:27–30.
79. Womack JW, Richardson DR, Murphy GA, Richardson EG, Ishikawa SN. Long- term evalua-
tion of interdigital neuroma treated by surgical excision. Foot Ankle Int. 2008;29:574–7.
80. Nery C, Raduan F, Del Buono A, Asaumi ID, Maffulli N. Plantar approach for excision of a
Morton neuroma: a long-term follow-up study. J Bone Joint Surg Am. 2012;94(7):654–8.
81. Kasparek M, Schneider W. Surgical treatment of Morton’s neuroma: clinical results after open
excision. Int Orthop. 2013;37:1857–61.
82. Bucknall V, Rutherford D, Macdonald D, Shalaby H, McKinley J, Breusch SJ. Outcomes
following excision of Morton’s interdigital neuroma: a prospective study. Bone Joint
J. 2016;98-B:1376–81.
83. Rosenberg G, Sferra J. Morton’s neuroma, primary and recurrent and their treatment. Foot
Ankle Clin. 1998;473–484
84. Shapiro SL. Endoscopic decompression of the inter-metatarsal nerve for Morton’s neuroma.
Foot Ankle Clin. 2004;9:397–407.
85. Abdelaziz M, Whitelaw K, Waryasz G, Guss D, Johnson A, Di Giovanni C. Isolated interm-
etarsal ligament release as a primary surgical management for Morton neuroma: the carpal
tunnel of the foot? Foot Ankle Orth. 2018;3(3):2473011418S0013.
86. Park EH, Kim YS, Lee HJ, Koh YG. Metatarsal shortening osteotomy for decompression of
Morton’s neuroma. Foot Ankle Int. 2013;34(12):1654–60.
87. Bauer T, Gaumetou E, Klouche S, Hardy P, Maffulli N. Metatarsalgia and Morton's disease:
comparison of outcomes between open procedure and neurectomy versus percutaneous meta-
tarsal osteotomies and ligament release with a minimum of 2 years of follow-up. J Foot Ankle
Surg. 2015;54(3):373–7.
88. Akermark C, Crone H, Skoog A, Weidenhielm L. A prospective randomized controlled trial
of plantar versus dorsal incisions for operative treatment of primary Morton’s neuroma. Foot
Ankle Int. 2013;34(9):1198–204.
89. Benedetti RS, Baxter DE, Davis PF. Clinical results of simultaneous adjacent interdigital neu-
rectomy in the foot. Foot Ankle Int. 1996;17:264–8.
90. Wolfort SF, Dellon AL. Treatment of recurrent neuroma of the interdigital nerve by
implantation of the proximal nerve into muscle in the arch of the foot. J Foot Ankle Surg.
2001;40(6):404–10.
91. Johnson JE, Johnson KA, Unni KK. Persistent pain after excision of an interdigital neuroma:
results of reoperation. J Bone Joint Surg Am. 1988;70:651–7.
92. Alexander IJ, Johnson KA, Parr JW. Morton’s neuroma: a review of recent concepts.
Orthopedics. 1987;10(1):103–6.
93. Su E, Di Carlo E, O'Malley M, Bohne WH, Deland JT, Kennedy JG. The frequency of digital
artery resection in Morton interdigital neurectomy. Foot Ankle Int. 2006;27(10):801–3.
94. Faraj AA, Hosur A. The outcome after using two different approaches for excision of Morton's
neuroma. Chin Med J (Engl). 2010;123(16):2195–8.
95. Sharp RJ, Wade CM, Hennessy MS, Saxby TS. The role of MRI and ultrasound imaging
in Morton’s neuroma and the effect of size of lesion on symptoms. J Bone Joint Surg (Br).
2003;85-B:999–1005.
96. Wagner E, Ortiz C. The painful neuroma and the use of conduits. Foot Ankle Clin N Am.
2011;16:295–304.
Bunionette
1 Introduction
The term “bunionette” refers to the lateral prominence of the fifth metatarsal (M5)
head and the abnormality of its surrounding soft tissues. Such condition has been
found frequently in tailors, due to the cross-legged position adopted at their work,
thus being also commonly designated as “tailor’s bunion” [1] (Fig. 1).
1.1 Epidemiology
Although the incidence and prevalence in the general population are not known, the
bunionette deformity is three to ten times more common in women than men and
has a peak incidence during the fourth and fifth decades of life [6, 7].
In one series 66% of the patients also had pes planus [15]. Other common associ-
ated forefoot abnormalities include adducted fifth toe, digital rotational component
to the axial deformity, hammer fifth toe, and hallux valgus. When the latter occurs
with a bunionette due to an increased angle between the fourth and the fifth
M. Resende Sousa (*)

Foot and Ankle Unit at Hospital da Luz, Lisbon, Portugal
D. Ribeiro Mendes
Foot and Ankle Unit at Hospital Cuf Tejo, Lisbon, Portugal
J. Vide
Foot and Ankle Surgeon at Hospital da Luz, Lisbon, Portugal

Switzerland AG 2022
518 M. Resende Sousa et al.
Fig. 1 Bunionette
metatarsals (4–5 IM angle), a wide splayed foot deformity results [5, 12, 23, 32, 50].
A splayed foot is present in up to 7.4% of patients with hallux valgus, of which
60.7% meet surgical criteria and are sometimes overlooked [13]. The identification
and appropriate treatment of this and other symptomatic foot pathology are para-
mount to success.
2 Anatomy and Etiology
Fifth metatarsal shape, rotation, and alignment, as well as exogenous factors, may
predispose patients to a painful bunionette. These factors, adapted from Koti [30],
are summarized in Table 1.
Bunionette 519
Table 1 Contributing factors for bunionette

Endogenous factors
A. M5 rotation
Abnormal foot position (lateral aspect of the foot resting on the ground)
Excessive pronation
Fifth tarsometatarsal joint hypermobility
Associated pronation of subtalar and midtarsal joints
Pes planus
B. M5 alignment – varus/increased 4–5 IM angle
Incomplete insertion or development of the transverse metatarsal ligament
Supernumerary ossicles attached to the lateral fourth metatarsal, pushing the fifth metatarsal
laterally
C. M5 shape
Prominent lateral fifth metatarsal head
“Dumbbell”-shaped fifth metatarsal head
Lateral bending/deviation of the fifth metatarsal
Congenital plantar or dorsiflexed fifth ray deformities
D. Hypertrophy of soft tissues overlying the lateral aspect of the M5 head
Exogenous factors
Tight footwear causing pressure around the M5 head
2.1 Clinical Symptoms and Signs
Bunionette is usually a static deformity. Repeated activities such as running or jog-

ging cause friction between the bunionette and a constrictive footwear, leading to
inflammation of soft tissues surrounding the fifth metatarsal head, including the
overlying bursa [29, 53, 54]. Three main painful areas have been described in rela-
tion to the head of fifth metatarsal: the lateral, the dorsolateral, and plantar aspects.
Over time, continued friction and inflammation can evolve to an ulceration or
keratosis. In patients with diabetes, advanced Charcot-Marie-Tooth disease, or spi-
nal dysraphism with poor sensibility, can result in superinfection and loss of the
entire fifth ray or even the foot [25].
Patients may present plantar keratosis (10–33%), lateral keratosis (50–70%), or
a combination of the previous (17–20%) [11, 15, 20, 23, 26, 38]. This differentiation
may affect the surgical procedure.
The clinical examination should include a thorough assessment of the patient’s
past and present medical history, with special emphasis placed on the chronicity of
the symptoms, effect of the condition on the activities of daily living, employment
responsibilities, and progression of the deformity.
A detailed evaluation of the fifth metatarsal cuboid joint and fifth metatarsal
phalangeal joint range of motion, global forefoot posture, and palpation of the peri-
articular structures to determine areas of maximum signs and symptoms should be
performed [44]. Assessment of the neurologic and vascular status is of paramount
importance, as adequate peripheral circulation and protective sensation are neces-
sary for postsurgical healing.
MTP - 5 angle
C
F
D Width of the
foot
4-5 IM angle
Intermetatarsal
(<9˚) angle
Fig. 2 Radiographic measurements
2.2 Diagnostic and Classification
The bunionette evaluation includes standing dorsoplantar (Fig. 2) and lateral radio-
graphs. Occasionally, a medial oblique (MO) view is performed to assess lateral
flare, metatarsal head, lateral tubercle, and lateral soft tissues.
Anatomic variations found in the fifth metatarsal define the classification and
guide the treatment recommendations. Coughlin [9] described three types of bunio-
nette deformities based on weight-bearing dorsoplantar radiographs.
Type I deformity (Fig. 3) is an enlargement of the lateral surface of the M5 head
and occurs in 27% of cases, either due to an exostosis, a prominent lateral condyle,
or a round, or dumbbell-shaped, metatarsal head. The normal width of the metatar-
sal head is 13 mm or less [17].
However, the radiographic shape of the fifth metatarsal head changes with the
metatarsal pronation, just as does the shape of the first metatarsal head with increas-
ing rotation in hallux valgus. With increasing pronation, the lateral plantar tubercle
of the fifth metatarsal head becomes more prominent, creating the radiographic
impression of an enlarged head [15, 54] and an increase of up to 3° in the 4–5 IM
angle [17]; therefore, the radiographic technique may influence significantly the
preoperative and postoperative assessment [4]. In fact, Nestor [40] defends that
hypertrophy of the metatarsal head is not the cause of tailor’s bunion. Diebold [15]
Bunionette 521
Fig. 3 Classification
defends that the more or less bowed appearance of the fifth metatarsal is in fact due
to its position when the X-ray is taken. Indeed, inversion and eversion of the foot
modify this metatarsal appearance [17].
Type II deformity is secondary to abnormal lateral bowing of the distal fifth meta-
tarsal and occurs in 23% of cases. The lateral bowing, or deviation, occurs at the
distal third of the fifth metatarsal shaft and is measured between the line drawn from
the center of the fifth metatarsal head to its neck and the line made along the medial
cortex of the fifth metatarsal. The average lateral deviation angle is normally 2.6°
(range, 0°–7°). Symptomatic patients with bunionette deformities have an average
value of 8.05° (range, 0–16°) [10].
Type III deformity is an increased in the fourth to fifth intermetatarsal (4–5 IM)
angle and occurs in 50% of cases. The 4–5 IMA is measured by bisecting the axis
of both bone shafts. The average 4–5 IMA is 6.2° (range 3–11°). In symptomatic
patients, the average IMA is 9.6° (range, 5–14°) [10, 13]. In general, a 4–5 IM angle
greater than 8° is felt to be abnormal [36].
Differently from Coughlin, Kitaoka et al. [11] reported that fifth metatarsal bow-
ing or an enlarged fifth metatarsal head was observed to be a cause in less than 10%
of these cases, with most of the cases being caused by an increased 4–5 IMA (type III).
A type IV deformity suggested by Koty [30] consists of two or more components
of the other three deformities. Although rare, it is most commonly seen in the rheu-
matoid patients [1, 8] and does not aid in selecting the appropriate treatment.
The fifth metatarsal-phalangeal (MTP-5) angle expresses the magnitude of the
medial deviation of the fifth toe in relation to the axis of the fifth metatarsal. A nor-
mal MTP-5 angle is 14° or less [51], averaging 10.2 degrees [40].
The MTP-5 status should be assessed, as pain and swelling may be caused by
inflammatory or degenerative pathology [14].
Sagittal plane deformities, although not so common, may also influence the sur-
gical treatment.
3 Treatment
No evidence-based guidelines exist for the conservative management of bunionette

deformity; nevertheless, nonsurgical management should be considered initially.
This includes padding or shaving the keratotic lesion. Patients should wear
altered shoes with wider toe box, to accommodate the lateral deformity. Nonsteroidal
oral analgesics and corticosteroid injections can be used for the acutely inflamed
bursa. Custom orthotics may be used to decrease pronation of the subtalar joint,
hence decreasing pressure over the fifth metatarsal head [14].
Surgery is indicated in the refractory patient (10–23% of all cases) [5]. Several sur-
gical techniques have been described for deformity: lateral condylectomy, distal
metatarsal osteotomy, diaphyseal osteotomy, and proximal fifth metatarsal osteot-
omy (Fig. 4). Other options, like metatarsal head resection, fifth metatarsal ray
resection, and isolated soft tissue procedures, are of limited use.
Bunionette
deformity
Type I Type II Type III

Large M5 Large M5 Increased
head deviation 4-5 IM angle
Lateral Distal Midshaft

Proximal
condylectomy Osteotomy Osteotomy
Chevron
osteotomy
- Transverse - Oblique
- Weil - SCARF
- Chevron - Closing
- Oblique wedge
Fig. 4 Surgical treatment options

Bunionette 523
The goals of surgical intervention are resolution of the symptoms, decreased

width of the forefoot as well as the prominence of the bunionette [14], and avoid-
ance of complications [24].
3.2.1 Lateral Condylectomy
This technique was first presented by Davies in 1949 [12]. It is indicated in type I
deformity and isolated or as part of other surgical techniques and can be done by
either open or percutaneous approach. It is also indicated when more aggressive
procedures are not tolerated, and the patient is allowed to immediately ambulate in
a postoperative shoe for 3 weeks. A lateral condylectomy is often successful in
relieving symptoms. Kitaoka and Holiday [27] reported that 71% of the patients
were satisfied with their result.
In isolation, it is not effective in the presence of an intractable plantar keratosis.
The presence of pes planus or forefoot pronation is considered a relative contraindi-
cation as the pressure will continue due to the position of the hindfoot and forefoot.
The most common complications are recurrence of the deformity, MTP joint sub-
luxation and poor weight bearing, the last due to excessive resection [31]. A tight
capsule closure with excision of redundant soft tissue (or pant-over-vest suture) plus
attention to repair the abductor digiti quinti muscle minimizes medial MTP joint
subluxation [26, 29, 50]. Any angle correction is mostly due to associated soft tissue
procedures, an effect that decreases over time. Therefore, to avoid deformity recur-
rence, this technique should be avoided if MTP5/4–5 IM angle is elevated [21, 23,
31, 33, 38, 50, 57].
3.2.2 Fifth Metatarsal Resections
Resection of the fifth metatarsal head, resection of the distal half of the metatarsal,
and fifth ray resection have all been used to treat a bunionette deformity, but a high
complications rate makes it inappropriate as an initial treatment. Common compli-
cations are transfer metatarsalgia to the fourth metatarsal head [16, 19, 31] (75%),
malalignment (59%) [16], an average fifth toe retraction of 10 mm (36%) [16, 28,
31], continued symptoms (27%), stiffness (25%), toe subluxation [26, 28], and a
flail fifth toe.
These procedures are used as a salvage procedure for infection, ulceration
(excellent results in diabetic patients [2]), severe deformity, severe osteopenia,
extensive degenerative joint changes, previous failed surgery, or poor medical
health [14].
3.2.3 Osteotomy Procedures
Several fifth metatarsal osteotomies have been recommended for the treatment of
symptomatic bunionettes. The choice depends on the case-specific anatomic vari-
ants and the surgeon’s preference. Patients should weight-bear in a postoperative or
Barouk shoe for 6 weeks (Fig. 5).
Distal Fifth Metatarsal Osteotomies
The main contraindication to a distal metatarsal osteotomy is a moderate or severe

angular deformity.
In the distal transverse medializing osteotomy, a transverse vertical osteotomy,
perpendicular to the long axis of the fifth metatarsal, is made from lateral to medial,
completely transecting the metatarsal neck. The cut creates a shelf that tends to
minimize dorsal translation of the capital fragment. A 1.8 mm Kirschner wire (K
wire) is inserted into the soft tissue adjacent to the toe on the lateral aspect and
driven distally out the tip of the fifth toe. With the capital fragment displaced as far
Fig. 5 M5 osteotomies. (1) Capital oblique; (2) chevron; (3) modified Weil; (4) scarfette – gray
dots represent the dorsal projection of the plantar surface cut; (5) Ludloff; (6) proximal chevron
Bunionette 525
medialward as desired, the Kirschner wire is then driven proximal into the diaphy-
seal canal until it penetrates the proximal metaphyseal region. The K wire is
removed 4–6 weeks after surgery. Weitzel et al. [56] reported on 21 patients (30 feet)
who were noted to have 81% good and excellent results at an average follow-up of
more than 7 years. Giannini et al. [21] reported on 32 patients (50 feet) at almost
5 years follow-up with 90% good and excellent results.
Smith and Weil [49] described a distal oblique medializing osteotomy without
fixation, and later Steinke and Boll [52] added fixation. The osteotomy is oriented
in a distal-lateral to proximal-medial direction at an angle of 70° and undercut by
15° (Fig. 5.1). The purpose of this angle is to have the bone slide medially and to
avoid dorsal migration of the head. The osteotomy site is fixed with a K wire or with
one or two mini-fragment screws.
The bone cut orientation of the distal chevron osteotomy is similar to the one
performed in the first metatarsal (Fig. 5.2). The distal fragment is displaced medi-
ally and fixed according to the surgeon’s preference. The remaining metaphyseal
flare is shaved. In a case series by Kitaoka et al. [29] with a mean follow-up of
7.1 years, the authors reported improvement in pain control, IMA, forefoot width,
and fifth MTP angle after distal chevron osteotomy. Satisfaction rate was 89.5% in
17 of 19 patients. Although the osteotomy is stable by design, fixation and a secure
capsule closure are recommended to prevent malunion, nonunion, and recurrence.
Barouk [3] recommends the capital oblique osteotomy (modified Weil osteotomy)
because of the inherent stability and ease of performance. However, like the chevron
procedure, it has limitations in the narrow metatarsal head [55]. Similar to the Weil
osteotomy of the lesser metatarsals, the bone cut is parallel to the plantar aspect of
the foot (Fig. 5.3). The osteotomy is fixed with a dorsal-plantar mini-fragment
screw. Radl et al. [43] reported an improvement in the AOFAS score from 42 to 87
points, no nonunions, and no transfer lesions.
The percutaneous distal metatarsal osteotomy is performed through the same
incision as for the exostectomy, using a straight burr 2–15, following a 45° oblique
angle from dorsal-distal to plantar-proximal. A lateral wedge osteotomy is per-
formed, sparing the medial cortical. A valgus movement is performed on the fifth
toe and metatarsal, thus completing the osteotomy with osteoclasis. The post-op
bandage must be worn day and night for about 3 weeks [42].
Diaphyseal Fifth Metatarsal Osteotomies
In the presence of a type III deformity or a severe type II deformity, a diaphyseal

osteotomy combined with a distal soft tissue procedure affords an excellent means
of correction.
The scarfette osteotomy is similar to the SCARF osteotomy of the first ray
(Fig. 5.4). The osteotomy is fixed with two vertical mini-fragment screws. The
remaining lateral shelf of bone is resected with a sagittal saw. Seide and Petersen
[46] reported successful results in a follow-up of 10 feet. Maher et al. [35] reported
on 28 patients (36 feet) at a mean of 6.5 years. Eighty-six percent were completely
satisfied. The mean AOFAS score improved from 44 to 92 points. The most reported
complications are shaft fracture [34] and the need for hardware removal [22].
Ludloff first described an oblique osteotomy from the dorsal proximal to the
plantar distal aspect of the first metatarsal in 1918 as a treatment option for hallux
valgus. Coughlin [11] described a diaphyseal oblique osteotomy to correct an
increased 4–5 IMA and/or an increased lateral bowing (Figs. 5.5 and 5.6). This
oblique osteotomy is rotational rather than translational, which helps to maintain
metatarsal length and avoid shortening. Two mini-fragment screws are used to fix
the osteotomy site. The initial screw serves as the center of rotation for the osteot-
omy. Once the osteotomy has been aligned, a second screw is placed to further sta-
bilize the osteotomy site (Fig. 6). Prominent bone at the osteotomy site is resected
with a sagittal saw. The fifth MTP joint capsule is repaired, and the fifth toe is
brought into proper alignment (Fig. 7). An unreliable patient may be treated with a
below-knee walking cast for 6 weeks. Coughlin [11] reported on 30 feet (20 patients)
with 31 months follow-up. Ninety-three percent had excellent or good clinical
results; all osteotomies healed within 8 weeks, with only one case of a mild transfer
lesion. In a report on 11 pediatric patients with a mean follow-up of 32 months,
Masquijo et al. [37] noted all results were rated as excellent or good, and the final
AOFAS score averaged 92 points (Fig. 6).
Several authors modified the oblique osteotomy to be more bio-mechanically
stable with reverse Ludloff osteotomy. The theoretical benefit over the traditional
Ludloff osteotomy is the force generated across the osteotomy with weight-bearing,
which is a compression force rather than a distraction force across the osteotomy.
Mariano De Prado described the “DRP osteotomy” [42], a percutaneous diaphy-
seal osteotomy performed between the middle third and the distal third with the
straight burr 2–15.The osteotomy starts at the medial cortical surface of the fifth
metatarsal in a dorsal-distal to plantar-proximal direction at 45°, sparing the lateral
cortical bone and creating a medial wedge. Once the desired size is reached, the
Fig. 6 Ludloff osteotomy

Bunionette 527
Fig. 7 Clinical result after

bilateral Ludloff M5
osteotomies
wedge is closed by pressing on the head of the fifth metatarsal to produce osteocla-
sis of the lateral cortical bone. The post-op bandage must be worn day and night for
about 3 weeks (Fig. 7).
In 1972, Gerbert et al. [19] described a long oblique closing wedge osteotomy of
the fifth metatarsal. The osteotomy runs from distal-medial to proximal-lateral end-
ing at the junction of the lateral shaft and base of the fifth metatarsal and maintain-
ing the proximal-lateral cortical-periosteal hinge. A small 2–3 mm medially based
wedge of the bone is then resected from the proximal and medial portion of the fifth
metatarsal. The osteotomy is closed with a small bone clamp, and fixation is done
with a small, oblique screw, oriented from distal-lateral to proximal-medial. Patient
is non-weight-bearing in either a short-leg cast or removable immobilization boot
for 6–8 weeks.
Distal fifth metatarsal osteotomy complications are usually a result of either
inappropriate soft tissue handling, fixation failure, or inappropriate end position of
the M5 head.
After lateral capsulotomy, the remaining blood supply enters the metatarsal head
from its medial aspect, so excessive dorsal and plantar soft tissue stripping should
be avoided, as it increases the risk of AVN, instability, and fixation failure [41].
Excessive soft tissue tightening to compensate an insufficient bone procedure may
result in recurrence of deformity due to progressive tissue attenuation.
The most common causes of fixation failure are no postsurgical protection, the
choice of a lower stability osteotomy (transverse < oblique < modified Weill/chev-
ron/scarfette) or the use of a weak implant (screws better the K wires). This may
result in a delayed/nonunion with excessive callus formation and an inappropriate
end position of the M5 head. Inappropriate surgical technique can also be the cause
for failure. On the transverse plane, the M5 head can be located too medially
(overcorrected – rare) or too laterally (undercorrection or deformity recurrence –

common). On the sagittal plane, an excessive plantar displacement causes plantar
keratosis, and a dorsal displacement may translate in transfer metatarsalgia.
Pontious et al. [41] compared distal fifth metatarsal osteotomies that were inter-
nally fixed to those not fixed. They concluded that osteotomies that were internally
fixed healed more predictably and that fixation prevented displacement. Kitaoka
and Holiday [29] and Frankel et al. [18] concluded that floating fifth metatarsal
osteotomies that seek their own level in an uncontrolled manner have a significant
incidence of transfer metatarsalgia.
Proximal Fifth Metatarsal Osteotomy
Fifth metatarsal base osteotomies may be used for severe type III deformities, but
nonunion is a serious concern. Shereff et al. [47] investigated the extraosseous and
intraosseous arterial vascular supply of the proximal fifth metatarsal. The authors
suggested that an osteotomy or fracture in the proximal 2 cm of the fifth metatarsal
can injure both the extraosseous and the intraosseous supply, leading to delayed
union or nonunion.
A medial-to-lateral proximal chevron osteotomy performed with the apex 1 cm
distal to the tip of the fifth metatarsal and its horizontal cut oriented distally
(Fig. 5.6). The distal fragment is translated medially and stabilized to the fourth
metatarsal with small Steinmann pins placed lateral to medial. The pins exit through
the skin. Any prominent bone at the osteotomy site is beveled. A below-knee cast is
applied for 6 weeks, when Steinmann pins are removed, and the patient is allowed
to walk weight-bearing.
Diebold and Bejjani [15] reported excellent results in 90% of cases (12 patients
with 1 year average follow-up). No nonunions were reported. Later, in a follow-
up report, the same authors confirmed that 22 osteotomies had all success-
fully healed.
Minimal Incision Surgery
Techniques for minimally invasive osteotomy with or without fixation continue to

emerge, with good to excellent results [48]. Postoperative dressings must keep the
4–5 IM angle closed and the fifth toe in the correct position in the first 3 weeks. The
first dressing change occurs 7–10 days postoperatively. A postoperative shoe is used
for 4 weeks [39].
Delayed bone healing is a well-known phenomenon after percutaneous sur-
gery on the lateral metatarsals. Clinical healing usually precedes radiographic
evidence of bone healing by several weeks. In most patients, the osteotomy site
was pain free at 6 weeks postoperatively, despite only limited callus formation on
X-ray [39].
Bunionette 529
Concerns of inferior outcomes after minimally invasive correction of type II and

III deformities are possibly the result of the inability to address the underlying
pathology.
The great majority of cases yielded an acceptable cosmetic result with no scar-
ring or dorsal contracture, but because of the limited outcomes studies available and
the tendency toward dorsal malunion, it is difficult to recommend this technique
routinely until more extensive data are reported.
Intractable Plantar Keratosis
In the presence of a plantar keratosis (Fig. 8), the chosen osteotomy should allow
a controlled elevation of the metatarsal head. This is possible in most osteotomies,
as in the distal chevron osteotomy, the modified Weil osteotomy, the scarfette oste-
otomy, the diaphyseal oblique osteotomy, or the proximal chevron osteotomy.
Instead of a horizontal cut, the saw blade is oriented from lateral-plantar to medial-
dorsal, so that the capital fragment elevates as it is translated in a medial direction
(Fig. 9b).
The amount of sagittal plane M5 head translation increases with the inclination
of the osteotomy cut and with the osteotomy site: more proximal osteotomies allow
a larger translation. One should be mindful about excessive dorsal translation as
transfer metatarsalgia may occur.
Deformity Correction Power
The ability to correct the deformity varies with the type and site of the osteotomy.
Proximal procedures are reported to have a larger 4–5 IM angle and MTP5 angle
correction power (Table 2).
Surgical Pearls
1. Soft tissue:
(a) Avoid excessive soft tissue stripping
(b) Avoid additional correction with soft tissue tightening
2. Use internal fixation device
3. Select correct procedure
(a) Enough correction power – adequate site
(b) Address sagittal plane
(c) Stable enough and low risk of delayed or nonunion
Fig. 8 Intractable plantar

keratosis
4 Summary
Most painful bunionette deformities respond to nonsurgical management. When

intractable symptoms are refractory to nonsurgical treatment, operative intervention
may be necessary. Lateral eminence resection is reserved for patients with a focal
prominence and no angular deformity of the metatarsal. Metatarsal osteotomies nar-
row the forefoot, maintain the length of the metatarsal, and preserve function of the
Bunionette 531
Fig. 9 M5 head translation

with medialization (a)
none; (b) dorsal
translation; (c) plantar
translation
Table 2 Deformity correction power

Bone procedure 4–5 IM A MTP5 A Power
Lateral condyle resection None Low Very lowa
Distal osteotomy 4–5° 8° (55b, 71b) Low
Percutaneous 4,5° 12° Low to average
Mid-diaphyseal osteotomy Scarfette 5–10° (14, 47, 62) 15° (62) Average
Oblique 10° [9, 45] 15–17° Average
Proximal osteotomy Highest N/A High
Correction due to soft-tissue procedure
a
MTP joint. When appropriate correction can be achieved with the chevron osteot-
omy, it should be the procedure of choice, because it has the greatest strength and
fails in the same manner as the intact fifth metatarsal. Diaphyseal oblique osteotomy
and scarfette osteotomy are indicated to treat mild to moderate transverse and sagit-
tal plane deformities and have inherent stability that allow early weight-bearing.
Proximal osteotomies allow for larger correction of the IMA compared with distal
osteotomies but carry a risk of potential injury to the already tenuous proximal fifth
metatarsal blood supply. Newer minimally invasive techniques with expanded cor-
rective power have been reported, with promising results; however, sufficiently
powered, prospective, randomized, controlled trials related to surgical bunionette
correction are not available.
References
1. Addante JB, Chin M, Makower BL, Lescosky FA, Nowick AR. Surgical correction of tailor’s
bunion with resection of fifth metatarsal head and silastic sphere implant: an 8-year follow-up
study. J Foot Surg. 1986;25:315–20.
2. Armstrong DG, Rosales MA, Gashi A. Efficacy of fifth metatarsal head resection for treatment
of chronic diabetic foot ulceration. J Am Podiatr Med Assoc. 2005;95:353–6.
3. Barouk LS. Some pathologies of the fifth ray: tailor’s bunion. In: Barouk LS, editor. Forefoot
reconstruction. Paris: Springer-Verlag; 2002. p. 276–83.
4. Baumhauer JF, Benedict FD. Osteotomies of the fifth metatarsal. Foot Ankle Clin. 2001;6:3.
5. Bishop J, Kahn A 3rd, Turba JE. Surgical correction of the splayfoot: the Giannestras proce-
dure. Clin Orthop Relat Res. 1980;146:234–8.
6. Boyer ML, Deorio JK. Bunionette deformity correction with distal chevron osteotomy and
single absorbable pin fixation. Foot Ankle Int. 2003;24:834–7.
7. Buchbinder IJ. DRATO procedure for tailor’s bunion. J Foot Surg. 1982;21:177–80.
8. Catanzariti AR, Friedman C, DiStazio J. Oblique osteotomy of the fifth metatarsal: a five-year
review. J Foot Surg. 1988;27:316–20.
9. Cohen BE, Nicholson CW. Bunionette deformity. J Am Acad Orthop Surg. 2007;15:300–7.
10. Coughlin MJ. Etiology and treatment of the bunionette deformity. Instr Course Lect.
1990;39:37–48.
11. Coughlin MJ. Treatment of bunionette deformity with longitudinal diaphyseal osteotomy with
distal soft tissue repair. Foot Ankle. 1991;11:195–203.
12. Davies H. Metatarsus quintus valgus. Br Med J. 1949;1:664.
13. Deveci, et al. An overlooked deformity in patients with hallux valgus: Tailor’s bunion.
JAPMA. 2015;15(3):233–7.
14. Didomenico, et al. Revisiting the Tailor’s bunion and adductovarus deformity of the fifth digit.
Clin Podiatr Med Surg. 2013;30:397–422.
15. Diebold PF, Bejjani FJ. Basal osteotomy of the fifth metatarsal with intermetatarsal pinning: a
new approach to tailor’s bunion. Foot Ankle. 1987;8:40–5.
16. Dorris MF, Mandel LM. Fifth metatarsal head resection for correction of tailor’s bunions and
sub-fifth metatarsal head keratoma: a retrospective analysis. J Foot Surg. 1991;30(269):275.
17. Fallat LM, Buckholz J. An analysis of the tailor’s bunion by radiographic and anatomical
display. J Am Podiatry Assoc. 1980;70:597–603.
18. Frankel JP, Turf RM, King BA. Tailor’s bunion: clinical evaluation and correction by distal
metaphyseal osteotomy with cortical screw fixation. J Foot Surg. 1989;28:237–43.
19. Gerbert J, Sgarlato TE, Subotnick SI. Preliminary study of a closing wedge osteotomy of
the fifth metatarsal for correction of a Tailor’s bunion deformity. J Am Podiatry Assoc.
1972;62:212–8.
20. Giannestras NJ. Other problems of the foot. In: Giannestras NJ, editor. Foot disorders: medical
and surgical management. Philadelphia: Lea and Febiger; 1973. p. 420–1.
21. Giannini S, Faldini C, Vannini F, et al. The minimally invasive osteotomy “S.E.R.I.” (sim-
ple, effective, rapid, inexpensive) for correction of bunionette deformity. Foot Ankle Int.
2008;29:282–6.
22. Glover JP, Weil L Jr, Weil LS Sr. Scarfette osteotomy for surgical treatment of bunionette
deformity. Foot Ankle Spec. 2009;2:73–8.
23. Haber JH, Kraft J. Crescentic osteotomy for fifth metatarsal head lesions. J Foot Surg.
1980;19:66–7.
24. Haddon TB, SJ LP. Relative strength of Tailor’s bunion osteotomies and fixation techniques. J
25. Ishikawa SN, Murphy GA. Lesser toe abnormalities. In: Canale ST, editor. Campbell’s opera-
tive orthopaedics. 10th ed. Philadelphia: Mosby; 2003. p. 4652–60.
26. Kaplan EG, Kaplan G, Jacobs AM. Management of fifth metatarsal head lesions by biplane
osteotomy. J Foot Surg. 1976;15:1–8.
27. Kitaoka HB, Holiday AD Jr. Lateral condylar resection for bunionette. Clin Orthop Relat Res.
1992;278:183–92.
28. Kitaoka HB, Holiday AD Jr. Metatarsal head resection for bunionette: long-term follow-up.
Foot Ankle. 1991;11:345–9.
29. Kitaoka HB, Holiday AD Jr, Campbell DC 2nd. Distal chevron metatarsal osteotomy for bun-
ionette. Foot Ankle. 1991;12:80–5.
30. Koti M, Maffulli N. Bunionette. J Bone Joint Surg Am. 2001;83-A:1076–82.
Bunionette 533
31. Leach RE, Igou R. Metatarsal osteotomy for bunionette deformity. Clin Orthop.
1974;100:171–5.
32. Legenstein R, Bonomo J, Huber W, Boesch P. Correction of tailor’s bunion with the Boesch
technique: a retrospective study. Foot Ankle Int. 2007;28:799–803.
33. Lelièvre J: [Exostosis of the head of the fifth metatarsal bone; tailor’s bunion].Concours Med.
1956;78:4815–16.
34. Magnan B, Samaila E, Merlini M, Bondi M, Mezzari S, Bartolozzi P. Percutaneous dis-
tal osteotomy of the fifth metatarsal for correction of bunionette. J Bone Joint Surg Am.
2011;93:2116–22.
35. Maher AJ, Kilmartin TE. Scarf osteotomy for correction of Tailor’s bunion: mid- to long-term
followup. Foot Ankle Int. 2010;31:676–82.
36. Mann RA. Keratotic disorders of the plantar skin. In: Mann RA, editor. Surgery of the foot. St
Louis: Mosby; 1986. p. 194–8.
37. Masquijo JJ, Willis BR, Kontio K, Dobbs MB. Symptomatic bunionette deformity in adoles-
cents: surgical treatment with metatarsal sliding osteotomy. J Pediatr Orthop. 2010;30:904–9.
38. McKeever DC. Excision of the fifth metatarsal head. Clin Orthop. 1992;278:183–92.
39. Michels F, Bauwhede J, Guillo S, Oosterlinck D, Lavigne C. Percutaneous bunionette correc-
tion. Foot Ankle Surg. 2013;19:9–14.
40. Nestor BJ, Kitaoka HB, Ilstrup DM, Berquist TH, Bergmann AD. Radiologic anatomy of the
painful bunionette. Foot Ankle. 1990;11:6–11.
41. Pontious J, Brook JW, Hillstrom HJ. Tailor’s bunion. Is fixation necessary? J Am Podiatr Med
Assoc. 1996;86:63–73.
42. Prado M, Ripoll PL, Golanó P. Cirurgía percutánea del pie 2003.
43. Radl R, Leithner A, Koehler W, Scheipl S, Windhager R. The modified distal horizontal meta-
tarsal osteotomy for correction of bunionette deformity. Foot Ankle Int. 2005;26:454–7.
44. Roukis TS. The tailor’s bunionette deformity: a field guide to surgical correction. Clin Podiatr
Med Surg. 2005;22:223–45.
45. Schabler JA, Toney M, Hanft JR, Kashuk KB. Oblique metaphyseal osteotomy for the correc-
tion of Tailor’s bunions: a 3-year review. J Foot Surg. 1992;31:79–84.
46. Seide HW, Petersen W. Tailor’s bunion: results of a scarf osteotomy for the correction of an
increased intermetatarsal IV/V angle. A report on ten cases with a 1-year follow-up. Arch
Orthop Trauma Surg. 2001;121:166–9.
47. Shereff MJ, Yang QM, Kummer FJ, Frey CC, Greenidge N. Vascular anatomy of the fifth
metatarsal. Foot Ankle. 1991;11:350–3.
48. Shi GG. Management of Bunionette Deformity. J Am Acad Orthop Surg. 2018;26:e396–404.
49. Smith SD, Weil LS. Fifth metatarsal osteotomy for tailor’s bunion deformity: minor surgery of
the foot. Mt. Kiscoe: Futura; 1971.
50. Sponsel KH. Bunionette correction by metatarsal osteotomy: preliminary report. Orthop Clin
North Am. 1976;7:809–19.
51. Steel MW 3rd, Johnson KA, DeWitz MA, Ilstrup DM. Radiographic measurements of the
normal adult foot. Foot Ankle. 1980;1:151–8.
52. Steinke MS, Boll KL. Hohmann-Thomasen metatarsal osteotomy for tailor’s bunion (bunio-
nette). J Bone Joint Surg Am. 1989;71:423–6.
53. Stewart M. Miscellaneous affections of the foot. In: Edmonson SA, Crenshaw AH, editors.
Campbell’s operative orthopaedics. St Louis: Mosby; 1980. p. 1733.
54. Throckmorton JK, Bradlee N. Transverse V sliding osteotomy: a new surgical procedure for
the correction of tailor’s bunion deformity. J Foot Surg. 1978;18:117–21.
55. Weil L, Consul D. Fifth metatarsal osteotomies. Clin Podiatr Med Surg. 2015;32:333–53.
56. Weitzel S, Trnka HJ, Petroutsas J. Transverse medial slide osteotomy for bunionette deformity:
long-term results. Foot Ankle Int. 2007;28:794–8.
57. Yancey HA Jr. Congenital lateral bowing of the fifth metatarsal. Report of 2 cases and opera-
tive treatment. Clin Orthop Relat Res. 1969;62:203–5.
Part IV
Adult Orthopaedics: Midfoot, Rearfoot
and Ankle
Progressive Collapsing Foot
Deformity – Flatfoot
Jaeyoung Kim and Jonathan T. Deland
1 Introduction
The flatfoot deformity in adults comprises a wide spectrum of ligament and poste-
rior tibial tendon (PTT) failure that results in significant deformity and disability.
Because dysfunction of the PTT has been considered the culprit of flatfoot defor-
mity in adults, this condition was initially termed posterior tibialis tendon dysfunc-
tion (PTTD) and later renamed adult-acquired flatfoot deformity (AAFD). However,
the dysfunction of the PTT has not been proven to be the cause of the condition.
Results from new imaging modalities have revealed that the shape of the tarsal
bones and slope of the posterior facet may be an important predisposing factor con-
tributing to why certain flatfeet get this condition and others do not. Also, because
the most debilitating problem is the collapse of the foot secondary to the ligament
failure and the tendon can be graded separately, there is now a proposal to rename
this condition in order to emphasize the progressive collapse of the foot appropri-
ately. In 2020, an expert consensus group proposed progressive collapsing foot
deformity (PCFD) as the better name for the condition with the tendon failure
graded separately [1]. Therefore, this book chapter will use the term PCFD when
referring to this condition. Paralleling the changes in terminology, the treatment for
PCFD has also evolved to shift the focus away from the tendon to increased empha-
sis on how to treat the collapsing foot deformity. The collapse of the foot and its
treatment are the most important determinants of a patient’s outcome.
J. Kim · J. T. Deland (*)

Hospital for Special Surgery, New York, NY, USA

Switzerland AG 2022
538 J. Kim and J. T. Deland
2 Etiology and Pathophysiology
As this condition has long been thought to be associated with the PTT problem, much
of the previous description of its etiology has primarily focused on factors that cause
attenuation, tear, or dysfunction of the PTT [2]. However, this does not describe the
failure of the ligamentous structures in the medial longitudinal arch, such as the
spring and deltoid ligaments. Although degeneration of the PTT is a common finding
and is often a presenting symptom, the timing of the failure of the ligaments is not
necessarily in parallel with that of the tendon. The failure of the ligaments that sup-
port the medial longitudinal arch of the foot can occur before, during, or after tendon
failure. Multiple factors have been described as associated with the PTT abnormality,
which can be fallen into two categories: extrinsic or intrinsic. The extrinsic factors
exert more physical force on the tendon, and these include preexisting flatfoot defor-
mity [3], accessory navicular [4, 5], obesity [6, 7], and acute traumatic injury [8]. The
intrinsic factors make the tendon more susceptible to degeneration, and these include
inflammatory disorders (rheumatoid arthritis or seronegative spondyloarthropathy)
[9–11], vascular insufficiency (steroid use), diabetes mellitus, hypertension [7], and
polymorphisms at genes involved in collagen degeneration (matrix metalloprotein-
ases 13 & 18) [12, 13]. Also the morphology of the talus with its effect on the valgus
angulation of the subtalar joint may be an important predisposing factor.
There are several underlying etiologies in which patients with a normal PTT can
develop PCFD. Failure of the spring ligament has been identified as a potential
cause of PCFD in patients in which the PTT is normal based on imaging and intra-
operative exploration [14, 15]. Some researchers have proposed that medial column
instability can be a primary driving force rather than the result of PTT dysfunction
in the development of the flatfoot deformity [16, 17]. Certainly, that could contrib-
ute as well as a more valgus subtalar joint axis.
Once the PTT becomes insufficient, the foot is subject to the unopposed pull of the
peroneus brevis, which is the primary antagonist of the posterior tibial muscle. This
results in increased abduction through the talonavicular joint, leading to increased stress
on the medial ligaments and abduction deformity seen in PCFD [18, 19]. A tight
Achilles tendon or gastrocnemius muscle may be causally related, a result of the defor-
mity or both. The force vector of the Achilles becomes lateral relative to the center of
the subtalar joint. This contributes to stress on medial ligaments and the resultant peri-
talar subluxation mentioned above. Thordarson et al. demonstrated that the triceps surae
has the most significant arch flattening effect in the sagittal plane [20]. Tight triceps
surae is also associated with abduction deformity of the forefoot in the transverse plane.
In later stages, the deltoid ligament may fail, causing ankle instability and talar tilt.
3 Anatomy
Through its medial course to the subtalar axis and multiple insertions in the mid-
foot, the posterior tibialis functions as plantarflexor and inverter of the hindfoot and
adductor and supinator of the forefoot [21]. There are several proposed anatomical
Progressive Collapsing Foot Deformity – Flatfoot 539
theories why the PTT is prone to develop degenerative or inflammatory changes.

First, the PTT courses directly behind the medial malleolus at a relatively acute
angle [22]. This creates excessive frictional forces with physical activity. Second,
the PTT courses underneath the tight overlying flexor retinaculum which can cause
compression and constriction of the tendon through synovial enlargement [23]. This
can affect the circulation of the tendon, leading to degenerative changes. Finally, a
cadaveric study demonstrated a hypovascular zone in the retromalleolar region,
with fibrocartilaginous changes in tendon structure identified in this region [24].
The spring ligament complex (SLC) is one of the static ligamentous structures
frequently involved in PCFD. The primary function of the SLC is to support the
head of the talus, an essential part of the articular surface of the talocalcaneonavicu-
lar joint. Alterations of the spring ligament are commonly seen with PTT degenera-
tion or tears, making them the most common secondary abnormality seen in PCFD
[25]. While acute tears of the spring ligament are uncommon, degeneration, plastic
deformation, and/or tears occur. The SLC has been known to be composed of two
distinct bands: a stronger superior medial calcaneonavicular (SMCN) ligament and
an inferior calcaneonavicular (ICN) ligament just lateral to it. Recently, a third addi-
tional component (third ligament) or midplantar oblique ligament has been described
as a distinct structure within the SLC. It runs from the notch between the anterior
and middle calcaneal facets to the tubercle of the navicular in the lower layer of the
SLC, lying beneath the cartilaginous surface of the complex [26].
The interosseous ligament also functions to maintain the alignment of the calca-
neus relative to the talus. In a magnetic resonance imaging (MRI) study, the talocal-
caneal interosseous ligament was the third most commonly involved ligament in
patients with PCFD, after the SMCN and ICN ligaments of the SLC [25]. Unlike the
SLC, it is located near the center of the subtalar joint and therefore likely has an
important role in resisting anterior/posterior and medial/lateral displacement rather
than inversion/eversion rotatory displacement. In advanced cases, subtalar sublux-
ation with both eversion rotation presumably from SLC failure and lateral calcaneal
drift from interosseous failure becomes apparent.
4 Diagnosis
4.1 Clinical
The typical patient with PCFD is an overweight, middle-aged woman. Patients may
describe the insidious onset of vague, activity-induced pain on the medial side of the
foot due to posterior tibial tendon degeneration and failure. In later stages, symp-
toms may include lateral-sided pain, which may be attributed to talocalcaneal or
calcaneofibular impingement. At advanced stages of the disease, patients may have
little to no pain along the PTT course due to elongation or rupture of the tendon.
Therefore, the absence of medial pain does not preclude the diagnosis of PCFD.
Physical examination is especially important in evaluating the degree of actual
deformity, as radiographs may not fully reflect the deformity. The examination begins
with the patient standing barefoot and allowing the foot to fully pronate. Asymmetrical
swelling and fullness about the medial ankle and hindfoot may be present. In advanced
stages, abduction of the forefoot is evident, resulting in a characteristic “too many
toes” sign. The function and strength of the posterior tibialis muscle can be tested in
a standing position by performing the heel-rise test. On bilateral heel rise, the exam-
iner looks for symmetric hindfoot inversion. Lack of symmetry indicates that the
affected PTT is incompetent in inverting the subtalar joint, locking the transverse
tarsal joint, and allowing heel rise through the gastrocnemius-soleus complex power.
A more sensitive and specific finding is the inability to perform a single heel-rise test,
but it can still be a false positive with other causes of midfoot pain. A sensation of
weakness or medial pain along the course of the PTT may also be appreciated. At the
earlier stages of disease progression, a repetitive single heel-rise test with comparison
to the contralateral uninvolved side may be helpful.
Patients with chronic deformity may have enlarged tendon size upon palpation,
especially at the retromalleolar region. The motor strength of the PTT can be
assessed by asking the seated patient to invert the foot against resistance. The foot
should be fully plantarflexed to ensure that the anterior tibial tendon is not substitut-
ing for the PTT. Tenderness over the joint line may be identified when there is a
valgus tilt of the talus within the tibiotalar joint. Heel cord tightness should be
checked, most commonly with the Silfverskiöld test. This test is considered positive
when ankle dorsiflexion increases with the knee in flexion, and the foot and ankle
cannot go into any dorsiflexion with the knee straight. The rigidity of the midfoot
and hindfoot should be checked under a range of motion assessment. A fixed fore-
foot varus should be checked with the heel in the neutral position. Dorsal instability
of the first tarsometatarsal (TMT) joint should also be evaluated.
4.2 Radiographic
When taking radiographs, it is especially important to educate patients to fully load

their weight on the involved foot and let it pronate completely; otherwise the defor-
mity can be underestimated. Four studies are commonly recommended for radio-
graphic assessment: weight-bearing anteroposterior (AP) and lateral views of the
foot, hindfoot alignment view, and weight-bearing AP view of the ankle. The abduc-
tion deformity of the foot is best visualized on the AP view of the foot. Talonavicular
coverage angle, talo-first metatarsal angle, and talar incongruency angle are radio-
graphic parameters that represent the amount of abduction deformity of the forefoot
[27–29]. Collapse of the medial longitudinal arch is best evaluated on the lateral
view of the foot. The talo-first metatarsal angle (Meary’s angle; flatfoot >20 degrees)
is an angle between the longitudinal axis of the talus and the first metatarsal bone
[27, 30]. The calcaneal pitch angle is formed by the line parallel to the ground and
the line along the inferior inclination axis of the calcaneus [27, 30]. When evaluat-
ing the lateral view, the location of collapse within the medial column should be
carefully inspected. Failure to fully address the apex of the instability may lead to
persistent postoperative deformity and poor patient outcomes. Instability at the first
TMT joint often presents as plantar gapping. However, there may be dorsal dis-
placement of the metatarsal bone in relation to the medial cuneiform without angu-
lation of the joint. Bony impingement at the sinus tarsi can also often be identified
at the angle of Gissane in the sinus tarsi in patients with advanced hindfoot valgus
deformity on the weight-bearing lateral X-ray. Hindfoot alignment view, frequently
called the Saltzman view, can quantify hindfoot valgus and guide operative plan-
ning on how much medial slide of the calcaneus will be needed [31]. The hindfoot
moment arm is measured by the shortest orthogonal distance between the axis of the
tibia and the most inferior point of the calcaneus. Hindfoot alignment angle is
formed by the intersection of the longitudinal axis of the tibial shaft and the axis of
the calcaneal tuberosity. On the AP view of the ankle, the height of the tibiotalar
joint line of the involved side may be lower than the uninvolved contralateral side
due to collapse of the medial arch and eversion of the calcaneus. Valgus talar tilt and
evidence of ankle arthritis can be observed in the later stages of PCFD. Calcaneofibular
bony impingement can sometimes be identified in the case where there is severe
subluxation at the subtalar joint but may not be able to be seen on plain X-rays and
is best seen on a weight-bearing computed tomography (WBCT) scan. In addition,
a whole limb radiograph can be beneficial to rule out other causes of the deformity
that might be associated with malalignment of the lower limb.
Although not universally available, MRI and WBCT are increasingly being used
to understand the extent of PCFD. MRI can be used as an adjunctive diagnostic test
in identifying soft tissue involvement, such as the PTT, deltoid ligament, SLC, and
interosseous ligaments. The information obtained from MRI can aid in determining
surgical treatment. WBCT is an emerging technique that has been proven to more
precisely measure bone position than conventional weight-bearing radiographs due
to its ability to evaluate multiplanar deformity with the patient weight-bearing [32].
When compared to conventional radiographs, WBCT is free from superimposition
and can minimize rotational errors. WBCT helps identify subluxation of joints
within the medial column as well as findings of hindfoot deformity such as sinus
tarsi impingement and calcaneofibular impingement (Fig. 1) [33].
4.3 Clinical Staging
The classification system is helpful because it aids in describing the deformity and
therefore directs the method of surgical treatment. There have been several classifi-
cation systems previously described, depending on the etiology and the location of
the deformity. A four-stage classification system popularized by Johnson and Strom
and later modified by Myerson is commonly cited [34, 35].
Stage I refers to the mildest form of the deformity within this classification sys-
tem, with an absence of abnormal alignment. It is the alignment of the flatfoot they
have had all their adult life without any progressive deformity. Tenosynovitis or
tendinosis with pain over the PTT tendon is the most important finding in this stage.
a b
Fig. 1 Weight-bearing computed tomography analysis reveals sinus tarsi impingement (a) and
calcaneofibular impingement (b), potentially explaining the presence of lateral hindfoot symptoms
However, in actual practice, the patients who truly fit into Stage I are relatively rare.
Radiographs are of a normal flatfoot, although MRI may show inflammation or
early signs of degeneration of the PTT. Stage II, with its different amounts and types
of deformity, is the most controversial part of this classification system. Stage II is
associated with an elongated or torn PTT and ligament failure, the latter of which
results in structural deformity. The deformity in Stage II is still flexible, which
makes it different from Stage III, and favors joint-preserving surgical methods
rather than joint arthrodesis. Depending on the amount of forefoot abduction, Stage
II is further divided into IIA and IIB. Stage IIA deformity is characterized by mini-
mal abduction at the midfoot with less than 40% talonavicular uncoverage on the
standing AP radiograph. In Stage IIB, there is greater forefoot abduction, 40% or
more talonavicular uncoverage. This division is useful in the determination of the
type of osteotomy, as lateral column lengthening is known to be more effective in
addressing abduction deformity than the medial displacement calcaneal osteotomy.
Stage III signifies a more rigid or fixed deformity, in which the malalignment at the
triple joint complex cannot be corrected past neutral with passive inversion. The
stiffness of each joint is not objectively measurable, and it is unclear exactly how
much stiffness defines a Stage III presentation. However, if the talonavicular joint
cannot be placed in neutral and the talonavicular joint is passively incapable of
inversion, a tendon transfer will not be of benefit, and deformity should be consid-
ered Stage III. Finally, Stage IV is a deformity of the ankle joint with talar tilt due
to the attenuation of the deltoid ligament. The foot deformity in Stage IV can be
either fixed or flexible.
Despite its wide use, this classification system has significant limitations. A limi-
tation of this classification system is that Stage I is a misnomer and is not typically
encountered in the outpatient clinic. Another is that PCFD is a progressive disorder,
and, interestingly, the deformity described in the current classification system is not
on a continuum. For example, Stage III refers to rigid flatfoot, which frequently
requires double or triple arthrodesis, whereas Stage IV includes deformities that are
still flexible which can be treated with osteotomy and ligament reconstruction.
Table 1 Consensus group classification of progressive collapsing foot deformity (2020)

Stage of the deformity
Stage I (flexible) Stage II (rigid)
Types of deformity (classes – isolated or combined)
Deformity type/location Consistent clinical/radiographic findings
Class A Hindfoot valgus deformity Hindfoot valgus alignment
Increased hindfoot moment arm, hindfoot
alignment angle, foot and ankle offset
Class B Midfoot/forefoot abduction Decreased talar head coverage
deformity Increased talonavicular coverage angle
Presence of sinus tarsi impingement
Class C Forefoot varus deformity/ Increased talus-first metatarsal angle
medial column instability Plantar gapping first TMT joint/NC joints
Clinical forefoot varus
Class D Peritalar subluxation/ Significant subtalar joint subluxation/
dislocation subfibular impingement
Class E Ankle instability Valgus tilting of the ankle joint
Reprinted from Myerson et al. [1]
Abbreviations: NC naviculocuneiform; TMT tarsometatarsal
In light of these limitations, in 2020, the expert consensus group proposed a new
classification system based on the flexibility and the type and location of the defor-
mity. In this new classification system, the deformity is designated into Stage I
(flexible) or Stage II (rigid) depending on the flexibility stage of the deformity [1].
In addition, depending on the type and location of the deformity, this is further clas-
sified into A through E (Table 1).
In most circumstances, initial treatment should start with nonoperative measures.

However, as the majority of symptomatic patients present with a deformity that will
progress, conservative treatment, in general, has a limited role. The goal for conser-
vative treatments would be to decrease the force exerted through the posteromedial
soft tissues theoretically. This can be done by encouraging weight loss, using ortho-
sis, and reducing repetitive loading by activity modifications. Often, this is usually
supplemented with nonsteroidal anti-inflammatory drugs. For patients with acute
symptoms, a short period of immobilization may be indicated in a removable boot or,
in severe cases, a cast. After immobilization, patients may be transitioned to a custom
brace or orthosis and begin a rehabilitation program. A variety of orthotic options are
available. These options include off-the-shelf orthoses, customized arch supports,
customized UCBL (University of California Biomechanics Laboratory), Arizona
brace, and Ritchie brace. Although braces may slow down deformity progression,
none of them have been shown to stop it. In our opinion, they do not stop the progres-
sion of deformity, and patients should be made aware of this. However, it is also true
that the rate of progression is variable. Physical therapy and rehabilitation protocols
can be helpful after initial inflammation dissipates. Goals for rehabilitation center
around mechanically strengthening ankle inversion power, stretching the Achilles
and gastrocnemius, and minimizing further tendon lengthening and foot deformity.
6 Surgical Management
Surgical treatment is recommended for patients who have failed conservative man-
agement. In reality, many patients who present with symptoms already have a defor-
mity from PCFD and therefore will highly likely need surgery. A wide breadth of
surgical treatment options for PCFD has been reported in the literature. In general,
a combination of procedures is preferred to address the complex multiplanar defor-
mity. The two most important things to check when determining the surgical plan
are (1) whether the deformity is still flexible or rigid and (2) the location of the
deformity. When the deformity is rigid and cannot be corrected back to neutral, this
favors arthrodesis of the involved joint. Joint instability or sagging within the medial
column is not always appreciable preoperatively. Therefore, this should be carefully
examined intraoperatively, and an effort should be made to address deformities
within the medial column. An exception is a naviculocuneiform joint, which in the
case of a mild to moderate sag in our experience is not necessary to fuse. The choice
of procedures must depend on the specific deformity to be addressed. Therefore, it
is essential to understand the strengths and weaknesses of each procedure.
6.1 Hindfoot Valgus Deformity
6.1.1 Medial Displacement Calcaneal Osteotomy
Medial displacement calcaneal osteotomy (MDCO) is a commonly employed tech-

nique to correct hindfoot valgus. By translating the posterior tuber of the calcaneus
medially, this repositions the axis of the Achilles and subsequently decreases strain
on the medial column. In one study investigating the factors associated with postop-
erative hindfoot alignment, MDCO was the only significant predictor. This can be
performed as an isolated bony procedure when there is an isolated hindfoot valgus
in the setting of mild talonavicular joint uncoverage (less than 40% uncovered) and
a lack of significant forefoot supination, varus, or abduction. Since some patients
can hold up their arch or lean back and do not let their arch fully sag, the X-ray can
be an underestimation of the true deformity. If no WBCT is available and no subta-
lar impingement seen on plain X-rays, use the preoperative standing clinical exam
as a possible alert to significant talonavicular abduction or plantar sag to suggest a
lateral column lengthening or subtalar arthrodesis may be necessary. A 7–15 mm of
medial slide osteotomy is recommended, and clinically straight heel (hindfoot
moment arm 0–5 mm by X-ray) is known to be associated with better clinical out-
comes. A lateral oblique incision along the suspected line of osteotomy is most
Fig. 2 Clinically straight

heel alignment should be
obtained after osteotomy
fixation for better patient
outcomes
commonly employed, but some endorse an L-shaped incision. Various types of fixa-
tion can be utilized, such as compression screws, step plates, or blade plate.
Regardless of the method, union rates are high. Lateral column lengthening (LCL)
can also correct the hindfoot valgus deformity but to a much smaller degree. The
key is achieving a clinically straight heel (Fig. 2).
6.2 Midfoot/Forefoot Abduction Deformity
6.2.1 Lateral Column Lengthening
LCL is a powerful procedure to correct forefoot abduction deformity as well as

restore the medial arch. Lengthening of the lateral column can be performed through
either an arthrodesis of the calcaneocuboid joint or an osteotomy of the anterior cal-
caneus. However, the former can lead to nonunion, stiffness, and lateral foot over-
load, causing residual discomfort, and has largely been abandoned. Theoretically,
lengthening through the anterior process preserves motion at the calcaneocuboid
joint, but overlengthening can lead to stiffness of the lateral column when an ade-
quate amount of eversion is not preserved. Therefore, performing the correct amount
of lengthening is a critical portion of the operation. The amount will vary depending
on the individual deformity, but the range of ideal graft size is recommended to be
5–7 mm. Hintermann pin distractor can be placed across the osteotomy and opened
gradually to allow for correction of forefoot abduction. The ideal amount of correc-
tion is assessed both visually and with a simulated anteroposterior weight-bearing
fluoroscopic view (Fig. 3). A moderate amount of eversion motion from neutral
should be maintained in the subtalar joint, approximately 15 degrees. If necessary,
give less correction to the alignment in the arch to allow this critical motion to remain,
or the patient will complain of excessive stiffness or lateral overload of the foot.
Once an ideal amount of correction has been achieved, passive hindfoot motion,
particularly eversion, should be assessed. When an adequate degree (usually 10 degrees)
a b
Fig. 3 A metal trial wedge is especially helpful in titrating the amount of correction. Any possibil-
ity of overcorrection should be checked and avoided to obtain better patient outcomes. There is a
high probability of overcorrection in our clinical experience when the lateral talar neck aims lateral
to the proximal-medial corner of the second metatarsal base (arrow, a). Some residual amount of
talonavicular uncoverage is allowed when the complete correction leads to stiffness in eversion (b)
a b
Fig. 4 Physical examination on the passive motion of the subtalar joint (a, b). Passive hindfoot
motion, at least 10 degrees of eversion (b), should be preserved; otherwise the patient will com-
plain of stiffness and possibly excessive lateral weight-bearing and pain
of eversion is not obtained, the graft size should be decreased to prevent overcorrection.
We aim to avoid adduction at the talonavicular joint, and avoidance of this adduction
has been shown to lead to better clinical results [36]. To get the most accurate size
measurement of the actual wedge to be implanted, the use of trial wedges is helpful.
While an Evans-type osteotomy is performed parallel and 1 cm posterior to the calca-
neocuboid joint, other osteotomies such as the central Hintermann-type or step-cut
lengthening osteotomies have been described with comparable outcomes. Regardless,
subtalar/talonavicular eversion motion should be maintained, or the patient will com-
plain of stiffness and possibly excessive lateral weight-bearing and pain (Fig. 4).
In the senior author’s experience, a difference of 1–2 mm of lengthening can

make the difference between a happy patient with good eversion motion remaining
and an unhappy patient with stiffness and possible lateral excessive weight-bearing.
Unfortunately, it is a very sensitive procedure. Either an autograft or allograft can be
used, while the use of trabecular metal wedges has also been described with low
nonunion rates. Metal wedges make the revision of LCL procedures very problem-
atic and should be avoided. The fixation of the osteotomy can be achieved in the
form of screws or plates.
6.3 Forefoot Varus or Supination Deformity/Medial

Column Instability
6.3.1 Cotton Osteotomy and Tarsometatarsal Joint Fusion
Forefoot varus or supination refers to the condition in which there is an elevation of

the first ray and/or rotation of forefoot in the coronal plane. Generally, it is consid-
ered as a correction for an elevated first ray but does not correct or counteract hind-
foot stiffness from excessive stiffness from LCL. Through a dorsal approach, the
medial cuneiform is osteotomized from dorsal to plantar, and the plantar hinge of
the cortex is left intact. The typical amount of correction ranges from 5 to 7 mm, and
an allograft, autograft, or metal implant can be inserted [37]. This is usually indi-
cated for patients with stable first TMT joints to correct both forefoot varus defor-
mity. However, when the TMT joint is unstable with excessive motion (plantar
gapping or dorsal instability in lateral radiographs), arthrodesis of the TMT joint is
needed. In cases when there is concomitant instability at other joints in the medial
column, an additional arthrodesis may be required, although this may not be neces-
sary. Mild to moderate naviculocuneiform plantar sag can be tolerated. More
recently, a technique which Recent study has established a technique for success-
fully transferring the flexor hallucis longus tendon to the first metatarsal base. This
method has been shown to successfully correct the entire medial arch, with the
added benefit of correcting medial arch instability even in the presence of gapping
or arthritic changes without undergoing joint arthrodesis.
6.3.2 Flexor Hallucis Longus Tendon Transfer and LapiCotton Procedure
Kim et al. described a procedure called dynamic medial column stabilization in

which the flexor hallucis longus tendon is transferred to the first metatarsal base
[38]. This method has been shown to successfully correct the entire medial arch as
well as three-dimensional deformities associated with PCFD, with the added benefit
of correcting medial arch instability even in the presence of plantar gapping or
arthritic changes in the first TMT joint. More recently, de Cesar Netto et al. described
another technique called LapiCotton as a surgical technique that combines the
mechanical advantages of a Cotton osteotomy with a modified Lapidus procedure to
treat medial column collapse by fusing the first TMT with a dorsal opening wedge
distraction allograft [39]. The procedure has the potential benefit of maintaining/
increasing the length of the first ray and plantarflexing the medial column, as well
as restoring the first ray’s mechanical competence in the foot tripod. Although their
outcomes are limited to short-term follow-up or reporting on surgical technique,
these two procedures have the potential to treat PCFD without or with a smaller
amount of LCL, thereby reducing the risk of complications such as foot stiffness.
6.4 Peritalar Subluxation/Dislocation (Rigid Deformity)
6.4.1 Double or Triple Arthrodesis
Subtalar joint arthrodesis is indicated when there are severe arthritic changes or
peritalar instability characterized by subtalar coronal subluxation or subfibular
impingement. This may be caused by laxity or failure of the interosseous talocalca-
neal ligament. In patients of older age, lower physical demand, or excessive weight,
arthrodesis may be an acceptable surgical option than LCL as fusing the subtalar
joint in neutral/mildly everted position makes lateral column overcorrection less
likely. When performing subtalar arthrodesis, it is imperative to correct the joint to
neutral as the deltoid ligament may otherwise fail in a poorly positioned fusion
(Fig. 5).
An MDCO should be added to obtain an ideal heel position, a clinically straight
heel. Talonavicular joint arthrodesis can be added when there is a severe arthritic
change at the joint or excessive abduction after hindfoot correction. If more than
50% of the abduction is corrected, spring ligament reconstruction is an option to
avoid talonavicular joint fusion. Whether or not the talonavicular joint is fused,
the calcaneocuboid joint can usually be spared. Unfortunately, even in the setting
of a double arthrodesis, patients are still at an increased risk for adjacent joint
arthritis.
6.5 Ankle Instability
6.5.1 Deltoid Ligament Reconstruction
When there is valgus talar tilt in the tibiotalar joint in PCFD, there is likely to be an
insufficiency of the deltoid ligament as long as there is not lateral tibial bone defect.
When used as a supplement to complete the correction of the flatfoot deformity,
deltoid reconstruction has been shown to result in good clinical outcomes as well as
correction of valgus talar tilt (Fig. 6) [40, 41].
Reconstruction can be achieved using either peroneus longus autograft or
Achilles tendon allograft. It is imperative to address all deformities in the foot when
performing deltoid reconstruction in order to minimize the risk of failure from
a b c
d e f
Fig. 5 Pre- (a–c) and postoperative (d–f) images following double arthrodesis in a 74-year-old
male patient. Heel alignment should be in the right position (straight) to make deltoid ligament
failure less likely
increased strain on the medial soft tissues in the longer term. Before proceeding
with deltoid reconstruction either at the same operation or as a staged procedure if
necessary, there must be a clinically straight heel in relation to the tibial and a mod-
erately plantarflexed first ray with moderate prominence of the first metatarsal head
in relation to the lesser metatarsal heads.
6.6 Soft Tissue Procedures
6.6.1 Flexor Tendon Transfer
The purpose of flexor tendon (flexor digitorum longus [FDL] or flexor hallucis lon-
gus [FHL]) transfer is to substitute or augment the function of the impaired PTT and
to balance the force of the peroneus muscle. The FDL is usually utilized due to its
proximity to the PTT and because there are fewer comorbidities associated with
harvesting the FDL tendon compared to the FHL. Although tendon transfer is a
widely performed technique in PCFD treatment, it alone fails to correct the
a b
Fig. 6 Pre- (a) and 7-year postoperative (b) ankle standing radiographs show a successful out-
come of deltoid ligament reconstruction in an 81-year-old female patient
deformity, and the correction would deteriorate over time. Therefore, it is combined
with bony realignment procedures such as LCL or MDCO. The optimal location of
tendon transfer has also been discussed, with options including the navicular, medial
cuneiform, or PTT. These locations have been shown to be biomechanically similar
in a cadaveric study. FHL transfer?
6.6.2 Gastrocnemius Recession/Achilles Tendon Lengthening
Heel cord tightness or equinus contracture is a common pathology observed in

PCFD and may lead to worsening hindfoot valgus deformity if heel alignment is not
fully corrected to a clinically straight heel. During PCFD correction, gastrocnemius
recession is usually performed first before performing other bony or tendinous pro-
cedures, while percutaneous tri-cut lengthening is most often performed at the end
of the procedure. The former is performed when the Silfverskiöld test is positive
(isolated gastrocnemius tightness), and the latter is performed to address both gas-
trocnemius and soleus tightness.
6.6.3 Spring Ligament Reconstruction
Spring ligament reconstruction is indicated when non-fusion bony procedures such

as LCL or subtalar fusion most often combined with medial heel slide correct at
least 50% of the abduction/plantarflexion deformity, but adequate correction is not
achieved. In cadaveric and clinical studies, spring ligament reconstruction resulted
in the correction of talonavicular deformity and talonavicular arthrodesis avoided
[42–44]. Multiple techniques have been described for spring ligament reconstruc-
tion, including allograft, autograft, and synthetic materials. However, this is techni-
cally demanding, and the data supporting this procedure is not yet sufficient. A
long-term study of spring ligament reconstruction is underway by the senior author
of this chapter.
7 Complication of Treatment
There are numerous surgical options in the treatment of PCFD, and all of these
procedures have the potential for a range of complications. Complications may be
due to poor presurgical planning, intraoperative errors, and inherent complications
of each procedure, such as delayed union, nonunion, over- or undercorrection, or
neurovascular injury.
7.1 Medial Displacement Calcaneal Osteotomy
While this procedure yields a high rate of osseous union, lateral incision risks injury
to the sural nerve. Several studies have described alternative incisions to minimize
the risk of sural nerve injury. In addition, the medial neurovascular bundle can also
be compromised when performing the osteotomy. A safe zone for the osteotomy has
been described as being within 11.2 ± 2.7 mm anterior to the line connecting the
posterosuperior apex of the calcaneal tuberosity to the origin of the plantar fascia
[45]. However, there is still some debate on whether a safe zone truly exists due to
inherent variation in anatomy. Finally, irritation from prominent hardware is also a
frequently described complication following MDCO.
7.2 Lateral Column Lengthening
Much of the concern for complications following PCFD reconstruction is associ-

ated with the LCL procedure. Due to the nature of non-anatomical lengthening, this
procedure can result in stiffness of the adjacent joints. Subsequently, lateral column
overload, fifth metatarsal stress fracture, and calcaneocuboid joint arthritis have all
been reported following this procedure. It is known that overcorrection leads to a

higher rate of lateral column pain and increased lateral foot pressures with a higher
rate of patient dissatisfaction. Therefore, as mentioned above, slight undercorrec-
tion of the abduction deformity and maintaining an adequate amount of eversion
after lengthening are paramount. Adequate eversion motion remaining is much
more important than arch height. Given the choice between an X-ray with a fully
restored Meary’s angle with stiffness and adequate eversion motion with a mild
talonavicular sag remaining, the latter is preferable and will usually result in a hap-
pier patient.
7.3 Arthrodesis
When an arthrodesis is chosen, the potential for adjacent joint overload and subse-
quent arthritis or secondary collapse should be explained to patients, and this should
be carefully assessed during the follow-up period. For example, triple arthrodesis
will limit the motion of the foot through arthrodesis of the talonavicular and calca-
neonavicular joints, resulting in more stress placed on the midfoot joints. One
should always be aware of possible arthritis as a source of patient’s recurrent symp-
toms in the long term. Preservation of talonavicular motion is particularly important
as it is not only a key motion to the foot but is associated with the development of
ankle arthritis over the long term. Triple arthrodesis, of which talonavicular fusion
is a key part, has been shown to cause ankle arthritis over the long term. Talonavicular
motion is also a motion that most patients in one way or another will miss.
Preservation of even some of this motion, whether by early correction of PCFD or
the use of spring ligament reconstruction when needed, will preserve important
motion and probably lessen the chance of adjacent joint arthritis.
8 Summary
In treating patients with PCFD, prompt early nonsurgical or surgical management is

essential to avoid deformity progression. The location and the severity of the defor-
mity may vary between the patients; therefore, an individualized approach is
required. Generally, the goal of treatment is to achieve good correction of the defor-
mity while maintaining as much as normal motion as possible both in the medial
and the lateral column of the foot. Poor alignment of joints, particularly the talona-
vicular, subtalar, or first metatarsal joints, or over- or undercorrection of heel align-
ment or lateral column lengthening correction leads to a dissatisfied patient.
References
1. Myerson MS, Thordarson D, Johnson JE, Hintermann B, Sangeorzan BJ, Deland JT, et al.
Classification and nomenclature: progressive collapsing foot deformity. Foot Ankle Int.
2020;1071100720950722.
2. Beals TC, Pomeroy GC, Arthur MI. Posterior tibial tendon insufficiency: diagnosis and treat-
ment. JAAOS-J Am Acad OrthopSurg. 1999;7(2):112–8.
3. Cody EA, Williamson ER, Burket JC, Deland JT, Ellis SJ. Correlation of talar anatomy and
subtalar joint alignment on weightbearing computed tomography with radiographic flatfoot
parameters. Foot Ankle Int. 2016;37(8):874–81.
4. KIDNER FC. The prehallux (accessory scaphoid) in its relation to flat-foot.
JBJS. 1929;11(4):831–7.
5. Kim J, Day J, Seilern, Aspang J. Outcomes following revision surgery after failed kidner pro-
cedure for painful accessory navicular. Foot Ankle Int. 2020:1071100720943843.
6. Fuhrmann R, Trommer T, Venbrocks R. The acquired buckling-flatfoot. A foot deformity due
to obesity? Der Orthopade. 2005;34(7):682–9.
7. Holmes GB, Mann RA. Possible epidemiological factors associated with rupture of the poste-
rior tibial tendon. Foot Ankle. 1992;13(2):70–9.
8. Giblin MM. Ruptured tibialis posterior tendon associated with a closed medial malleolar frac-
ture. Aust N Z J Surg. 1980;50(1):59–60.
9. Myerson M, Solomon G, Shereff M. Posterior tibial tendon dysfunction: its association with
seronegative inflammatory disease. Foot Ankle. 1989;9(5):219–25.
10. Downey DJ, Simkin PA, Mack LA, Richardson ML, Kilcoyne RF, Hansen ST. Tibialis poste-
rior tendon rupture: a cause of rheumatoid flat foot. Arthritis Rheum. 1988;31(3):441–6.
11. Michelson J, Easley M, Wigley FM, Hellmann D. Posterior tibial tendon dysfunction in rheu-
matoid arthritis. Foot Ankle Int. 1995;16(3):156–61.
12. Godoy-Santos A, Ortiz R, Junior RM, Fernandes TD, Santos M. MMP-8 polymorphism is
genetic marker to tendinopathy primary posterior tibial tendon. Scand J Med Sci Sports.
2014;24(1):220–3.
13. de Araujo Munhoz FB, Baroneza JE, Godoy-Santos A, Fernandes TD, Branco FP, Alle LF,
et al. Posterior tibial tendinopathy associated with matrix metalloproteinase 13 promoter geno-
type and haplotype. J Gene Med. 2016;18(11–12):325–30.
14. Orr JD, Nunley JA. Isolated spring ligament failure as a cause of adult-acquired flatfoot defor-
mity. Foot Ankle Int. 2013;34(6):818–23.
15. Tryfonidis M, Jackson W, Mansour R, Cooke P, Teh J, Ostlere S, et al. Acquired adult flat foot
due to isolated plantar calcaneonavicular (spring) ligament insufficiency with a normal tibialis
posterior tendon. Foot Ankle Surg. 2008;14(2):89–95.
16. Greisberg J, Assal M, Hansen ST Jr, Sangeorzan BJ. Isolated medial column stabilization
improves alignment in adult-acquired flatfoot. Clin Orthop Relat Res®. 2005;435:197–202.
17. Cohen BE, Ogden F. Medial column procedures in the acquired flatfoot deformity. Foot Ankle
Clin. 2007;12(2):287–99.
18. Funk DA, Cass J, Johnson K. Acquired adult flat foot secondary to posterior tibial-tendon
pathology. J Bone Joint Surg Am. 1986;68(1):95–102.
19. Imhauser CW, Siegler S, Abidi NA, Frankel DZ. The effect of posterior tibialis tendon dys-
function on the plantar pressure characteristics and the kinematics of the arch and the hindfoot.
Clin Biomech. 2004;19(2):161–9.
20. Thordarson DB, Schmotzer H, Chon J, Peters J. Dynamic support of the human longitudinal
arch: a biomechanical evaluation. Clin Orthop Relat Res (1976–2007). 1995;316:165–72.
21. Kelikian AS, Sarrafian SK. Sarrafian’s anatomy of the foot and ankle: descriptive, topographic,
functional. Lippincott Williams & Wilkins; 2011.
22. Supple KM, Hanft JR, Murphy BJ, Janecki CJ, Kogler GF. Posterior tibial tendon dysfunction.
Semin Arthritis Rheum: Elsevier. 1992:106–13.
23. Jahss MH. Spontaneous rupture of the tibialis posterior tendon: clinical findings, tenographic
studies, and a new technique of repair. Foot Ankle. 1982;3(3):158–66.
24. Frey C, Shereff M, Greenidge N. Vascularity of the posterior tibial tendon. J Bone Joint Surg
Am. 1990;72(6):884–8.
25. Deland JT, de Asla RJ, Sung I-H, Ernberg LA, Potter HG. Posterior tibial tendon insufficiency:
which ligaments are involved? Foot Ankle Int. 2005;26(6):427–35.
26. Taniguchi A, Tanaka Y, Takakura Y, Kadono K, Maeda M, Yamamoto H. Anatomy of the
spring ligament. JBJS. 2003;85(11):2174–8.
27. Ellis SJ, Yu JC, Williams BR, Lee C. Chiu Y-l, Deland JT. New radiographic param-
eters assessing forefoot abduction in the adult acquired flatfoot deformity. Foot Ankle Int.
2009;30(12):1168–76.
28. Williamson ER, Chan JY, Burket JC, Deland JT, Ellis SJ. New radiographic parameter
assessing hindfoot alignment in stage II adult-acquired flatfoot deformity. Foot Ankle Int.
2015;36(4):417–23.
29. Sangeorzan BJ, Mosca V, Hansen ST Jr. Effect of calcaneal lengthening on relationships
among the hindfoot, midfoot, and forefoot. Foot Ankle. 1993;14(3):136–41.
30. Younger AS, Sawatzky B, Dryden P. Radiographic assessment of adult flatfoot. Foot Ankle Int.
2005;26(10):820–5.
31. Saltzman CL, El-Khoury GY. The hindfoot alignment view. Foot Ankle Int. 1995;16(9):572–6.
32. Conti MS, Ellis SJ. Weight-bearing CT scans in foot and ankle surgery. JAAOS-J Am Acad
Orthop Surg. 2020;28(14):e595–603.
33. de Cesar NC, Myerson MS, Day J, Ellis SJ, Hintermann B, Johnson JE, et al. Consensus for
the use of weightbearing CT in the assessment of progressive collapsing foot deformity. Foot
Ankle Int. 2020;1071100720950734.
34. Johnson KA, Strom DE. Tibialis posterior tendon dysfunction. Clin Orthop Relat Res.
1989;239:196–206.
35. Bluman EM, Myerson MS. Stage IV posterior tibial tendon rupture. Foot Ankle Clin.
2007;12(2):341–62.
36. Conti MS, Chan JY, Do HT, Ellis SJ, Deland JT. Correlation of postoperative midfoot position
with outcome following reconstruction of the stage II adult acquired flatfoot deformity. Foot
Ankle Int. 2015;36(3):239–47.
37. Ellis SJ, Johnson JE, Day J, de Cesar NC, Deland JT, Hintermann B, et al. Titrating the amount of
bony correction in progressive collapsing foot deformity. Foot Ankle Int. 2020;41(10):1292–5.
38. Kim J, Kim J-B, Lee W-C. Dynamic medial column stabilization using flexor hallucis longus
tendon transfer in the surgical reconstruction of flatfoot deformity in adults. Foot Ankle Surg.
2021;27(8):920–7.
39. de Cesar Netto C, Ahrenholz S, Iehl C, Vivtcharenko V, Schmidt E, Lee H, et al. Lapicotton
technique in the treatment of progressive collapsing foot deformity. J Foot Ankle. 2020;14(3):
301–8.
40. Deland JT, de Asla RJ, Segal A. Reconstruction of the chronically failed deltoid ligament: a
new technique. Foot Ankle Int. 2004;25(11):795–9.
41. Ellis SJ, Williams BR, Wagshul AD, Pavlov H, Deland JT. Deltoid ligament reconstruction
with peroneus longus autograft in flatfoot deformity. Foot Ankle Int. 2010;31(9):781–9.
42. Deland JT, Arnoczky SP, Thompson FM. Adult acquired flatfoot deformity at the talonavicular
joint: reconstruction of the spring ligament in an in vitro model. Foot Ankle. 1992;13(6):327–32.
43. Choi K, Lee S, Otis JC, Deland JT. Anatomical reconstruction of the spring ligament using
peroneus longus tendon graft. Foot Ankle Int. 2003;24(5):430–6.
44. Williams BR, Ellis SJ, Deyer TW, Pavlov H, Deland JT. Reconstruction of the spring ligament
using a peroneus longus autograft tendon transfer. Foot Ankle Int. 2010;31(7):567–77.
45. Talusan PG, Cata E, Tan EW, Parks BG, Guyton GP. Safe zone for neural structures in medial
displacement calcaneal osteotomy: a cadaveric and radiographic investigation. Foot Ankle Int.
2015;36(12):1493–8.
Latest Trends in Flatfoot Management:
Contributions of the Spring Ligament
Complex and the Deltoid Ligament
Brian T. Sleasman and Anish R. Kadakia
1 Introduction
Flatfoot deformity is a common complaint of patients presenting to a foot and ankle

surgeon. It has long been accepted as a source of pain and disability and affects
upwards of five million Americans [1]. Originally, flatfoot was described as poste-
rior tibial tendon dysfunction (PTTD) due to the contribution of posterior tibial
tendon (PTT) insufficiency to the deformity. This idea was conceptualized in the
original flatfoot classification in 1989 by Johnson and Strom [2] and later refined by
Bluman [3] in 2007 to include a broader spectrum of pathologies. Despite the
breadth of this classification, it still failed to incorporate some components of the
deformity, specifically the spring and deltoid ligaments. Regardless, this classifica-
tion is well known and frequently referenced when discussing treatment algorithms.
Recently, a group of experts on flatfoot advocated for the use of the term progres-
sive collapsing foot deformity (PCFD) to include adults and children and to state the
progressive nature of this condition [4]. With continued research it has become evi-
dent that the medial stabilizers of the ankle provide essential support to the arch and
are critical in the prevention of this deformity. Several authors have noted that in
patients who have progressed to this deformity, the spring ligament is almost uni-
versally compromised [5–7]. The deltoid ligament, which was included in the late
stage disease in Bluman’s classification, may have implications in the earlier dis-
eased states. For these reasons, understanding and treatment of PCFD must include
an evaluation of these two medial soft tissue structures, and they should be addressed
at the time of correction.
B. T. Sleasman (*) · A. R. Kadakia

Northwestern University – Feinberg School of Medicine, Northwestern Memorial Hospital,
Department of Orthopedic Surgery, Chicago, IL, USA

Switzerland AG 2022
556 B. T. Sleasman and A. R. Kadakia
In this chapter we will focus on how to address the medial soft tissue structure
damage in PCFD. Please refer to the previous chapter for a more detailed analysis
of the clinical history, physical examination findings, and bone deformity correction.
2 Etiology: Pathophysiology
PCFD is a complex problem which results in the compromise of the soft tissue and
osseous structures in the foot. This compromise ultimately leads to the classic pro-
gressive collapse of the medial longitudinal arch.
Historically, the PTT has been implicated in the development of PCFD. This
tendon is a powerful plantar flexor and inverter of the hindfoot. It originates in the
posterior aspect of the intermuscular septum, and its tendon passes posterior to the
axis of rotation of the ankle and medial to the subtalar axis. Thus, it acts as a strong
plantarflexor and inverter of the hindfoot. Through the stages of gait, this tendon is
responsible for locking the transfer tarsal joints during gait which allows for effi-
cient propulsion. In patients without this tendon, the hindfoot is not effectively
inverted, and thus medial ligaments can be attenuated [8]. However, several authors
noted that it is not uncommon for patients with a normal PTT to have a planovalgus
deformity of the hindfoot [9, 10]. Additionally, we do not see PCFD in patients in
which the PTT is transferred for foot drop.
In an MRI study, evidence of spring ligament dysfunction was strongly associ-
ated with the planovalgus deformity, alongside with multiple other soft tissue insuf-
ficiencies like the deltoid ligament and subtalar interosseous ligament [7]. The
spring ligament has a crucial role as the soft tissue hammock in which the talar head
rests. The structure provides static stability to the talar head, and thus, when intact,
the foot cannot abduct nor the talus plantar flex at the TN joint. Therefore, it is not
without failure or attenuation of the spring ligament that the classic flatfoot defor-
mity should occur.
2.1 Relevant Anatomy
The medial soft tissue stabilizers of the ankle and talus include the spring ligament
complex (SLC) and the deltoid ligament, which are intimately related. The SLC is
comprised of a group of ligaments that connect the sustentaculum tali of the calca-
neus to the navicular bone. Together these ligaments support the head of the talus
and form part of the articular cavity of the talocalcaneonavicular joint, which is
referred to as the acetabulum or coxa pedis [11]. The SLC is comprised of three
main components. The most important of which is the superomedial band (SMCN).
This band is the longest and most medial of the components originating on the
medial sustentaculum tali and projecting anteromedially to attach over a broad spec-
trum to the navicular. Its deep surface is covered in fibrocartilage and is the specific
Latest Trends in Flatfoot Management: Contributions of the Spring Ligament Complex… 557
portion of the SLC primarily responsible for articulating with the talar head. The
inferoplantar (ICN) band is the shortest and most lateral part of the SLC. It is slightly
thicker than the SMCN, and biomechanical analysis shows that it does play a minor
role in stabilizing the talocalcaneonavicular joint as well as the medial arch of the
foot [12]. The medioplantar oblique band (MPO) is a distinct band that lies between
the SMCN and the ICN.
The deltoid ligament is composed of two main components, namely, the superfi-
cial and deep components. The deep deltoid originates on the distal aspect of the
medial malleolus and inserts over a wide non-articular portion of the medial and
posteromedial aspect of the talus. Its main function is to prevent lateral displace-
ment and external rotation of the talus. The superficial deltoid ligament is broad and
sends distinct bands to the navicular, the spring ligament, the calcaneus, and the
talus. The tibiospring and tibionavicular portions of the superficial deltoid ligament
highlight the intimate relationship between these two medial soft tissue structures
[13]. The tibionavicular band helps to suspend the spring ligament and works in
conjunction with the SLC to prevent inward displacement of the talus. The talocal-
caneal portion helps to prevent valgus.
As with most conditions of the foot and ankle, flatfoot treatment begins with nonop-
erative management. These options typically focus on alleviating pain and symp-
toms by attempting to off-load the medial foot and arch. This can be done with a
combination of weight loss, activity modification, and improving footwear. Orthoses
are often incorporated into early treatment algorithms to improve symptoms.
Typically, these included a medial post to support the medial arch. The University
of California Biomechanics Laboratory (UCBL) semirigid orthosis was created to
control the valgus of the hindfoot as well as support the medial arch. In biomechani-
cal studies the UCBL was effective in partially correcting these deformities [14].
In patients who are inflamed, or who have severe pain, a period of rest in a cast
or CAM boot immobilization combined with NSAIDs may be helpful. It is impor-
tant to note however that in most instances, in patients with true flatfoot deformity,
rather than PTT tendinitis, these treatments will not affect the long-term position of
the foot. Nonoperative treatment is most effective for patients with Stage I disease.
Surgical treatment of PCFD is determined by the level of deformity and the radio-
graphic and clinical findings. While there are many described treatments for PCFD,
we will focus on the medial ligamentous structures, specifically the SLC and the
deltoid.
4.1 Isolated Spring Ligament Injury
While it is much more common that the spring ligament is injured in conjunction
with the PTT, there have been several case reports which suggest that an isolated
injury to the SLC is enough to cause PCFD. In these cases, patients often present
with pain anterior to the medial malleolus and deep in the medial arch as opposed
to along the PTT. Patients often typically maintain their ability to perform a single
heel raise [15]. Due to the paucity of literature, there is no well-established recom-
mendation on how to treat these patients. Despite the literature on these isolated
injuries being very limited, good results have been published with surgical treatment.
In a case series of nine patients with PCFD with normal PTT function, Tryfonidis
et al. reported on three patients who went on to have surgery. One patient with an
acute spring ligament injury underwent direct repair of the torn spring and deltoid
ligaments, while the remaining two patients underwent a spring ligament repair in
conjunction with a flexor digitorum longus (FDL) transfer and medializing calca-
neal osteotomy (MCO). He noted good results with both techniques [15]. In two
separate case reports of high-level athletes with isolated spring ligament injury with
no evidence of PTT dysfunction, the patients returned to their prior level of compe-
tition after undergoing a repair of the sprained ligament. In one case the spring liga-
ment repair was supplemented with an FDL transfer [16, 17]. In 2013, Orr and
Nunley reported on six patients with PCFD with isolated spring ligament dysfunc-
tion [18]. In their cohort ligament repair was done in conjunction with LCL, MCO,
or cuneiform osteotomy as determined by pre-op deformity.
4.2 Spring Ligament Repair in Flexible PFCD
Stage II of PCFD is characterized by a valgus deformity of the hindfoot, flattening on

the medial arch of the foot, and a variable degree of abduction of the forefoot. The
amount of forefoot abduction differentiates between IIA and IIB deformities and is
based on the amount of talonavicular uncoverage. Historically, this stage is treated
with a FDL transfer, MCO, and/or LCL. However, in order for the forefoot to abduct,
and the talus to plantarflex, we know there has to be an attenuation of the SLC. Therefore,
in the flexible Stage II-A/B of PCFD, the ligament complex should be addressed to
correct abduction deformity directly. LCL has traditionally been done for this defor-
mity and, while effective [19, 20], can lead to lateral column overload, pain, and a rigid
hindfoot [21, 22]. In 2015, Conti et al. [23] showed that excess abduction correction,
by LCL, can lead to worse patient outcome, and this should be avoided. Additionally,
we know that the lateral column is not necessarily short in patients with PCFD.
Studies have looked at SLC repair and reconstruction in the acute and chronic
setting and concluded that it can be an effective treatment for forefoot abduction. In
some cases, the spring ligament repair with or without augmentation can reduce the
need to perform a LCL [24]. There are many different approaches to repair and
reconstruct the SLC. In a cadaver model, Tan et al. [25] performed augmentation
from the talar head to the navicular and found correction of the AP talo-first meta-
tarsal angle, lateral talo-first metatarsal angle, and medial cuneiform height. Aynardi
et al. in 2019 [26] compared SLC repair vs repair plus augmentation in eight cadav-
eric models. In their group, all of the ligament repairs failed, while only one of the
augmented repairs failed. Several other authors have had success in vivo with vari-
ous reconstruction techniques [26–30]. Most recently, Haye et al. [31] in 2020 com-
pared SLC reconstruction with hamstring allograft with synthetic ligament
augmentation and found patient outcomes were better with synthetic reconstruction.
Historically, a LCL is performed in patients with greater than 30% uncoverage of
the talar head. With new SLC reconstruction techniques with improved outcomes
and a better understanding of the consequences of over lengthening the lateral col-
umn, we feel that SLC reconstruction should be the preferred technique and LCL
only reserved for greater deformities of greater than 50% uncovering, given the
power of modern medial soft tissue reconstruction.
4.2.1 Author’s Recommended Technique
When performing this reconstruction, we developed a technique to reconstruct both

the calcaneonavicular and tibiospring components due to the intimate relationship of
the spring and deltoid ligaments. We chose to use the internal brace for our recon-
struction technique due to the superior radiographic results with synthetic ligament
reconstruction. A standard medial approach over the PTT is assessed for disease. If
there is disease or attenuation, a FDL transfer is first performed in the standard fash-
ion. If the PTT is found to be intact and in good condition, it can be left alone. After
addressing the PTT, attention is turned to the SLC. The SLC is incised, and the sus-
tentaculum of the calcaneus is identified. Utilizing the cannulated InternalBrace
System (Arthrex®), a guide wire is placed into the sustentaculum and confirmed
using fluoroscopy (Fig. 1). The sustentaculum is then further prepared with a drill and
tap in a standard fashion, and a 3.5 mm SwiveLock®, loaded with a single long
FiberTape®, is inserted. A wire is then placed from plantar to dorsal through the
navicular and again confirmed with fluoroscopy (Fig. 2). A 2.7 mm drill is passed over
the wire to create a passage for the FiberTape® (from the sustentaculum) which is
routed from plantar to dorsal through the navicular (Fig. 3). The spring ligament com-
ponent is then tensioned with the foot held in neutral dorsiflexion and neutral adduc-
tion by pulling on both limbs of the FiberTape® as it exits the dorsal navicular. After
obtaining appropriate tension, the FiberTape® is secured by placing a SwiveLock® in
the navicular tunnel. Attention is then turned to the deltoid component of our recon-
struction. A guide wire is first placed into the tip of the medial malleolus and con-
firmed with fluoroscopy (Fig. 4). The bone is then prepped with a drill and tap for a
4.75 SwiveLock®. Again, the foot is held in neutral dorsiflexion and neutral adduc-
tion, and both limbs of the FiberTape® are appropriately tensioned and inserted into
the medial malleolar tunnel (Fig. 5). We then imbricate the native spring ligament in
a pants-over-vest fashion using 0 Vicryl suture to complete the reconstruction.
Fig. 1 An axial view of

the calcaneus demonstrates
appropriate fluoroscopy
image to confirm
placement of the guide
wire into the sustentaculum
tali. Care must be taken to
place the wire from
proximal to distal to avoid
violation of the subtalar
joint
Fig. 2 An AP view of the

foot demonstrates wire
placement within the
navicular for creation of
the navicular tunnel
Fig. 3 Intraoperative
photograph demonstrating
the passage of the
FiberTape® from the
sustentaculum tali, plantar
to the stump of the
posterior tibial tendon, and
routed from plantar to
dorsal through the
navicular tunnel. The
sustentaculum tali are
marked with a white dotted
line and the letters “ST.”
The navicular bone is
marked with a white dotted
line and the letter “N”
Fig. 4 A mortise view of

the ankle demonstrating
appropriate drilling
position within the medial
malleolus for insertion of
the tibiospring component
of the reconstruction
4.3 Medial Ligament Reconstruction in Rigid PCFD
As the progression of flatfoot deformity continues, the medial arch collapses, there
is increased forefoot abduction, the hindfoot becomes rigid with subtalar arthritis
(Stage III), and ultimately the deltoid will fail leading to asymmetry of the ankle
the tibiospring component
of the reconstruction with
the FiberTape® now
anchored into the medial
malleolus. The medial
malleolus is marked with a
white dotted line and the
letters “MM.” The
navicular is marked with a
white dotted line and the
letter “N”
mortise with increased talar tilt. This ankle asymmetry is the hallmark of Stage IV
of PCFD and was further subdivided by Bluman in 2007 into IV-A and IV-B, based
on the presence or absence of ankle arthritis [3]. Historically, IV-A deformity is
treated with deltoid reconstruction in conjunction with bony procedures, often a
triple arthrodesis. When the ankle becomes arthritic, the tibiotalar joint is involved,
and thus patients are historically treated with a pantalar arthrodesis. While this may
be required to effectively correct deformity, extensive hindfoot fusions have a high
morbidity, and when possible, joint sparing procedures should be attempted [32].
During surgical decision-making for patients with III and IV-A disease, there are
several factors that must be considered. These include the ability to fully correct the
hindfoot valgus and to realign and restore the ankle mortise and the identification
and treatment of concomitant lateral ankle instability. We know through cadaveric
studies that flatfoot deformity causes a shift and reduction in tibiotalar contact areas
which can lead to point loading and development of arthritis [33]. In Stage III dis-
ease, the subtalar and talonavicular arthrodesis procedure or triple arthrodesis has
had good results as the deformity has not progressed to include the tibiotalar joint.
However, the increased rigidity of the construct will place increased stress on the
deltoid ligament and medial-sided structures which may ultimately lead to failure
and progression of deformity [34, 35]. Therefore, it is critical that the hindfoot
deformity is completely corrected to decrease the risk of progression to Stage IV of
disease despite arthrodesis. In patients with existing deltoid function and ankle
asymmetry, but with intact cartilage (Stage IV-A) successful alignment of the mor-
tise must be obtained. This can be obtained through reconstruction of deltoid liga-
ment. Several procures have been described and have had good success [29, 30,
36–38]. In general, these procedures involve a reconstruction of some or all of the
components of the tibiocalcaneonavicular ligament, term given to the functional
ligament comprising the superficial and deep deltoid and spring ligament complex
[39] which spans the tibiotalar, tibiocalcaneal, tibionavicular, and calcaneonavicu-
lar segments. This triangularly shaped complex reconstruction has been described
using autograft, allograft, with or without augmentation due to the attenuation of the
native ligament [30]. While often not considered a hallmark of early PCFD, Presaud
et al. showed that there is MRI evidence of lateral ligament injury in approximately
63% of patients with Stage II or III disease [40]. When present this should be
addressed.
Stage IV-B deformity, which is defined by the presence of ankle arthritis is a
unique situation. In these patients joint-sparing procedures are often limited.
Typically, when patients reach this stage, we surgeons are limited to ankle fusion vs
total ankle replacement (TAR). Although TAR has been contraindicated in patients
with deformity, as our understanding of deformity correction has improved, and our
techniques have evolved, indications have expanded. In this instance most authors
would recommend staged procedures that initially address the deformity and stabil-
ity of the ankle and hindfoot, followed by TAR after complete recovery, to address
the coexisting ankle arthritis [41].
4.3.1 Author’s Recommended Technique
In our practice we attempt to avoid hindfoot fusion when possible in the early Stage
IV disease. This can only be accomplished when there is not significant subtalar
arthrosis. In these instances, both the superficial and deep deltoid ligaments must be
reconstructed to provide stability. We prefer a technique that was described by Nery
et al. in which the deep and superficial deltoid ligaments are reconstructed along
with the spring ligament. This procedure involves anchoring a FiberTape® into the
medial malleolus. One of the limbs is then anchored to the talus to reconstruct the
deep deltoid, while the other is anchored, with a second FiberTape®, into the sus-
tentaculum to reconstruct the superficial limb. This second FiberTape® is then
routed through the navicular (in a similar fashion as described in detail above) to
reconstruct the SLC. In all cases this reconstruction must be combined with a
MCO. Alternatively, a double-loaded 3.5 mm SwiveLock® can be placed into the
sustentaculum, and the use of the longer FiberTape® is recommended. Two limbs
are taken into the navicular as described previously, tensioned with foot in neutral
adduction, and secured with a 3.5 mm SwiveLock®. The superficial deltoid and
tibiospring components are then reconstructed by taking the two limbs from the
sustentaculum and the two limbs from the navicular and securing them into the
medial malleolus with a 4.75 SwiveLock® with the foot held in slight inversion.
The deep deltoid is then reconstructed immediately anterior to the MM with a 3.5
SwiveLock® with two of the four limbs that were anchored into the medial
malleolus.
In cases in which the arthrosis of the hindfoot progresses to end-stage disease
and a hindfoot fusion is required, a MCO is also performed to further medialize the
forces on the ankle. In these cases, the deltoid ligament should also be reconstructed
as we know this ligament must be attenuated or torn for this deformity to occur and
repair is not sufficient. For this technique a medial incision is made, and the native
deltoid ligament is elevated of the medial malleolus. Augmentation is completed by
placing a 4.75 mm double loaded SwiveLock® into the medial malleolus. One of
the limbs is anchored into the talus 5 mm distal and 5 mm anterior to the tip of the
medial malleolus, and the second is inserted into the sustentaculum, reconstructing
the deep and superficial deltoid ligaments, respectively. In these instances, fusion of
the subtalar and talonavicular joints obviates the need for SLC reconstruction. It is
imperative that the ankle is held in neutral dorsiflexion with a reduced mortise,
while each limb of the reconstruction is separately tensioned. This reconstruction is
then imbricated with the native deltoid ligament using anchors and additional
0 Vicryl.
In instances of Stage IV-B deformity where the ankle has progressed to end-stage
arthritis, we feel that this should be treated in a staged fashion using the techniques
described above to correct deformity and provide stability during the index proce-
dure. When the patient has a stable and aligned foot, a TAR can be performed,
understanding that there is still persistent risk of recurrent valgus in this case. In all
cases, it is our protocol to utilize an ASO and an arch support for 3–6 months to
protect the soft tissue repair.
References
1. Coughlin M, Mann R. Surgery of the foot and ankle. 7th ed. St. Louis: Mosby; 1999.
2. Johnson KA, Strom DE. Tibialis posterior tendon dysfunction. Clin Orthop Relat Res.
1989;239:196–206.
3. Bluman EM, Title CI, Myerson MS. Posterior tibial tendon rupture: a refined classification
system. Foot Ankle Clin. 2007;12(2):233–49, v. https://doi.org/10.1016/j.fcl.2007.03.003.
4. de Cesar NC, Deland JT, Ellis SJ. Guest editorial: expert consensus on adult-acquired flatfoot
deformity. Foot Ankle Int. 2020;41(10):1269–71. https://doi.org/10.1177/1071100720950715.
5. Deland JT. The adult acquired flatfoot and spring ligament complex. Pathology and impli-
cations for treatment. Foot Ankle Clin. 2001;6(1):129–35, vii. https://doi.org/10.1016/
s1083-7515(03)00086-x.
6. Deland JT, de Asla RJ, Sung IH, Ernberg LA, Potter HG. Posterior tibial tendon insuf-
ficiency: which ligaments are involved? Foot Ankle Int. 2005;26(6):427–35. https://doi.
org/10.1177/107110070502600601.
7. Williams G, Widnall J, Evans P, Platt S. Could failure of the spring ligament complex be
the driving force behind the development of the adult flatfoot deformity? J Foot Ankle Surg.
2014;53(2):152–5. https://doi.org/10.1053/j.jfas.2013.12.011.
8. Funk DA, Cass JR, Johnson KA. Acquired adult flat foot secondary to posterior tibial-tendon
pathology. J Bone Joint Surg Am. 1986;68(1):95–102.
9. Oburu E, Myerson MS. Deltoid ligament repair in flatfoot deformity. Foot Ankle Clin.
10. Hintermann B, Knupp M, Pagenstert GI. Deltoid ligament injuries: diagnosis and manage-
ment. Foot Ankle Clin. 2006;11(3):625–37. https://doi.org/10.1016/j.fcl.2006.08.001.
11. Omar H, Saini V, Wadhwa V, Liu G, Chhabra A. Spring ligament complex: illustrated normal
anatomy and spectrum of pathologies on 3T MR imaging. Eur J Radiol. 2016;85(11):2133–43.
https://doi.org/10.1016/j.ejrad.2016.09.023.
12. Davis WH, Sobel M, DiCarlo EF, Torzilli PA, Deng X, Geppert MJ, et al. Gross, histological,
and microvascular anatomy and biomechanical testing of the spring ligament complex. Foot
13. Campbell KJ, Michalski MP, Wilson KJ, Goldsmith MT, Wijdicks CA, LaPrade RF, et al. The
ligament anatomy of the deltoid complex of the ankle: a qualitative and quantitative anatomi-
cal study. J Bone Joint Surg Am. 2014;96(8):e62. https://doi.org/10.2106/JBJS.M.00870.
14. Havenhill TG, Toolan BC, Draganich LF. Effects of a UCBL orthosis and a calcaneal oste-
otomy on tibiotalar contact characteristics in a cadaver flatfoot model. Foot Ankle Int.
15. Tryfonidis M, Jackson W, Mansour R, Cooke PH, Teh J, Ostlere S, et al. Acquired adult flat
foot due to isolated plantar calcaneonavicular (spring) ligament insufficiency with a nor-
mal tibialis posterior tendon. Foot Ankle Surg. 2008;14(2):89–95. https://doi.org/10.1016/j.
fas.2007.11.005.
16. Borton DC, Saxby TS. Tear of the plantar calcaneonavicular (spring) ligament causing flat-
foot. A case report. J Bone Joint Surg Br. 1997;79(4):641–3. https://doi.org/10.1302/0301-620
x.79b4.7396.
17. Chen JP, Allen AM. MR diagnosis of traumatic tear of the spring ligament in a pole vaulter.
Skelet Radiol. 1997;26(5):310–2. https://doi.org/10.1007/s002560050242.
18. Orr JD, Nunley JA. Isolated spring ligament failure as a cause of adult-acquired flatfoot defor-
mity. Foot Ankle Int. 2013;34(6):818–23. https://doi.org/10.1177/1071100713483099.
19. Dumontier TA, Falicov A, Mosca V, Sangeorzan B. Calcaneal lengthening: investigation of
deformity correction in a cadaver flatfoot model. Foot Ankle Int. 2005;26(2):166–70. https://
doi.org/10.1177/107110070502600209.
20. Sangeorzan BJ, Mosca V, Hansen ST. Effect of calcaneal lengthening on relationships
among the hindfoot, midfoot, and forefoot. Foot Ankle. 1993;14(3):136–41. https://doi.
org/10.1177/107110079301400305.
21. Oh I, Imhauser C, Choi D, Williams B, Ellis S, Deland J. Sensitivity of plantar pressure and
talonavicular alignment to lateral column lengthening in flatfoot reconstruction. J Bone Joint
Surg Am. 2013;95(12):1094–100. https://doi.org/10.2106/JBJS.K.01032.
22. Benthien RA, Parks BG, Guyton GP, Schon LC. Lateral column calcaneal lengthening,
flexor digitorum longus transfer, and opening wedge medial cuneiform osteotomy for flex-
ible flatfoot: a biomechanical study. Foot Ankle Int. 2007;28(1):70–7. https://doi.org/10.3113/
FAI.2007.0013.
23. Conti MS, Chan JY, Do HT, Ellis SJ, Deland JT. Correlation of postoperative midfoot position
with outcome following reconstruction of the stage II adult acquired flatfoot deformity. Foot
24. Acevedo J, Vora A. Anatomical reconstruction of the spring ligament complex: “internal brace”
augmentation. Foot Ankle Spec. 2013;6(6):441–5. https://doi.org/10.1177/1938640013499404.
25. Tan GJ, Kadakia AR, Ruberte Thiele RA, Hughes RE. Novel reconstruction of a static medial
ligamentous complex in a flatfoot model. Foot Ankle Int. 2010;31(8):695–700. https://doi.
org/10.3113/FAI.2010.0695.
26. Aynardi MC, Saloky K, Roush EP, Juliano P, Lewis GS. Biomechanical evaluation of spring
ligament augmentation with the fiber tape device in a cadaveric flatfoot model. Foot Ankle Int.
27. Baxter JR, LaMothe JM, Walls RJ, Prado MP, Gilbert SL, Deland JT. Reconstruction of the
medial talonavicular joint in simulated flatfoot deformity. Foot Ankle Int. 2015;36(4):424–9.
28. Pasapula C, Devany A, Fischer NC, Wijdicks CA, Hübner T, Reifenscneider F, et al. The resis-
tance to failure of spring ligament reconstruction. Foot (Edinb). 2017;33:29–34. https://doi.
org/10.1016/j.foot.2017.05.006.
29. Nery C, Lemos AVKC, Raduan F, Mansur NSB, Baumfeld D. Combined spring and deltoid
ligament repair in adult-acquired flatfoot. Foot Ankle Int. 2018;39(8):903–7. https://doi.
org/10.1177/1071100718770132.
30. Brodell JD, MacDonald A, Perkins JA, Deland JT, Oh I. Deltoid-spring ligament reconstruc-
tion in adult acquired flatfoot deformity with medial peritalar instability. Foot Ankle Int.
31. Heyes G, Swanton E, Vosoughi AR, Mason LW, Molloy AP. Comparative study of spring liga-
ment reconstructions using either hamstring allograft or synthetic ligament augmentation. Foot
32. Taylor R, Sammarco VJ. Minimizing the role of fusion in the rigid flatfoot. Foot Ankle Clin.
33. Friedman MA, Draganich LF, Toolan B, Brage ME. The effects of adult acquired flatfoot
deformity on tibiotalar joint contact characteristics. Foot Ankle Int. 2001;22(3):241–6. https://
doi.org/10.1177/107110070102200312.
34. Miniaci-Coxhead SL, Weisenthal B, Ketz JP, Flemister AS. Incidence and radiographic predic-
tors of valgus tibiotalar tilt after hindfoot fusion. Foot Ankle Int. 2017;38(5):519–25. https://
doi.org/10.1177/1071100717690439.
35. Song SJ, Lee S, O'Malley MJ, Otis JC, Sung IH, Deland JT. Deltoid ligament strain after cor-
rection of acquired flatfoot deformity by triple arthrodesis. Foot Ankle Int. 2000;21(7):573–7.
36. Deland JT, de Asla RJ, Segal A. Reconstruction of the chronically failed deltoid ligament: a new
technique. Foot Ankle Int. 2004;25(11):795–9. https://doi.org/10.1177/107110070402501107.
37. Haddad SL, Dedhia S, Ren Y, Rotstein J, Zhang LQ. Deltoid ligament reconstruction: a
novel technique with biomechanical analysis. Foot Ankle Int. 2010;31(7):639–51. https://doi.
org/10.3113/FAI.2010.0639.
38. Jeng CL, Bluman EM, Myerson MS. Minimally invasive deltoid ligament reconstruction
for stage IV flatfoot deformity. Foot Ankle Int. 2011;32(1):21–30. https://doi.org/10.3113/
FAI.2011.0021.
39. Cromeens BP, Kirchhoff CA, Patterson RM, et al. An attachment-based description of the
medial collateral and spring ligament complexes. Foot Ankle Int. 2015;36(6):710–21. https://
doi.org/10.1177/1071100715572221.
40. Persaud S, Hentges MJ, Catanzariti AR. Occurrence of lateral ankle ligament disease with
stage 2 to 3 adult-acquired flatfoot deformity confirmed via magnetic resonance imag-
ing: a retrospective study. J Foot Ankle Surg. 2019;58(2):243–7. https://doi.org/10.1053/j.
jfas.2018.08.030.
41. Dodd A, Daniels TR. Total ankle replacement in the presence of talar varus or valgus deformi-
ties. Foot Ankle Clin. 2017;22(2):277–300. https://doi.org/10.1016/j.fcl.2017.01.002.
Cavus Foot
1 Introduction
The cavus foot represents an incredibly complex spectrum of deformities all caused
by muscle imbalance leading to structural changes in the foot. There is no classic
presentation of the cavus foot, since cavus, cavovarus, cavoadductovarus, and cavo-
equinovarus are all different types of structural deformity associated with muscle
imbalance and soft tissue contracture [1–5]. To add to this, there is a very wide and
varied spectrum of the severity of deformity even within each of the above subtypes.
There are references to the mild or subtle cavus foot in the literature, those which
appear to be idiopathic [6–12] and those which we easily recognize as being quite
severe. The keys to understanding all of these deformities are based on some very
straightforward principles, since treatment is determined by recognition of the flex-
ibility or rigidity of the hindfoot, midfoot, and forefoot, the structural changes of the
foot, the apex of each of these separate deformities, and the inherent muscle imbal-
ance which is the cause of every neurological cavus foot deformity [13–15]. The
management of the cavus foot does not have to be complicated provided one under-
stands this muscle imbalance and the role of correction in multiple planes at the
apex of each structural deformity. One should not rely on correction of deformity
with osteotomy or arthrodesis alone since balancing the muscle forces with tendon
transfer(s) should be considered fundamental for many procedures and in all cases
of neuromuscular cavus deformity [5].
This chapter will focus on the neurological cavus foot deformities, and the prin-
ciples of deformity correction can be summarized here:
M. S. Myerson (*) · S. Li
Department of Orthopaedics, University of Colorado Anschutz Medical Campus,
Aurora, CO, USA
https://www.steps2walk.org

Switzerland AG 2022
568 M. S. Myerson and S. Li
• Tendon transfer(s) must be performed to improve muscle imbalance in neuro-

logical cavus foot.
• A tenotomy of the posterior tibial tendon may be necessary if there is severe
scarring of the foot and ankle.
• A plantar fascia release is routinely performed.
• Osteotomies or arthrodesis must be performed at the apex of deformity.
• A triplanar calcaneal osteotomy may be necessary in addition to hindfoot
arthrodesis.
• Resection of the base of the fifth metatarsal combined with triple or pantalar
arthrodesis is useful to correct fixed midfoot varus deformity.
2 Examination of the Foot
Is the deformity rigid or flexible? How will one use this information? The classic
clinical test of rigidity is the Coleman “block test” where the lateral forefoot and
heel rest on a block of wood, while the plantarflexed first ray is allowed to drop off
the edge of the block [16–18]. If the hindfoot varus remains uncorrected after
removing the plantarflexed first ray as a deforming force, then the hindfoot varus is
considered to be rigid. The challenge to effectively and predictably use this test is
that there is a spectrum to flexibility and rigidity, and it is difficult to know what to
do when the hindfoot partially corrects. While the Coleman block test can tell you
if there is some flexibility, its downfall is that it does not give the examiner a “feel”
for how correctable the hindfoot really is [5]. The Coleman block is not the only
way to assess hindfoot rigidity, and others have suggested maneuvers for evaluating
hindfoot flexibility while the patient is non-weight-bearing. One described method
is performed by placing the patient in a prone position with the knee flexed 90° [19].
In this position, the foot is allowed to move freely without the influence of the first
ray, and hindfoot manipulation is easily performed allowing for determination of
rigidity. We agree that while a test of rigidity while weight-bearing is relevant, it is
not nearly as useful as the “feel” that one obtains when examining the foot in the
seated position. We therefore always perform the examination of the foot by manip-
ulating the heel with the patient in a seated position and the foot dangling from the
exam table. With the foot in equinus, it takes out the effect of any Achilles or gas-
trocnemius contracture as well as the position of the first metatarsal. We believe that
this method gives the examiner a better sense for the amount of retained hindfoot
motion and is easier to perform than the Coleman block test or by having the patient
lie prone [20]. With this method, if the heel is correctable to a valgus position, then,
regardless of what happens to the forefoot, there is still the likelihood that an
arthrodesis can be avoided. If the hindfoot is only partially correctible, then it is our
practice to lean toward arthrodesis rather than trying to “push the limits” of a joint-
sparing procedure. One should also realize that final decision-making regarding
flexibility of the foot can sometimes only be made intraoperatively following medial
soft tissue release. Some surgeons use the Coleman block test to determine whether
Cavus Foot 569
a single dorsal closing wedge osteotomy at the base of the first metatarsal can cor-
rect the varus deformity of the heel, based on a concept that this is a “forefoot-
driven hindfoot varus deformity.” However, there are very no neurologic cavovarus
deformities which are caused by a fixed equinus of the first metatarsal in the absence
of muscle imbalance. Secondly, in order to correct a “forefoot-driven hindfoot
varus” deformity with a single first metatarsal osteotomy, the midfoot and hindfoot
must be flexible to allow sufficient derotation, which is very difficult to achieve due
secondary medial and plantar soft tissue contracture. It is a general principle of
deformity correction to commence with the most proximal deformity, and heel
varus is no different where an osteotomy of the calcaneus may be the ideal way to
start. We suggest that if one wants to start by correcting the first metatarsal plantar
flexion, always check intraoperatively under simulated weight-bearing if the hind-
foot is corrected. If the foot is not able to be reduced under anesthesia during the
surgery, then it is unlikely to do so after surgery.
Standard anteroposterior, oblique, and lateral weight-bearing radiographs of the
foot and ankle should be taken, and often forgotten, but most important, are weight-
bearing radiographs of the ankle [21]. We know that the foot is deformed, but if
deformity, instability, or arthritis of the ankle persists, this will significantly affect
the outcome of treatment. Weight-bearing computerized tomography (WBCT) scan
can give us three-dimensional detailed information of the alignment, structure, bio-
mechanics, and condition of the joints. It is always helpful to quantify the amount
of deformity. For example, on weight-bearing radiographic images, using the calca-
neal pitch angle, Meary’s angle, Hibbs angle, to evaluate pes cavus; using hindfoot
alignment, talonavicular coverage, metatarsus adductus, and Kite’s angle to assess
varus deformities, and on three-dimensional WBCT scan images using foot and
ankle offset (FAO), parameters of peritalar subluxation and the arch index to assess
the general cavovarus deformity [22, 23].
The apex of the deformity, which is nearly always multiplanar, will be very use-
ful to decide where and which procedure(s) need to be performed [24]. The location
of the apex in the sagittal plane will determine whether the deformity is an anterior
(midfoot) or posterior (hindfoot) cavus (or both since there can be more than one
apex). One must plan for correction in the coronal plane as well in particular adduc-
tion and rotational malalignment. The hindfoot alignment view is a very useful
adjunct in radiographic evaluation. It is helpful in measuring the amount of defor-
mity present and can provide an objective gauge of the amount of correction of
hindfoot varus achieved after surgical intervention. When one chooses to use WBCT
scans in helping surgical planning, it is critical to realize that the foot and ankle
offset (FAO) which was developed based on the tripod theory of the foot should not
be used to substitute for the hindfoot alignment view. The FAO is a three-dimensional
parameter which gives the reader a general idea of how well the foot is balanced as
a tripod, but one cannot say that a patient with a higher negative FAO value has a
more severe cavus or varus deformity than another patient with a lower negative
FAO value. Several recent publications [25–27] were designed by grouping patients
using FAO as a direct substitution for the assessment of hindfoot alignment which
is misleading. In treating a cavus deformity, one must see the whole picture, that is,
you cannot see the forest for the trees, since one should address each individual
problem by taking the whole picture apart and then reassembling it. One can use the
peritalar subluxation assessment in the subtalar, talonavicular, calcaneocuboid, and
ankle joints and the relationship between the first and the fifth metatarsal and the
floor to help with preoperative planning [23]. Ideally, after derotation around those
joints, the declination of the first metatarsal and the height of the medial cuneiform
to the floor should decrease postoperatively, and the position and height of the fifth
metatarsal from the floor should increase postoperatively.
3 Approach to Correction
As the heel moves into varus, the first metatarsal has to compensate for the hindfoot
position by dropping into equinus, in order to maintain the forefoot in a plantigrade
position. This equinus position of the first metatarsal is perpetuated and aggravated
by contracture of the plantar fascia, and in cases where there is weakness of the
anterior tibial muscle as in Charcot-Marie-Tooth (CMT) disease, the equinus of the
first metatarsal is worsened. With increasing contracture of the plantar fascia, and in
particular as a result of atrophy of the intrinsic muscles of the foot when associated
with CMT, the forefoot deformity worsens. In neurological cavus deformity, there
is frequently an imbalance between the peroneus longus and the anterior tibial mus-
cles, and the posterior tibial muscle is always stronger than the peroneus brevis
muscle in more severe deformities, with a variable degree of contracture of the
gastrocnemius and soleus muscles present. Understanding this will be very useful
for planning the structural changes in the foot [28]. In order to successfully correct
structural deformity, it is useful to perform a release of any contracted soft tissue,
including the plantar fascia release, which can be the initial procedure followed by
preparation of the posterior tibial tendon for transfer, since the calcaneus is difficult
to move with osteotomy if the plantar fascia remains contracted. The sagittal apex
is either in the midfoot or the hindfoot or both and will determine the location as
well as the type of the procedure. Recognize that whatever is done to correct one
plane of deformity will have an impact on the rest of the foot. For example, as the
hindfoot varus is corrected through eversion and pronation, the medial forefoot
equinus worsens. The medial column of the foot is always more plantarflexed than
the lateral column, but the lateral column tends to be more fixed, rotated, and slightly
adducted. Thus, when correcting the plantarflexion of the first ray, rotational
malalignment must also be addressed or else the midfoot will be left in a supinated
position with continued overload of the lateral column. The assessment of muscle
strength is important to plan the tendon balancing which will be a necessary part of
the correction. While this is understood in the setting of the joint-sparing procedures
for a flexible deformity, it has often been overlooked when treating a rigid defor-
mity. It has been our observation that without proper soft tissue balancing, bony
procedures alone are likely to fail in the long run [4].
Cavus Foot 571
One can simplistically approach deformity correction based on the flexibility of

the foot and the severity of the deformity [29]. Although it is difficult to quantify
flexibility, it implies that the subtalar joint is easily correctable to neutral, there is
mild forefoot equinus deformity, and no fixed adductovarus. For a flexible foot asso-
ciated with a mild deformity, we perform a combination of a plantar fascia release,
a calcaneal osteotomy, a transfer of the peroneus longus to brevis, and then what-
ever else is necessary to complete the correction, which may have to include a dor-
sal closing wedge osteotomy of the first metatarsal, an arthrodesis or the first TMT
joint, or a dorsal closing wedge osteotomy of the medial cuneiform. There is often
an associated equinus deformity, and the correction is performed with either a per-
cutaneous Achilles lengthening or a gastrocnemius recession depending on the
nature of the contracture. For a moderate deformity, we perform the same sequence
of procedures above but recognize that the midfoot deformity is greater with an
increased cavus of the medial part of the midfoot as well as increased rotation of the
lateral foot which creates a much greater load along the entire length of the fifth
metatarsal. If present, adductovarus is mild, and a transfer of the posterior tibial
tendon is unusual in these cases unless the cavus is caused by CMT disease associ-
ated with a drop foot, in which case the posterior tibial tendon is transferred through
the interosseous membrane to the midfoot. The most important aspect of correcting
a moderate deformity is a midfoot osteotomy-arthrodesis. For severe deformity cor-
rection, the sequence of steps includes the same approach as outlined above but
performed with one or another modification of a triple arthrodesis and additional
procedures which are necessary including peroneus brevis repair and a lateral ankle
ligament reconstruction. It is easy to distinguish between a mild and a severe defor-
mity, but the difficulty lies in the approach to correct a moderate deformity where
the foot appears to be correctible on a Coleman block test, the hindfoot is flexible
on examination, and one tries to avoid an arthrodesis leading to less-than-ideal
results.
3.1 The Plantar Fascia Release
Correcting the malposition of the calcaneus is difficult without first releasing the
plantar fascia, and this is part of the overall soft tissue releases medially which
include the posterior tibial tendon transfer. This simplest fasciotomy is done percu-
taneously through a 1 cm medial longitudinal incision adjacent to the heel, at the
junction of the dorsal and plantar skin (Fig. 1). Although uncommon, this may lead
to a small area of numbness on the medial aspect of the heel pad but of no clinical
relevance. Following the skin incision, a pair of scissors is inserted to bluntly push
above and below the fascia to separate and to locate the fascia which will also avoid
any injury to the branch of the lateral plantar nerve. The fascia is then cut with scis-
sors by advancing the scissors without a cutting motion, but simply allowing the
scissors to split the fascia until both the medial and lateral bands are completely
released. For severe adductovarus deformity, the fascia of the abductor hallucis
Fig. 1 Plantar fascia

release
tendon also must be completely released. This release must be very carefully
planned because multiple incisions cannot be used for the posterior tibial tendon
transfer, the plantar fascia release, the abductor hallucis tendon release, and the
talonavicular joint capsule and the spring ligament release. By carefully planning,
these procedures can be completed through the same medial approach.
3.2 Calcaneus Osteotomy
The calcaneus osteotomy is a very utilitarian procedure to correct a cavus foot and,
depending on the magnitude of the deformity, is always required in one form or
another. When correcting a very severe hindfoot varus deformity, in addition to a
subtalar or triple arthrodesis, a triplanar calcaneus osteotomy can be added. This
triplane osteotomy corrects the varus with a laterally based wedge and then moves
the tuberosity laterally as well as cephalad [30]. One has to be careful with the
extent of the lateral shift of the calcaneus, since this can cause tarsal tunnel syn-
drome [31]. If the varus is severe, we think that a prophylactic release of the tarsal
tunnel is useful and can be performed by extending the medial incision for the
exposure of the posterior tibial tendon. At times one can perform the osteotomy and
then palpate the skin on the medial side of the foot to determine if it remains soft,
and if so a release may not be necessary.
The incision for the calcaneal osteotomy varies according to the type of procedure
performed (Fig. 2a). If an osteotomy alone is performed, then a shorter incision is
made directly inferior to the peroneal tendons. Invariably however, the calcaneal
Cavus Foot 573
osteotomy often needs to be performed with additional lateral procedures, including

repair of the peroneal tendon(s), reconstruction of lateral ankle instability, a peroneus
longus-to-brevis tendon transfer, and a cuboid osteotomy. For these cases, the incision
is simply extended posteriorly along the axis of the peroneal tendons behind the fibula.
The incision is deepened through subcutaneous tissue in the plane between the
peroneal tendon and the sural nerve. The peroneal tendon repair or transfer is per-
formed before the osteotomy (Fig. 2b). The nerve can be retracted either superiorly
or inferiorly, depending on its position. The periosteum needs to be elevated over a
broad area, because a wedge of bone is going to be removed. Two small, curved
retractors are used on either side of the incision to expose the entire lateral tuberos-
ity. A saw should be used to make the wedge cuts, with the first cut perpendicular to
the axis of the calcaneus at a 45-degree angle to the tuberosity and the second at an
angle of approximately 20 degrees, but this depends on the size of the wedge. It is
far easier to start out with a smaller wedge and then remove more bone if the cor-
rection is not sufficient. The osteotomy rarely closes down perfectly at this time, so
additional perforation of the calcaneus typically is necessary to permit it to close
down smoothly. Depending on the deformity, the calcaneus is moved in two or three
planes as described above (Fig. 2c-e). The valgus closing wedge osteotomy consti-
tutes the first plane. The tuberosity is then shifted laterally by 8–10 mm, and cepha-
lad movement is the third plane which is added according to the pitch angle of the
calcaneus. We use two guide pins to hold the calcaneus in the corrected position.
The first guide pin is inserted centrally into the body of the posterior tuberosity,
which can then be manipulated into the corrected position. While the guide pin is
being held and the heel held in the desired position, a second guide pin is introduced
for screw fixation. It is best to insert the screw from slightly posterior lateral to
slightly anterior and medial to gain maximal compression. Tamping the overhang-
ing inferior ledge of the bone is unnecessary.
3.3 Tendon Transfers
Cavovarus deformities tend to be both dynamic and progressive, and only a well-
balanced foot will be stable over time. Soft tissue balancing contributes to the long-
term success of the bony structural correction, as it will remove the major deforming
forces going forward [32]. In cavovarus deformities the deforming forces are the
posterior tibial and the peroneus longus tendons, which overpower the peroneus
brevis and anterior tibial tendon, respectively. This imbalance leads to a varus hind-
foot and a pronated and plantarflexed medial column. However, this muscle imbal-
ance is always a little different in each patient, and variations in muscle strength will
always be encountered, and therefore, evaluation of their relative differences is
important. The peroneus longus-to-brevis transfer is an important part of correction,
and without release of the force of the peroneus longus, recurrence of first metatar-
sal plantarflexion will occur even if a midfoot or triple arthrodesis is performed. We
transfer the peroneus longus to the weakened peroneus brevis to increase eversion
a b
c d
Fig. 2 (a) An extensile incision is used laterally to approach the calcaneus, the peroneal tendon
transfer, and also expose the cuboid for osteotomy. (b) The peroneus longus-to-brevis tendon
transfer is performed and the calcaneal osteotomy marked out with electrocautery. (c) The calca-
neus osteotomy is performed as a triplane shift. A wedge is removed laterally, (d) and the calca-
neus shifted cephalad and fixed with a fully threaded screw. (e) Note the lateral shift of the
tuberosity
Cavus Foot 575
strength. Ideally, this procedure is done in younger patients and even in children to
achieve maximal advantage or when the foot is more flexible. One must be careful
using this transfer to augment the eversion strength when a posterior tibial tendon
transfer is performed simultaneously in the absence of a hindfoot arthrodesis. In this
situation, one can cause an irreversible flatfoot deformity. If the peroneus brevis
tendon is scarred, torn, or absent, the longus tendon can still be transferred to the
stump of the base of the brevis tendon into the fifth metatarsal. This is the first ten-
don transfer to be performed, and we usually do it before commencing with the
calcaneus osteotomy. The technique for this transfer involves pulling the longus
tendon distally while suturing both tendons together before cutting the longus to
achieve the appropriate tension. If the longus is cut before suture, it is more difficult
to find the correct resting tension for the transfer. Additional tendons to consider for
transfer are the anterior tibial tendon, the extensor hallucis longus, and extensor
digitorum longus. Even though the anterior tibial tendon is overpowered by the
peroneus longus, it still has some strength and contributes to the deformity by creat-
ing a dorsal apex in the midfoot. In certain deformities, without release and transfer
of the tendon, it may be impossible to unwind the foot adequately for correction.
A typical tendon transfer for the cavus foot is to use the posterior tibial tendon (PTT)
and place it in a position that is beneficial for function and stability of both the foot and
the ankle. There are two reasons to perform a tendon transfer: the first is to remove a
deforming force, and the second is to gain power in a direction that is missing. Muscle
power of any commonly transferred tendon in the cavus foot, particularly the posterior
tibial, is variable, and when the posterior tibial muscle is weak, surgeons commonly do
not perform a transfer judging it to lack sufficient power for transfer. However, there is
always some power left in the muscle that will overcome its antagonist and gradually
lead to recurrence of deformity, and we perform a posterior tibial tendon transfer rou-
tinely, regardless of the type of bony surgery chosen. If not transferred, an arthrodesis
will eventually fail since overpull by the posterior tibial tendon will cause adduction at
the level of the talonavicular joint if a midfoot arthrodesis is planned or at the naviculo-
cuneiform joint if a triple is done. In either setting, a new apex of deformity is created
by the intact insertion of the tendon. We try to use whatever tendon is available and, in
particular, whichever muscle is a deforming force on the foot or ankle. This applies to
the extensor hallux longus, the extensor digital longus, the posterior tibial tendon, the
peroneus longus, and any other tendon that may be used to correct deformity. The prin-
ciples of tendon transfer are similar to those performed for paralytic deformities; how-
ever, the incisions must be planned more carefully when calcaneal and midfoot
osteotomies are performed simultaneously. We prefer not to use an interference screw
or bone suture anchor to secure the posterior tibial tendon to the midfoot, but use a
broad rubber button which is used over a gauze pad. We use the syringe top from a 20
or 30 syringe and then take off the rubber cap and perforate it with two clamps to make
a hole and then pass sutures attached to the posterior tibial tendon transfer through the
rubber cap which are then tied over a gauze pad on the under surface of the foot.
3.4 Midfoot Osteotomy-Arthrodesis
Midfoot osteotomy and arthrodesis are ideally suited for a deformity where the apex
is located distal to the transverse tarsal joint. A triple arthrodesis will not correct the
forefoot and midfoot present in this deformity and is therefore the incorrect proce-
dure in this situation. For so many moderate to severe deformities, rigid or flexible,
one can perform correction with soft tissue procedures, a triplanar osteotomy of the
calcaneus, an osteotomy through the cuneiforms and cuboid, or an arthrodesis of the
naviculocuneiform joints and an osteotomy of the cuboid (Fig. 3). Concerns about
wound healing, nonunion, and technical difficulty of the operation have led sur-
geons away from midfoot arthrodesis, but one cannot correct the forefoot only with
an osteotomy of the first metatarsal since this is at a point distal to the apex and will
only create a banana shape to the medial forefoot.
Several techniques for dorsal wedge osteotomy have been described including
Jahss [33] who performed the procedure at the level of the tarsometatarsal (TMT)
joints and Cole [34] and Jappas [35] who performed correction at the naviculocunei-
form/cuboid joints [36]. Our preferred technique is similar to that proposed by Cole,
since this provides correction at the apex of the deformity, and it allows for multipla-
nar correction including the plantarflexion and adductus. The midfoot arthrodesis
must be performed with a release of the plantar fascia. An extensile dorsal midline
incision from the ankle to the mid-metatarsal is made. One should not compromise
wound healing by limiting the length of the incision, because skin retraction and
wound dehiscence are potential risks with a shorter incision. The superficial pero-
neal nerve is retracted laterally, and the deep peroneal nerve and dorsalis pedis artery
are elevated via a subperiosteal plane and retracted medially followed by tenotomy
of the extensor hallucis brevis tendon if necessary, to visualize the midfoot. The
apex of the deformity is identified under fluoroscopy, and an electrocautery is used
to mark out the wedge of bone which is removed with a saw (Fig. 4). Predicting the
size of the wedge is not easy, so we always begin with a small amount of bone resec-
tion and then gradually increase this as necessary for correction. The entire osteot-
omy-arthrodesis of the midfoot and cuboid can be performed through one dorsal
incision, but this requires a lot of retraction laterally to visualize the cuboid. We will
frequently use two incisions to approach correction, the first one dorsally and the
second by extending the incision used for the calcaneus osteotomy distally to the
fifth metatarsal. In this way the cuboid can be very easily visualized and cut. It is rare
that the wedge correction can be obtained with a single bone cut, because the first
metatarsal declination is always more depressed than the fifth, and the wedge is
biplanar, with more bone removed from the dorsal than from the lateral midfoot. It
is very important to understand that one cannot remove a medially based wedge
which will cause or worsen any adductus deformity. The wedge is therefore based
dorsally toward the middle and medial cuneiform but tapered laterally into the
cuboid where no wedge is removed. However, more of a dorsal wedge will need to
be removed medially than laterally – the medial correction is achieved mostly by
dorsiflexion through the wedge resection, whereas the lateral correction through the
cuboid is achieved more by dorsal translation and rotation. A very useful technique
Cavus Foot 577
b c
d e
Fig. 3 (a) The wedges are marked out here to illustrate the size and orientation from the navicular
cuneiform joint, the cuboid, and calcaneus. It is not always necessary to remove a wedge from the
cuboid, and a vertical osteotomy in the center of the cuboid with dorsal translation may be suffi-
cient. (b, c) The location and extent of the wedge from the naviculocuneiform joints and the cuboid
is illustrated. Note the plantar fasciotomy and the position of the calcaneus tuberosity. (d) A key
part of the correction of the midfoot deformity is to push up under the base of the fifth metatarsal
and cuboid in order to derotate the supination of the midfoot. (e) Final fixation is demonstrated
a b
c d
e f
Fig. 4 (a, b) This is a partially rigid deformity associated with Charcot-Marie-Tooth disease. (c)
Following the plantar fascia release and the harvest of the posterior tibial tendon for transfer, the
lateral incision is made for calcaneal osteotomy and peroneus longus-to-brevis transfer. (d). The
triplane calcaneal osteotomy is performed and shifted laterally and cephalad. (e, f) The midfoot is
exposed, and a guide pin is inserted across marking out the osteotomy both clinically and under
fluoroscopy to ensure that the osteotomy is performed in the center of the naviculocuneiform joint
and across into the cuboid at the correct level. (g) Following the osteotomy and fixation with 3 mm
pins, a drill hole is made to pass the posterior tibial tendon from dorsal to plantar, in this case
through the medial edge of the cuboid. (h, i) The posterior tibial tendon is secured on the plantar
surface of the foot over soft tissue bolster and a rubber stopper from a 30 mL syringe. (j) Note the
correction obtained with the naviculocuneiform arthrodesis, the dorsal translation of the cuneiform
on the navicular, and the triplanar calcaneal osteotomy
Cavus Foot 579
g h
i j
Fig. 4 (continued)
now is to close the wedge but add additional dorsal translation of the forefoot. This
can usually be done, but depends on the plantar soft tissue contracture, and the size
of the wedge resected. More dorsal translation should be obtained medially, but this
depends on the severity and location of the equinus. This step will significantly
reduce the residual forefoot deformity and decrease the likelihood of metatarsalgia
(Fig. 5). Because the first metatarsal declination is always more depressed than the
fifth, the wedge is biplanar, with more bone removed from the dorsal than from the
lateral midfoot. Also note that one should not try to remove a huge wedge medially
in order to elevate the first metatarsal since this will unnecessarily shorten the foot,
and it is easier to perform a double osteotomy, one in the midfoot and an additional
osteotomy of the first metatarsal. If the latter is performed with a long oblique wedge
instead of a vertical wedge, the length of the metatarsal can also be preserved. Be
careful of the location of the anterior tibial tendon which must be retracted out of the
way of the excursion of the saw blade. If adductus needs to be corrected in addition
to the cavus, a biplanar correction is achieved by resecting more bone laterally, in
a b
Fig. 5 (a) Following the biplanar osteotomy, an alternative technique for closure of the osteotomy
is to adjust the distal aspect of the midfoot which is pushed dorsally. (b) The thumb on the right
hand is pushing down on the navicular, while the forefoot and midfoot are elevated. Bone contact
with this elevation is quite adequate. (c) Following fixation, one can appreciate the dorsal transla-
tion of the cuneiforms on the navicular which simultaneously elevates the forefoot to correct
the equinus
Cavus Foot 581
particular through the cuboid. The osteotomy cut is shaped such that the medial limb
forms one aspect of a wedge that is 8 mm in diameter and at a 15–20-degree angle
to the dorsal plane of the midfoot. The first lateral osteotomy cut is made extending
the saw cut toward the cuboid from the middle or lateral cuneiform, and then the
second osteotomy cut is made at a much smaller angle so that the apex is in the
cuboid without removing much of the cuboid at all. It is far easier to perform the
lateral correction by dorsally translating the cuboid and then rotating it slightly to
elevate the base of the fifth metatarsal.
Once the midfoot has been corrected through dorsiflexion, elevation, and translation
as well as lateral column rotation, good bony apposition can be achieved with any avail-
able fixation (Fig. 6). Typically, we use multiple 3 mm Steinmann pins. Using pins in
a c d
Fig. 6 Note the preoperative non-weight-bearing X-ray (a, b) of this severely deformed foot asso-
ciated with Charcot-Marie-Tooth disease. The hindfoot and the midfoot were quite rigid. Note the
severely supinated midfoot with a dorsal apex at the naviculocuneiform joint. The subtalar joint is
open, and in varus, and the fifth metatarsal is close to the floor with a marked change in the arch
height index. (c, d) Even though these are not weight-bearing X-rays, it is easy to see the marked
change in appearance of all of the features of the cavus foot in the postoperative X-ray. The subta-
lar joint is no longer in varus, and the arch height index (the ratio between the height of the medial
cuneiform and fifth metatarsal to the floor) has been completely restored. On the anteroposterior
review, the talus-first metatarsal angle, the adductus, and supination have all been corrected
this location is easier than plates, staples or screws because of the plane of the osteot-
omy and the small bone segments between each articulation. The pins are inserted from
the medial and lateral portion of the foot, from distal to proximal, and then removed at
4–6 weeks in children and 8 weeks in adults, once ambulation begins. Once the oste-
otomy has been stabilized, the tendon transfer(s) can be completed. We typically place
the posterior tibial tendon into the lateral cuneiform, although if severe adductus is
present and some anterior tibial muscle power is present, we will insert it into the cuboid.
3.5 Correction of Forefoot Equinus
As the heel is brought into valgus, increased pronation of the forefoot occurs, with an
increased plantar flexion of the first metatarsal which is counterproductive in a cavus
foot. For a flexible deformity, the worsening of the first metatarsal equinus occurs
commonly but may also be required following a midfoot osteotomy-arthrodesis or
even a triple arthrodesis. One must understand that the apex of the cavus deformity is
never in the first metatarsal and is either at the first TMT joint, the cuneiform, the
naviculocuneiform (NC), or the talonavicular (TN) joint. Why then is a dorsiflexion
osteotomy of the first metatarsal so frequently performed? Although this is an easy
procedure to perform, and intentionally elevates the first metatarsal to correct the
distal overload, it is technically incorrect. It is our preference therefore to perform the
osteotomy or arthrodesis directly at the apex of the deformity which will either be the
first TMT joint, the medial cuneiform, or the NC joint, and a first metatarsal osteot-
omy will be used for convenience purposes only for minor deformities or after hind-
foot correction. One should consider the balance of the foot with the combination of
a calcaneal osteotomy, a peroneus longus-to-brevis tendon transfer, and a first meta-
tarsal osteotomy. With the peroneus longus tendon transfer, the plantar flexion of the
first ray is clearly weakened, and this weakening has to be considered when the oste-
otomy is performed to prevent overcorrection with ultimate shift of weight to the
second metatarsal. Another issue is whether the forefoot cavus deformity is global or
limited to one or two metatarsals. More frequently, the first metatarsal alone is in
equinus, so this single forefoot osteotomy is most commonly used.
An incision is made on the dorsal medial aspect of the first metatarsal extending
to the metatarsal cuneiform joint. The periosteum is stripped, and the extensor hal-
lucis longus tendon is retracted laterally. The osteotomy cut is made 1 cm distal to
the articulation in the metaphyseal bone with an oblique saw cut on the metatarsal
from distal and dorsal to proximal and plantar. It is useful to preserve the plantar
cortex to maintain stability, although one can even gain some length by allowing the
metatarsal to shift distally before fixation. Once the bone wedge has been resected,
the first metatarsal is pushed up dorsally, and the plantar surface of the forefoot is
palpated with the foot in maximal dorsiflexion. More bone can be shaved through
the osteotomy itself until an appropriate amount of the wedge has been resected.
The easiest way to secure this osteotomy is with a vertically inserted screw which is
why one uses a long oblique osteotomy cut. If the bone fractures with insertion of
the screw, a two-hole plate is used. Frequently, the first metatarsal osteotomy is
Cavus Foot 583
performed in conjunction with an arthrodesis of the hallux interphalangeal joint and

transfer of the extensor hallux longus tendon for correction of a claw hallux. In this
situation, the extensor hallux longus should be cut first, the dorsal capsule of the
hallux metatarsophalangeal joint released, and then the first metatarsal osteotomy
performed. At the completion of the osteotomy, the extensor hallux longus can be
transferred into the first metatarsal or the midfoot (which is our preference).
3.6 Triple Arthrodesis
The triple arthrodesis is a safe and reliable option for the management of severe and
rigid cavus regardless of the subtype of deformity. Triple arthrodesis has not had
enough focus in the recent literature. Older reports [37, 38] demonstrated poor long-
term outcomes associated with degenerative changes of the ankle and joints of the
midfoot. These deformities were caused by muscle imbalance since many feet that
initially had had satisfactory alignment and deformity developed as a result of inade-
quate muscle balance at the time of the triple arthrodesis. The posterior tibial tendon
inserts distal to the talonavicular joint, and unless it is transferred, the medial foot
deformity will gradually recur, with onset of adductovarus. Therefore, if a triple
arthrodesis is thought to be the procedure of choice, it should be performed with
appropriate transfer of the posterior tibial tendon, as well as additional tendon trans-
fers as required. We have previously reported that one cannot rely on a triple arthrod-
esis to correct as well as maintain correction of deformity secondary to a neuromuscular
disease process [4]. As noted above, if performed in isolation, a triple arthrodesis may
fail since the arthrodesis must be accompanied by additional procedures to address the
muscle imbalance and soft tissue contractures. There are several techniques of triple
arthrodesis described in the literature. The original description by Hoke utilized a lat-
eral incision and fused only the subtalar and talonavicular joints. He described making
a cut through the neck of the talus and removing the head and neck for preparation for
arthrodesis. The neck portion had to be shortened because when the equinus deformity
was corrected with dorsiflexion, the head and neck piece was too long to go back in
[39]. Ryerson’s technique involves taking a wedge from the transverse tarsal joint for
correction of transverse or sagittal plane deformity [40]. Lambrinudi’s technique [41]
creates a notch in the posteroinferior portion of the navicular and then an oblique cut
through the talar head. The cut surface of the neck of the talus is then plantarflexed
down to the anterior process of the calcaneus and wedged under the notch that was
made in the navicular. The angle produced posteriorly by the flexed talus on the calca-
neus is filled with the bone graft piece obtained from the talar head and neck [41].
The Siffert “beak” triple arthrodesis [42] was described specifically for correc-
tion of the cavus deformity. In this technique, the dorsal cortex of the navicular is
removed. An osteotomy of the anterior calcaneus and talar head and neck are per-
formed in order to create the talar “beak.” The forefoot is then displaced downward,
and the navicular is locked under the talar “beak” for correction of the deformity.
Despite its appearance, this arthrodesis actually gains length of the foot. It works
extremely well when the apex is dorsal, directly at the talonavicular joint.
Our method of triple arthrodesis for the cavus foot is to utilize a single lateral
incision to the three joints, although one can use the medial incision used for the
posterior tibial tendon transfer for more visualization of the talonavicular joint.
Furthermore, there is frequently a separate dorsal incision used for the posterior
tibial tendon transfer, and the dorsal surface of the talonavicular joint is visible and
can be approached under more direct vision. The lateral incision is begun at the tip
of the fibula and extended distally toward the base of the fifth metatarsal long
enough to expose the calcaneocuboid (CC) joint. It is important to watch for the
sural nerve during the dissection, and it should be retracted plantarward along with
the peroneal tendons. The extensor digitorum brevis is retracted dorsally, and the
soft tissues are elevated sharply from the floor of the sinus tarsi. The sinus tarsi is
then distracted with a toothed laminar spreader allowing visualization of the inter-
osseous ligament, which can be sharply divided and removed with a rongeur. This
allows access to the posterior and middle facets of the subtalar joint. Preparation of
the subtalar joint is begun by removing the cartilage, and then a curved osteotome
is used to rigorously “fish-scale” the surfaces of the middle and posterior facets.
Next, a large periosteal elevator is used to strip the lateral surfaces of the calcaneus
and cuboid at the level of the calcaneocuboid joint. The peroneal retinaculum is
retracted inferiorly, and a knife is swept vertically through the calcaneocuboid joint
and rotated dorsally through the bifurcate ligament. Preparation of the joint is per-
formed in the same manner as for the subtalar joint. For most severe deformities, the
talonavicular joint is easy to visualize from the lateral approach, and a separate inci-
sion medially is not necessary. After the cartilage is denuded with a chisel, we will
often use a burr in order to break through the subchondral plate while still maintain-
ing the overall shape of the joint. Once all the joints have been prepared, one must
plan the deformity correction which will include a wedge resection of the lateral
subtalar and calcaneocuboid joints and a lateral rotation of the talonavicular joint
(Fig. 7). In more severe cases, a saw can be used to remove a wedge from the
Fig. 7 (a) This is an extremely rigid deformity fixed in equinovarus. The posterior tibial tendon
has been transferred through the interosseous membrane to the anterolateral compartment. (b)
With the foot in adductovarus, it is easy to see the subluxation of Chopart’s joint with both the
talonavicular and calcaneocuboid joint easily visible. (c) The correction is begun with a wedge cut
through the calcaneocuboid joint using a saw. (d) The size of the wedge is approximately 8–10 mm,
which should start on the smaller size and then more bone taken out as needed once the correction
has been done. (e) A wedge has now been removed from the posterior facet of the subtalar joint as
the second step in the sequence of correction. This too is between 8 and 10 mm in diameter at the
base of the wedge. (f) The wedge across the talonavicular joint begins with an angled cut across
the talar head. All of the head is removed as part of this wedge. (g) Following wedge resection of
all three joints, it is easy to see that the forefoot has been corrected and well aligned but the heel
remains in varus. (h) The hindfoot alignment also demonstrates the persistent varus indicating that
more needs to be done to correct this persistent heel deformity. (i) A wedge has now been repeated,
this time by adding a calcaneal osteotomy to the resection of the subtalar joint. Although further
bone removal from the subtalar joint could have been attempted, the joint was coming together
very well, and it was felt to be easier to correct the remaining varus through calcaneal osteotomy.
(j, k) The final appearance of the foot is shown here from the plantar and lateral surface after the
completion of internal fixation for the triple arthrodesis and the posterior tibial tendon transfer to
the dorsocentral aspect of the foot.
Cavus Foot 585
a b
c d
e f
g h
i j
Fig. 7 (continued)
Cavus Foot 587
calcaneocuboid joint across to the talonavicular joint. The position of the heel is
then assessed and corrected at the subtalar joint to approximately 5 degrees of val-
gus. Fixation of the subtalar joint is then performed with a partially threaded large
cannulated screw inserted from the heel but off the weight-bearing surface of the
calcaneus into the body of the talus. The talonavicular joint is not easy to palpate nor
visualize for screw insertion, but one should use two cannulated partially threaded
screws or a single screw and dorsal two-hole plate depending on the quality of the
bone and the purchase and compression achieved by the first screw. The compres-
sion screws are inserted from distal to proximal beginning at the medial tuberosity
of the navicular. It is important to make sure that the screw head sits flush with the
margin of the joint so as not to protrude into the naviculocuneiform joint. Finally,
fixation of the calcaneocuboid joint is performed. The cuboid has a tendency to
subluxate plantarward and if fixed in this position, it will tend to cause lateral col-
umn overload with weight-bearing. It is therefore vital to elevate the lateral forefoot
to make sure that the plantar surface of the cuboid is even with that of the calcaneus
on the lateral fluoroscopic view prior to fixation. The calcaneocuboid joint can be
fixed in an antegrade or retrograde fashion, and we generally use screw(s) placed
across the joint from proximal to distal after creating a lateral notch in the calcaneus
approximately 1 cm proximal to the calcaneocuboid joint in order to recess the
screw head. If screw purchase or compression across the joint is poor, a four-hole
plate can be applied to the dorsolateral surface of the joint for added stability and
compression.
Sometimes, even though the calcaneocuboid joint has been reduced completely,
the rotation of the forefoot is such that the base of the fifth metatarsal is still very
plantar, and in this situation resection of the base of the fifth metatarsal will be
required [43]. In these cases, there is typically a large hard callus under the base of
the fifth metatarsal, and the ostectomy can be done in conjunction with any addi-
tional necessary procedure (Fig. 8). The incision that is used for the calcaneal oste-
otomy, peroneal tendon procedure, or triple arthrodesis is extended, or an additional
incision is made from the base of the fifth metatarsal distally along the course of the
dorsal shaft of the metatarsal. A saw cut is made obliquely in the shaft of the fifth
metatarsal in two planes so that the starting point of the osteotomy is dorsal and
slightly lateral. With this orientation of the osteotomy, no bone prominence remains
on the plantar lateral weight-bearing surface. The metatarsal base is grasped with a
clamp, rotated on its pedicle, and then cut sharply by detaching the short plantar
ligament and the remnant of the attachment of the peroneus brevis tendon. The
peroneus brevis tendon can be detached from the fifth metatarsal and can be left
with its attachment to the adjacent soft tissues, because it is generally nonfunctional
with these more severe deformities. If a peroneus longus-to-brevis tendon transfer
is performed, however, then the longus tendon needs to be securely attached to the
cuboid using a suture anchor for fixation. At the completion of the ostectomy, the
hypertrophic callus needs to be shaved, and it is helpful to soften the hard callus
with a moist sponge before it is cut. Finally, always assess the stability of the ankle,
and if the posterior tibial tendon transfer does not hold the foot stable, then it may
be necessary to add lateral ligament stabilization.
a b
c d
Fig. 8 (a–c) Following fixation of the triple, one should get a sense of the alignment of the foot.
Note here that there’s a large prominence at the base of the fifth metatarsal. This needs to be
addressed since a maximum supination has already been obtained through rotation of the calcaneo-
cuboid joint. Note also the severely torn peroneus brevis tendon, which was split and routed
through the fibula as part of a non-anatomic ankle ligament reconstruction which was necessary in
this case for severe ankle instability. (d, e) The ostectomy is made obliquely at the base of the
metatarsal removing as much as is necessary to address the bone prominence. Note also the split
half of the peroneus brevis tendon attached to the insertion point of the tendon distally. This is not
a problem, since the tendon is easily reattached to the soft tissues adjacent to the base of the
metatarsal
Cavus Foot 589
4 Conclusions
• Rigid deformity is usually treated with a triple arthrodesis although a midfoot

correction in combination with a triplanar calcaneus osteotomy may be sufficient.
• A triple arthrodesis is a good procedure, provided that the foot is correctly bal-
anced with additional osteotomy and tendon transfers.
• Be careful of causing a tarsal tunnel syndrome with correction of the hind-
foot varus.
• Even with a large wedge resection in the midfoot, the foot will usually be longer
and not shorter.
• Persistent and recurrent deformity will occur if soft tissue and muscle balance is
not achieved.
• Posterior tibial tendon transfer and peroneus longus transfer are nearly always
required for correction.
• Soft tissue procedures (such as anterior tibial tendon transfer, plantar fascia
release, Achilles tendon lengthening, gastrocnemius recession) may be necessary.
References
1. Barg A. The cavus foot. Foot Ankle Clin. 2019;24(2):xiii–xiv.

2. Younger AS, Hansen ST Jr. Adult cavovarus foot. J Am Acad Orthop Surg. 2005;13(5):302–15.
3. Chesler SM, Grumbine NA. An examination procedure for cavo-adducto-varus. J Foot Surg.
1979;18(1):1–6.
4. Li S, Myerson MS. Failure of surgical treatment in patients with cavovarus deformity: why
does this happen and how do we approach treatment? Foot Ankle Clin. 2019;24(2):361–70.
5. Li S, Myerson MS. Managing severe foot and ankle deformities in global humanitarian pro-
grams. Foot Ankle Clin. 2020;25(2):183–203.
6. Brewerton DA, Sandifer PH, Sweetnam DR. Idiopathic. Pes Cavus Br Med
J. 1963;2(5358):659–61.
7. Harris N, Stevens M. A cavovarus foot is a predisposing factor for rather than a result of pero-
neus longus tendinopathy. Foot Ankle Int. 2001;22(6):525.
8. Larsen E, Angerman P. Association of ankle instability and foot deformity. Acta Orthop Scand.
1990;61:136–9.
9. Vienne P, Schöniger R, Helmy N, et al. Hindfoot instability in cavovarus deformity: static and
dynamic balancing. Foot Ankle Int. 2007;28:96–102.
10. Fortin PT, Guettler J, Manoli A. 2nd idiopathic cavovarus and lateral ankle instability: recogni-
tion and treatment implications relating to ankle arthritis. Foot Ankle Int. 2002;23:1031–7.
11. Manoli A 2nd, Graham B. The subtle cavus foot, “the underpronator”. Foot Ankle Int.
2005;26:256–63.
12. Di Fabio R, Lispi L, Santorelli FM, et al. Idiopathic pes cavus in adults is not associated with
neurophysiological impairment in the lower limbs. Neurol Sci. 2015;36(12):2287–90. https://
doi.org/10.1007/s10072-015-2334-7.
13. Heron JR. Neurological syndromes associated with pes cavus. Proc R Soc Med. 1969
Mar;62(3):270–1.
14. Nagai MK, Chan G, Guille JT, Kumar SJ, Scavina M, Mackenzie WG. Prevalence of
Charcot-Marie-Tooth disease in patients who have bilateral cavovarus feet. J Pediatr Orthop.
2006;26(4):438–43.
15. Krause FG, Wing KJ, Younger AS. Neuromuscular issues in cavovarus foot. Foot Ankle Clin.
2008;13(2):243–vi.
16. Coleman SS, Chesnut W. A simple test for hindfoot flexibility in the cavovarus foot. Clin
17. Deben SE, Pomeroy GC. Subtle cavus foot: diagnosis and management. J Am Acad Orthop
Surg. 2014;22(8):512–20.
18. Dreher T, Beckmann NA, Wenz W. Surgical treatment of severe cavovarus foot deformity in
Charcot-Marie-Tooth disease. JBJS Essent Surg Tech. 2015;5(2):e11.
19. Price BD, Price CT. A simple demonstration of hindfoot flexibility in the cavovarus foot. J
Pediatr Orthop. 1997;17(1):18–9.
20. Myerson MS. Cavus foot correction. In: Myerson MS, editor. Reconstructive foot and ankle
surgery: management of complications. 2nd ed. Philadelphia: Elsevier; 2010. p. 155–73.
21. Perera A, Guha A. Clinical and radiographic evaluation of the cavus foot: surgical implica-
tions. Foot Ankle Clin. 2013;18(4):619–28.
22. Lintz F, Welck M, Bernasconi A, et al. 3D biometrics for hindfoot alignment using weightbear-
ing CT. Foot Ankle Int. 2017;38(6):684–9.
23. Li S, Myerson MS, Netto CC. Peritalar Subluxation: A Key Finding for Both Cavovarus and
Flatfoot Deformities. Foot Ankle Orthop. 2022;7(1):2473011421S00316.
24. Joseph TN, Myerson MS. Correction of multiplanar hindfoot deformity with osteotomy,
arthrodesis, and internal fixation. Instr Course Lect. 2005;54:269–76.
25. Lintz F, Bernasconi A, Baschet L, et al. Relationship between chronic lateral ankle instability
and hindfoot varus using weight-bearing cone beam computed tomography. Foot Ankle Int.
2019;40(10):1175–81.
26. Lintz F, Mast J, Bernasconi A, et al. 3D, weightbearing topographical study of periprosthetic
cysts and alignment in total ankle replacement. Foot Ankle Int. 2020;41(1):1–9.
27. Zhang JZ, Lintz F, Bernasconi A; Weight Bearing CT International Study Group, Zhang S. 3D
biometrics for hindfoot alignment using weightbearing computed tomography. Foot Ankle Int.
2019;40(6):720–6.
28. Aminian A, Sangeorzan BJ. The anatomy of cavus foot deformity. Foot Ankle Clin.
2008;13(2):191-v.
29. Myerson MS, Myerson CL. Cavus foot: deciding between osteotomy and arthrodesis. Foot
Ankle Clin. 2019;24(2):347–60.
30. Myerson M, editor. Current therapy in foot and ankle surgery. St Louis: Mosby Year
Book; 1993.
31. VanValkenburg S, Hsu RY, Palmer DS, Blankenhorn B, Den Hartog BD, DiGiovanni
CW. Neurologic deficit associated with lateralizing calcaneal osteotomy for cavovarus foot
correction. Foot Ankle Int. 2016;37(10):1106–12.
32. Huber M. What is the role of tendon transfer in the cavus foot? Foot Ankle Clin.
2013;18(4):689–95.
33. Jahss MH. Tarsometatarsal truncated-wedge arthrodesis for pes cavus and equinovarus defor-
mity of the fore part of the foot. J Bone Joint Surg Am. 1980;62(5):713–22.
34. Cole WH. The classic. The treatment of claw-foot. By Wallace H. Cole. 1940. Clin Orthop
Relat Res. 1983;181:3–6.
35. Japas LM. Surgical treatment of pes cavus by tarsal V-osteotomy. Preliminary report. J Bone
Joint Surg Am. 1968;50(5):927–44.
36. Sullivan RJ, Aronow MS. Different faces of the triple arthrodesis. Foot Ankle Clin.
2002;7(1):95–106.
37. Wetmore RS, Drennan JC. Long-term results of triple arthrodesis in Charcot-Marie-Tooth dis-
ease. J Bone Joint Surg Am. 1989;71(3):417–22.
38. Wukich DK, Bowen JR. A long-term study of triple arthrodesis for correction of pes cavovarus
in Charcot-Marie-Tooth disease. J Pediatr Orthop. 1989;9(4):433–7.
39. Hoke M. An operation for stabilizing paralytic feet. J Orthop Surg. 1921;3:494–507.
40. Ryerson EW. Arthrodesing operations on the feet. J Bone Joint Surg. 1923;5:453–71.
Cavus Foot 591
41. Lambrinudi C. New operation on drop-foot. British J Surg. 1927;15:193–200.

42. Siffert RS, Forster RI, Nachamie B. “Beak” triple arthrodesis for correction of severe cavus
deformity. Clin Orthop Relat Res. 1966;45:101–6.
43. Shariff R, Myerson MS, Palmanovich E. Resection of the fifth metatarsal base in the severe
rigid cavovarus foot. Foot Ankle Int. 2014;35(6):558–65.
“Management of Severe Untreated
and Recurrent Clubfoot Deformity
in the Child and Adult”
1 Introduction
The approach to treatment of severe untreated or recurrent clubfoot deformities is

very different in the world where patients are mobile and have access to repeated
return visits for follow-up treatment and where more sophisticated options for grad-
ual correction with external fixation are available [1–4]. While the Ponseti treatment
can be applied to untreated deformity even in older children and young adults [5],
many of these patients do not have the ability to return from rural regions for repeated
casting and bracing following this treatment [1, 6]. The spectrum of these deformi-
ties in children and adults is tremendous, ranging from minor procedures such as an
anterior tibial tendon transfer, tendon transfers with or without osteotomy, to
arthrodesis or even talectomy. The goal of treatment for these severe deformities is
to obtain a plantigrade foot with no likelihood for recurrent deformity. Our extensive
experience with these deformities has been on global humanitarian programs where
we have very limited resources and a lack of availability of implants and where the
needs of patients are quite different from those we as surgeons are accustomed to in
the Western world. This setting will affect decision-making since resorting to a
Ponseti treatment is invariably not possible and prolonged treatments with external
fixation is not practical for these patients. These deformities are so variable that a
simplistic algorithm for surgical treatment is not possible (Fig. 1a, b). There are
those with a fixed equinus and no dorsiflexion of the ankle due to a flat-top talus.
Addressing the foot alone will not correct the deformity and where an anterior clos-
ing wedge osteotomy of the tibia is required in addition to tri-planar correction of
M. S. Myerson (*) · S. Li
Department of Orthopaedics, University of Colorado Anschutz Medical Campus,
Aurora, CO, USA
https://www.steps2walk.org

Switzerland AG 2022
a b
Fig. 1 (a, b) These are multiplanar deformities, and this untreated clubfoot in an adolescent typi-
fies how challenging correction can be. The ankle is in equinus, the heel in varus, and the midfoot
is adducted as well as in cavus. This would correctly be termed an equino-cavo-adductovarus
deformity, and each component of this deformity must be corrected
the foot. In patients with some range of motion of the ankle but an equinus defor-
mity, it may be very difficult to regain dorsiflexion because of severe scarring of the
Achilles tendon which may even be adherent to the skin. Provided that some ankle
range of motion is present, most deformities of the foot no matter how severe can be
corrected with a combination of osteotomies and tendon transfers or arthrodesis, and
a triple arthrodesis would be the procedure of choice. For rigid severe deformities of
the foot and ankle where no motion whatsoever is present, talectomy is preferable.
The indications for talectomy in the setting of an untreated or recurrent club foot
deformity are nowadays uncommon and rarely necessary with the use of modern
external fixation techniques [7, 8]. As noted however, this is not a treatment option
for our patients in rural settings where continuous monitoring of fixation is necessary.
2 Patient Evaluation
Decision-making is based on the mobility of the foot and ankle, the presence of
scarring from prior surgeries, the presence of bilateral deformity, and the overall
needs of the patient. These feet are already small; therefore, anything other than
gradual correction with external fixation will further reduce the foot size, since lat-
eral shortening is always safer and easier than medial lengthening. One has to antic-
ipate a significant leg length discrepancy following talectomy which averages
2.5 cm and approximately 3 cm if a tibiocalcaneal (TC) arthrodesis is performed.
For this reason, a unilateral talectomy must be a last resort. If bilateral deformities
are present, this decision-making is easier since both limbs will be shorter, and leg
length discrepancy will not be a concern [9, 10]. If some albeit limited ankle range
of motion is present and the foot can be passively corrected into neutral, a talectomy
is not indicated since a triple arthrodesis combined with tendon transfers and
“Management of Severe Untreated and Recurrent Clubfoot Deformity in the Child… 595
additional osteotomies can be performed regardless of the magnitude of deformity.

If a flat-top talus is present in the child associated with a fixed equinus deformity
and limited dorsiflexion, it is quite reasonable to perform an anterior closing wedge
osteotomy of the distal tibia to regain dorsiflexion which is similar to the procedure
of anterior distal tibial epiphysiodesis performed in children with residual or recur-
rent equinus deformity [11]. Therefore, it is the magnitude of the equinus deformity,
the associated soft tissue scarring or contracture, and the possibility of ischemia
with an attempt of correction with alternative methods that will determine the need
for a talectomy. Scarring can be quite daunting and will limit the ability to perform
a revision with additional soft tissue release procedures, and if so, one may need to
be versatile with the use of skin Z-plasty due to the medial contracture (Fig. 2).
Bear in mind that active dorsiflexion will rarely be present in these very severe
equinovarus deformities. It is rare that any of the extensor muscles of the foot are
functional, and following any procedure whether arthrodesis (triple, tibiotalocalca-
neal (TTC), or pantalar), although the hindfoot position may be recovered from
equinus to neutral, no active dorsiflexor is present, and a static and dynamic equinus
of the midfoot or forefoot may persist. Equinus of the forefoot is usually not fixed,
but dynamic following correction of the ankle and hindfoot, and generally the foot,
can be passively pushed up into a neutral position. However, the forefoot will drop
back down into equinus. In such cases, a tendon transfer can be used as a dynamic
or static force to help correcting the mid- and forefoot equinus [12].
The same philosophy of muscle rebalancing will apply to correcting the defor-
mity in the midfoot. This is difficult to determine preoperatively due to rigidity of
the contracture, but an effort should be made to try to carefully examine the foot for
function of various muscles since these will determine the need for a tendon transfer.
Transfer of the posterior tibial tendon is indicated if one can demonstrate that
some posterior tibial muscle function remains, in which case the tendon can be
transferred through the interosseous membrane to the dorsum of the foot to provide
a b
Fig. 2 Note the severe fixed equinus deformity in both these feet associated with significant scar-
ring along the posteromedial foot and the length of the Achilles tendon. The scars are thick, hyper-
trophic, and in the skin completely adherent to the Achilles tendon (a, b)
some degree of active dorsiflexion or at least to change its deforming force into a
static dorsiflexion power. Tendon transfer is very difficult to perform in the feet
which have undergone a few prior surgeries. If there is little identifiable posterior
tibial tendon, a tenotomy is more useful. If there is no functioning muscle (either the
anterior or posterior tibial or the peroneus brevis and/or longus) to consider for a
tendon transfer to increase dorsiflexion, then a tenodesis should be considered using
one of the extensor tendons, generally the extensor digitorum longus.
3 Anterior Tibia Closing Wedge Osteotomy
If the equinus deformity cannot be fully corrected due to a flat-top talus but range of
motion in the ankle is however present, one can consider a closing wedge anterior
distal tibial osteotomy. Most of the time, this procedure will be performed in older
adolescents or adults, in which case a combination of screw and plate fixation will
be ideal. The bone cut is made in the metaphysis, leaving enough room in the distal
metaphysis for application of a T-shaped or L-shaped plate. We begin with a small
wedge, approximately 4 mm in diameter, and see how much dorsiflexion is obtained
since dorsiflexion to 10° is preferable. It is important to translate the distal tibia
posteriorly following the wedge resection in order to center the ankle under the tibia
(Fig. 3). If not, the foot will move forward after the wedge resection, which is not
ideal biomechanically. An osteotomy of the fibula is also required, and generally we
will make a small oblique cut on the distal fibula almost at the same level as the
tibial osteotomy. The fibula osteotomy does not require fixation.
A lengthening of the Achilles tendon should be performed before the tibial oste-
otomy which is made through an anterior incision centered over the distal tibia. In
many of these feet, the equinus is difficult to manage because of scarring around the
Achilles tendon posteromedially, which limits the ability to perform a further
lengthening. The Achilles tendon can be scarred, ropelike, and adherent to the skin,
and one has to be careful with the lengthening procedure chosen. Tenotomy is not a
good choice here, since one wants to preserve whatever push-off strength remains
in the Achilles.
Fig. 3 Note the severe equinovarus in this 8-year-old child following three failed attempts at
Ponseti treatment. There was no dorsiflexion associated with a flat-top talus and severe scarring
posteriorly (a–c). A closing wedge osteotomy including both distal tibia and fibula was performed.
Note the size of the wedge (d), and with dorsiflexion of the foot, the distal tibia translated anteri-
orly (e), and the foot and distal tibia needed to be translated posteriorly in order to center the foot
under the tibia (f). The final appearance of the foot is shown following a lateral transfer of the
anterior tibial tendon, the tibia and fibula osteotomy, and a closing wedge osteotomy of the
cuboid (g, h)
b c
d
e f
g h
Fig. 3 (continued)
4 Triple Arthrodesis
This topic is discussed elsewhere in the book (Chap. 26), as well as a brief overview
in the section on the cavus foot (Chap. 26). A triple arthrodesis is an option for cor-
rection of severe equinovarus deformity, but only when range of motion is present
in the ankle. Ideally, one would want the ankle to reach at least a neutral position,
even in the presence of a flat-top talus. Because of the adductovarus of the Chopart
joint and the fixed varus of the subtalar joint, much larger wedges need to be
removed from these joints than one may be accustomed to doing with a more rou-
tine triple arthrodesis (Fig. 4a). The deformities that are amenable to a triple arthrod-
esis vary significantly, but are generally fixed in equinovarus, but with some passive
range of motion of the ankle present (Fig. 4b–e).
Other than a tenotomy of the posterior tibial tendon which may be necessary, no
medial incision is required, and if a tenotomy is performed, we prefer to do it behind
the medial malleolus and not over the medial foot. The procedure is performed in
conjunction with a plantar fascia release and tendon transfers or tenotomies as neces-
sary. The steps for the triple arthrodesis are illustrated here in sequence (Fig. 5). The
b c
d e
Fig. 4 The triple arthrodesis was performed through an extensile lateral incision. Note the large
wedge that was first taken out of the calcaneocuboid and talonavicular joints (a). This patient had
bilateral equinovarus deformities which were treated simultaneously with a plantar fascia release,
a posterior tibial tendon transfer, Achilles lengthening, and a triple arthrodesis (b, c) and the wedge
removed from the calcaneocuboid joint (d). The final plantigrade position of the hindfoot was
accomplished by pushing up under the base of the fifth metatarsal and cuboid in order to elevate
through translation the lateral column of the foot (e)
a b
c d
e f
Fig. 5 The sequence of steps for the triple arthrodesis is illustrated here beginning with an exten-
sile incision (a). Planning for the wedge resection is illustrated noting a large wedge removed from
the subtalar joint and a biplanar wedge removed from the calcaneocuboid and talonavicular joints
with more bone resected laterally and dorsally across the Chopart joints (b–e). Prior to commenc-
ing with fixation, it is important to manipulate the foot into the correct position maintaining hind-
foot valgus and pressure underneath the lateral column of the foot, generally directly under the
cuboid. This dorsal translation of the lateral column is important (f). Note that a calcaneal osteot-
omy may be required in addition to the subtalar arthrodesis. One may have to translate the calca-
neus slightly cephalad to improve the pitch angle as well as laterally if any persistent valgus is
present (g). The options for fixation are presented (h, i)
g h
Fig. 5 (continued)
entire triple arthrodesis procedure should be performed through an extensile lateral

approach beginning at the distal fibula and ending at the base of the fourth metatarsal.
Beginning with the calcaneocuboid joint, a wedge of approximately 8 mm is resected,
followed by debridement of the subtalar joint and then the talonavicular joint. It is
often possible to extend the saw cut on the calcaneocuboid joint directly across the
navicular and the head of the talus, but this may have to be cut separately depending
on the size of the wedge required for correction. Once these wedges have been
removed, it should be quite easy to shift the foot into the correct position. The heel
should be placed in a few degrees of valgus, and there should be no residual pressure
under the lateral border of the foot. The adduction should be completely corrected
with the wedge resection of Chopart joint. A useful tip is to push up under the fifth
metatarsal and cuboid in order to correct the supination deformity across the midfoot.
Screw fixation is preferable, and the size, type, and number of screws are surgeon
preference. Since the medial screw(s) are inserted percutaneously, depending on
access to the navicular, it is sometimes necessary to add a two-hole plate dorsally to
the talonavicular joint to improve stability of fixation of the talonavicular fusion.
5 Talectomy
Talectomy is not by any means a physiologic procedure, but because of the ankylo-
sis that it creates between the tibia and calcaneus and the ability to accept full body
weight, it is a very reasonable procedure despite the limb shortening [7–10, 13].
Most patients are free of pain and fairly functional and ambulate satisfactorily.
Another option is to correct the deformity gradually with an external fixator, which
does maintain limb length; however, the foot is no more functional following cor-
rection of the deformity since rigidity persists (Fig. 6).
A talectomy should only be performed with very specific indications, and
although always associated with severe foot deformity, a rigid ankle often associ-
ated with a flat-top talus is invariably present [10]. Talectomy is rarely performed as
an isolated procedure, since this will only correct a severe equinus deformity of the
ankle and hindfoot and to a lesser extent the changes in the transverse tarsal joint.
Frequently, the adduction deformity of the Chopart joints is too severe to permit
correction without an additional procedure which abducts the foot at the apex of the
deformity, usually the calcaneocuboid joint. In addition to the talectomy and
a b
c d
Fig. 6 This patient was treated on one of the our humanitarian programs with severe bilateral
deformities, a flat-top talus, and no range of motion in either the foot or ankle (a, b). In this case
an Ilizarov fixator was used to gradually correct the deformity with a well-aligned plantigrade foot
at the completion of treatment (c, d). (Case courtesy of Dr. Saad Ilyas, on Steps2Walk humanitar-
ian programming, Lahore Pakistan)
calcaneocuboid wedge arthrodesis, there are further procedures which must be con-
sidered to correct any residual adduction or equinus deformity of the midfoot and
forefoot, as well as balance the soft tissue contracture. These could involve a trans-
fer of the posterior tibial tendon, the anterior tibial tendon, or the peroneus longus
to the peroneus brevis. Rarely, the deformity is in the ankle and hindfoot, and there
is no severe midfoot deformity. In these cases, correction of the equinus deformity
and the hindfoot varus can be addressed with a tibiotalocalcaneal (TTC) arthrodesis.
A decision will need to be made preoperatively and then again intraoperatively
as to whether or not an isolated talectomy will be performed or whether this will be
done in conjunction with a TC or a TC and tibionavicular (TN) arthrodesis [14, 15].
In general, a talectomy without arthrodesis is preferred since the residual motion is
generally painless and functional. The decision is based on stability of the hindfoot
following temporary pin fixation and the age of the patient, since it is very rare that
an arthrodesis is necessary in childhood or even in adolescence. The range of motion
after a talectomy is generally not significant, but it does improve function.
We have found that the anterolateral approach for performing an isolated talec-
tomy is the most versatile, since one has the opportunity to obtain a complete lateral
exposure, extending the incision distally to include the calcaneocuboid joint and the
peroneal tendons as necessary. This extensile approach permits a complete removal
of the talus successfully (Fig. 7). One has to always consider the potential for skin
complications with any approach to correction of these very severe deformities, but
a laterally based incision is not likely to lead to problems as a result of decompres-
sion of the soft tissue contracture following the talectomy. The extensile lateral
approach has to be long, commencing behind the fibula towards the fifth metatarsal.
One can either leave the fibula intact or remove the distal 2 cm for visualization. The
main advantage of the transfibular approach is easy visualization and removal of the
talus and molding of the tibia and calcaneus for an arthrodesis. It is also easy to
mold the anterior tibia and the navicular to include a tibionavicular arthrodesis.
Most importantly, access to the lateral foot for a wedge resection of the calcaneocu-
boid joint can be done with an extensile approach (Fig. 8). When considering a
talectomy without arthrodesis, one can consider an anterior approach to the ankle.
This is more useful for deformities which are predominantly locked in equinus,
without midfoot adductus caused by a rigid contracture medially and which does
not necessitate many additional procedures. By removing the talus from the anterior
approach, both malleoli can be left intact, which may serve to provide some stability
to the periarticular tissues as the calcaneus gradually scars into position. Occasionally,
the anterior approach may lead to impingement between the margins of the malleo-
lus and either the calcaneus or navicular medially and less laterally. If this is the
case, a subsequent secondary procedure may need to be performed with an ostec-
tomy of the offending bone causing the impingement. The one disadvantage of
approaching a talectomy anteriorly is that it is not as easy to remove the talus as
through a lateral approach since the talus has to be cut into pieces with an osteotome
and then gradually removed.
Thick skin flaps should be maintained. If one is certain that a TC arthrodesis will
be performed, then the distal fibula can be resected to gain access to the talectomy
a b
c d
Fig. 7 The sequence of steps for the talectomy is illustrated in a very typical foot with severe rigid
equinovarus, weight-bearing on the dorsal surface of the foot noted by hypertrophy of the dorso-
lateral skin (a). It is not just the magnitude of the deformity of the foot that determines the need for
talectomy but the fixed rigid deformity of the ankle in equinus (b). Following an extensile lateral
approach, the talus is exposed with or without removing the distal 2 cm of the fibula (c–e). Often,
additional wedges need to be removed, one from the calcaneocuboid joint and the other from the
anterior tibia and dorsal surface of the navicular (f). Provisional fixation is performed with can-
nulated guide pins if available (g) and the screw fixation demonstrated after molding the tibia to
the calcaneus and inserting bone graft as noted between the tibia and calcaneus (h)
e f
g h
Fig. 7 (continued)
and preparation of the joint surfaces. All of the ligaments and capsules connecting
the talus to the adjoining bones are divided, trying to avoid any injury to the articu-
lar surfaces, particularly in children. The anterior talofibular ligament is first cut
followed by the calcaneofibular ligament which should be detached as much as pos-
sible off the fibula so as to reattach it at the completion of the procedure if there is
any coronal plane instability. It is generally not possible to maximally invert the foot
and expose the talus without cutting the calcaneofibular ligament. The main liga-
ment that anchors the talus is the talocalcaneal interosseous ligament which is easier
to cut from the lateral approach, thereby freeing up lateral attachments and subse-
quently dislocating the foot to remove the talus. This is not as easy if an anterior
approach is used. After freeing up the lateral ligaments, the foot can be manipulated
into more equinus and varus, and by holding the talus with a large towel clamp, the
medial capsule of the subtalar joint and the deep portion of the deltoid ligament as
well as the posterior ankle and posteromedial calcaneal capsule are cut. A posterior
capsulotomy is easier to perform under direct vision noting however the position of
the flexor hallucis longus and the neurovascular bundle posteromedially. It is impor-
tant to remove the entire talus and not leave any small bone fragments behind, which
can lead to secondary deformity.
The foot should now be quite mobile and can easily reach a neutral position
without any residual equinus or adductovarus. By manipulation the foot is posi-
tioned under the tibia ensuring that there’s no residual equinus nor any tension in the
a b
c d
Fig. 8 This patient was a 26-year-old with a fixed and rigid equinovarus deformity with no motion
in either the ankle or foot (a–d). Note the ostectomy of the terminal fibula (e,1) and the articular
surface of the distal tibia (e, 2), with the osteotome perforating through the interosseous ligament
to lever out the talus (e). Saw cuts were made on the articular surface of the calcaneus, the tibia
across to and including the medial malleolus, and then finally the anterior aspect of the tibia where
it would articulate with the navicular (f–h). A wedge was removed from the calcaneocuboid joint
followed by provisional fixation of the foot (i, j). The final clinical and radiographic appearance of
the foot 5 months following surgery is demonstrated. Note that there is very little limb length
inequality as a result of prior surgery on the contralateral foot (k–n)
e f
g h
Fig. 8 (continued)
i j
k l
m n
Fig. 8 (continued)
posterior ankle capsule. Division of the anterior inferior tibiofibular ligament in the
syndesmosis has been described to widen the ankle mortise and more easily fit the
calcaneus underneath the tibia, but we do not have experience with this step [16]. It
is essential that the foot is positioned correctly, and it should be translated slightly
posteriorly under the tibia. Adequate posterior capsular release needs to be per-
formed in order to move the foot posteriorly. At times this requires additional release
as well as tenotomy of the Achilles tendon if contracture still presents. As the foot
is moved posteriorly, the tip of the medial malleolus will be immediately adjacent
to the navicular and the tip of the fibula just posterior to the calcaneocuboid joint.
The goal is to provide a long lever to the foot by shifting the foot posteriorly to give
mechanical advantage to the gastrocnemius-soleus [17]. Once positioned, the foot
is fixed to the tibia with two 3 mm Steinman pins. If any impingement occurs
between the calcaneus and the fibula and prevents correction, one can remove the tip
of the fibula or the medial malleolus to decrease the jamming. Occasionally, the
tibia will abut against the navicular with the posterior shift of the calcaneus, but in
a child an arthrodesis should be avoided, and to regain a neutral position, the ante-
rior tibia can be shaved with an ostectomy in order to permit slightly more posterior
translation. Slight dorsiflexion and plantarflexion may be possible despite the anky-
losis and can provide some function.
Dorsiflexion may not be possible because the anterior tibia is impinging against
the navicular. The same may occur because of a medially rotated navicular where it
is impinging against the medial malleolus. In either of these situations one has to
trim the anterior distal tibia or the dorsal and medial navicular. Both of these proce-
dures are necessary if one is performing a tibionavicular arthrodesis. The latter pro-
cedure is only occasionally necessary in conjunction with a tibiocalcaneal arthrodesis
and never with an isolated talectomy. The incision is then extended more distally to
the base of the fifth metatarsal and a large wedge removed from the calcaneocuboid
joint. The distal cut can be extended medially to include the navicular as one cut if
a tibionavicular arthrodesis is going to be considered. Once the calcaneocuboid
wedge has been removed, the foot should now assume a perfectly neutral position.
Prior to completing the tendon transfer dorsally, the hindfoot is fixed to the tibia
using two or three 3 mm pins. The one is introduced from the posterior and inferior
calcaneus passing through the anterior cortex of the distal tibia, and the second is
inserted vertically through the calcaneus into the tibia (Fig. 9).
6 Additional Procedures
An equinus deformity of the forefoot may still persist following the talectomy, and
if present, it is helpful to stabilize the deformity with a tenodesis using the extensor
tendons. A 2 cm incision is made over the midfoot, and the longus extensor tendons
to the second, third, and fourth toes are cut, sutured together, and inserted into the
midfoot using either an interference screw, a suture anchor, or a soft tissue bolster
on the plantar surface of the foot. In children, we prefer to use a padded bolster and
not a suture button, which can cause necrosis of the skin. A 4 mm drill through the
lateral cuneiform is made, and the tendons are passed through to the plantar surface.
A useful technique to pass the tendon is to insert a guide pin through the cuneiform,
hold the guide pin with a clamp below the foot, and then drill through the bone.
Using a #15 blade, a small skin incision is made over the guide pin; then, a metallic
a b
c d
e f
Fig. 9 The surgical steps of talectomy are demonstrated in this 26-year-old female who was walk-
ing on the dorsolateral surface of the foot (a, b). An anterolateral extensile incision was made fol-
lowed by manipulation of the foot into varus. With further manipulation the talus can be extruded
laterally (c–e). Note that at completion of the talectomy and articular surface resection, the foot
remains in adduction and equinus (f). Large wedges were then removed from the calcaneocuboid
joint as well as the anterior distal tibia in order to bring the foot into a neutral plantigrade position
(g, h). When the tourniquet was deflated, severe ischemia of the foot was present. Nitroglycerin
paste was applied to the foot as shown (i) which resulted in reperfusion (j)
g h
i j
Fig. 9 (continued)
suction tip is passed over the guide pin from plantar to dorsal and pushed out dor-
sally [18]. The suture attaching the tendons is then inserted into the suction which is
then pulled out into the drill hole through to the plantar surface. The foot is then
positioned in neutral and the sutures tied over a soft tissue bolster. We use the rubber
stopper from a 30 mL syringe which is perforated twice with a small clamp, and the
sutures are passed through the rubber stopper, and a soft tissue bolster is inserted
between the stopper and the skin and then again over the stopper to prevent the
suture from cutting through the rubber, thereby losing tension. In children, it is use-
ful to reinforce this with a 2.0 absorbable suture through the dorsal bone and into the
tendon. The bone may be too hard to accomplish this in the adult, in which case
small holes are made with a 1.6 mm K wire, or a suture anchor can be inserted into
the cuneiform directly. If a suture anchor is used, one should ensure that this does
not pull out with very vigorous tension on the suture.
Talectomy without arthrodesis will provide sufficient laxity of the soft tissue
contracture to permit correction of the equinus and various associated deformities.
Occasionally however, an Achilles tenotomy needs to be performed simultaneously
and only needs to be performed at the completion of the talectomy if equinus defor-
mity persists. The tendon can easily be reached posterolaterally, grasped with a
curved clamp, and cut with the blade moving from outside to inside to avoid inad-
vertently cutting the skin. Following the talectomy, regardless of whether it is done
with or without an arthrodesis, it is useful to shorten the peroneal tendons. The
peroneal muscles will not function if the tendons are left alone due to considerable
laxity following reduction of the foot, and one may want to restore muscle balance
by shortening the tendons as necessary. Certainly, the peroneus brevis should be
tightened, and a transfer of the peroneus longus to the brevis can also be considered.
Talectomy will correct the majority of the equinus deformity and some of the
adductovarus deformity but is occasionally not sufficient to decompress the defor-
mity, and additional procedures must be considered. The simplest would be to trans-
fer the posterior tibial tendon which ensures that recurrent adductovarus deformity
does not occur and also may help provide an active dorsiflexor albeit weak to the
foot. It is rare that the extensor muscles are functional. If one is not able to perform a
transfer of the posterior tibial tendon, a tenotomy of the tendon will need to be per-
formed. Harvesting the tendon may not be easy because of prior scarring if a postero-
medial incision has been used in early childhood. Since it is never clear what has
been previously performed, we initiate the incision at the level of the medial malleo-
lus and try to find the posterior tibial tendon in its sheath which is opened. The tendon
is usually firmly adherent to the posterior aspect of the medial malleolus, and a
smooth small clamp is inserted underneath the tendon to visualize it. From here, one
can work distally by opening the sheath as far as possible distally. Because of scar-
ring, one may not be able to harvest the entire tendon, but it is essential to attempt to
obtain as long a piece of tendon possible for the interosseous transfer. If so, the distal
2 or 3 cm may have to be shaped and narrowed knowing that this is predominantly a
scar tissue. Once the tendon has been dissected free and sutured, one should take note
of any persistent adduction contracture. In cases where on examination one is certain
that either the anterior tibial or extensor tendon function is present, then these can be
considered for use as an active transfer in combination with the talectomy. Essentially,
the foot must be balanced so that recurrent deformity of the midfoot and forefoot is
less likely to occur. Bear in mind that the peroneal tendons are also not likely to be
functioning in these advanced cases, but one can perform a longus-to-brevis transfer
in an effort to aid eversion and balance the hindfoot. This transfer should not be con-
sidered however if the peroneal muscles are functioning strongly and the posterior
and anterior tibial tendons are scarred or the muscles dysfunctional.
At this stage one should check the alignment of the toes since a flexion contracture
may now be present. To some extent this will always occur because of the pre-existing
equinus deformity, and as the foot is dorsiflexed, the long flexor tendons are contracted.
Since passive dorsiflexion of the toes of 45° is desirable, the contracture may be decom-
pressed by virtue of the talectomy in which case nothing needs to be done. Since these
muscles may still be functional, if there are residual flexion contractures after the
talectomy, one can consider a lengthening at the musculotendinous junction or through

the tendon depending on the magnitude of the contracture. If severe scarring is present
posteromedially, then lengthening is not necessary, and tenotomies can be performed.
If so, we find it easier to perform the tenotomy of the flexor hallucis longus looking
through the ankle from posterior to anterior under direct vision. Needless to state, make
sure that one is grasping the flexor tendon and not the tibial nerve.
At the completion of the above procedures, the tourniquet must be left down to
ensure adequate circulation to the foot. This is frequently compromised because of
the magnitude of the deformity, the inevitable traction on the neurovascular bundle,
hypoplasia of the dorsalis pedis artery, or prior scarring around the posteromedial
ankle from prior surgeries. If perfusion does not return immediately, apply warm
moist cloths to the foot and ankle, and wait for 10 minutes. It is also useful to drop
the foot down slightly off the side of the table to a dependent position. If circulation
does not improve following 10 minutes, we recommend applying nitroglycerin
paste (Nitro-Bid) (Fig. 9h–j). This promotes vasodilatation and may sufficiently
improve venous return such that the ischemia is resolved. If not, use a Doppler to
mark out the tibial artery, and if there is an appreciable change at the level of the
ankle, open posteromedially and perform a complete tarsal tunnel release. When
releasing the tibial nerve and artery, it is important to trace the bundle distally
beyond its bifurcation to the medial and lateral branches since the flexor retinacu-
lum may be constricting either or both vessels.
7 Conclusions
The spectrum of severe untreated or recurrent clubfoot deformities that one encoun-
ters makes it impossible to provide a clear algorithm for treatment. We have high-
lighted a few of the more common approaches that are used on our global
humanitarian programs including tendon transfer, tibial osteotomy, triple arthrode-
sis, and talectomy. By no means are these the only options for treatment, since
combinations of procedures and additional osteotomies of the cuboid and calcaneus
and other soft tissue procedures must be considered on a case-by-case basis. As we
noted above, the approach to treatment of these deformities may be quite different
where patients have access to regular return visits for follow-up treatment and where
more sophisticated options for gradual correction with external fixation are available.
References
1. Li S, Myerson MS. Managing severe foot and ankle deformities in global humanitarian pro-
grams. Foot Ankle Clin. 2020;25(2):183–203.
2. Dobbs MB, Morcuende JA, Gurnett CA, Ponseti IV. Treatment of idiopathic clubfoot: an his-
torical review. Iowa Orthop J. 2000;20:59–64.
3. Radler C, Mindler GT. Treatment of severe recurrent clubfoot. Foot Ankle Clin.
2015;20(4):563–86.
4. Thomas HM, Sangiorgio SN, Ebramzadeh E, Zionts LE. Relapse rates in patients with club-
foot treated using the Ponseti method increase with time: a systematic review. JBJS Rev.
2019;7(5):e6.
5. Dragoni M, Farsetti P, Vena G, Bellini D, Maglione P, Ippolito E. Ponseti treatment of
rigid residual deformity in congenital clubfoot after walking age. J Bone Joint Surg Am.
2016;98(20):1706–12.
6. Eidelman M, Kotlarsky P, Herzenberg JE. Treatment of relapsed, residual and neglected club-
foot: adjunctive surgery. J Child Orthop. 2019;13(3):293–303.
7. Holmdahl HC. Astragalectomy as a stabilising operation for foot paralysis following poliomy-
elitis; results of a follow-up investigation of 153 cases. Acta Orthop Scand. 1956;25(3):207–27.
8. Joseph TN, Myerson MS. Use of talectomy in modern foot and ankle surgery. Foot Ankle Clin.
2004;9(4):775–85.
9. Letts M, Davidson D. The role of bilateral talectomy in the management of bilateral rigid
clubfeet. Am J Orthop (Belle Mead NJ). 1999;28(2):106–10.
10. El-Sherbini MH, Omran AA. Midterm follow-up of talectomy for severe rigid equinovarus
feet. J Foot Ankle Surg. 2015;54(6):1093–811.
11. Ebert N, Ballhause TM, Babin K, Schelling K, Stiel N, Stuecker R, Spiro AS. Correction of
recurrent equinus deformity in surgically treated clubfeet by anterior distal tibial hemiepiphys-
iodesis. J Pediatr Orthop. 2020;40(9):520–5.
12. Malik SS, Knight R, Ahmed U, Prem H. Role of a tendon transfer as a dynamic checkrein
reducing recurrence of equinus following distal tibial dorsiflexion osteotomy. J Pediatr Orthop
B. 2018;27(5):419–24.
13. Cooper RR, Talectomy CW. A long-term follow-up evaluation. Clin Orthop Relat Res.
1985;201:32–5.
14. Mirzayan R, Early SD, Matthys GA, Thordarson DB. Single-stage talectomy and tibio-
calcaneal arthrodesis as a salvage of severe, rigid equinovarus deformity. Foot Ankle Int.
2001;22(3):209–13.
15. Mann RA, Chou LB. Tibiocalcaneal arthrodesis. Foot Ankle Int. 1995;16(7):401–5.
16. Arthrogryposis. In: McCarthy JJ, Drennan JC, editors. Drennan’s the child’s foot and ankle.
Vol. 2. Philadelphia: Lippincott Williams & Wilkins; 2009. p. 252–253.
17. Hsu LC, Jaffray D, Leong JC. Talectomy for club foot in arthrogryposis. J Bone Joint Surg Br.
1984;66(5):694–6.
18. Melamed EA, Myerson MS, Schon LC. A review of tendon passing techniques and introduc-
tion of a new method using a suction tip. Foot Ankle Int. 2000;21(8):693–6.
Muller Weiss Disease
Manuel Monteagudo and Ernesto Maceira
1 Introduction
Müller-Weiss disease (MWD) is defined as a dysplasia of the navicular bone, a

consequence of abnormal development during its ossification in childhood, the
pathomechanical consequences of which are experienced in adulthood. There are
several possible origins for MWD, but all combine an environmental factor
(e.g., malnutrition) with a predisposing mechanical factor (e.g., a short first metatar-
sal), during the ossification stage of the navicular. The progressive thinning of the
lateral region of the bone produces a progressive lateral translation of the head of
the talus until it is positioned over the calcaneus, thus generating a subtalar varus.
This subtalar varus, together with the medial prominence of the medial navicular
tuberosity, creates a “paradoxical varus flatfoot” pathognomonic of MWD. Dysplastic
changes and altered talonavicular coverage are evident on plain weightbear-
ing radiographs. There is no direct correlation between radiological and clinical
involvement. The patient usually complains of pain in the dorsal talonavicular
region, over the anterior chamber of the ankle, lateral instability due to subtalar
varus effect, and pain in the tarsal sinus and peroneal tendons. Some patients with
MWD do not have much pain or dysfunction and do not require treatment. When
pain and functional limitation are present, the most effective conservative treatment
is the use of insoles with a varus/pronator wedge in the hindfoot and internal longi-
tudinal arch support. The varus/pronator wedge promotes passive medial displace-
ment of the talar head to take advantage of healthy (“virgin”) cartilage in the medial
M. Monteagudo (*)
E. Maceira
Orthopaedic Foot and Ankle Unit, Complejo Hospitalario La Mancha Centro,
Alcázar de San Juan, Ciudad Real, Spain

Switzerland AG 2022
616 M. Monteagudo and E. Maceira
region of the navicular. Most patients improve with orthotic treatment. Patients who
show limiting pain, despite insoles, may require surgery. Since this is an asymmetric
talonavicular joint osteoarthritis, surgery should provide the necessary mechanical
change to take advantage of the medial region of healthy joint cartilage. Performing
a calcaneal valgus osteotomy allows translation of the talar head medially to achieve
good talonavicular coverage. In most patients, clinical improvement allows us to
avoid arthrodesis. In patients with no clinical response to calcaneal valgus osteot-
omy, we can perform an arthrodesis which, depending on the location and extent of
osteoarthritic involvement, can be talonavicular, talonaviculocuneiform, or double/
triple tarsal.
2 Epidemiology
Understanding the epidemiology and historical development of MWD is very

important in order to understand the origin, pathogenesis, and diagnosis of the dis-
ease. In 1925, Schmidt reported a compressed and flattened tarsal navicular in a
patient with a multiple endocrine deficiency syndrome but did not publish
any x-ray images [1]. In 1927, Walther Müller a German surgeon did publish the
first images of a fragmented, compressed, and condensed tarsal navicular [2].
Konrad Weiss, an Austrian radiologist, studied the radiological signs of the frag-
mented, compressed, and condensed tarsal navicular to conclude that it was osteo-
necrosis [3]. This was a logical deduction because the radiological details pointed to
poor bone vitality but also because of professional bias since Weiss was a disciple
of Kiemböck who had described a similar condition in the lunate bone of the wrist
(lunatomalacia). However, in later studies no necrotic changes were found in histo-
logical analysis of biopsies of navicular bones affected by this pathology [4, 5].
MWD was named after the findings of these two physicians. Since then, numerous
etiopathogenic theories have been suggested to explain its development (congenital
malformation, anomalous evolution of Köhler’s disease, posttraumatic migration of
an accessory cuboid, etc.) [6].
Brailsford proposed that a history of previous trauma was an important factor for
the development of MWD and named it “listhesis navicularis” because of the crush-
ing and sliding of the fragments after their separation from the bone [7]. This author
had a large series of cases for the time (5 patients in 1935, 17 in 1945, and 20 in
1953). He also reported that it was predominantly bilateral and asymmetric between
the feet, and 88% of the patients were women. Interestingly, he commented that the
disease was more prevalent than previously thought and that many cases were not
correctly diagnosed. This is something we fully subscribe to in our experience to
date. MWD is largely unknown in many parts of the world. Understanding its epi-
demiology explains to a large extent why it is underdiagnosed.
In 1948, Fontaine et al. coined the term “adult tarsal scaphoiditis,” and it became
the most popular non-eponymic name in Europe [8]. In 1981, Willey and Brown
published the longest series in North America (Ottawa) and suggested that it was
Muller Weiss Disease 617
not an osteonecrosis but the result of heterogeneous ossification centers inducing

dysplasia [9].
In a seminar paper (2004) for MWD, Maceira and Rochera described the types
of radiological presentation and also analyzed epidemiological data that pointed to
environmental factors, interacting with a mechanical predisposition of the foot, for
the development of the disease [10]. The authors studied the clinical records of
191 cases of MWD registered at the Hospital de San Rafael in Barcelona, and
from the analysis of the data, they realized several very interesting facts. Eighty-
five percent of the patients were born outside Barcelona and had migrated from
different rural areas of southern Spain to Barcelona in the 1950s, with a homoge-
neous distribution of birth dates. Most were born around 1932, about 4 years
before the outbreak of the Spanish Civil War. However, 70% of the controls seen
for other foot and ankle reasons in the same hospital and the same time period
were born in Barcelona. Most of the patients with MWD were immigrants whose
families had escaped from conditions of extreme poverty and hunger in southern
Spain after the Spanish Civil War (1936–1939). Southern Spain (Andalusia,
Extremadura, Castilla-La Mancha) suffered devastating war and postwar condi-
tions of extreme poverty and hunger. Environmental and nutritional stress in chil-
dren with a growing navicular may have played a fundamental role in the later
development of a navicular that, for a time until complete ossification, may have
been subjected to abnormal loads that eventually deformed it. Poverty and lack of
food were also due to the disappearance of traditional agriculture in Spain, due to
the progressive mechanization of agricultural techniques that required less labor.
For all these reasons, in the 1950s, there were massive migratory movements from
the most disadvantaged areas of southern Spain to the big capitals – Madrid,
Barcelona, and Valencia – and the new inhabitants occupied the lower-skilled jobs.
Some 73% of the patients with MWD in Maceira and Rochera’s study were
women, housewives, or housekeeping staff [10]. Müller and Weiss’s patients had
also suffered a very similar situation with the First World War, which raged in
Europe between 1914 and 1918 [1–3]. Their published cases had the same tempo-
ral pattern with respect to a war as those in Barcelona. The low incidence of MWD
in some countries such as the United States can be explained by the absence of the
predisposing environmental factors already explained. They have not suffered
wars (on their territory) in the last century, and they have not suffered poverty or
hunger, so cases of MWD in the United States are usually “imported” in immi-
grants who did suffer hardships during their childhood in their countries of origin
[10]. It is interesting how archeological studies have been able to identify cases of
MWD and how the stigmata of malnutrition coincided in our ancestors and in our
epidemic patients [11]. Anthropologists believe that the presence of Harris lines
(radiological striations indicating tortuous bone growth due to malnutrition), den-
tal enamel hypoplasia (which will cause severe dental problems at early ages), and
cribra orbitalia (porotic hyperostosis of the orbital roof due to childhood stress)
represents episodes of nutritional stress among populations of children in different
civilizations throughout history [12]. Most patients with MWD show these signs
of nutritional stress.
The authors, after studying more than 600 cases of MWD over the last 20 years
(including those in the study by Maceira and Rochera), can explain that there are
different types of MWD, which are due to different etiological factors, although all
of them share the fundamental characteristics of navicular dysplasia and subtalar
varus [10, 13]:
1. Cases of unknown origin
2. Epidemic environmental stress during childhood
3. Individual environmental stress during childhood
4. Obvious or less obvious anatomical deformities, such as metatarsus adductus or
varus hindfoot
5. Athletes with intensive training during childhood
6. A special type of adult-onset MWD known as “Müllerweissoid foot”
These different types of MWD will be discussed in the following section in order to
understand their pathomechanics and development.
3 Pathomechanics
Once the epidemiology of MWD is understood, the most important question to

understand its pathomechanics would be: Is delayed navicular ossification a suffi-
cient condition to develop MWD? The answer would be no. There must also be an
abnormal (“nonideal”) mechanical factor that irregularly compresses a matur-
ing (ossifying) navicular. Children who, subjected to severe nutritional environmen-
tal stress, did not develop MWD underwent compressive forces that were
homogeneously distributed along the entire length and width of the navicular,
whereby the ossifying cartilage structure could accommodate these loads and not
deform, except if we occasionally consider a symmetrical flattening in its antero-
posterior width. This scenario is found in Köhler’s disease, a benign, self-limiting
condition also known as naviculare pedis retardatum.
Environmental factors alone are not a sufficient condition for developing MWD;
otherwise, the prevalence would be higher and more homogeneous in risk groups. It
is necessary for a mechanical factor to act on the slowly maturing navicular to cause
asymmetric load distribution and consequent dysplasia. The most frequent predis-
posing mechanical factor (almost 100% of cases) is the presence of a short first
metatarsals (metatarsal index minus formula) [8, 10, 14]. When the first ray of the
foot is not able to transmit the loads to the ground due to the short length of the first
metatarsal, the compressive moments are transferred to the second-third-fourth
metatarsal producing a “nutcracker” effect on the immature navicular to eventually
cause dysplasia with crushing in the lateral region. A more or less marked metatar-
sus adductus (metatarsus adductus) or the sequel of a clubfoot can also cause the
same effect on the navicular (Fig. 1).
At this stage of bony stress, during ossification of the navicular, it is common for
some orthopedic surgeons unfamiliar with MWD to diagnose as a navicular stress
a b
Fig. 1 Representation of the pathogenic mechanism in Müller-Weiss disease. The navicular bone
is compressed between the head of the talus and the central cuneiforms producing a “nutcracker”
effect. (a) In a foot with a non-dysplastic navicular, compressive forces during gait act between the
head of the talus and the first metatarsal through the medial cuneiform, maintaining the shape of
the coxa pedis. (b) In a dysplastic navicular due to Müller-Weiss disease, with a short first metatar-
sal, compressive forces act between the head of the talus and the medial cuneiforms producing
bony stress in the lateral region of the navicular
fracture what is actually the natural evolutionary process of the disease [15]. The
progressive compression, condensation, and crushing of the lateral region of the
navicular cause the head of the talus to progressively migrate laterally and plantarly,
progressively overlapping the calcaneus (decreased kite angle). The overlapping of
the talus and calcaneus is physiological during the third rocker of gait (“propulsive
calcaneal foot”), but is not physiological when maintained throughout the gait cycle.
The superimposition of the talus over the calcaneus results in subtalar varus. The
forces transmitted by the triceps and those of ground reaction are transformed into
varus moments that end up damaging the lateral structures of the ankle and foot.
Peroneal tendon pathology and calcaneocuboid pain are common among patients
with MWD [13]. Subtalar varus also leads to the loss of the shock-absorbing
“talar foot” during the first and second rocker gait. The shock-absorbing work dur-
ing the first and second rocker gait must be then performed by an upper segment, the
knee extensor apparatus. This extensor apparatus will be forced to work with rota-
tion and greater compression than usual against the femoral trochlea in order to
compensate for subtalar varus. This load transfer explains the high incidence of
patellofemoral problems and patellar tendinopathies in patients with MWD [13].
When an insole is modified to achieve a greater valgus effect, the foot improves, and
the knee worsens. Conversely, when the valgus effect is reduced, the knee improves,
and the foot worsens. If for years the knee has to compensate and assume the cush-
ioning that the midtarsal joint does not do, not only the patellofemoral joint will
suffer but also the femorotibial joint will eventually be damaged, which justifies that
the incidence of total knee arthroplasty in patients with MWD is much higher than
in the general population (without MWD) (Fig. 2) [10].
Talonavicular osteoarthritis may also be responsible for pain, but in many cases
it is also due to the mechanical compression causing damage to the deteriorated
bone and soft tissue [16]. Today we know the beneficial effects on pain and function
of joint preservation surgeries in cases of asymmetric osteoarthritis. Similarly, with
conservative or surgical treatment, when we manage to transfer loads to the most
preserved region of the joint, the patient improves pain and function. With a com-
mon pathomechanical basis, the asymmetric compression of a navicular with
delayed ossification due to various predisposing factors, we can differentiate some
special pathomechanical pathways that would justify that not all patients with
MWD are the same, although they all share common clinical findings:
1. Cases of unknown origin.
In very few patients, we do not find a clear cause for the development of
MWD. Surely there was some subtle mechanical problem that acted in child-
hood (but later disappeared by development) on the growing navicular and
caused dysplasia.
2. Epidemic environmental stress during infancy.
This group includes the cases of the so-called “epidemic group” described by
Müller, Weiss, Brailsford, Maceira, and other authors in which the “children
of war” were unable to ossify their naviculars normally [1–3, 7, 10]. Nowadays
wars are far from the Western world in which many of us live, but there are con-
tinents with millions of children in a situation of famine and nutritional stress
silently generating new cases of MWD. In malnourished children, the fragility of
the navicular during its maturation (last tarsal bone to ossify) makes it sensitive
to any mechanical factor, banal in any other stage of life, to end up developing
dysplasia. Nutritional stress in children is also associated with Harris lines,
enamel hypoplasia, and cribra orbitalia, and these findings are very frequent in
adult patients with MWD and very rare in the general population [10, 13].
a c
Fig. 2 Lack of cushioning of the foot with Müller-Weiss disease leads to load transfer to the knee.
(a) Dorsoplantar view of weightbearing radiograph of a patient showing bilateral involvement,
already operated with an unsuccessful attempt at arthrodesis and without varus correction. (b)
X-ray in lateral weightbearing view of the same case. (c) Anteroposterior view of weightbearing
radiographs of both knees showing gonarthrosis. (d) The patient required a total knee replacement.
(e) Total knee replacement is a common and an early event in patients with Müller-Weiss disease
3. Individual environmental stress during childhood.

There are non-epidemic cases in which a child may suffer malnutrition or
malabsorption and produce altered navicular ossification. Some diseases, such
as inflammatory bowel disease and chronic kidney disease, which can occur in
childhood, produce a decreased appetite and increased energy expenditure, with
consequent alteration of navicular ossification [17]. Some of these children may
later, as adults, have good control of the underlying disease, and the pathome-
chanical correlation described above may be difficult.
4. Obvious or less obvious anatomical deformities such as metatarsus adductus or
varus hindfoot.
Sometimes the mechanical causes are obvious and sufficient to “take advan-
tage” of any slight delay in navicular ossification and cause dysplastic develop-
ment. A very short first metatarsal (brachymetatarsia of the first metatarsal), a
marked metatarsus adductus, a cavovarus foot, can cause a great imbalance of
compressive and shearing forces on a navicular with “normal” development to
end up deforming it (Delpech’s law).
5. Athletes with intensive training during childhood.
Another scenario in which the pathomechanics have more to do with non-
epidemic factors is found in high-level athletes who, during childhood with their
developing naviculars, were subjected to intensive training. These “non-epi-
demic” cases show no Harris lines, no dental problems, and no orbital cribra [10,
13]. The vast majority of these child athletes, some of them later elite profession-
als, have a short first ray, and their naviculars were subjected to “too much work,
too soon.” The short first ray can be explained by the existence of a short first
metatarsal or by the secondary relative shortening of the medial column of the
foot as a result of the internal rotation of the navicular in the transverse plane and
the relative retroposition of the first cuneometatarsal joint with respect to the
second. Kidner and Muro already indicated to us that children with metatarsal
palette adduction had delayed ossification of their naviculars [18]. Spontaneous
correction of the adductus in some children involves external rotation of the
cuboid and of the “en bloc” cuneiforms. This rotation is possible if the medial
region of the navicular acts as a fulcrum and the rotation is at the expense of
compression of the lateral region of the navicular and a medial subluxation of the
cuboid. It would simulate the “nutcracker effect” already outlined, the arms
being the talus and cuneiforms, the fulcrum the medial region of the navicular,
and the nut the lateral region of the navicular. The lack of cushioning of the foot
means that, during the “adult” phase of their sporting career (between 25 and
35 years of age), many suffer from patellofemoral problems and tendinopathies
of the extensor apparatus of the knee. It is not easy for some of these patients,
many of them professional athletes and some of them elite athletes, to find a bal-
ance for the correct functioning of the foot-knee pair with adequate insoles.
Some of them have several insoles with pronator wedges of different heights,
which they change during the competition or the season to increase the work of
the foot or knee according to their symptoms. Some of these athletes compete in
environments with a low historical prevalence of MWD, and their pain is mis-
taken for navicular stress fractures, when radiological studies leave no doubt
about their problems [19]. Sometimes, misdiagnosed athletes are treated by fixa-
tion (osteosynthesis) with grafting, and many of these surgeries fail because they
do not heal, and the athlete maintains pain and functional limitation. The subtalar
varus and the “nutcracker effect” will cause distraction forces on the focus of
injury and with the result of a nonunion in many of these athletes. The newspaper
archives (see the American professional basketball league players with navicular
stress fractures on the Internet) have plenty of examples of failures of supposed
navicular stress fractures in elite athletes, which are a “career-ending” injury
because of treating the consequence and not the cause of their problem.
6. A special type of adult-onset MWD known as “Müllerweissoid foot”.
A less obvious scenario of MWD development can be observed in adult life
on the basis of a healthy navicular. The combined existence of a constitutional
subtalar varus and a short first metatarsal stimulates repeated pronation of the
forefoot during gait and results in subtle osteoarthritis of the Lisfranc joint.
Lisfranc arthrosis and midfoot abduction and pronation create a dorsomedial
prominence in the midfoot and a false valgus flatfoot appearance. Lisfranc
arthropathy may divert our attention away from subtalar varus and direct damage
to the lateral region of the acetabulum pedis. These “Müllerweissoid” feet do not
show lateral navicular fragmentation, and the bone dysplasia is very subtle, but
they share the pathomechanics and clinical and treatment strategy of a patient
with “conventional” MWD (Fig. 3). If MWD goes undiagnosed in many cases,
the “Müllerweissoid” foot is even more complicated to diagnose. Many cases are
a b
Fig. 3 The “Müllerweissoid” foot is the result of a combination of constitutional subtalar varus
and a short first metatarsal. There is no obvious navicular dysplasia, but it shares the pathogenetic
mechanisms of Müller-Weiss disease. The radiological signs are identifiable on a weightbear-
ing radiograph. (a) In a dorsoplantar view we can appreciate the existence of a short first metatarsal
and a subtle varus of the hindfoot. (b) In the lateral view, we can see the dorsal prominence in the
midfoot. (c) And an associated arthropathy at the Lisfranc joint that almost always accompanies
the “Müllerweissoid” foot
treated as flat feet instead of subtalar varus feet. When the type of treatment is
changed, the response is often comparable to that of classic MWD.
4 Diagnosis
As in any other mechanical pathology of the foot, the combination of a good physi-
cal examination with the reading of radiographs of both feet should allow us to
make a diagnosis of MWD.
5 Clinical Examination
The examination should begin by observing the patient walking in the office, bare-
foot and with the ankles free. In many patients we observe what we call a “para-
doxical varus flatfoot,” because it is usual for the flatfoot to be valgus and the pes
cavus to be varus. However, in MWD, the flatfoot appearance is conferred by the
protrusion of the medial tuberosity of the navicular that simulates a collapse of the
medial arch, unlike true flatfoot in which the medial protrusion is due to the head
of the talus. The varus may be obvious or subtle. When the varus is subtle, a good
examination maneuver for diagnosis is to grasp the patient’s heel while asking the
patient to do a bipodal toe-off. The “palpable” varus is maintained throughout the
entire length of the toe-off and up to the plantigrade position of the foot, unlike
valgus flatfoot in which (when the subtalar is mobile) a change into valgus position
of the heel is noticed with the bipodal or monopodal toe-off. Pain in the dorsal
region of the talonavicular joint is frequent, as well as pain attributable to lateral
overload due to subtalar varus, such as pain in the peroneal tendons, in the sinus
tarsi, and in the calcaneocuboid region. Often the patient reports a sensation of
ankle instability, also related to subtalar varus. The existence of an associated equi-
nus can be assessed by the Silfverskiöld maneuver. The presence of a third rocker
metatarsalgia in the context of an index minus is also common in patients
with MWD.
6 Imaging Studies
It is essential to obtain a reliable weightbearing radiograph of both feet. The

“mechanical reading” of the radiographs gives us almost all the information neces-
sary to complete the diagnosis and to know the existence of other typical changes of
MWD [20, 21]. After analyzing the radiological variants of MWD, Maceira formu-
lated a radiological classification that allows us to identify the different evolutionary
changes of navicular dysplasia [10]. The radiological classification has no direct
correlation with clinical findings or with pain, but it is very useful to identify differ-
ent evolutionary stages of the same problem. The degree of asymmetry and frag-
mentation of the navicular is more visible in the dorsoplantar view of the
feet weightbearing. In this projection we can see the existence of an index minus,
with a first metatarsal much shorter than the second, in the great majority of patients
with MWD. The overlapping of the talus and calcaneus reduces the visible surface
of the calcaneocuboid joint and exposes most of the medial tuberosity of the navicu-
lar which is “uncovered” without articulating with the talus. The head of the talus
faces the heads of the second-third (and even fourth) metatarsals instead of facing
the first metatarsal, as in a mechanically normal foot (Fig. 4). CT can help quantify
arthropathy and fragmentation of the lateral region of the navicular and check for
the absence of osteoarthritis in neighboring joints, including the subtalar. MRI often
reveals bone edema in the lateral talonavicular region and the lateral region of the
subtalar joint [22]. MRI is also useful to assess for tendinopathy or longitudinal
tears in the peroneals and to assess the status of the lateral collateral ligament of the
ankle. Talonavicular joint asymmetry usually preserves the medial region of the
joint with healthy cartilage that will be the basis for improving patient’s symptoms
using a joint preservation surgery (calcaneal osteotomy). Other tests such as
SPECT-CT scintigraphy or weightbearing CT scan (WBCT) can help to assess sub-
talar joint congruency and associated injuries in neighboring joints but are not nec-
essary for diagnosis [23].
a b
Fig. 4 The “mechanical reading” of a weightbearing X-rays allows the diagnosis of Müller-Weiss
disease. (a) Weightbearing dorsoplantar view of a patient showing greater radiological involve-
ment of the right foot. It is important to see that the head of the talus “faces” the second metatarsal
and the presence of a bilateral short first metatarsal. (b and c) Lateral view of a weightbearing
radiograph of the same case
7 Treatment
Regardless of the evolutionary stage or the patient’s pain at the first consultation, we
should always try to exhaust the resources of conservative treatment before consid-
ering surgery. There is no minimum time of effect of conservative therapies to con-
sider surgery. The surgical decision will depend above all on the limitation of quality
of life and poor pain control experienced by the patient during the evolution of MWD.
7.1 Conservative
As with any mechanical pathology of the foot, conservative treatment should always
precede any surgical indication. Physical means of rehabilitation and anti-
inflammatory medication generally have little effect in the treatment of MWD. When
there is a lot of bone edema, some patients improve with magnetotherapy [13].
Conservative treatment in mechanical foot disorders has as a fundamental ele-
ment the use of insoles. When we were aware of the importance of hindfoot varus,
our indication of the type of insoles focused on using pronator/valgus wedges of
about 10–12 mm of lateral base in the hindfoot, to try to counteract the subtalar
varus moments during the first rocker of gait, and the use of a medial longitudinal
arch support to stop the collapse of the medial tuberosity of the navicular. With the
correct insoles, most patients experience marked improvement in their symptoms
and improve their function (Fig. 5) [13]. With a mobile and healthy subtalar joint,
the pronator wedge forces subtalar pronation and the head of the talus to move
toward the more medial region of the joint. Loading on a region of the bone with
healthy cartilage allowed patients’ pain and function to improve. Many patients with
MWD present with incorrect insoles, with the heel wedge being supinator/varus
rather than pronator/valgus. Switching to the correct wedge improves most patients.
Although it would be logical to think that patient response to insole use might antici-
pate response to surgery, we have not seen a direct correlation in our patients [13].
Some did not respond adequately to insoles but were much improved by surgically
correcting the hindfoot varus. The same situation applies to the degree of radiologi-
cal compromise. We have not found a direct relationship between the degree of
osteoarthritic involvement and deformity and the response to the use of insoles,
which leads us to indicate them in any evolutionary situation of the disease before
surgery is considered. In a short series with ten patients, Ruiz-Escobar et al. report a
significant improvement in seven of the patients, with the remaining three requiring
surgery [24].
Footwear may also be important in some cases of MWD. Rocker-bottom shoes
allow a smoother transition from the first to the third rocker of the gait, with less
energy expenditure and reduced joint work [25]. Some patients improve with
rocker-bottom shoes. Some of our patients have also improved with the use of ankle
braces to limit anterolateral instability associated with MWD.
Fig. 5 Insoles used in

Müller-Weiss disease with
pronator/valgus wedges for
the hindfoot and with
internal longitudinal arch
support
7.2 Surgical
When the patient is unable to perform basic activities of daily living because of pain
and functional limitation, and conservative treatments have been reasonably
exhausted, surgery can functionally improve patients with MWD. About 20 years
ago, the gold standard of treatment was to perform arthrodesis of the painful arthritic
segments. We associated then (about 25 years ago) osteoarthrosis and arthrodesis as
an appropriate diagnosis-treatment pair in MWD.
7.2.1 Arthrodesis
The most common arthrodesis in our past treatments was talonavicular. This selec-
tive arthrodesis could be considered in cases of isolated talonavicular involvement
and with a healthy naviculocuneiform joint, but it is associated with a high risk of
nonunion. From a technical point of view, it was not easy to perform an isolated
talonavicular arthrodesis in a foot with MWD. The most common approach was
the medial approach. To achieve an adequate valgus, the talar head had to be
“pushed” from lateral to medial to achieve a favorable alignment between the talar
head and the first metatarsal head. And then the talus had to be held in position
with adequate stable fixation with plate and screws. But the varus moments were
still acting on a dysplastic talonavicular, which explained the high percentage of
nonunions and malunions in medial column arthrodesis in patients with
MWD. Some of our patients required salvage surgery after attempted arthrodesis
due to nonunion or malunion. A few years ago, Hintermann et al. added lateral
fixation with a tension band and screws that neutralized the varus forces in the
talonavicular region to be arthrodesed, obtaining homogeneously good results
[26]. Other authors have reported good results in this type of arthrodesis in MWD
[27, 28].
Triple tarsal arthrodesis was indicated in the few patients with added involve-
ment of subtalar and calcaneocuboid arthrosis and, occasionally, to avoid nonunion
of the isolated talonavicular arthrodesis. Triple arthrodesis can have good results
both with an open approach and arthroscopically in patients with MWD, although
there were patients with residual lateral pain attributable to residual uncorrected
varus [29–31].
With a dysplastic navicular, with frequent involvement of the naviculocuneiform
joint, and with little bone stock for arthrodesis, we often expanded the number of
joints to be included in the arthrodesis block and frequently resorted to performing
a talonaviculocuneiform (medial column) arthrodesis. Watson-Jones described
internal longitudinal arch arthrodesis for the treatment of navicular fracture sequelae
[32]. Restoration of medial column length of the foot is desirable in a posttraumatic
setting but is challenging to achieve in MWD. Improved length in the medial col-
umn has been associated with a better clinical outcome in this type of arthrodesis
[33]. Several authors have achieved good results with talonaviculocuneiform
arthrodesis in MWD, most using a tricortical iliac crest graft to connect the seg-
ments to be arthrodesed [34–37]. Some authors opted for complete removal of the
navicular and replacement with a femoral head allograft to cover the defect and fixa-
tion with an eight-hole plate with solid union [38]. The poor vitality of the navicular
has led some authors to try using a vascularized femoral condyle graft to success-
fully perform a medial column arthrodesis, replacing the nonviable part of the
navicular [39].
Our overall experience with arthrodeses in MWD was variable. We learned from
the technical difficulty of fusion and used a talonaviculocuneiform arthrodesis with
“Watson-Jones” grafting in most of our cases. But objectively, the arthrodesis
required long postoperative unloading times, slow recovery, the need for grafting, a
non-negligible percentage of nonunions, and some malunions with residual subtalar
varus (Fig. 6). By 2003, our perception of pathomechanics in MWD changed from
considering osteoarthritis as the problem causing the pain to hindfoot varus as the
true culprit. Asymmetric talonavicular osteoarthritis led us to believe that, if we
a b
Fig. 6 In tarsal arthrodesis for the treatment of Müller-Weiss disease, it is common to find non-
union and malposition without hindfoot varus correction. (a) In the dorsoplantar view we can
appreciate the presence of nonunion. In one of the feet, a screw (“talus-stop”) was used to stop the
lateral displacement of the talus. (b and c) Lateral weightbearing view of the same case
could modify the moments acting on the lateral region of the joint toward the medial
region, the existing “virgin” cartilage in the medial region of the navicular could
allow an improvement in joint conditions and pain relief. The same was true for
other asymmetric osteoarthritis such as the knee in genu varum after valgus osteot-
omy of the proximal tibia. The use of pronator wedge inserts achieved this goal in
most patients [13]. We went from operating on 10–15 cases per year to only 2–4.
The next question was then logical: could we achieve the same effect of the insoles
with surgery?
7.2.2 Joint Preservation Osteotomies/Surgery
The response was to perform a calcaneal valgus osteotomy to allow the triceps to
function by generating valgus moments rather than favoring varus moments. The
Dwyer-type calcaneal valgus osteotomy was a simple technique and allowed early
loading in patients with MWD. And it worked, in most cases with mild varus, but
not to the same extent when the varus was significant. We then made two modifica-
tions that allowed improvement in cases of more accentuated varus. The first modi-
fication in our surgical technique to achieve greater valgus with the Dwyer-type
osteotomy was to perform it in the most anterior region of the calcaneus. When we
perform a varus osteotomy of the calcaneus, the translation has the same effect if it
is performed on the posterior tuberosity as if it is placed closer to the sinus of the
tarsus. The triceps will act in the same way, generating the same varus moments.
However, in a Dwyer-type osteotomy, the location of the osteotomy does matter.

The same lateral base wedge of about 8–10 mm will produce a greater varus effect
the further forward the osteotomy cut is placed. The lever arm from the osteotomy
to the insertion of the Achilles at the posterior calcaneal tuberosity will be greater
the further the distance from the Achilles insertion in the calcaneus and the greater
the valgus effect. The second modification was to add a lateral displacement
(reverse Koutsogiannis effect) to the Dwyer osteotomy to achieve an even greater
valgus effect. When attempting to shift the posterior region of the calcaneus later-
ally, it is necessary to stretch/weaken the medial soft tissues. In our experience it is
not necessary to section the plantar fascia to achieve a “valguizating” osteotomy.
Sectioning the plantar fascia can also have unpredictable consequences, such as
medial arch collapse and lateral column overload syndrome of the foot. It is suffi-
cient to spend about 2 minutes during surgery, using a laminar spreader, to open
and close the osteotomy several times, resulting in a controlled fractional elonga-
tion of the medial soft tissues including the plantar fascia. When this effect is
achieved, it is easy to gain about 8–10 mm of lateral translation in the osteotomy,
achieving the desired valguizating effect that has given us considerably better
results than those obtained with the Dwyer osteotomy alone [13]. Fixation of the
osteotomy is performed with two 6.5 or 7.0 millimeter cannulated screws (Fig. 7).
The immediate postoperative period includes non-weightbearing for 2 weeks until
the wounds and soft tissues are healed. At 2 weeks, weightbearing is started with an
orthopedic boot and crutches according to the patient’s tolerance. The boot is aban-
doned between the second and third month. In recent years, and in view of our
results, this “supervalgus” osteotomy – very anterior lateral closing wedge and
lateral translational calcaneal osteotomy – has become our surgery of choice for
patients with MWD, regardless of the radiological stage at the time of surgery [13].
Any modification to the calcaneus-triceps loading axis requires a minimum of
6 months of “brain habituation” so that our cortex receives reliable mechanical
stimuli and can develop an effective and homogeneous motor plan for the patient to
gain gait fluidity and reflex speed with the operated foot. Most of the patients oper-
ated on with an isolated calcaneal osteotomy improved without the need for sec-
ondary surgery [40]. But, as is obvious and as we explain to our surgical patients,
some patients may require secondary arthrodesis after an osteotomy that did not
produce the desired effect or that produced it for a time only to worsen later. When
talonavicular coverage improves, arthrodesis over a previous osteotomy is quicker
and easier and possibly more likely to be successful than primary arthrodesis over
the original deformity.
The first series in our case series with an isolated “supervalgus” osteotomy was
the subject of a joint study with Myerson’s group series with 13 patients in total
(14 feet) treated with a calcaneal valgus osteotomy [40]. The mean age at the time
of surgery was 56 years, with a mean of 10.6 years of previous symptomatology.
With a mean follow-up of 3.7 years (1–8.5 years), the visual analog pain scale
improved from 8 (7–9) preoperatively to 2 (0–4), and the hindfoot AOFAS scale
improved from 29 (20–44) to 79 (70–88). Most patients were very satisfied with the
a b
c
d
Fig. 7 The valguizating osteotomy for varus correction in a patient with Müller-Weiss disease has
several key steps. (a) Radioscopy image showing the optimal location of the osteotomy, as anterior
as possible, to achieve the greatest valgus effect. (b) The osteotomy already performed and provi-
sional fixation with k-wires can be seen. (c) Axial view of the intraoperative fluoroscopy shows the
lateralizing effect of the osteotomy. (d) Intraoperative image showing the lateral step after dis-
placement of the osteotomy and provisional fixation with k-wires. E: Radioscopy showing fixation
of the osteotomy with two cannulated 6.5 mm screws
outcome of surgery. When we published this study, no patient had had to be reoper-
ated, but we have subsequently had to perform a salvage arthrodesis in the patient
who showed a worse outcome.
We have recently reviewed our series of joint preservation surgeries in 17 cases
with very satisfactory results and comparable to those obtained in the bi-center
study discussed above, with one patient reintervened with an arthrodesis 4 years
after osteotomy (Fig. 8) [41]. With these results, supervalgus calcaneal osteotomy
has become our surgery of choice in MWD regardless of radiological and clinical
involvement, although it is clear that some patient will need a salvage arthrodesis
some time after the osteotomy.
7.2.3 Other Surgeries
Some authors have proposed joint preservation surgery for MWD, consisting of
performing a calcaneal osteotomy to lengthen the lateral column [42]. In their work
they confuse MWD with a valgus flatfoot and adopt a solution contrary to the
pathomechanics of the disease. It is clear that an Evans-type lengthening of the lat-
eral column can only increase lateral translation of the talar head and increase sub-
talar varus and the clinical problems of MWD. The work was challenged shortly
thereafter, and the authors of this chapter believe that the starting error was the
confusion of a paradoxical varus flatfoot with a conventional valgus flatfoot [43].
Other authors have reported a good outcome after decompression with biopsy/for-
ages of the navicular with MWD [44].
8 Conclusions
MWD is a dysplasia of the navicular that develops during childhood and is suf-
fered in adulthood. Epidemiologic study of many cases over the past 25 years has
allowed us to understand that not all patients have the same origin of their defor-
mity, but they all share common pathomechanics that includes translation of the
talar head laterally to lie over the calcaneus, inducing subtalar varus. Confusion in
the clinical diagnosis of a paradoxical varus flatfoot instead of a conventional val-
gus flatfoot will lead to inadequate treatment and failure to respond to conservative
and surgical treatment. Plain weightbearing radiographs are the most cost-effective
diagnostic tool in MWD. Conservative treatment consists primarily of the use of
pronator/valgus wedge insoles in the rearfoot to reduce subtalar varus effects and
internal longitudinal arch support. Joint preservation surgery in asymmetric osteo-
arthritis of MWD, by means of a supervalgus osteotomy of the calcaneus, allows
in most cases a good clinical and radiological result and thus avoids the need for
arthrodesis. Arthrodesis could be reserved for cases that do not improve with
osteotomy.
a b
Fig. 8 Progressive medial displacement of the talar head after a valguizating calcaneal osteotomy
is evident by comparing the radiographs shown. (a) Preoperative dorsoplantar weightbearing view
showing significant involvement of the left foot. (b) Lateral view of the same foot where the talo-
navicular degenerative changes can be seen, and it is not possible to visualize the joint. (c) One
year after surgery, the improvement in the talonavicular coverage can be seen after the medial
displacement of the talus produced by the osteotomy. (d) Lateral view 1 year after surgery where
the talonavicular joint is already visible
References
1. Müller W. On a typical deformity of the tarsal navicular and its clinical presentation [in
German]. ROEFO. 1928;37:38–42.
2. Müller W. On an odd double-sided change of the tarsal navicular [in German]. Deutsche
Zeitschrift für Chirurgie Leipzig. 1927;201:84–7.
3. Weiss K. On the malacia of the tarsal navicular [in German]. Fortschr Geb Rontgenstr.
1927;45:63–7.
4. Maceira E. Clinical and biomechanical aspects of Müller Weiss disease [in Spanish]. Revista
de Medicina y Cirugía del Pie. 1996;10:53–65.
5. Zimmer EA. Diseases, injuries and varieties of the tarsal navicular [in German]. Arch Orthop
Trauma Surg. 1937;38:396–411.
6. Viladot A, Rochera R, Viladot A Jr. Necrosis of the navicular bone. Bull Hosp Jt Dis Orthop
Inst. 1987;47(2):285–93.
7. Brailsford JF. Osteochondritis of the adult tarsal navicular. J Bone Joint Surg Am.
1939;26(1):111–20.
8. Fontaine R, Warter P, de Lange CH. The adult tarsal scaphoiditis (Müller-Weiss disease) [in
French]. J Radiol Électrol. 1948;29:540–1.
9. Wiley JJ, Brown DE. The bipartite tarsal scaphoid. J Bone Joint Surg. 1981;63B(4):583–6.
10. Maceira E, Rochera R. Müller-Weiss disease: clinical and biomechanical features. Foot Ankle
Clin. 2004;9(1):105–25.
11. Chiavegatti R, Canales P, Saldias E, Isidro A. Earliest probable case of Mueller-Weiss disease
from ancient Egypt. J Foot Ankle Surg. 2018;57(5):1034–6.
12. Nowak O. The influence of conditions of life on the formation of morphological features of
human long bones in historical populations. Variabil Evol. 2000;8:129–34.
13. Monteagudo M, Maceira E. Management of Müller-Weiss disease. Foot Ankle Clin.
2019;24(1):89–105.
14. Vilaseca JM, Casademunt M. Escafoidopatı’a tarsiana del adulto [Adult tarsal scaphoidopa-
thy]. Anales de Medicina Sección Médica Barcelona. 1957;43:157–72. [In Spanish]
15. Frosch L. The pathologic fracture of the tarsal navicular [in German]. Deutsche Z für Chirurgie.
1931;232:487–92.
16. Doyle T, Napier RJ, Wong-Chung J. Recognition and management of Müller-Weiss disease.
Foot Ankle Int. 2012;33(4):275–81.
17. Sylvester FA, Wyzga N, Hyams JS, Davis PM, Lerer T, Vance K, Hawker G, Griffiths
AM. Natural history of bone metabolism and bone mineral density in children with inflamma-
tory bowel disease. Inflamm Bowel Dis. 2007;13(1):42–50.
18. Kidner FC, Muro F. Köhler’s disease of the tarsal scaphoid or os naviculare pedis retardatum.
JAMA. 1924;83(21):1650–4.
19. Khan M, Madden K, Burrus MT, Rogowski JP, Stotts J, Samani MJ, Sikka R, Bedi
A. Epidemiology and impact on performance of lower extremity stress injuries in professional
basketball players. Sports Health. 2018;10(2):169–74.
20. Wong-Chung J, McKenna R, Tucker A, Gibson D, Datta P. Radiographic analysis of Müller-
Weiss disease. Foot Ankle Surg. 2020:S1268–7731(20)30119–3. https://doi.org/10.1016/j.
fas.2020.06.009. Online ahead of print.
21. Samim M, Moukaddam HA, Smitaman E. Imaging of Mueller-Weiss syndrome: a review of
clinical presentations and imaging spectrum. Am J Roentgenol. 2016;207(2):W8–W18.
22. Nguyen AS, Tagoylo GH, Mote GA. Diagnostic imaging of the mueller-weiss syndrome: find-
ings of a rare condition of the foot. J Am Podiatr Med Assoc. 2014;104(1):110–4.
23. Welck MJ, Kaplan J, Myerson MS. Müller-Weiss syndrome: radiological features and the role
of weightbearing computed tomography scan. Foot Ankle Spec. 2016;9(3):245–51.
24. Ruiz-Escobar J, Viladot-Pericé R, Álvarez-Goenaga F, Ruiz-Escobar P, Rodríguez-Boronat
E. Tratamiento con soportes plantares en la enfermedad de Müller-Weiss. Reporte preliminar
Acta Ortopédica Mexicana. 2020;34(2):112–8.
25. Myers KA, Long JT, Klein JP, et al. Biomechanical implications of the negative heel rocker
sole shoe: gait kinematics and kinetics. Gait Posture. 2006;24(3):323–30.
26. Fornaciari P, Gilgen A, Zwicky L, Horn Lang T, Hintermann B. Isolated talonavicular fusion
with tension band for Müller-Weiss syndrome. Foot Ankle Int. 2014;35(12):1316–22.
27. Cao HH, Lu WZ, Tang KL. Isolated talonavicular arthrodesis and talonavicular-cuneiform
arthrodesis for the Müller-Weiss disease. J Orthop Surg Res. 2017;12:83. https://doi.
org/10.1186/s13018-017-0581-4.
28. Harnroongroj T, Chuckpaiwong B. Müller-Weiss disease: three- to eight-year follow-up out-
comes of isolated talonavicular arthrodesis. J Foot Ankle Surg. 2018;57(5):1014–9.
29. Cao HH, Tang KL, Xu JZ. Peri-navicular arthrodesis for the stage III Müller-Weiss disease.
Foot Ankle Int. 2012;33(6):475–8.
30. Hetsroni I, Nyska M, Ayalon M. Plantar pressure distribution in patients with Müller-Weiss
disease. Foot Ankle Int. 2007;28(2):237–41.
31. Lui TH. Arthroscopic triple arthrodesis in patients with Müller Weiss disease. Foot Ankle
Surg. 2009;15(3):119–22.
32. Watson-Jones R. Fractures of the tarsal navicular bone. In: Watson-Jones R, editor. Fractures
and joint injuries, vol. 2. 4th ed. Edinburgh: E & S Livingstone; 1955. p. 900.
33. Fernández de Retana P, Maceira E, Fernández-Valencia JA, Suso S. Arthrodesis of the
talonavicular-cuneiform joints in Müller-Weiss disease. Foot Ankle Clin. 2004;9(1):65–72.
34. Mohiuddin T, Jennison T, Damany D. Müller-Weiss disease - review of current knowledge.
Foot Ankle Surg. 2014;20(2):79–84.
35. Yu G, Zhao Y, Zhou J, Zhang M. Fusion of talonavicular and naviculocuneiform joints for the
treatment of Müller-Weiss disease. J Foot Ankle Surg. 2012;51(4):415–9.
36. Yuan C, Wang C, Zhang C, Huang J, Wang X, Ma X. Derotation of the talus and arthrodesis
treatment of stages II-V Müller-Weiss disease: midterm results of 36 cases. Foot Ankle Int.
2019;40(5):506–14.
37. Zhang H, Li J, Qiao Y, Yu J, Cheng Y, Liu Y, Gao C, Li J. Open triple fusion versus TNC
arthrodesis in the treatment of Mueller-Weiss disease. J Orthop Surg Res. 2017;12(1):13.
38. Tan A, Smulders YC, Zöphel OT. Use of remodeled femoral head allograft for tarsal recon-
struction in the treatment of Müller-Weiss disease. J Foot Ankle Surg. 2011;50(6):721–6.
39. Levinson H, Miller KJ, Adams SB Jr, Parekh SG. Treatment of spontaneous osteonecrosis
of the tarsal navicular with a free medial femoral condyle vascularized bone graft: a new
approach to managing a difficult problem. Foot Ankle Spec. 2014;7(4):332–7.
40. Li S, Myerson M, Monteagudo M, Maceira E. Efficacy of calcaneus osteotomy for treatment
of symptomatic Müller-Weiss disease. Foot Ankle Int. 2016;38(3):261–9.
41. Buendía I, Gaviria ME, Monteagudo M, Maceira E, Martínez de Albornoz P. Enfermedad de
Müller–Weiss, ¿cómo hemos cambiado? Rev Pie Tobillo. 2020;34(2):125–32. in press.
42. Ahmed AA, Kandil MI, Tabl EA. Preliminary outcomes of calcaneal lengthening in adolescent
flatfoot in Müller-Weiss disease. Foot Ankle Int. 2019;40(7):803–7.
43. Myerson MS. Letter regarding: preliminary outcomes of calcaneal lengthening in adolescent
flatfoot in Muller-Weiss disease. Foot Ankle Int. 2019;40(7):808.
44. Janositz G, Sisák K, Tóth K. Percutaneous decompression for the treatment of Mueller-Weiss
syndrome. Knee Surg Sports Traumatol Arthrosc. 2011;19(4):688–90.
Surgical Techniques for Peritalar
Osteoarthrosis: Talonavicular, Subtalar,
Calcaneocuboid, and Midfoot
José Antônio Veiga Sanhudo and Marco Túlio Costa
1 Introduction
Osteoarthrosis of the peritalar joints is usually post-traumatic, secondary to pre-

existing deformities and/or systemic inflammatory diseases. Calcaneus fracture is
undoubtedly one of the major causes of arthrosis of the subtalar joint and, less fre-
quently, of the calcaneocuboid joint. The overload and alignment changes observed
in the cavus varus foot or flatfoot are often associated with degenerative changes of
the peritalar joints, especially the subtalar joint.
2 Anatomy and Biomechanics of the Subtalar Joint
The subtalar is a complex joint, with an important role in impact absorption, propul-
sion and adaptation to irregular surfaces during walking. Separated by a medially
cylindrical bone tunnel, called the tarsal canal, and laterally conical, called the sinus
tarsi, it can be divided into anterior, composed of the talocalcaneonavicular joint,
and posterior, composed of the talocalcaneal joint.
During walking, the joint is responsible for impact absorption in the heel contact
phase, when it is in valgus and with the transverse tarsal joints unlocked and flexi-
ble. As it progresses to the propulsion phase, the subtalar joint inverts, the transverse
tarsal joints lock to transform the hindfoot into a lever arm for impulse and
J. A. V. Sanhudo (*)
Hospital Moinhos de Vento de Porto Alegre, Porto Alegre, RS, Brazil
M. T. Costa
Hospital Santa Casa de Misericórdia de São Paulo, São Paulo, Brazil

Switzerland AG 2022
638 J. A. V. Sanhudo and M. T. Costa
locomotion. During walking, a complex triplane movement involving eversion/

inversion, abduction/adduction, supination/pronation of the middle and the hindfoot
alternate successively, involving mainly the talonavicular joint, but also the calca-
neocuboid and subtalar joints [1].
3 Diagnosis
3.1 Clinical
The typical history of subtalar osteoarthrosis is pain in the lateral subfibular region
and sinus of the tarsus, associated with difficulty in walking on uneven surfaces.
The diagnostic investigation begins with the clinical examination, observing the
alignment of the lower limb as a whole, especially the alignment of the knee, ankle
and hindfoot, the medial longitudinal arch and the presence of increased volume,
common in more advanced cases. Valgus or varus deviations of the hindfoot are
often associated with subtalar degeneration and it is important to remember that the
varus deviation of the hindfoot is often associated with fibular tendinopathy, which
can simulate subtalar arthropathy.
Dynamic inspection is of paramount importance in the identification of gait
changes, often associated with pain, muscle imbalance and neurological
disorders.
In the physical examination, the palpation of the pain site, as well as the evalua-
tion of the active and passive ankle, subtalar and midfoot joints range of motion
allows the identification of joint degeneration, among other causes. The pain in sub-
talar osteoarthrosis usually worsens with active and passive eversion/inversion of the
hindfoot. Silfverskiöld test, comparing the degree of ankle dorsiflexion with the
flexed and extended knee, should be routinely performed in these patients, since the
shortening of the calf muscle is often associated with hindfoot misalignment, espe-
cially in valgus [2].
4 Imaging
The initial image evaluation involves an anteroposterior, oblique and lateral

foot weight bearing radiographs. Narrowing of the joint space, sclerosis and/or
subchondral cysts and formation of osteophytes are the most frequent findings
in degenerative changes of the hindfoot. Additional incidences, such as the
axial calcaneus or the long leg view, are requested in selected cases for evalua-
tion of the mechanical axis. An anteroposterior ankle x-ray with 40° internal
rotation allows an excellent visualization of the subtalar joint. Nuclear mag-
netic resonance is extremely useful for demonstrating incipient degenerative
Surgical Techniques for Peritalar Osteoarthrosis: Talonavicular, Subtalar… 639
changes and in evaluating soft tissues, especially tendons and ligaments of the
hindfoot. The emerging weight bearing computed tomography (WBCT) has
been proving extremely useful in the evaluation of hindfoot disorders, espe-
cially regarding functional alignment and joint incongruity. The demonstration
of changes in subtalar joint orientation in flatfoot was possible with the advent
of WBCT [3–6].
Infiltration of the subtalar joint with anesthetic (xylocaine or ropivacaine 2%)

guided or not by radioscopy or another imaging method may be useful in confirm-
ing the source of pain. The association of anesthetic with steroid can also be used
aiming at a combined therapeutic effect [7]. The intra-articular injection of hyal-
uronic acid at weekly intervals for 21 days was shown to be beneficial, with pain
improvement, AOFAS score and greater tolerance for walking, in 18 of 20 patients
aged between 22 and 72 years with subtalar ostheoarthritis. The benefit of the treat-
ment lasted more than six months [8]. The association of hyaluronic acid and intra-
articular chondroitin sulfate was beneficial in patients with knee and hip
osteoarthrosis, but there are no studies demonstrating the same benefits in other
joints of the lower limb [9, 10].
The conservative treatment is the first choice for osteoarthrosis of the foot and
involves the modification of the activity and the footwear, as well as the use of
orthoses aiming at a better load distribution. Decreasing high demand physical
activities and losing weight help with symptoms relief as well. The treatment of
osteoarthrosis involves the use of painkillers, anti-inflammatory drugs and chondro-
protectors, but the efficacy of the latter in the treatment of degenerative foot disor-
ders has not yet been proven.
6 Subtalar Joint Osteoarthrosis
Few options exist between conservative treatment and arthrodesis in the manage-
ment of subtalar joint osteoarthritis. Thus, after conservative treatment failure, the
most performed surgical procedure is arthrodesis, which can be in situ or modelling,
depending on the existence or not of associated deformity. The use of bone block
grafting is indicated for correction of malunion with flattening of the calcaneus and
loss of height on the hindfoot [11].
Although less invasive procedures, such as arthroscopy, are procedures per-
formed in many centers, few cases present in a phase of osteoarthrosis that
would benefit from this less invasive approach that does not involve subtalar
arthrodesis.
6.1 Biomechanics
Although widely used in the treatment of flatfoot, subtalar arthrodesis alone has
been shown, in a cadaveric study, to be less effective in promoting support for the
medial and lateral longitudinal arch than combined calcaneocuboid and talonavicu-
lar arthrodesis. However, the most effective support for both arches was obtained
through triple arthrodesis [12]. The biomechanical stress caused by hindfoot
arthrodesis on local bone and soft tissue structures was studied through a finite ele-
ment model. It was observed that in situ talonavicular arthrodesis alone is superior
to subtalar arthrodesis alone and equivalent to triple arthrodesis in relation to the
biomechanical stress on bone and soft tissue structures supporting the plantar arch.
Isolated subtalar arthrodesis was, among the isolated arthrodesis of the hindfoot, the
one that contributed less to stress reduction in both the plantar fascia and the spring
ligament and it was associated with higher stress in the forefoot and hindfoot. The
triple arthrodesis is the one that has provided the most stress reduction in soft tissues
and bones [13]. The blockage of the talonavicular joint, as in an arthrodesis, practi-
cally eliminates mobility of the subtalar joint. On the other hand, arthrodesis of the
subtalar joint maintains 74% of mobility in the talonavicular joint and 44% of
mobility in the calcaneocuboid joint [14].
6.2 Surgical Technique for Subtalar Arthrodesis
The procedure is usually performed under sedation and popliteal block or spine
anesthesia. The use of tourniquet in the thigh or above the ankle, depending on the
level of anesthesia, is practiced by most surgeons, after the limb is exsanguinated
with Smarch band.
6.2.1 Approach
The subtalar joint approach is determined, among other factors, by the necessity or
not of associated procedures. Subtalar arthrodesis by lateral approach is indicated
for cases of primary or post-traumatic arthrosis of this joint and can be extended to
the calcaneocuboid and even talonavicular joints. The incision starts at the fibula
distal end and extends anteriorly parallel to the sole of the foot to the base of the
fourth metatarsal. The subcutaneous tissue is dissected up to the subtalar joint pro-
tecting the sural nerve and moving the fibular tendons plantarly and the superficial
fibular nerve dorsally. The capsule is incised exposing the joint and the cervical
ligament, which is sectioned to facilitate access to all joint facets, using a bone
spreader. This lateral approach, through the sinus tarsi, demonstrated in studies
with cadavers to be adequate for exposure of the three facets of the subtalar joint
[15, 16].
Subtalar arthrodesis performed in cases of talo-calcaneal coalition, a medial

approach is used to remove the bone bridge and perform the arthrodesis. The inci-
sion is made following the upper edge of the posterior tibial tendon, extending from
the medial malleolus to the navicular bone. Galli and collaborators studied the prox-
imity of the neurovascular and tendon structures through this medial approach and
observed that the distance from the medial facet to the flexor digitorum longus ten-
don was 5 mm, to the flexor hallucis longus was 19 mm and to the neurovascular
bundle was 21 mm [17]. In the treatment of rigid flatfoot, common in advanced
phases of posterior tibial tendon dysfunction, arthrodesis through a medial approach
presents the advantages of easy facilitate incision closure, which is performed in the
region of lower tension after correction of the deformity. Access to the joint is
obtained by displacing the posterior tibial tendon plantarly or by resection of the
diseased portion of it in cases of advanced tendinosis (Fig. 1). Double arthrodesis,
subtalar and talonavicular, using a medial approach is an excellent alternative for the
treatment of degenerative disorders of the hindfoot with or without deformity. The
ability to correct deformities with double arthrodesis is the same as triple arthrode-
sis, and the approach has proven to be safe regarding the risk of neurovascular injury
[18, 19]. This approach allows access to 90% or more of the hindfoot joints [20]. In
summary, besides being technically simpler, the medial approach for double arthrod-
esis of the hindfoot avoids lateral incision and its complications, maintains the cal-
caneocuboid mobility, with clinical results similar to triple arthrodesis [21].
The posterior approach, lateral to the Achilles tendon, is an alternative in cases
of inadequate skin conditions or higher risks of incisional complications, as in dia-
betics and smokers. Patients who need arthrodesis to the ankle as well (tibio-talar
Fig. 1 Medial approach

with exposure of the
subtalar joint by
dislocating the posterior
tibial tendon plantarly
arthrodesis), with a previous lateral approach and/or poor skin conditions will also
benefit from the posterior approach, since the implants are better protected in a
deeper plane and the location of the incision facilitates the drainage of the hema-
toma in the postoperative period.
Regardless of the approach, we must keep in mind that joint preparation is one
of the most important steps for the arthrodesis success. Using curette and osteo-
tome, the joint cartilage is removed, the subchondral bone is exposed and perfo-
rated with a 1.5 mm Kirchner or with a narrow osteotome. The use of supplementary
grafting in subtalar arthrodesis is debatable, but most authors agree that the main
recommendation is restricted to cases of cysts, major bone defects and/or associ-
ated deformities.
The arthroscopic approach with lateral and/or posterior portals is described
for the treatment of cartilage lesions, including subtalar joint arthrodesis [22, 23].
According to some studies, arthroscopic subtalar arthrodesis presents results
comparable to open technique for in situ arthrodesis, but requires a longer learn-
ing curve and sophisticated equipment. In the lateral arthroscopic approach, the
patient is positioned in lateral decubitus position, and the joint is accessed
through the anterolateral portals; the anterior, 1 cm distal and 2 cm anterior to the
tip of the fibula; the middle, at the sinus tarsus level 1 cm anterior to the tip of the
fibula; and the posterolateral, 5 mm proximal to the tip of the fibula immediately
lateral to the calcaneal tendon. In the posterior arthroscopic approach, with the
patient in prone position and with the foot out of the operating table, two portals
are performed. One immediately medial and another immediately lateral to the
calcaneus tendon in line with the tip of the fibula. The posterolateral portal is
performed first, and the trocar instrument is directed to the first intermetatarsal
space. The posteromedial portal is performed following the path of the postero-
lateral portal to protect the medial structures, especially the neuro-vascular bun-
dle. The most important reference point in this approach is the flexor hallucis
longus tendon, which represents the medial limit of the working area. The subta-
lar joint is easily visualized through this approach, but distraction of the joint by
introducing a 4.0 mm trocar instrument is necessary sometimes for proper access
to the joint surface [22]. The average healing rate of arthroscopic subtalar arthrod-
esis is 93% [24]. Earlier return to work and sports activities is one of the advan-
tages of the arthroscopic over the open approach, but it is important to observe
that arthroscopic subtalar arthrodesis, although less invasive, presents more
implant related complications [23–27]. Sural nerve lesion, which is located 4 mm
anterior to the posterolateral portal, is described in 6% of the cases, as well as the
tibial nerve bundle lesion, which is located 6.4 mm from the posteromedial por-
tal [28].
Since bone block grafting cannot be performed arthroscopically, subtalar arthro-
sis with associated deformity should be approached openly [27, 29]. In these cases,
the graft is preferably removed from the posterosuperior apophysis of the calcaneus
through a longitudinal incision lateral to the Achilles tendon (Gallie approach)
Fig. 2 Longitudinal lateral

para-Achilles approach for
bone harvest from the
posterosuperior apophysis
of the calcaneus
(Fig. 2). Alternatively, an extended L approach may be used in cases of calcaneus

fracture sequelae, in which a block graft arthrodesis is programmed. This broad
approach, allows lateral calcaneal wall removal, access to the graft donor area and
wide view of the subtalar joint (Fig. 3) [30, 31].
6.2.2 Fixation of the Subtalar Arthrodesis
The internal fixation of the subtalar arthrodesis is one of the most important fac-
tors for successful consolidation. Although staple fixation is employed in some
centers, fixation with screws of at least 6.5 mm in diameter is employed by most
authors [7, 18, 22, 32].
6.2.3 Number of Screws
Single screw fixation distributes stress better at the subtalar joint, but has lower
rotational and inversion/version stress resistance than double screw fixation [33].
Double screw fixation has higher compression, torsional stiffness and strength than
single screw fixation [34]. Jastifer et al. demonstrated that torsional stiffness and
maximum torque are higher with two screws compared to a single screw fixation,
and that the more divergent these screws are introduced the better the stability
obtained [35]. Subtalar fixation with two angled screws was superior to fixation
with two parallel screws also in a biomechanical study applying cyclic loads in the
three main mobility planes of the subtalar joint [36]. Wirth and collaborators
observed a higher rate of nonunion, 35% versus 14%, when the fixation was per-
formed with two compared to the fixation with three screws. The third screw can be
a b
Fig. 3 (a) Extended L-shaped approach for removal of the enlarged portion of the calcaneus lat-
eral wall, exposure of the subtalar joint, and use of the retractor blade to estimate the size of the
block graft needed; (b) removal of the block graft from the posterosuperior apophysis of the calca-
neus; (c) placement of the block graft from the posterior superior region of the calcaneus on the
posterior facet of the subtalar
added depending on the position of the two screws initially introduced and the need
to improve stability due to higher risk of nonunion, as in diabetics and smokers
[37, 38].
6.2.4 Direction of Screws
Although the bone density of the neck of the talus and the tuberosity of the calcaneus
are not the same, the direction of the screws from plantar to dorsal or from dorsal to
plantar has not shown any biomechanical difference. From the clinical point of view
the introduction of the screws from dorsal to plantar increases the risk of neurovasu-
lar injury [36, 39–41]. The disadvantages of the plantar to dorsal screw is that at least
one of the screws must be short threaded to promote compression between the frag-
ments and the risk of re-interventions to remove the implants is greater, especially in
cases where a washer is added [38]. The use of headless screws can minimize this
complication, but the cost of the procedure could rise [42].
6.2.5 Technical Considerations
Regardless of the fixation method chosen, it is very important to correct the subtalar
alignment before fixation, especially the correction of talo-calcaneal divergence. It
is of utmost importance to correct the alignment of the hindfoot when performing
the arthrodesis, since the varus fixation leads to overload of the lateral column and
the valgus fixation overloads the deltoid ligament. Both possibilities may require
revision of the arthrodesis.
It is essential to use fluoroscopy to insert and check the correct positioning of the
implants. The fixation is done from plantar to dorsal with two 6.5 mm cancellous
screws, one partially thread initially to promote compression and another fully
thread for rotational stability. At the time of in situ arthrodesis fixation, however, it
is important to insert one screw (cannulated or not) first and only then start the fixa-
tion with the second screw, because the compression of the initial fixation may be
impaired by the presence of a guide wire or Kirchner [22]. After the screw length is
determined, a 6.5 mm cancellous screw with a short thread of 16 mm is introduced,
obtaining compression between the fragments. A second 6.5 mm cancellous screw
with full thread must be inserted 1–2 cm below the entry point of the first screw,
preferably in divergent direction, below the Achilles insertion and above the plantar
contact point, for rotational control of the fixation. Alternatively, this second screw
may be inserted at the lateral edge of the calcaneus, approximately 1 cm proximal
to the calcaneocuboid joint towards the talus head, or it may be the third screw,
inserted after the two described above. The position and depth of the screws are
checked by fluoroscopy in the sagittal and frontal plane.
6.3 Results
Subtalar arthrodesis, is a procedure that presents high success and low complication
rates [43–45].
Radnay demonstrated that subtalar arthrodesis in patients with a fractured calca-
neus obtained better results than patients who had been conservatively treated, due
to the improved anatomy of the first group [46]. Worse results were obtained in
subtalar arthrodesis if smoking, high-energy trauma and concomitant same limb
fracture were associated [47].
In the treatment of calcaneus malunion with height loss, subtalar arthrodesis with
bone block grafting can be performed with iliac crest, tibia or even from the supe-
rior calcaneus apophysis (Haglund area). The latter is an excellent alternative being
in the same surgical field (Fig. 4) [30, 31, 46].
Fig. 4 Schematic
representation of the bone
block graft removal of the
posterosuperior apophysis
of the calcaneus
7 Talonavicular Osteoarthrosis
The talonavicular joint (TN) is considered the key articulation of the hindfoot. The
arthrodesis of this joint leads to a limitation of 91% of the hindfoot mobility and
eliminates 75% of the posterior tibial tendon excursion [14, 48]. To have an idea of
its importance, the TN arthrodesis alone is as effective as double (talonavicular and
calcaneocuboid) or triple arthrodesis to correct the deformity in the valgus
plane [49].
The treatment of talonavicular osteoarthrosis mostly involves the arthrodesis of
this joint, but good clinical and radiological results have been obtained with the use
of calcaneus osteotomies in cases of localized talonavicular osteoarthrosis associ-
ated with Muller Weiss disorder [50].
7.1 Diagnosis
7.1.1 Clinical
Osteoarthrosis of the TN is often associated with degenerative conditions in other

hindfoot joints. As described for the subtalar joint, the inspection of the alignment
of the entire lower limb is paramount. Swelling in the dorsal medial aspect of the
foot, associated or not with varus/valgus foot deviations and medial longitudinal
arch colapse are frequently observed. During gait analysis claudication and antalgic
position of the limb, as external rotation of the affected lower limb can be detected.
Pain in the TN joint is common on palpation of the dorsal region, as well as with
mobilization in adduction-abduction. During the physical examination is very
important to identify the exact point of greatest pain, whether in the joint line or
more distal, at the level of the navicular bone itself. The latter, suggests a navicular
stress fracture.
7.1.2 Imaging
The image evaluation of the talonavicular joint involves a weight-bearing antero-

posterior lateral and oblique view of the foot. Degenerative changes, with narrowing
of the joint space, subchondral sclerosis with or without subchondral cysts are
expected in cases of ostheoarthritis. Resonance magnetic imaging and computed
tomography scan are useful in case of incipient desease.
7.2 Surgical Technique for Talonavicular Arthrodesis
Surgical procedures at the talonavicular joint level are performed under sedation
and popliteal block anesthesia whenever possible. Tourniquet is used by most
surgeons.
7.2.1 Approach
The most commonly used approach for talonavicular arthrodesis is the isolated medial
approach, but the association of a lateral incision to stabilize the lateral portion of the
joint is very useful biomechanically, and seems to promote better consolidation rates
[51]. However, percutaneous fixation by lateral approach presents high rates of neuro-
vascular injury, around 30–35% of cases [52, 53].
7.2.2 Internal Fixation
Through traditional medial exposure, the classical fixation of talonavicular arthrod-

esis is performed with two or three retrograde screws from the medial region of the
navicular to the lateral region of the talus. The technique does not stabilize the lat-
eral portion of the talonavicular joint, allowing some local micromobility, with
increased chance of nonunion. Jarrell et al. did not observe any significant biome-
chanical difference when comparing fixation with medial screws and fixation with
a medial plate and a dorsal screw in a study with cadavers [54]. In another similar
study, however, Granata and collaborators observed that fixation with a locked dor-
sal plate and a retrograde screw was more effective in blocking 3D mobility than
fixation with two retrograde screws [55].
7.2.3 Technical Considerations
The crucial points for a successful talonavicular arthrodesis are joint preparation
and internal fixation. Due to its concave shape, the exposure of joint surfaces and
subchondral bone makes the talonavicular joint the most difficult to prepare among
a b
Fig. 5 Schematic representation of talonavicular fixation with two retrograde screws and one
anterograde in anteroposterior (a) and lateral (b)
the hindfoot joints. The use of a bone spreader or Hintermann-type retractor is very
useful to facilitate joint access, but care must be taken, especially in older patients,
not to cause local bone sinking. Once the joint surface of the talus and navicular
head is prepared, the joint is positioned in the desired position, provisionally fixing
it with 1.5 mm Kirschner wires or guide wires. Once the adequate position of the
joint is confirmed, fixation with three 4.5 mm cannulated screws is performed. The
third screw can be partially threaded to confer additional compression to the lateral
portion of the TN joint or fully thread, conferring rotational stability (Fig. 5). The
direction and depth of the screws are controlled by fluoroscopy in the anteroposte-
rior and lateral planes. To close the operative wound, meticulous hemostasis is per-
formed to reduce bleeding, swelling and related complications (Fig. 6).
7.3 Results
Calcaneous osteotomy for TN osteoarthritis in Muller Weiss disease have shown

good functional scores. This will be presented in another chapter [50].
Talonavicular arthrodesis is the most performed procedure and has a high rate of
success in the treatment of arthrosis of this joint, as well as in the correction and sta-
bilization of deformities of the hindfoot. Harper and collaborators published a study
including 29 patients with talonavicular arthrodesis alone showing 86% of good
results after 26 months of follow-up [56]. Chen and collaborators obtained fusion in
15 out of 16 patients submitted to arthrodesis using staples or screws after a mean
follow-up of 51 months. Osteoarthrosis was observed in the neighboring joints of 5
of the 16 operated patients, but without symptoms and without affecting the clinical
results obtained [57].
Through a minimally invasive dorsal approach and fixation by posterior approach,
Carranza-Bencano et al. obtained healing in 10 cases of 11 performed, with signifi-
cant improvement of clinical parameters evaluated, but patients with angular defor-
mities were excluded in this study [58].
Lechler and collaborators obtained good and excellent results in 26 of 30 feet
submitted to talonavicular arthrodesis fixed with a locked mini-plate [59].
a b
Fig. 6 (a) Anteroposterior X-ray with TN arthrosis; (b and c) anteroposterior and lateral image of
the arthrodesis with triplanar fixation performed with two retrograde screws and one antero-
grade screw
Harnroongroj and Chuckpaiwong obtained fusion in all 16 patients diagnosed with

Muller-Weiss disorder submitted to isolated talonavicular arthrodesis. Improvement
was also observed in the visual analog pain scale and in the Foot & Ankle Outcome
Score (FAOSs) [60].
8 Treatment Complications
The most common complications of arthrodesis for surgical treatment of subtalar

and talonavicular osteoarthrosis are delayed healing, nonunion, malunion, deep
vein thrombosis, vasculo-nervous injury and infection [23, 43–45]. The occurrence
of nonunion in the subtalar joint according to the literature varies from 2 to 30%,
with higher rates reported in smokers and diabetic patients [39, 40]. Among the
modifiable factors associated with the development of nonunion, possibly the joint
preparation is one of the most important. The approach and the surgeon’s experi-
ence are important as well. Although some authors recommend the use of bone
grafting to decrease the chance of subtalar nonunion, this benefit is not fully proven.
Regarding the TN joint, due to its concave shape, its location in an area of
great stress at the junction of the midfoot and the hindfoot, and the weak lateral
stabilization with traditional fixation, this joint is the most prone to nonunion
between the hindfoot joints, with rates reported between 3.8 and 29% [61]. The
micromobility in the lateral portion of this joint after traditional fixation with
medial screws is one of the most important factors associated with delayed or no
unions [49, 62]. To decrease this micromobility, additional procedures involving
the hindfoot, such as arthrodesis of neighboring joints and osteotomies, have
been described, but they considerably increase the morbidity of the surgery [49,
62, 63]. Malik et al. have demonstrated that among the key points in talonavicu-
lar arthrodesis is a comprehensive and rigid fixation, but avoiding damage to the
underlying joints, especially the naviculo-cuneiform. In a study with cadavers
the author demonstrated that calcaneal osteotomy reduces the micromobility of
isolated talonavicular arthrodesis. According to the study, medializing calcaneal
osteotomy decreases the ground reaction forces medially by 57 to 91%, and rec-
ommends its addition step in patients at high risk of nonunion, like smokers,
obese and diabetics patients [62]. Resnick, also in a study with cadavers, demon-
strated that the association of triple arthrodesis with medializing calcaneal oste-
otomy decreases stress in the deltoid ligament by 56% compared to lateral
tuberosity sliding [64].
As previously mentioned, one factor associated with the TN nonunion risk is the
scarce fixation of the lateral joint region. Retrograde fixation with a lateral percuta-
neous screw through is recommended by some authors. In a cadaveric study, Lee
et al, demonstrated that lateral percutaneous TN fixation was associated with nerve
injury in 30% of cases and tibialis anterior tendon and extensor hallucis longus
tendon injury in 20 and 30 % of the cases, respectively [53].
Other complications described in talonavicular arthrodesis are malunion and
progressive osteoarthrosis of neighboring joints, described in up to 10% of cases.
9 Immobilization
The leg is immobilized with a well-padded splint and the patient must keep the foot
elevated. Thromboprophylaxis is indicated in selected patients, and the risks and
benefits of using anticoagulants should always be considered individually. When
used, it is usually recommended during the whole period of immobilization and/or
non weight bearing. 10 days postoperative, the first dressing change is performed
and, with the operative wound with good signs of healing, the leg is casted and
weight bearing as tolerated is allowed. Non weight bearing should be extended in
patients with high risk of nonunion, such as diabetics and smokers. The cast
removal is performed after joint fusion, usually between 8 and 12 weeks after sur-
gery. CT scan is useful in cases of doubtful healing [65]. Another way of
approaching the postoperative period, is not allowing weightbearing for 2 months
until bone healing is shown by a CT scan. During these 2 months, a removable boot
can be used.
10 Calcaneal-Cuboid Arthrosis
The calcaneocuboid joint integrates the lateral column of the foot. Its isolated
arthrodesis is not common and is usually associated with other procedures in the
foot [66, 67]. In this section we will discuss some particularities of this joint.
10.1 Anatomy and Biomechanics
It is a stable synovial joint formed by the anterior portion of the calcaneus and the
proximal portion of the cuboid. Together with the talonavicular joint, it forms what
we call the Chopart joint. In addition to the joint capsule, some ligaments confer
stability, both dorsal and plantar (dorsal and palntar calcaneo-cuboid ligaments).
The bifurcated ligament also aids in stability. This joint is not completely flat and
has a sinuous shape [1].
During walking the calcaneocuboid joint, together with the talonavicular and
talocalcaneal, plays a fundamental role in the accommodation of the foot on the
ground and during the toe-off phase. These joints are responsible for making the
foot a flexible structure in the beginning of stance phase and rigid one during the
toe-off phase [1]. Therefore, any factor that leads to loss of mobility, whether by
pathologies or surgeries, affects the biomechanical performance of the foot during
walking. The calcaneocuboid arthrodesis alone seems to be the one that least affects
the biomechanics of the foot [66]. Astion and collaborators [66], in study in ana-
tomical pieces, found that talonavicular arthrodesis decreases about 98% of the
inversion and eversion movement of the hindfoot. However, the calcaneocuboid
movement blockade reduces about 33% of the talonavicular inversion and eversion
movement. Apparently the talonavicular block significantly reduces the calcaneus-
cuboid movement, but the reverse is not true.
10.2 Indications for Arthrodesis
Indications for calcaneocuboid arthrodesis are multiple [66, 68–71]. Fractures may
lead to future osteoarthritis. Neurological diseases with loss of tendon function may
require arthrodesis to stabilize the foot. The correction of deformities caused by
congenital diseases, such as congenital clubfoot; or progressive collaspsing foot

deformity are also part of the indications for calcaneocuboid arthrodesis. As men-
tioned above, arthrodesis of this isolated joint is not common, and is usually associ-
ated with some other procedure in the foot.
In 1961, Evans [70, 72] described calcaneocuboid arthrodesis as a procedure
associated with the treatment of congenital clubfoot. Although currently this proce-
dure is not routinely employed, the long-term result of calcaneocuboid arthrodesis
in cases of congenital clubfoot with recurrent deformity, after failure of the initial
treatment, still seems to be acceptable [68].
Surgical approach The approach employed is the dorsal-lateral, centered on the

calcaneus-cuboid, extending between the anterior portion of the calcaneus and the
proximal portion of the cuboid [69, 73]. When subtalar arthrodesis is also scheduled
in the same procedure, the surgical access can be extended further proximal and the
two joints exposed through the same approach. Partial detachment of the extensor
digitorum brevis may be necessary. The fibular tendons are retracted to proximal
and plantar [69, 74, 75]. This joint has a saddle shape [66], which should be taken
into consideration when removing joint cartilage and subchondral bone.
Fixation Several fixation methods are described in the literature [66, 75–77].
One of the most used is the fixation with one or two oblique screws in the joint,
performing compression. These screws can be inserted from the calcaneus to the
cuboid or vice versa [75, 77, 78]. A 6.5 mm long screw, starting from the poste-
rior process of the calcaneus to the cuboid is also described. In an anatomical
study, Khann et al. [75] found that an axial screw provides better fixation than a
screw inserted obliquely. Staple fixation is also a possibility [66, 77]. Milshteyn
et al. [79], also in a study on cadavers, found that the fixation with locked plate
is more rigid than the fixation with oblique screws.
10.4 Calcaneo-Cuboid Arthrodesis with Lateral

Column Lengthening
Cuboid joint arthrodesis has been described as part of the surgical procedure for the
treatment of progressive collaspsing foot deformity. When correction of the abduc-
tion deformity is necessary, one of the options is calcaneocuboid arthrodesis with
bone grafting to lengthen the lateral column [69, 73, 76, 79–81]. Grunander and
Thordarson [73] believe that the potential for correcting the deformity with this
procedure is great. Deland et al. [69] observed that after calcaneocuboid arthrodesis
with lengthening of the lateral column, the talonavicular preserves about 48% of its
movement and the subtalar, about 70%. The surgical approach is the same used in
arthrodesis. Thomas et al. [82] recommend for this procedure that the surfaces to be
arthrodesed should be flat. Lateral column lengthening is performed through bone
graft interposition in the space created. Bone graft size varies between 8 and 15 mm
[69, 74, 82]. The intraoperative fluoroscopy helps measure the exact measurement
of the graft by forefoot adduction. The source of the tricortical graft is usually the
patient’s own iliac crest. Despite the theoretical advantage of the autograft, this
extra procedure increases the morbidity of the surgery [73]. Some authors report the
use of allograft [73] or synthetic substitutes [76]. It is important that the lateral sur-
face of the graft be molded to avoid peroneal tendons irritation [74]. In general, the
healing time of this arthrodesis is about 12 weeks. The lateral column lengthening
causes increased tension in the surgical scar, which may lead to dehiscence of the
suture and lesion of the sural nerve more frequently. Care should be taken in the
manipulation of soft tissues during surgery to reduce the incidence of these compli-
cations. The non-union of this arthrodesis varies from 11% to 20% in the literature
[74, 83]. Proper preparation of joint surfaces and rigid fixation are tactics that help
control non-union risk. Thomas et al. [82] recommend fixation with plate and
screws. Immobilization and non-weightbearing should be kept por 8 weeks postop-
eratively (Figs. 7, 8, 9, and 10).
10.5 Results
CC fusion without lengthening the lateral column occurs in almost all cases. In
literature, the possibility pseudoarthrosis varies from 0% to 11% [70, 71, 84],
however, these studies are related to calcaneocuboid arthrodesis in triple arthrod-
esis. Grunander and Thordarson [73] described calcaneocuboid arthrodesis with
Fig. 7 Weightbearing
radiography in lateral view
of a triple arthrodesis
demonstrating the fixation
of the calcaneal-cuboid
arthrodesis with a 6.5 mm
screw from posterior to
anterior
Fig. 8 Oblique view on

X-ray showing bone graft
in the calcaneal-cuboid
joint
the calcaneocuboid
arthrodesis with the
addition of a tricortical
graft block for lateral
column lengthening
Fig. 10 Lateral X-ray of a

case of triple arthrodesis in
which lengthening of the
lateral column with a
tricortical graft block was
employed in the calcaneus-
cuboid arthrodesis
lengthening of the lateral column using an allograft (femoral head) associated

with platelet-rich plasma and noted 7 cases of pseudoarthrosis in 16 patients.
They considered the number of complications high and recommended against
this technique. They commented that the use of the patient’s own iliac graft and
fixation with plate and screws should reduce the incidence of pseudoarthrosis.
However, as they observed good results with lateral column lengthening in the
anterior part of the calcaneal bone (Evans procedure), they did not opt for calca-
neocuboid arthrodesis anymore. Other possible complications are sural nerve
injury, fibular tendon injuries, stress fractures [66], suture dehiscence, symptom-
atic harware and infection [73].
11 Tarso-Metatarsal Arthrosis
Although not widely cited in the literature, midfoot arthrosis can cause chronic
pain with significant impact on daily life activities [84–86]. The intention of this
chapter is to describe briefly the anatomy and biomechanics of this region the diag-
nosis and the possible treatments of this problem.
11.1 Anatomy and Biomechanics
The midfoot includes the tarso-metatarsal, intercuneiform and naviculo-

cuneiform and cuboid-cuneiform joints. The Navicular has three articular facets
that articulate with the three cuneiforms. We can also consider a joint between
the cuboid and navicular, sometimes fibrous and more rarely even a synovial joint
[85, 87].
In this section we will not address the talonavicular and calcaneal-cuboid joints,
which are part of the hindfoot. The metatarsal tarsal joints can be divided into three
columns [84, 85, 87, 88].
–– Medial column: includes the medial cuneiform and the first metatarsal bone.
–– Intermediate column: includes the intermediate and lateral cuneiform and the
second and third metatarsal bone.
–– Lateral column: includes the cuboid and the fourth and fifth metatarsal bone.
The stability of the region, which is important for the gait biomechanics, is
given by the shape of the bone joints and the ligamentos strength [84, 87]. In a
cross section, the midfoot bones are arranged in the shape of a Roman arch, giving
intrinsic stability. The second metatarsal has a more proximal position, which also
confers stability. The bones of this region are united by strong plantar, interosse-
ous and dorsal ligaments [85]. However, there is no interosseous ligament between
the first and second metatarsal bone. In fact, instead of a ligament between the
base of the first and second metatarsal bone, there is a strong ligament between the
base of the second metatarsal bone and the medial cuneiform, known as the
Lisfranc ligament. This ligament plays a fundamental role in the stability and bio-
mechanics of the region [84, 85]. The peroneos longus tendon, which runs from
lateral to medial in the plantar region of the foot, also acts in the stabilization of
the midfoot [84, 87].
With less mobility than other regions of the foot, the midfoot is the link between
the forefoot and the hindfoot. It helps to keep the foot as a rigid structure during
propulsive phase and flexible one in the stance phase [1, 85, 86]. The smallest move-
ment occurs between the intermediate cuneiform and the second metatarsal, a place
of greater stability and where most of the load passes during walking [84, 87]. This
fact may explain these joints are the most frequent sites of midfoot osteoarthritis,
even in the absence of a traumatic event [84, 87]. The loss of midfoot stability can
be visualized with the collapse of the medial longitudinal plantar arch. This collapse
compromises the foot function decreasing its mechanical efficiency [2, 6].
11.2 Diagnosis and Clinical Chart
History, physical examination and X-rays exams are key to midfoot osteoarthritis
diagnosis.
Trauma is the most common cause of osteoarthritis in the Lisfranc region [84,
88, 90]. Patients with arthrosis of the midfoot usually report fractures or ligament
injuries in the past. In some cases, these ligament injuries may have been subtle,
having gone unnoticed [88, 90]. Primary arthrosis is not so common. Inflammatory
arthritis, such as gout and rheumatoid arthritis [87], also cause joint degeneration in
the midfoot and usually affects multiple joints. When the cause is suspected to be a
rheumatic disease, blood tests and a rheumatologist’s evaluation should be ordered.
Overload caused by ankle and/or hindfoot arthrodesis can also lead to arthrosis in
this region. Although it often does not cause painful symptoms, Charcot’s arthropa-
thy in insensitive foot can also lead to joint degeneration [84, 85, 87]. The progres-
sive collaspsing foot deformity, in advanced phases, can also end up in
tarso-metatarsal joint degeneration [85]. According to Nemec et al. [89], obesity is
another factor that can lead to the appearance of arthrosis.
The patient with typical midfoot arthrosis has pain that worsens when walking
on uneven ground [85]. There may be a feeling of instability [84]. In some cases,
collapse of the plantar arch occurs [89, 90], associated with abduction deformity.
Dorsal osteophytes, often painful, may appear on the dorsum of the foot [84, 85,
87]. Gastrosoleus shortening leads to loss of ankle and foot dorsiflexion, increasing
the midfoot pressure when walking and is also a factor that may be involved in the
appearance of arthrosis [86, 89].
Keiserman et al. [91] described the piano key test, which helps to better locate
which joint is symptomatic. Although the injection of local anesthetic can also help
identify which joint is symptomatic, these joints are small, making it difficult to
inject in the correct place, which would hinder accurate diagnosis [84, 88, 90].
Weightbearing x-rays, in AP, lateral and obliques views are the first exams to
order [84, 85, 87, 89]. In X-rays, correct alignment of the metatarsals with the cune-
iform and cuboid bones has to be confirmed. Decreased joint space, presence of
osteophytes, bone sclerosis and subchondral cysts are radiographic signs of osteo-
arthritis [90]. In the lateral X-ray observe whether the plantar arch has collapsed.
The angles between the talus and the first metatarsal bone, both in the dorsal-plantar
and lateral views, as well as the height from the medial cuneiform to the 5th meta-
tarsal base are used to measure the deformity [89]. Both magnetic resonance imag-
ing and computed tomography assist in mapping the severity and extent of arthrosis.
It is important, when arthrodesis is considered as treatment, to evaluate signs of
degeneration in neighboring joints [84].
The conservative treatment should always be the first choice [87, 89, 92]. Analgesics
and anti-inflammatory drugs, physiotherapy, local infiltrations, insoles, modifica-
tions in shoes and orthoses can be effective for pain relief [84, 87, 93]. The strategy
must be focused on pain relief, increase of midfoot stability and load relief in the
affected region [85].
Although analgesics and anti-inflammatory drugs can relieve the symptoms of
affected joints, the chronic use of this type of medication should be viewed with
caution due to the adverse effects of these medications, especially cardiovascular
system [85, 90, 94].
As orthoses and insoles have little adverse effects, they are an attractive method
in the initial approach to arthrosis of the midfoot [90]. Footwear with rigid soles
(trekking shoes) tend to facilitate the transfer of load during walking, decreasing the
overload in the midfoot and consequently relieving pain. The ankle foot orthosis
(AFO) also relieves pain, however, it causes great restriction of movement both in
the ankle and the foot, and they are not easily accepted by the patient [90]. Halstead
et al. found that the use of orthosis for 12 weeks led to clinical and biomechanical
improvements in patients with midfoot osteoarthritis [ 95].
Local injections with corticoids are also described in the treatment of arthrosis of
the midfoot. They assist in pain relief and the correct location of painful joints for
future arthrodesis [84]. However, the correct identification of the injection site can
be difficult, and sometimes the assistance of ultrasound is necessary.
The decision of surgical treatment should be guided by pain intensity, functional

restriction and failure of conservative treatment [84, 87, 88, 90, 96]. Komenda et al.,
[88] as well as Gougoulias and Lampridis [86], recommend that the surgical treat-
ment should only be chosen three to six months after the conservative treatment is
initiated. When dorsal osteophytes are the cause of pain, exostectomy i.e. removal
of these osteophytes, are effective for pain treatment. But the definitive treatment
for this osteoarthritis is joint arthrodesis [84, 93], mainly of the medial and interme-
diate midfoot columns [85, 87]. One of the challenges of arthrodesis in the midfoot
is the correct identification of which joints are painful, due to the large number of
joints that may be involved in the genesis of pain [84, 85]. For this reason some
authors advocate infiltration with local corticoid or anesthetic [87]. In the preopera-
tive planning one should consider whether the correction of any deformity is neces-
sary (modeling arthrodesis) or if the arthrodesis can be in situ [84, 88]. For Johnson
and Johnson [97], the correction of the initial deformity did not seem to present
advantages over in situ arthrodesis, and they do not recommend the correction of
deformities in midfoot arthrodesis. Sangeorzan et al. [98], as well as Mann et al.
[92], concluded that the reduction of joints with correction of deformities is an
important factor for a good result. They also observed more than 90% of good
results with midfoot arthrodesis, however, they noticed bad results when the initial
deformity was not corrected. The choice of implant for fixation also be considered.
There are several options, including Kirschner wires, cannulated screws, non-lock-
ing and locking plates, staples and hybrid systems [84, 86].
When the talo-medial cuneiform-first metatarsal (whole medial column) col-
lapses, the fusion of the entire medial column, from the talus to the first metatarsal,
can be an interesting option with satisfactory deformity correction and pain relief.
According to Horton and Olney [99], and Mann et al. [92], it is important to correct
residual deformities and restore the medial longitudinal arch.
Arthrodesis of the medial and intermediate columns is more frequent. It is impor-
tant here to adequately prepare the joint surfaces and if possible, achieve a rigid
stabilization [85]. Generally, a longitudinal approach is used between the base of the
first and second metatarsals and another between the base of the third and fourth
metatarsals. An adequate spacing between these two pathways is important to keep
the viability of local soft tissues. Several materials are described for fixation, plates
and screws or interfragmentary screws are the most employed [85, 90]. Nemec et al.
[89], recommended the use of interfragmentary screws when there is good bone
quality and the use of a plate with poor bone stock. Other studies report that there is
no evidence favoring the use of one implant or another [85, 86]. Buddha et al. [96]
found that the use of isolated dorsal plate, without the interfragmentary screw is
associated with both delayed healing and pseudoarthrosis. They also call attention
that the use of dorsal plates is associated with a greater possibility of skin problems.
In a study in anatomical specimens, Cohen et al. [100] identified that the fixation
with interfragmentary screws is also more rigid than the H-blocked plate. They
affirmed that the plate does not achieve compression in the joint that has to be fused.
This finding was the same of Baxter et al. [101], who also found in an anatomical
study that the dorsomedial plate does not achieve the same compression at the site
of the arthrodesis obtained with interfragmentary screws. Although interfragmen-
tary screws are the preferred method of fixation of this arthrodesis, when there is
bone gap or bone with poor quality (osteoporotic), some authors suggest the use of
plates, with or without interfragmentary screws [102]. The use of bone graft helps
with bone healing [89, 96] which generally takes around 12 weeks [3]. Gougoulias
and Lampridis [86] do not recommend the use of routine bone grafting unless there
is no bone contact. They reported 6.6% of pseudoarthrosis in 30 cases. Buddha and
collaborators consider the use of bone graft essential in midfoot [96] arthrodesis.
During the first 6 postoperative weeks, immobilization and non weightbearing is
recommended (Figs. 11, 12, 13, 14, and 15) [89, 90].
Fig. 11 Planning of the

access routes for medial
and intermediate columns
arthrodesis. The spacing
between the pathways
should be sufficient not to
compromise the circulation
of the local skin
Fig. 12 Intermediate
column exposure, with
signs of osteoarthritis
between the second and
third metatarsals and
cuneiforms. The plantar
bending of the metatarsals
facilitates the visualization
of the surface to be
prepared for arthrodesis
Fig. 13 Positioning of a
dorsal H-plate for midline
arthrodesis
Fig. 14 X-ray showing

arthrodesis of the medial
and intermediate columns,
consolidated, associated
with arthrodesis of the
intercuneiform and
naviculo-cuneiform joints
radiographic image of an
arthrodesis of the medial
and intermediate columns,
fixed with dorsomedial
plate and interfragmentary
screws
Complications of this arthrodesis range from non-union, neuroma, hardware

related pain, metatarsalgia, stress fractures of the metatarsals [85, 89] and osteoar-
thritis of the adjacent joints. The incidence of non-union in the literature varies from
2% to 10% [89, 92, 96, 103]. Smoking [96] and obesity [89] have been associated
with a higher possibility of pseudoarthrosis. Nemec et al. [89] observed, in a series
of cases, that patients with body mass index (BMI) higher than 30 kg/m2, had worse
clinical functional outcome according to the AOFAS score and more complications
than patients with BMI < 30 kg/m2. Gougoulias and Lampridis [86] reported that
despite a successful arthrodesis, 30% of the patients complain about pain in the
neighboring joints and that 34% needed to wear insoles after surgery to relieve
symptoms. The need for hardware removal varies in the literature between 9% and
25% [87, 89, 90].
The arthrodesis of the lateral column (lateral tarsus-metatarsal joints) is still
controversial in the literature [ 85, 87, 93]. The mobility of these joints is impor-
tant in the accommodation of the midfoot on the ground. The lateral column
fusion has been associated with chronic lateral pain, pseudoarthrosis and stress
fracture [84, 85, 93]. Raikin and Schon [93] stated that arthrodesis of the lateral
column (cuboid - fourth and fifth metatarsal) can improve pain and function.
However, in their study, most patients (22 arthrodesis) had deformity due to
Charcot’s arthropathy, which makes it difficult to evaluate the function and pain
in the postoperative result, since these patients have insensitive feet and do not
have the biomechanics of normal gait due to loss of proprioception. For this rea-
son, although there is no formal contraindication for lateral column arthrodesis,
there are descriptions in the literature of procedures that try to maintain the move-
ment of the region [85]. Berlet et al. [104] retrospectively evaluated the results of
joint resection of the lateral column and interposition of the peroneus tertius ten-
don. There are other studies that propose interposition of synthetic material in the
region. Many authors recommend that surgery should be postponed as much as
possible [84, 85]. Komenda et al. [88] affirm that the mobility of the lateral col-
umn is important for the function of the foot and many times, despite the radio-
graphic images showing signs of joint degeneration, the patient is asymptomatic
or has mild pain.
12 Summary
Arthrosis in the midfoot and hindfoot region are mostly post-traumatic or secondary
to systemic inflammatory diseases, and usually cause significant pain and func-
tional disability. Although conservative treatment is the first choice, it is often not
effective, which makes surgery, especially arthrodesis, the best alternative in many
cases. To achieve succesful results, the most important factors are joint preparation,
patient selection and counseling, bone contact at the fusion site, rigid internal fixa-
tion and an adequate postoperative protocol including non weightbearing and
immobilization.
References
1. Mann RA, Haskell A. Biomechanics of the foot and ankle. In: Coughlin MJ, Mann RA,
Saltzmann CL, editors. Surgery of the foot and ankle. 8th ed. Philadelphia: Elsevier Health;
200. p. 3–45.
2. Silfverskiöld N. Reduction of the uncrossed two-joints muscles of the leg to one-joint mus-
cles in spastic conditions. Acta Chir Scand. 1924;56:315–30.
3. Colin F, Lang TH, Zwicky L, et al. Subtalar joint configuration on weightbearing CT scan.
Foot Ankle Int. 2014;35:1057–62.
4. Hirschmann A, Pfirrmann CWA, Klammer G, et al. Upright cone CT of the hindfoot: com-
parison of the non-weight-bearing with the upright weight-bearing position. Eur Radiol.
2014;24:553–8.
5. Krähebühl N, Tschuck M, Bollinger L, et al. Orientation of the subtalar joint. Foot Ankl Int.
2015;37:109–14.
6. Probasco W, Hallen AM, Yu J, et al. Assessment of coronal plane subtalar joint alignment in
peritalar subluxation via weight-bearing multiplanar imaging. Foot Ankle Int. 2015;36:302–9.
7. Wirth SH, Zimmermann SM, Viehöfer AF. Open Technique for in situ subtalar fusion. Foot
Ankle Clin N Am. 2018;23:461–74.
8. Mei-Dan O, Carmont M, Laver L, Mann G, Maffulli N, Nyska M. Intra-articular injections
of hyaluronic acid in osteoarthritis of the subtalar joint: a pilot study. J Foot Ankle Surg.
2013;52(2):172–6.
9. Sadykov RI, Akhtyamov IF. Efficacy and safety of chondroitin sulfate therapy in patients
with knee and hip osteoarthritis. Khirurgiia (Mosk). 2020;7:76–81.
10. Alekseeva LI, Kashevarova NG, Taskina EA, Sharapova EP, Anikin SG, Strebkovan EA,
Raskina TA, Zonova EV, Otteva EN, Rodionova SS, Torgashin AN, Buklemishev UV, Shmidt
EI, Shesternya PA, Naumov AV, Zagorodniy NV, Lila AM. The efficacy and safety of intra-
articular application of a combination of sodium hyaluronate and chondroitin sulfate for
osteoarthritis of the knee: a multicenter prospective study. Ter Arkh. 2020;92(5):46–54.
11. Fletcher AN, Lilies JL, Steele JJ, Pereira GF, Adams SB. Systematic review of subtalar dis-
traction arthrodesis for the treatment of subtalar arthritis. Foot Ankle Int. 2020;41:437–48.
12. Chen Y, Zhang K, Quiang M, Hao Y. Maintenance of longitudinal foot arch after dif-
ferent mid/hindfoot arthrodesis procedures in a cadaveric model. Clin Biomech.
2014;29:170–6.
13. Cifuentes-De la Portilla C, Larrainzar-Garijo R, Bayod J. Analysis of biomechanical stresses
caused by hindfoot joint arthrodesis in the treatment of adult acquired flatfoot deformity: A
finite element study. Foot Ankle Surg. 2020;26:412–20.
14. Astion D, Deland J, Otis J, et al. Motion of the hindfoot after simulated arthrodesis. J Bone
Joint Surg. 1997;79:241–6.
15. Patel NB, Blazek C, Scanlan R, Manway JM, Burns PR. Common pitfalls in subtalar joint
preparation for arthrodesis via sinus tarsi approach. J Foot Ankle Surg. 2020;59(2):253–7.
16. Abyar E, McKissack HM, Pinto MC, Littlefield ZL, Moraes LV, Stefani K, Shah
A. Subtalar fusion preparation: what are we really doing? A cadaver study. Foot Ankle Spec.
2020;13(3):201–6.
17. Galli MM, Scott RT, Bussewitz BW, Hyer CF. A retrospective comparison of cost and
efficiency of the medial double and dual incision triple arthrodeses. Foot Ankle Spec.
2014;7:32–6.
18. Sammarco VJ, Magur EG, Sammarco GJ, Bagwe MR. Arthrodesis of the subtalar and
talonavicular joints for correction of symptomatic hindfoot malalignment. Foot Ankle Int.
2006;27:661–6.
19. DeVries JG, Scharer B. Hindfoot deformity corrected with double versus triple arthrodesis:
radiographic comparison. J Foot Ankle Surg. 2015;54:424–7.
20. Jeng CL, Tankson CJ, Myerson MS. The single medial approach to triple arthrodesis: a
cadaver study. Foot Ankle Int. 2006;27:1122–5.
21. So E, Reb CW, Larson DR, Hyer CF. Medial double arthrodesis: technique guide and tips. J
22. Wagner E, Melo R. Subtalar arthroscopic fusion. Foot Ankle Clin N Am. 2018;23:475–83.
23. Vilá-Rico J, Mellado Romero MA, Bravo-Giménez, Jiménez-Díaz V, Ojeda-Thies C. Subtalar
arthroscopic arthrodesis: technique and outcomes. Foot Ankle Surg. 2017;23:9–15.
24. Dutra JMG, Barcelos VA, Prata SDS, Rizzo MAG, Filho RLR. Oliveira DB arthroscopic
subtalar arthrodesis – results and complications. A systematic review. Journal of the. Foot and
Ankle. 2020;14:205–10.
25. Rungprai C, Phisitkul P, Femino JE, Martin KD, Saltzman CL, Amendola A. Outcomes and
complications after open versus posterior arthroscopic subtalar arthrodesis in 121 patients. J
26. Martín Oliva X, Falcão P, Fernandes Cerqueira R, Rodrigues-Pinto R. Posterior arthroscopic
subtalar arthrodesis: clinical and radiologic review of 19 cases. J Foot Ankle Surg.
2017;56:543–6.
27. Albert A, Deleu PA, Leemrijse T, Maldague P, Devos BB. Posterior arthroscopic subtalar
arthrodesis: ten cases at one-year follow-up. Orthop Traumatol Surg Res. 2011;97:401–5.
28. Beimers L, Frey C, van Dijk CN. Arthroscopy of the posterior subtalar joint. Foot Ankle Clin.
2006;11:369–90.
29. Mosca M, Caravelli S, Vannini F, Pungetti C, Catanese G, Massimi S, Fuiano M, Faldini C,
Giannini S. Mini bone block distraction subtalar arthrodesis (SAMBB) in the management
of acquired adult flatfoot with subtalar arthritis: a modification to the grice-green procedure.
Joints. 2019;13(7):64–70.
30. Sanhudo JAV. Artrodese subtalar com enxerto em bloco de osso local. Revista ABTPé.
2012;6:37–8.
31. Sanhudo JAV. Bone block graft from calcaneus for foot and ankle reconstruction. Foot &
Ankle Orthopaedics. 2016;1:1.
32. Herrera-Pérez M, Andarcia-Bañuelos C, Barg A, Wiewiorski M, Valderrabano V, Kapron AL,
De Bergua-Domingo JM, Pais-Brito JL. Comparison of cannulated screws versus compres-
sion staples for subtalar arthrodesis fixation. Foot Ankle Int. 2015;36:203–10.
33. Yuan CS, Chen W, Chen C, Yang GH, Hu C, Tang KL. Effects on subtalar joint stress dis-
tribution after cannulated screw insertion at different positions and directions. J Foot Ankle
Surg. 2015;54:920–6.
34. Chuckpaiwong B, Easley ME. Glisson RR screw placement in subtalar arthrodesis: A biome-
chanical study. Foot Ankle Int. 2010;30:133–41.
35. Jastifer JR, Alrafeek S, Howard P, Gustafson PA, Coughlin MJ. Biomechanical evalua-
tion of strength and stiffness of subtalar joint arthrodesis screw constructs. Foot Ankle Int.
2016;37:419–26.
36. Eichinger M, Schmöiz W, Brunner A, Mayr R, Bölderl A. Subtalar arthrodesis stabilization
with screws in an angulated configuration is superior to the parallel disposition: a biome-
chanical study. Int Orthop. 2015;39:2275–80.
37. Wirth SH, Viehöfer A, Fritz Y, Zimmermann SM, Rigling D, Urbanschitz L. How
many screws are necessary for subtalar fusion? A retrospective study. Foot Ankle Surg.
2020;26:699–702.
38. Riedl M, Glisson RR, Matsumoto T, Hofstaetter SG, Easley ME. Torsional stiffness after
subtalar arthrodesis using second generation headless compression screws: Biomechanical
comparison of 2-screw and 3-screw fixation. Clin Biomech. 2017;45:32–7.
39. Tuijthof GJ, Beimers L, Kerkhoffs GM, Dankelman J, Dijk CN. Overview of subtalar
arthrodesis techniques: options, pitfalls and solutions. Foot Ankle Surg. 2010;16:107–16.
40. Chaudhari N, Godoy-Santos AL, Netto CC, Rodriguez R, Dun S, He JK, McKissack H,
Fleisig GS, Pires EA, Shah A. Biomechanical comparison of plantar-to-dorsal and dorsal-to-
plantar screw fixation strength for subtalar arthrodesis. Einstein. 2020;18:1–6.
41. Pearce DH, Mongiardi CN, Fornasier VL, Daniels TR. Avascular necrosis of the talus: a
pictorial essay. Radiographics. 2005;25:399–410.
42. Kunzler D, Shazadeh Safavi P, Jupiter D, Panchbhavi VK. A comparison of removal
rates of headless screws versus headed screws in calcaneal osteotomy. Foot Ankle Spec.
2018;11:420–4.
43. Diezi C, Favre P, Vienne P. Primary isolated subtalar arthrodesis: outcome after 2 to 5 years
Followup. Foot Ankle Int. 2008;29:1195–202.
44. Yildrin T, Sofu H, Çamurcu Y, et al. Isolated subtalar arthrodesis. Acta Orthop Belg.
2015;81:155–60.
45. Easley ME, Trnka H-J, Schon LC, et al. Isolated subtalar arthrodesis. J Bone Joint Surg Am.
2000;82:613–24.
46. Radnay CS, Clare MP, Sanders RW. Subtalar fusion after displaced intra-articular
calcaneal fractures: does initial operative treatment matter? J Bone Joint Surg Am.
2009;91:541–6.
47. van der Vliet QMJ, Hietbrink F, Casari F, Leenen LPH, Heng M. Factors Influencing func-
tional outcomes of subtalar fusion for posttraumatic arthritis after calcaneal fracture. Foot
Ankle Int. 2018;39:1062–9.
48. Savory KM, Wulker N, Stukenborg C, Alfke D. Biomechanics of the hindfoot joints in
response to degenerative hindfoot arthrodeses. Clin Biomech. 1998;13:62–70.
49. O’Malley MJ, Deland JT, Lee KT. Selective hindfoot arthrodesis for the treatment of adult
acquired flatfoot deformity: an in vitro study. Foot Ankle Int. 1995;16:411–7.
50. Monteagudo M, Maceira E. Management of müller-weiss disease. Foot Ankle Clin.
2019;24:89–105.
51. Van den Broek M, Vandepitte G, Somville J. Dual window approach with two-side screw
fixation for isolated talonavicular arthrodesis. J Foot Ankle Surg. 2017;56:171–5.
52. Miller SD, Schon LC, Melvani RT, Atwater LC, Aynardi M. Evaluating the safety of
percutaneous dorsolateral talonavicular joint fixation in modified double arthrod-
esis: an anoatomic study. Foot & Ankle Orthopaedics. 1(1) https://doi.org/10.117
7/2473011416S00063.
53. Lee SR, Stibolt D, Patel H, Abyar E, Moon A, Naranje S, Shah A. Structures at risk during
percutaneous screw fixation for talonavicular fusion. Foot Ankle Int. 2018;39:1502–8.
54. Jarrel SE, Owen JR, Wayne JS, Adelaar RS. Biomechanical comparison of screw versus
plate/screw construct for talonavicular fusion. Foot Ankle Int. 2009;30(2):150–6.
55. Granata JD, Berlet GC, Ghotge R, Li Y, Kelly B, DiAngelo D. Talonavicular joint fixation: a
biomechanical comparison of locking compression plates and lag screws. Foot Ankle Spec.
2014;7(1):20–31.
56. Harper MC. Talonavicular arthrodesis for the acquired flatfoot in adult. Clin Orthop Relat
Res. 1999;65:8.
57. Chen C-H, Huang P-J, Chen T-B, Cheng Y-M, Lin S-Y, Chiang H-C, Chen L-C. Isolated
talonavicular arthrodesis for talonavicular arthritis. Foot & Ankle Int. 2001;22:633–6.
58. Carranza-Bencano A, Tejero S, Fernández Torres JJ, Del Castillo-Blanco G, Alegrete-Parra
A. Isolated talonavicular joint arthrodesis through minimal incision surgery. Foot Ankle Surg.
2015;21:171–7.
59. Lechler P, Graf S, Köck FX, Schaumburger J, Grifka J, Handel M. Arthrodesis of the
talonavicular joint using angle-stable mini-plates: a prospective study. Int Orthop.
2012;36:2491–4.
60. Harnroongroj T, Chuckpaiwong B. Müller-weiss disease: three- to eight-year follow-up out-
comes of isolated talonavicular arthrodesis. J Foot Ankle Surg. 2018;57:1014–9.
61. Xie M, Xia K, Zhang H, Cao H, Yang Z, Cui H, Gao S, Tang K. Individual headless compres-
sion screws fixed with three-dimensional image processing technology improves fusion rates
of isolated talonavicular arthrodesis. J Orthop Surg Res. 2017;12:1–8.
62. Malik A, Grant E, Rhodenizer J. Analysis of micromotion in a talonavicular arthrodesis with
and without a calcaneal displacement osteotomy in a cadaver model. J Foot Ankle Surg.
2020;59:91–4.
63. Lombardi CM, Dennis LN, Connoly FG, Silhanek AD. Talonavicular joint arthrodesis and
Evans calcaneal osteotomy for treatment of posterior tibial tendon dysfunction. J Foot Ankle
Surg. 1999;38:116–22.
64. Resnick RB, Jahss MH, Choueka J, Kummer F, Hersch JC, Okereke E. Deltoid ligament
forces after tibialis posterior tendon rupture: effects of triple arthrodesis and calcaneal dis-
placement osteotomies. Foot Ankle Int. 1995;16:14–20.
65. Coughlin MJ, Grimes JS, Traughber PD, Jones CP. Comparison of radiographs and CT
scans in the prospective evaluation of the fusion of hindfoot arthrodesis. Foot Ankle Int.
2006;27:780–7.
66. Astion DJ, Deland JT, Otis JC, Kenneally S. Motion of the Hindfoot after simulated arthrode-
sis*. J Bone Jt Surg. 1997;79(2):241–6. https://doi.org/10.2106/00004623-199702000-00012.
67. Barmada M, Shapiro HS, Boc SF. Calcaneocuboid arthrodesis. Clin Podiatr Med Sur.
2012;29(1):77–89. https://doi.org/10.1016/j.cpm.2011.11.002.
68. Chu A, Chaudhry S, Sala DA, Atar D, Lehman WB. Calcaneocuboid arthrodesis for recurrent
clubfeet: what is the outcome at 17-year follow-up? J Child Orthop. 2014;8(1):43–8. https://
doi.org/10.1007/s11832-014-0557-4.
69. Deland JT, Otis JC, Lee K-T, Kenneally SM. Lateral column lengthening with calcaneocu-
boid fusion: range of motion in the triple joint complex. Foot Ankle Int. 1995;16(11):729–33.
70. Evans D. Relapsed club foot. J Bone Jt Surg Br Volume. 1961;43-B(4):722–33. https://doi.
org/10.1302/0301-620x.43b4.722.
71. Graves SC, Mann RA, Graves KO. Triple arthrodesis in older adults. Results
after long-term follow-up. J Bone Jt Surg. 1993;75(3):355–62. https://doi.
org/10.2106/00004623-199303000-00006.
72. Grier KM, Walling AK. The use of Tricortical autograft versus allograft in lateral column
lengthening for adult acquired flatfoot deformity: an analysis of union rates and complica-
tions. Foot Ankle Int. 2010;31(9):760–9. https://doi.org/10.3113/fai.2010.0760.
73. Grunander TR, Thordarson DB. Results of calcaneocuboid distraction arthrodesis. Foot
Ankle Surg. 2012;18(1):15–8. https://doi.org/10.1016/j.fas.2011.01.004.
74. Haeseker GA, Mureau MA, Faber FWM. Lateral column lengthening for acquired adult flat-
foot deformity caused by posterior Tibial tendon dysfunction stage II: a retrospective com-
parison of calcaneus osteotomy with calcaneocuboid distraction arthrodesis. J Foot Ankle
Surg. 2010;49(4):380–4. https://doi.org/10.1053/j.jfas.2010.04.023.
75. Kann NJ, Parks BG, Schon LC. Biomechanical evaluation of two different screw posi-
tions for fusion of the calcaneocuboid joint. Foot Ankle Int. 1999;20(1):33–6. https://doi.
org/10.1177/107110079902000107.
76. Kobayashi H, Kageyama Y, Shido Y. Calcaneocuboid distraction arthrodesis with synthetic
bone grafts: preliminary results of an innovative bone grafting procedure in 13 patients. J
Foot Ankle Surg. 2017;56(6):1223–31. https://doi.org/10.1053/j.jfas.2017.07.003.
77. Van Der KA, Louwerens JWK, Anderson P. Adult acquired flexible flatfoot, treated by
calcaneo-cuboid distraction arthrodesis, posterior tibial tendon augmentation, and percutane-
ous Achilles tendon lengthening: a prospective outcome study of 20 patients. Acta Orthop.
78. Meyer MS, Alvarez BE, Njus GO, Bennett GL. Triple arthrodesis: a biomechanical eval-
uation of screw versus staple fixation. Foot Ankle Int. 1996;17(12):764–7. https://doi.
org/10.1177/107110079601701209.
79. Milshteyn MA, Dwyer M, Andrecovich C, Bir C, Needleman RL. Comparison of two fixa-
tion methods for arthrodesis of the calcaneocuboid joint: a biomechanical study. Foot Ankle
80. Pell RF, Myerson MS, Schon LC. Clinical outcome after primary triple arthrod-
esis*†. J Bone Jt Surgery-american Volume. 2000;82(1):47–57. https://doi.
org/10.2106/00004623-200001000-00006.
81. Sangeorzan BJ, Smith D, Veith R, Hansen ST. Triple arthrodesis using internal fixation in
treatment of adult foot disorders. Clin Orthop Relat R. 1993;294(NA):299–307. https://doi.
org/10.1097/00003086-199309000-00044.
82. Thomas RL, Wells BC, Garrison RL, Prada SA. Preliminary results comparing two
methods of lateral column lengthening. Foot Ankle Int. 2001;22(2):107–19. https://doi.
org/10.1177/107110070102200205.
83. Toolan BC, Sangerozan BJ, Hansen ST. Complex reconstruction for the treatment of dor-
solateral Peritalar subluxation of the foot. Early results after distraction arthrodesis of the
calcaneocuboid joint in conjunction with stabilization of, and transfer of the flexor Digitorum
longus tendon to, the midfoot to treat acquired pes Planovalgus in adults*. J Bone Jt Surg.
1999;81(11):1545–60. https://doi.org/10.2106/00004623-199911000-00006.
84. Kurup H, Vasukutty N. Midfoot arthritis- current concepts review. J Clin Orthop Trauma.
2020;11:399–405.
85. Patel A, Rao S, Nawoczenski D, Flemister AS, DiGiovanni B, Baumhauer JF. Midfoot arthri-
tis. Am Acad. Orthop Surg. 2010;18:417–25.
86. Gougoulias N, Lampridis V. Midfoot arthrodesis. Foot Ankle Surg. 2016;22:17–25.
87. Sayeed SA, Khan FA, Turner NS, Kitaoka HB. Midfoot arthritis. Am J Orthop. 2008;5:251–6.
88. Komenda GA, Myerson MS, Biddinger KR. Results of arthrodesis of the Tarsometatarsal
joints after traumatic injury*†. J Bone Jt Surg. 1996;78:1665–76.
89. Nemec SA, Habbu RA, Anderson JG, Bohay DR. Outcomes following midfoot arthrodesis
for primary arthritis. Foot Ankle Int. 2011;32:355–61.
90. Rao S, Nawoczenski DA, Baumhauer JF. Midfoot arthritis. Techniques. Foot Ankle Surg.
2008;7:188–95.
91. Keiserman LS, Cassandra J, Amis JA. The piano key test: a clinical sign for the identification
of subtle Tarsometatarsal pathology. Foot Ankle Int. 2003;24:437–8.
92. Mann RA, Prieskorn D, Sobel M. Mid-tarsal and Tarsometatarsal arthrodesis for primary
degenerative osteoarthrosis or osteoarthrosis after trauma*. J Bone Jt Surg. 1996;78:1376–85.
93. Raikin SM, Schon LC. Arthrodesis of the fourth and fifth Tarsometatarsal joints of the mid-
foot. Foot Ankle Int. 2003;24:584–90.
94. Da Costa BR, Reichenbach S, Keller N, Nartey L, Wandel S, Jüni P, et al. Retracted: effec-
tiveness of non-steroidal anti-inflammatory drugs for the treatment of pain in knee and hip
osteoarthritis: a network meta-analysis. Lancet. 2016;387:2093–105.
95. Halstead J, Chapman GJ, Gray JC, Grainger AJ, Brown S, Wilkins RA, et al. Foot orthoses
in the treatment of symptomatic midfoot osteoarthritis using clinical and biomechanical out-
comes: a randomised feasibility study. Clin Rheumatol. 2016;35:987–96.
96. Buda M, Hagemeijer NC, Kink S, Johnson AH, Guss D, DiGiovanni CW. Effect of fixation
type and bone graft on Tarsometatarsal fusion. Foot Ankle Int. 2018;39:1394–402.
97. Johnson JE, Johnson KA. Dowel arthrodesis for degenerative arthritis of the Tarsometatarsal
(Lisfranc) joints*. Foot Ankle Int. 1986;6:243–53.
98. Sangeorzan BJ, Verth RG, Hansen ST. Salvage of Lisfranc’s Tarsometatarsal joint by arthrod-
esis. Foot Ankle Int. 1990;10:193–200.
99. Horton GA, Olney BW. Deformity correction and arthrodesis of the midfoot with a medial
plate*. Foot Ankle Int. 1993;14:493–9.
100. Cohen DA, Parks BG, Schon LC. Screw fixation compared to H-locking plate fixation for
first Metatarsocuneiform arthrodesis: a biomechanical study. Foot Ankle Int. 2005;26:984–9.
101. Baxter JR, Mani SB, Chan JY, Vulcano E, Ellis SJ. Crossed-screws provide greater
Tarsometatarsal fusion stability compared to compression plates. Foot Ankle Specialist.
2015;8:95–100.
102. Filippi J, Myerson MS, Scioli MW, Hartog BDD, Kay DB, Bennett GL, et al. Midfoot
arthrodesis following multi-joint stabilization with a novel hybrid plating system. Foot Ankle
Int. 2012;33:220–5.
103. Jung HG, Myerson MS, Schon LC. Spectrum of operative treatments and clinical outcomes
for atraumatic osteoarthritis of the Tarsometatarsal joints. Foot Ankle Int. 2007;28:482–9.
104. Berlet GC, Anderson RB. Tendon arthroplasty for basal fourth and fifth metatarsal arthritis.
Foot Ankle Int. 2002;23:440–6.
Forefoot-Driven Hindfoot Deformity:
Coupled Deformity
Norman Espinosa and Georg Klammer
1 Introduction
The foot and ankle are fascinating and complex biomechanical structures of the
human body. They are composed of a multitude of bones, ligaments and tendons,
which shape various joints [1, 2]. The smooth interplay of those kinematic chains
allow a perfect bipedal gait.
Even in the presence of biomechanical alterations within this system, the foot
and ankle is able to compensate for them. All of them – of course – being three
dimensional and dynamic corrections. Sometimes those compensations may last for
a long time before they start to fail.
The talonavicular joint represents the link between hind- and mid-to forefoot. It
is crucial for the transfer of vertical forces into horizontal load distribution. Its
cardan-style construction and function categorizes it as one of the most important
joints in the foot and ankle [3–6].
The subtalar joint offers a large potential for corrections in patients suffering
from flatfeet, while its potential in varus hindfeet is quite more limited [7–14].
However, both joints are connected to each other and act in concert to adapt to any
motion and alteration within the system.
In this chapter the problem of forefoot-driven hindfoot deformities and patholo-
gies will be discussed. To understand those mechanical abnormalities, it is manda-
tory to distinguish between forefoot-driven hindfoot valgus and forefoot-driven
hindfoot varus deformities.
Whereas many scientific literature is available regarding the forefoot-driven
hindfoot varus deformity, almost nothing is found for the forefoot-driven hindfoot
N. Espinosa (*) · G. Klammer

Institute for Foot and Ankle Reconstruction Zurich, FussInstitut Zurich, Zurich, Switzerland

Switzerland AG 2022
670 N. Espinosa and G. Klammer
valgus deformity [15, 16]. To the opinion of the author the latter does exist as well
and could pose more challenging demands for any surgeon when treatment
is needed.
2 Definition of Forefoot-Driven Hindfoot Deformity
Any biomechanical alteration of kinematics within the fore-and midfoot can result
in compensatory misalignment of the hindfoot. Important to know is, that all hind-
foot deformities, which are provoked by the forefoot, are flexible.
The cause can either be static (e.g. plantarflexed first ray) or dynamic (e.g. hyper-
activity of the peroneus longus muscle). It is therefore crucial to properly identify
the origin of pathology to formulate an adequate treatment strategy.
3 Etiologies of Forefoot-Driven Hindfoot Deformities
The causes for any forefoot-driven hindfoot deformity are variable and require cor-
rect clinical and intellectual judgement. Sometimes, combinations of causes could
be responsible for the development of those pathologies and need therefore more
complex or expanded treatment strategies. If only one of those causes goes mis- or
undiagnosed the result of treatment may be unsatisfactory for the patient.
3.1 Forefoot-Driven Hindfoot Varus
The underlying causes should be classified into dynamic, static and combined
forms [16].
One of the most discussed etiologies of a dynamically forefoot-driven hindfoot
varus is a neurologic disorder resulting in an imbalance between agonists and antag-
onists. The peroneus longus, peroneus brevis, tibialis anterior and tibialis posterior
play an essential role [17].
Weakness of the tibialis anterior and peroneus brevis muscle group in combi-
nation with an overpowering peroneus longus and strong tibialis posterior muscle
lead to the characteristic deformation of the fore-, hind- and midfoot [16]:
Pronation of forefoot, supination of midfoot and elevation of longitudinal arch.
To compensate for the plantarflexed first ray the hindfoot needs to swing
into varus.
In contrast, static plantarflexion of the first ray causing structural rigidity of the
forefoot forces the flexible hindfoot also to push into varus [18]. The reason for a
static plantarflexion might be congenital, traumatic or iatrogenic (i.e. after surgical
interventions).
Forefoot-Driven Hindfoot Deformity: Coupled Deformity 671
3.2 Forefoot-Driven Hindfoot Valgus
In contrast to forefoot-driven hindfoot varus, forefoot-driven hindfoot valgus [19,

20] encompasses a completely different etiology.
The most important cause for a forefoot-driven hindfoot valgus is the instability
of the first ray [21–23]. Any excessive motion at the first tarsometatarsal, naviculo-
cuneiform or talonavicular joint can result in a hyper-supination of the forefoot and
midfoot [24, 25]. Other reasons encompass iatrogenically or traumatically induced
elevation of the first ray forcing the forefoot to rotate into malposition.
Therefore, the pattern of forefoot-driven hindfoot valgus is: Supination of the
forefoot, ± midfoot and decrease of the longitudinal arch. Consequently, the hind-
foot compensates for this abnormal motion by turning into valgus.
4 General Aspects of Clinical Assessment
Any patient should be examined in a barefoot situation during walking and in a

standing position. The bilateral evaluation of both legs and hindfeet helps to obtain
a detailed appreciation of the deformity type. Leg, hindfoot, midfoot, and forefoot
deformities should be identified, and the rigidity and corrective potential estimated.
Of course, throughout the clinical evaluation attention is paid to signs of other
pathologic conditions such as peroneal tendinopathy and lateral as well as medial
instability, osteochondral lesions, osteoarthritis including ankle impingement,
occult fractures, and neuropathy of the superficial peroneal nerve. At some times it
might be necessary to correct them to achieve a proper overall result.
4.1 Inspection
Hindfoot alignment is observed during stance and includes inspection of soft-tissue

conditions. Measurement of hindfoot alignment is performed while inspecting the
patient from posterior. The angle between long axis of the leg and axis of the calca-
neus is measured. Normal values range from 0° neutral to 5° valgus. Any varus is
pathologic. Valgus hindfoot deformities that exceed 10° can be seen as abnormal.
4.2 Palpation
Specific attention is paid to tender spots at the level of the ankle, subtalar, Chopart-
and Lisfranc joints. In addition, palpation should be continued along the course of
the medial and lateral ligament complexes around the ankle as well as along the
joint lines of the ankle, subtalar, and Chopart joints. Tenderness along the peroneal
tendons may indicate tendinopathy or partial rupture and needs specific imaging, for
example, magnetic resonance imaging (MRI). Occasionally a prominent osteophyte
formation points toward arthritic disorders. If local swelling is observed, palpation
allows identification of joint effusion, tenosynovitis, or ganglion formation. Besides
this, any tender spot at the site of the posterior tibial tendon insertion is important
because it may hint onto the existence of insertional tendinopathy as well as a
Spring-ligament insuffiency/- rupture.
4.3 Functional Testing
Range of motion (ROM) at the ankle, subtalar, and Chopart joints is assessed.
Reduced ROM at any of those joints helps to identify the locus of rigidity and
deformity.
An impaired ROM at the level of the ankle with associated equinus may be the
result of a short gastrocnemius-soleus muscle complex [19]. The contracture of a
short gastrocnemius-soleus complex, is best examined by means of the Silfverskjöld
test [26]. It is important to distinguish shortening of the Achilles tendon from con-
tractures of the triceps surae. Those structures may play a crucial role in correcting
the hindfoot and in determining whether additional surgery should be performed.
A proper neurologic assessment is mandatory to rule out any muscular imbal-
ance in the foot and ankle. Despite this vascular status should be checked (i.e. Aa.
popliteal, tibialis posterior, dorsalis pedis).
• Specific tests in forefoot-driven hindfoot valgus deformity
In patients suffering from forefoot-driven hindfoot valgus the so-called reversed
Coleman-block can be used (Fig. 1) [27, 28]. In addition to the reversed Coleman-
block Test any hypermobility of the first ray should be evaluated [21–23, 29–32].
Testing of hypermobility of the first ray can be done as reported by Glasoe and
Michaud [33].
• Specific tests in forefoot-driven hindfoot varus deformity
The most important functional test to assess the flexibility of hindfoot varus—in
case of a forefoot-driven hindfoot varus—is the Coleman block test [27, 28, 34].
One of the most debated pathologies or causes of a forefoot-driven hindfoot
varus is the hyperactivity of the peroneus longus. However, it can be function-
ally tested as follows: The patient sits in front of the examiner and is asked to
forcefully dorsiflex at the ankle joint with the knee in full extension. In this posi-
tion the examiner places one thumb underneath the first metatarsal head and the
other thumb underneath the second, third, and fourth metatarsal heads. The
patient then plantarflexes the foot maximally against resistance of the examiner
hand. The combined pronation of the forefoot with a strong plantarisation of the
first ray indicates the presence of a hyperactivity of the peroneus longus muscle.
In contrast, patients who plantarflex their foot without pronation of the forefoot
are considered to have a normal activity of the peroneus longus muscle [15,
17, 35].
a b
Fig. 1 (a) The image depicts a patient with a forefoot-driven hindfoot valgus on her right foot.
Please note the remarkable valgus hindfoot deformity. (b) The reversed-Coleman-Block Test cor-
rects the hindfoot valgus in neutral when the block is put underneath the greater toe joint
5 Imaging
Usually, surgeons start to analyse the deformities and pathologies of the foot and
ankle by using conventional radiography.
In general, conventional radiography includes the following techniques:
5.1 Conventional Imaging
Normally, standard weightbearing radiographs, including anteroposterior, lateral

views of the ankle and dorsoplantar, oblique and lateral views of the foot are per-
formed. To assess the hindfoot alignment, the author recommends hindfoot align-
ment or long axial views to measure the amount of varus deformity. Any arthritic
change around the foot and ankle should be identified. On the mortise view, the
congruency of the ankle joint can be judged, and the lateral distal tibial angle
(LDTA) measured (normal value 88°).
• Specific alterations in forefoot-driven hindfoot varus feet
On the lateral view of the foot, the deformity can be measured. In cavus feet most
commonly the talus–first metatarsal (Meary [36]) and talocalcaneal angles as well
as the calcaneal pitch angles are assessed to describe the deformity [37].
Usually, the slope of the first metatarsal bone is steep, indicating the driving-
force of the deformity. The sinus tarsi represents wide open and circular in shape on
lateral views of the ankle (Fig. 2).
• Specific alterations in forefoot-driven hindfoot valgus feet
Fig. 2 This image depicts

a cavus foot provoked by
the forefoot. The sinus tarsi
is wide open and the
angulation of the
metatarsals quite steep.
The Meary-angle is
positive
In flatfeet the Meary-angle [38, 39] serves to measure the deformity and to iden-
tify the sag of medial column. In valgus feet the sinus tarsi becomes almost not
visible or completely obliterated.
In patients with hypermobility of the first ray, it might be possible to see a plantar
gaping of the first tarsometatarsal joint and loss of parallelism between the dorsal
cortices of the first and second metatarsal bone (Fig. 3) [32, 33, 40].
5.2 Hindfoot Alignment
The classic radiographic hindfoot alignment view, as described by Saltzman and

el-Khoury, has been introduced to reduce the flaws as for example obtained from the
Cobey-view [41, 42].
Nowadays, there is quite a lot of scientific evidence revealing the usefulness of
the hindfoot view for visual judgment of the hindfoot alignment. In addition, the
hindfoot view shows good-to-excellent intraobserver reliability. However, interob-
server reliability is very low and is clearly surpassed when using the classic long
axial view only (Fig. 4) [43–45]. One of the major drawbacks of the hindfoot view
is its susceptibility to rotatory malpositioning of the foot. Thus, the measurements
obtained with the hindfoot view need to be interpreted with caution.
A far more reliable angle measurement can be done using the long axial view or
the medial and lateral borders of the calcaneus [43, 46].
Whereas preoperative assessment of hindfoot alignment under weight-bearing
conditions is done in a standardised fashion, there is not yet a technique available to
do so under non–weight-bearing conditions, for example, during surgery. More
recently, Min and Sanders described varus-valgus referencing relative to the medial
process of the posterior calcaneal tuberosity in the unloaded Mortise view. Its use-
fulness and feasibility will be subject of future research [47].
a c
Fig. 3 (a) Anteroposterior view of the ankle under full-weightbearing conditions. The ankle is
absolutely fine. (b) On the lateral view the sinus tarsi depicts itself as slightly obliterated while the
first metatarsal is elevated. Please note a slight sag within the naviculocuneiform joint. Diagnosis:
Forefoot-driven hindfoot valgus. (c) The dorsoplantar view of the foot in the same patient as under
Fig. 1b does not reveal any major forefoot abduction
Fig. 4 This is the

long-axial view of the
same patient’s hindfoot as
reported in Figs. 3a–c. The
valgus moment is clearly
visible
Full-length radiographs of both legs including the pelvis and hips are considered
when complex reconstructions are planned.
5.3 Computed Tomography and MRI
MRI and computed tomography (CT) allow precise three-dimensional depiction of

the bones and soft tissues. Both technologies are mainly indicated for evaluation of
the lateral ligamentous complex and concomitant pathologic conditions such as
peroneal tendinopathy, osteochondral lesions, and/or osteoarthritis.
MRI has been found to be highly specific in detecting lesions of the anterior
talofibular and calcaneofibular ligaments; however, sensitivity is poor [48].
Because of its superiority when compared with a simple arthro-CT examination

the authors perform CT only in selective cases, for example, to estimate the amount
of fibular malrotation; to measure the true extent of osteochondral lesions of the
talus or to evaluate presence of a tarsal coalition.
Weightbearing-CT has become a novel tool for the assessment of hindfoot deformi-
ties [49]. Burssens et al. presented a method of measuring the angular deformities [50].
And it seems to work well [51]. WBCT allows a clear depiction of where the apex of
the deformity is and how fore- and hindfoot interact. This helps surgeons to plan the
intervention as precise as possible. Recently, a consensus group defined the following
parameters in the assessment of the foot and ankle: If available, a hindfoot alignment
view is strongly recommended. ‘If available, WEIGHTBEARING computed tomog-
raphy is strongly recommended for surgical planning. When WEIGHTBEARING CT
is obtained, important findings to be assessed are sinus tarsi impingement, subfibular
impingement, increased valgus inclination of the posterior facet of the subtalar joint,
and subluxation of the subtalar joint at the posterior and/or middle facet’ [51].
Conservative treatment has always had its place in the treatment of foot and ankle
pathologies. While in the flexible forefoot-driven hindfoot deformity insoles and shoe
modification may have a certain benefit, they might not be very useful in the presence
of postural abnormalities or fixed mechanical deformities because they are not effec-
tive enough to correct those rigid anatomical alterations. Thus, they might fail very soon.
However, there will always be a group of individuals who do not qualify for any
operation due to their comorbidities, which increase health risks and outweigh the
benefits of surgery. This group encompasses elderly patients and those with inade-
quately adjusted diabetes mellitus, advanced peripheral vascular disease or cardio-
vascular disease, specific neurologic disorders, or respiratory disease.
Conservative treatment might not be able to address the underlying cause of a
mechanically induced hindfoot deformity but could be beneficial in cases of flexible
varus deformity.
Conservative treatment should be followed up for at least 6 months. If after a stan-
dardised nonoperative protocol there is no improvement, surgery may be considered.
6.1 Physical Therapy
Physical therapy has shown to influence functional instability by improving pro-

prioception, peroneal muscle preactivation, and eversion strength. This is mainly
useful in patients suffering from hindfoot varus associated with variable degrees of
hindfoot instability [52].
Aggressive stretching protocols maybe performed to lengthen the gastrocnemius-
soleus unit and to reduce tension exerted through the Achilles tendon. By so doing,
the inversion moment can be reduced, and stability improved [53].
6.2 Braces
Braces can decrease severity and frequency of ankle sprains in patients with chronic
instability. Laced braces have been shown to be most effective [54].
In addition, improved stability can be achieved by taping. Although the inversion
moments at the ankle are reduced by means of taping, the true mechanical stabilis-
ing effect of taping is limited. It has been shown that almost 50% of the stabilising
effect is gone after 10 minutes of exercise [55–59].
However, proprioception might remain improved due to other reflex mecha-
nisms. Braces may also help to stretch the gastrocnemius-soleus unit.
6.3 Shoe Modifications and Insoles
Equalisation of pressure distribution and offloading of painful areas are the primary
goals of insoles and orthoses.
Lateral wedging may partially correct flexible hindfoot varus and decrease sub-
jective instability [37]. In flexible hindfoot valgus medial arch supports may be
indicated to try to correct the deformity to some extent.
Prefabricated products are available, but custom-made devices have advantages,
especially in patients with rigid deformity. Additional support may be achieved with
specific shoe modifications, for example increased width of the heel sole. In case of
secondary degenerative changes, rocker-bottom soles could alleviate pain by reduc-
ing the propulsive work at the ankle joint.
The OSSA-orthosis is a very specific tool to stop rotation at the talonavicular
joint. In certain patients who are dealing with a forefoot-driven hindfoot valgus, this
treatment modality could be a valuable option to treat the condition. However, due
to the rigidity of the OSSA-orthosis, patients may complain about pain and stop
continuation of the treatment.
Surgical treatment is always warranted when conservative measures have failed.

This may specifically apply for postural, i.e. anatomically rigid, deformities. The
selection of treatment varies between forefoot-driven hindfoot varus and forefoot-
driven hindfoot valgus deformities. The goal of any of those treatments is to create
an equilibrium between fore-, mid- and hindfoot.
The surgeon needs to identify the origin of deforming force and restore anatomy
and biomechanics where needed. The primary goal is to strive for joint-preserving
surgery. However, in certain cases it might not be possible, and fusions should be
considered the better option.
7.1 Forefoot-Driven Hindfoot Varus
Goal of treatment: To unload the first ray and to restore an equilibrium between
fore- and hindfoot through the midfoot.
7.1.1 The Plantarflexed First Ray
A flexible plantarflexed first ray may arise from hyperactivity of the peroneus
longus, which can be decreased by means of a peroneus longus to brevis trans-
fer [17, 35]. The transfer is performed with a lateral incision between the
cuboid tunnel and the peroneal tubercle on the lateral calcaneal wall. The
sheaths of the peroneal tendons are opened and a side-to-side tenodesis achieved
suturing the peroneus longus to the peroneus brevis tendon with the foot in
neutral position. Pretensioning of the peroneus longus tendon in case of its
hyperactivity is not necessary. Side-to-side tenodesis may be continued more
proximally in case of a peroneus brevis degeneration or tear. After tenodesis the
peroneus longus tendon is cut at the cuboid groove and if present an os peroneal
excised. The peroneal tubercle may be removed to avoid impingement of the
tendons [60].
Otherwise fixed plantarflexion of the metatarsals, for example as seen in idio-
pathic cavovarus foot, can be addressed by a dorsiflexion osteotomy. Dorsiflexion
osteotomies, first described by Swanson et al., may involve a single metatarsal or
more metatarsals [61]. In forefoot-driven hindfoot varus, the deformity is caused
by a rigid and massively plantarflexed first ray. In such a situation a dorsiflexion
osteotomy of the proximal first metatarsal bone is recommended. We approach
the metatarsal bone with a dorsal incision. The dorsally based closing wedge
osteotomy is started 2–3 cm distal to the tarsometatarsal joint and angled 60°
distally. Fixation with a 2-hole plate is considered sufficient, as under weight-
bearing the osteotomy with a preserved plantar hinge is compressed and stable
(Fig. 5) [62]. Larger plantarflexion deformities might be better addressed using a
fusion of the first tarsometatarsal joint [63]. Correction of the 2nd and 3rd ray is
considered when simulated weightbearing indicates overload of the metatar-
sal heads.
7.1.2 Calcaneal Osteotomy
A lateralising calcaneal osteotomy is added if after soft tissue balancing by means

of the peroneal tendon transfer and/or metatarsal osteotomies the hindfoot varus
persists. Preoperatively this may be anticipated if hindfoot varus is incompletely
corrected with the Coleman block test.
Vienne and colleagues published the results of a consecutive series of patients with
cavo-varus deformity and recurrent ankle instability. All patients revealed a failed
a b
Fig. 5 (a) Lateral view of a patient with a forefoot-driven hindfoot varus. Note the wide sinus tarsi
and the steep course of the metatarsal bones. (b) Lateral view of the same patient as mentioned in
(a) after correction through a metatarsal elevation osteotomy. It is interesting how the hindfoot
corrects as seen on the sinus tarsi
prior ligament stabilisation surgery. The plantarflexed first ray and hindfoot varus
were flexible. Each patient was clinically detected to have a hyperactivity of the pero-
neus longus muscle. All were successfully treated by means of a lateralising calcaneal
osteotomy and peroneus longus to brevis transfer. In half of the patients, a Broström
procedure was added to address lateral ligament insufficiency. All patients showed
good results with subjective and objective lateral stability [64]. Similar results were
achieved by Fortin et al. adding dorsiflexion osteotomy in patients with flexible hind-
foot deformities [65].
8 Forefoot-Driven Hindfoot Valgus
Goal of treatment: To increase the competence of the medial column and thus to
restore an equilibrium between fore- and hindfoot through the midfoot.
8.1 Elevated First Ray Due to Traumatic or Iatrogenic Origin
Trauma or surgery can result in anatomical alterations of the first metatarsal bone.
In those cases, the elevation of the bone itself can force the forefoot to turn into
supination, which in turn accelerates the development of a flexible hindfoot valgus
deformity. In such cases it is needed to correct the deformity at its apex and to
straighten the first metatarsal bone in an anatomical manner.
8.2 Instability of the Medial Column
The stabilisation of the medial column is essential in patients who suffer from
forefoot-driven hindfoot valgus. The treatment should be chosen as efficient as pos-
sible to achieve minimal loss of joints but maximum secondary correction at the
hindfoot.
While the concept seems easy to understand, the treatment itself can pose signifi-
cant problems to the surgeons. The difficulty lies in the assessment of instability and
where it may occur. The first tarsometatarsal-, naviculocuneiform- and talonavicu-
lar joints are three different articulations, which can reveal isolated or combined
instabilities. It is therefore mandatory to evaluate the potential apex of deformity on
weightbearing lateral views of the foot.
Plantar gaping at the first tarsometatarsal joint, or a sag at the level of the navicu-
locuneiform and/or talonavicular joint indicate instability [32, 33]. In chronic
forefoot-driven hindfoot valgus deformities, even the deltoid and spring ligament
complex can become altered and insufficient [66–70].
By means of the reversed- Coleman-Block Test the amount of correction can be
anticipated. However, until today it is not yet clear whether based on this test a
simple stabilisation of the medial column would be sufficient or if other means (e.g.
calcaneal osteotomies, medial deltoid ligament repair, etc.) should be added. Thus,
the authors think that intraoperative judgment of the correction should always be
done and where needed liberal use of the forementioned techniques applied.
• Fusion of the first tarsometatarsal joint [71–73].
This is a very effective treatment to treat a forefoot-driven hindfoot valgus asso-
ciated with an isolated but severe hypermobility at the first tarsometatarsal joint.
Fusion of the first tarsometatarsal joint is done through a medial approach. It is
in most cases an in-situ arthrodesis. In case of co-existing valgus deformities, it
can also help to provide a correction. The subcutaneous tissues should be divided
and then the distal margins of the retinaculum (lying over the tibialis anterior
tendon) become visible. The retinaculum is cut, and the tibialis anterior tendon
protected. Afterwards the first tarsometatarsal joint can be reached and the cap-
sule of it is incised. The cartilage should be removed by means of osteotomes and
curettes. The authors do not use a saw to prepare the joint surfaces to avoid any
risk of over-shortening [73]. After this procedure the subchondral bone plate is
freshened up using a 2.0 mm burr. The joint surfaces, i.e. their subchondral parts,
are brought together and a K-wire (1.6–2.0 mm diameter) inserted to lock the
joint in the position needed. First a laterally placed lag-screw that runs from
distal-dorsal to proximal-plantar through the first tarsometatarsal joint is put in.
After this a medially placed plate is laid over the first tarsometatarsal joint to
secure the construct.
• Fusion of the naviculocuneiform joint [25, 39, 74–77]
The approach is similar to that of the first tarsometatarsal joint fusion but more
proximal. After subcutaneous preparation the retinaculum over the tibialis ante-
rior tendon is incised and the tendon pulled distally by means of Langenbeck-
hooks. The naviculocuneiform joint capsule should be opened up completely. By
means of osteotomes and mini curettes, the cartilage is removed. It is essential
not to remove too much of the subchondral bone because the larger the defect the
more difficult to close the joint during fusion. If this situation occurs, the authors
recommend adding autologous cancellous bone graft from the proximal and/or
distal tibia. Fixation of the naviculocuneiform joint is tricky: According to
Hansen, the fusion can be achieved by means of 3.5 mm screws. However, con-
temporary plates and fixation systems allow even more stable means to achieve
proper union.
• Fusion of the talonavicular joint [78–84].
For this fusion, a medial approach is done right over the talar head and navicular
tuberosity. The incision of the skin parallels with the course of the posterior tibial
tendon. During subcutaneous preparation the surgeon needs to take care of the
venous vessels and sometimes ligations of those structures are important. The
capsule of the talonavicular joint should be opened without harming the insertion
site of the posterior tibial tendon. The authors do not extend the preparation and
separation of the capsule beyond the joint line. To the opinion of the authors, it is
essential to preserve the vascular supply to the talar head. Therefore, any strip-
ping of the capsule at the level of the talar neck is forbidden.
By means of a curved osteotome and curettes the cartilage is removed.
Sometimes specific distractors are needed to open up the talonavicular joint. As
with every other joint the subchondral bone is freshened up using a 2.0 mm drill.
The authors usually reduce the hindfoot through the so-called ‘Myerson’-
reduction-maneuver. Fixation can be done by means of 5.5 and/or 3.5 mm
screws. The medially placed screw represents a true lag-screw while the other
two function as positioning screws.
• Combined fusions of the medial column [85, 86]
Sometimes, when the instability cannot be precisely found at one of the afore-
mentioned joints, it is necessary to fuse the tarsometatarsal ± naviculocuneiform
± the talonavicular joint. The combination of fusion enhances the medial stabil-
ity and provides a powerful tool to restore the longitudinal arch by ensuring
durable correction at the hindfoot (Fig. 6).
• Calcaneal osteotomy [3, 87–93]
The authors are quite liberal in terms of using a medialising calcaneal osteotomy.
If there is a residual valgus found, during intraoperative evaluation, the medialis-
ing calcaneal osteotomy can help to correct the hindfoot, while turning it into
neutral. The surgeon should be cautious not to overcorrect the hindfoot into
varus. Thus, intraoperative judgement by help of an axial calcaneal view is
recommended.
The simplest way to perform is the medial sliding calcaneal osteotomy, which
is performed by an oblique cut of the calcaneus. The approach is chosen laterally
over the calcaneal tuberosity. The line of skin incision can be straight or slightly
curved (preferred by the authors). After meticulous subcutaneous preparation two
Hohmann-hooks are placed over the dorsum of the calcaneus tuberosity and plan-
tar to the insertion site of the aponeurosis. The surgeon should hold the calcaneus
in one hand to control the depth of cut during the osteotomy (which is performed
by means of an oscillating saw). Holding the knee in 90° of flexion and the ankle
in full plantarflexion the calcaneal tuberosity can be shifted easily to the medial
side. Once the planned shift is reached the foot and knee are straightened up to
neutral. By so doing, the tuberosity gets temporarily secured until final fixation is
done by means of screws, which are inserted from posteriorly.
a b
Fig. 6 (a) Lateral view of a foot with forefoot-driven hindfoot valgus deformity. A remarkable
plantar gaping at the first tarsometatarsal joint and sag at the naviculocuneiform can be appreci-
ated. The sinus tarsi is not visible anymore. (b) The dorsoplantar view of the foot demonstrates a
small forefoot abduction and presence of a hallux valgus deformity. (c) Dorsoplantar view of the
same foot after medial column fusion. The plate expands from the first tarsometatarsal over the
naviculocuneiform joint. Note the correction of the forefoot. (d) On the lateral view of the foot the
sinus tarsi has opened and the midfoot has been put in line with the forefoot and talar axis
In patients who require a more three-dimensional correction a so-called

z-shaped osteotomy could be performed [94–96]. This type of calcaneal osteot-
omy allows correction in all three planes including medial shift, transversal and
coronal rotation. It is a very powerful osteotomy. However, fixation can be some-
what difficult due to the course of the osteotomy-lines. It can also be used
together with a talonavicular fusion (in the literature an Evans-osteotomy has
been used for this purpose) [97].
• Deltoid and Spring-Ligament-reconstruction [98, 99]
In patients who suffer from chronic forefoot-driven hindfoot valgus deformity
the medial collateral ligament complex can become insufficient. This is specifi-
cally the case when a decompensation takes place at the talonavicular joint. In
those cases, the forefoot starts to rotate and shift laterally while increasing stretch
onto the deltoid and spring ligament is exerted. The diagnosis of a medial deltoid
and spring ligament insufficiency can best be made using an MRI.
The authors adopted and modified the techniques described by Haddad et al. [99]
and Nery et al. [98] Both techniques base on anatomic reconstruction of the deltoid
ligament including the option to repair the Spring-ligament where needed. While in
their original papers the techniques have been performed using tendon grafts the
current method can be performed utilising non-resorbable fiber sutures.
A posteromedial approach is chosen for this specific technique. Skin incision
follows the course of the posterior tibial tendon and is placed slightly dorsal to it.
The posterior tibial tendon sheath is exposed and incised. The posterior tibial ten-
don should then be moved plantarly using a Langenbeck-hook. This maneuver
allows direct inspection of both, the deltoid and Spring ligament. Two essential
anatomical regions need now to be exposed: First the part dorsal to the insertion
of the posterior tibial tendon at the navicular tuberosity and second the sustentacu-
lum tali. Both loci are important for the suture anchor placement. When exposing
the sustentaculum tali, it is important not to injure the tendon of the flexor digito-
rum longus or flexor hallucis longus. In addition, the anterior and medial part of
the calcaneus as well as the tip of the medial malleolus needs to be exposed. Two
drill holes are made in the medial malleolus (close to its tip). The reconstruction
needs two autologous or allografts (minor morbidity). Alternatively, new tools,
e.g. the InternalBrace™ (Arthrex Inc.; Naples, FL, USA) can be used. Additional
drill holes are made in the navicular tuberosity, the anteromedial part of the calca-
neus (underneath the anteromedial facet of the subtalar joint) and sustentacu-
lum tali.
The first graft is inserted with its one end into the medial surface of the talus and
secured with an interference screw. The foot is hold in neutral position. Afterwards
the graft is brought close to the inferior drill hole in the medial malleolus and its
limb secured by means of another interference screw. This reconstructs the tibiota-
lar ligament. Afterwards the distal graft limb is inserted into the drill hole, which
has been made in the anteromedial portion of the calcaneus and passed from medial
to lateral to achieve proper tension. The graft is then secured by means of an addi-
tional interference screw. This part reconstructs the tibiospring-ligament.
The second graft will then be inserted with its one end into the sustentaculum
tali and secured with an interference screw. The distal part of the graft is then
inserted into the anterior drill hole of the medial malleolus and secured. This
reconstruction creates a band that connects the tibia and calcaneus. It corre-
sponds to the tibiocalcaneal ligament and enhances the construct. Now the rest
of the graft can be inserted, under tension, within the navicular tuberosity and
fixed with an interference screw. This last step reconstructs the tibionavicular
ligament.
By so doing, the surgical technique allows the reconstruction of 4 ligaments. In
case of a complete rupture of the spring-ligament an additional graft/suture might
be used, which is driven from the navicular tuberosity to the sustentaculum tali.
Nery et al. [98] described their technique and evaluated 10 consecutive patients
with flatfoot deformity and insufficient ankle and midfoot ligaments. No postopera-
tive complications, stiffness, or loss of correction were found. Therefore, the group
stated that the novel technique to reconstruct the failed deltoid and spring ligament
during flatfoot correction could have merit.
In contrast to Nery et al. [98], Haddad and co-workers [99] investigated their
technique on six pairs of fresh frozen cadaveric lower extremities. As a result of the
biomechanical testing angular displacement at a 2 Nm level torque was significantly
greater in the sectioned group compared to the deltoid reconstruction group in exter-
nal rotation and eversion (p = 0.006 and p = 0.017, respectively). The authors did
not find a statistical difference in angular displacement between the deltoid intact
and reconstructed group in external rotation and eversion when tested at 2 Nm of
torque (p = 0.865 and p = 0.470, respectively). The stiffness of the reconstruction
was 136.4 ± 40.2% compared to the intact ligament. Stiffness data were statistically
insignificant in both plantar flexion and dorsiflexion between the reconstructed and
sectioned groups (p = 0.050 and p = 0.126). As a final result the authors were able
to demonstrate that the described reconstruction technique under low torque was
able to restore eversion and external rotation stability to the talus, which was statis-
tically similar to the intact deltoid ligament [100].
All those techniques, which have been described and discussed in brief help to
correct the entire foot and ankle and can – if properly planned – be highly successful.
9 Summary
Forefoot-driven hindfoot deformities represent a highly interesting field in foot and

ankle surgery. The most amazing fact is, that the hindfoot deformity itself is mainly
corrected at the level of the fore- and midfoot.
The causes for each type are different and therefore the distinction into varus and
valgus deformities is important. The same applies for the general rules of surgical
treatment: Varus hindfoot corrections can be achieved by unloading the first ray,
while valgus hindfoot corrections can reliably be achieved through stabilisation of
the medial column.
The surgical armamentarium to correct those deformities has already been pub-
lished for other pathologies and can be applied in the current types of pathology.
Thus, a surgeon should feel quite familiar with those techniques. The main discrep-
ancy, however, lies in the clinical and radiographic assessment of those patients and
to identify the underlying cause and apex of deformity.
Once these basics are appreciated, it will be easy to treat any of those patients
while ensuring a high probability for a good outcome.
References
1. Golano P, et al. Ankle anatomy for the arthroscopist. Part II: role of the ankle ligaments in soft
tissue impingement. Foot Ankle Clin. 2006;11(2):275–96. v-vi
2. Golano P, et al. Ankle anatomy for the arthroscopist. Part I: the portals. Foot Ankle Clin.
2006;11(2):253–73. v
3. Sizensky JA, Marks RM. Medial-sided bony procedures: why, what, and how? Foot Ankle
Clin. 2003;8(3):539–62.
4. Knupp M, Stufkens SA, Hintermann B. Triple arthrodesis. Foot Ankle Clin. 2011;16(1):61–7.
5. Amaha K, et al. Anatomic study of the medial side of the ankle base on the joint capsule: an
alternative description of the deltoid and spring ligament. J Exp Orthop. 2019;6(1):2.
6. MacDonald, A. et al., Peritalar kinematics with combined deltoid-spring ligament recon-
struction in simulated advanced adult acquired flatfoot deformity. Foot Ankle Int, 2020:
p. 1071100720929004.
7. Noguchi K. Biomechanical analysis for osteoarthritis of the ankle. Nihon Seikeigeka Gakkai
Zasshi. 1985;59(2):215–22.
8. Karlsson J, Eriksson BI, Renstrom P. Subtalar instability of the foot. A review and results after
surgical treatment. Scand J Med Sci Sports. 1998;8(4):191–7.
9. Mittlmeier T, Rammelt S. Update on subtalar joint instability. Foot Ankle Clin.
2018;23(3):397–413.
10. Sangeorzan BJ, et al. Contact characteristics of the subtalar joint: the effect of talar neck mis-
alignment. J Orthop Res. 1992;10(4):544–51.
11. Wagner UA, et al. Contact characteristics of the subtalar joint: load distribution between the
anterior and posterior facets. J Orthop Res. 1992;10(4):535–43.
12. Sangeorzan BJ, Ananthakrishnan D, Tencer AF. Contact characteristics of the subtalar joint
after a simulated calcaneus fracture. J Orthop Trauma. 1995;9(3):251–8.
13. Sangeorzan A, Sangeorzan B. Subtalar joint biomechanics: from normal to pathologic. Foot
Ankle Clin. 2018;23(3):341–52.
14. Krahenbuhl N, et al. The subtalar joint: a complex mechanism. EFORT Open Rev.
2017;2(7):309–16.
15. Klammer G, Benninger E, Espinosa N. The varus ankle and instability. Foot Ankle Clin.
2012;17(1):57–82.
16. Krahenbuhl N, Weinberg MW. Anatomy and biomechanics of cavovarus deformity. Foot
Ankle Clin. 2019;24(2):173–81.
17. Vienne P, et al. Hindfoot instability in cavovarus deformity: static and dynamic balancing. Foot
Ankle Int. 2007;28(1):96–102.
18. Seaman TJ, Ball TA. Pes Cavus. Treasure Island: StatPearls; 2020.
19. Espinosa N, Brodsky JW, Maceira E. Metatarsalgia. J Am Acad Orthop Surg.
2010;18(8):474–85.
20. Maceira E, Monteagudo M. Mechanical basis of metatarsalgia. Foot Ankle Clin.
2019;24(4):571–84.
21. Myerson MS, Badekas A. Hypermobility of the first ray. Foot Ankle Clin. 2000;5(3):469–84.
22. Roukis TS, Landsman AS. Hypermobility of the first ray: a critical review of the literature. J
Foot Ankle Surg. 2003;42(6):377–90.
23. Cowie S, et al. Hypermobility of the first ray in patients with planovalgus feet and tarsometa-
tarsal osteoarthritis. Foot Ankle Surg. 2012;18(4):237–40.
24. Kadakia AR, et al. Did failure occur because of medial column instability that was not recog-
nized, or did it develop after surgery? Foot Ankle Clin. 2017;22(3):545–62.
25. Metzl JA. Naviculocuneiform sag in the acquired flatfoot: what to do. Foot Ankle Clin.
2017;22(3):529–44.
26. Strayer LM Jr. Recession of the gastrocnemius; an operation to relieve spastic contracture of
the calf muscles. J Bone Joint Surg Am. 1950;32-A(3):671–6.
27. Fortin PT, Guettler J, Manoli A 2nd. Idiopathic cavovarus and lateral ankle instability: recogni-
tion and treatment implications relating to ankle arthritis. Foot Ankle Int. 2002;23(11):1031–7.
28. Younger AS, Hansen ST Jr. Adult cavovarus foot. J Am Acad Orthop Surg. 2005;13(5):302–15.
29. Klaue K, Hansen ST, Masquelet AC. Clinical, quantitative assessment of first tarsometatar-
sal mobility in the sagittal plane and its relation to hallux valgus deformity. Foot Ankle Int.
1994;15(1):9–13.
30. Prieskorn DW, Mann RA, Fritz G. Radiographic assessment of the second metatarsal: measure
of first ray hypermobility. Foot Ankle Int. 1996;17(6):331–3.
31. Bierman RA, Christensen JC, Johnson CH. Biomechanics of the first ray. Part III. Consequences
of Lapidus arthrodesis on peroneus longus function: a three-dimensional kinematic analysis in
a cadaver model. J Foot Ankle Surg. 2001;40(3):125–31.
32. King DM, Toolan BC. Associated deformities and hypermobility in hallux valgus: an investi-
gation with weightbearing radiographs. Foot Ankle Int. 2004;25(4):251–5.
33. Glasoe WM, Michaud TC. Measurement of dorsal first ray mobility: a topical historical review
and commentary. Foot Ankle Int. 2019;40(5):603–10.
34. Coleman SS, Chesnut WJ. A simple test for hindfoot flexibility in the cavovarus foot. Clin
35. Ramseier LE, et al. Treatment of late recurring idiopathic clubfoot deformity in adults. Acta
Orthop Belg. 2007;73(5):641–7.
36. Boffeli TJ, Schnell KR. Cotton osteotomy in flatfoot reconstruction: a review of consecutive
cases. J Foot Ankle Surg. 2017;56(5):990–5.
37. Sammarco GJ, Taylor R. Cavovarus foot treated with combined calcaneus and metatarsal oste-
otomies. Foot Ankle Int. 2001;22(1):19–30.
38. Lin YC, et al. Imaging of adult flatfoot: correlation of radiographic measurements with
MRI. AJR Am J Roentgenol. 2015;204(2):354–9.
39. Aiyer A, et al. Radiographic correction following reconstruction of adult acquired flat foot
deformity using the cotton medial cuneiform osteotomy. Foot Ankle Int. 2016;37(5):508–13.
40. Koury K, et al. Radiographic assessment of first tarsometatarsal joint shape and orientation.
Foot Ankle Int. 2019;40(12):1438–46.
41. Saltzman CL, el-Khoury GY. The hindfoot alignment view. Foot Ankle Int. 1995;16(9):572–6.
42. Cobey JC. Posterior roentgenogram of the foot. Clin Orthop Relat Res. 1976;118:202–7.
43. Buck FM, et al. Hindfoot alignment measurements: rotation-stability of measurement tech-
niques on hindfoot alignment view and long axial view radiographs. AJR Am J Roentgenol.
2011;197(3):578–82.
44. Buck FM, et al. Diagnostic performance of MRI measurements to assess hindfoot malalign-
ment. An assessment of four measurement techniques. Eur Radiol. 2013;23(9):2594–601.
45. Sutter R, et al. Three-dimensional hindfoot alignment measurements based on bipla-
nar radiographs: comparison with standard radiographic measurements. Skelet Radiol.
2013;42(4):493–8.
46. Reilingh ML, et al. Measuring hindfoot alignment radiographically: the long axial view is
more reliable than the hindfoot alignment view. Skelet Radiol. 2010;39(11):1103–8.
47. Min W, Sanders R. The use of the mortise view of the ankle to determine hindfoot alignment:
technique tip. Foot Ankle Int. 2010;31(9):823–7.
48. Chandnani VP, et al. Chronic ankle instability: evaluation with MR arthrography, MR imaging,
and stress radiography. Radiology. 1994;192(1):189–94.
49. Hirschmann A, et al. Upright cone CT of the hindfoot: comparison of the non-weight-bearing
with the upright weight-bearing position. Eur Radiol. 2014;24(3):553–8.
50. Burssens ABM, et al. Is lower-limb alignment associated with hindfoot deformity in the coro-
nal plane? A weightbearing CT analysis. Clin Orthop Relat Res. 2020;478(1):154–68.
51. de Cesar Netto C, et al. Consensus for the use of weightbearing CT in the assessment of pro-
gressive collapsing foot deformity. Foot Ankle Int. 2020;41(10):1277–82.
52. Tourne Y, et al. Chronic ankle instability. Which tests to assess the lesions? Which therapeutic
options? Orthop Traumatol Surg Res. 2010;96(4):433–46.
53. Taddei UT, et al. Effects of a therapeutic foot exercise program on injury incidence, foot func-
tionality and biomechanics in long-distance runners: feasibility study for a randomized con-
trolled trial. Phys Ther Sport. 2018;34:216–26.
54. Lin YC, et al. The hindfoot arch: what role does the imager play? Radiol Clin N Am.
2016;54(5):951–68.
55. Cramer EA, Friedhoff K. Taping--a safe alternative in the early functional treatment of all liga-
ment instabilities of the proximal ankle joint? Results of a prospective study. Unfallchirurg.
1990;93(6):275–83.
56. Jerosch J, Bischof M. The effect of proprioception on functional stability of the upper ankle
joint with special reference to stabilizing aids. Sportverletz Sportschaden. 1994;8(3):111–21.
57. Jerosch J, et al. The influence of orthoses on the proprioception of the ankle joint. Knee Surg
Sports Traumatol Arthrosc. 1995;3(1):39–46.
58. Jerosch J, et al. Is prophylactic bracing of the ankle cost effective? Orthopedics.
1996;19(5):405–14.
59. Callaghan MJ. Role of ankle taping and bracing in the athlete. Br J Sports Med.
1997;31(2):102–8.
60. Huber M. What is the role of tendon transfer in the cavus foot? Foot Ankle Clin.
2013;18(4):689–95.
61. Krause FG, Iselin LD. Hindfoot varus and neurologic disorders. Foot Ankle Clin.
2012;17(1):39–56.
62. Reddy VB. Metatarsal Osteotomies: Complications. Foot Ankle Clin. 2018;23(1):47–55.
63. Jung HG, Park JT, Lee SH. Joint-sparing correction for idiopathic cavus foot: correlation of
clinical and radiographic results. Foot Ankle Clin. 2013;18(4):659–71.
64. Vienne P, Schöniger R, Helmy N, Espinosa N. Hindfoot instability in cavovarus deformity:
static and dynamic balancing. Foot Ankle Int. 2007;28(1):96–102.
65. Fortin PT, Guettler J, Manoli A 2nd. Idiopathic cavovarus and lateral ankle instability: recogni-
tion and treatment implications relating to ankle arthritis. Foot Ankle Int. 2002;23(11):1031–7.
66. Alshalawi S, et al. Medial ankle instability: the deltoid dilemma. Foot Ankle Clin.
2018;23(4):639–57.
67. Bastias GF, et al. Spring Ligament Instability. Foot Ankle Clin. 2018;23(4):659–78.
68. Pellegrini MJ, et al. Chronic deltoid ligament insufficiency repair with internal brace augmen-
tation. Foot Ankle Surg. 2019;25(6):812–8.
69. Brodell JD Jr, et al. Deltoid-spring ligament reconstruction in adult acquired flatfoot deformity
with medial peritalar instability. Foot Ankle Int. 2019;40(7):753–61.
70. Guerra-Pinto F, et al. The tibiocalcaneal bundle of the deltoid ligament – prevalence and varia-
tions. Foot Ankle Surg. 2021;27:138–42.
71. Claassen L, et al. Surgical procedures for the correction and stabilization of pes planovalgus.
Orthopade. 2020;49(11):968–75.
72. Conti MS, Garfinkel JH, Ellis SJ. Outcomes of reconstruction of the flexible adult-acquired
flatfoot deformity. Orthop Clin North Am. 2020;51(1):109–20.
73. Dahlgren N, et al. First tarsometatarsal fusion using saw preparation vs. standard preparation
of the joint: a cadaver study. Foot Ankle Surg. 2020;26(6):703–7.
74. Catanzariti AR. Modified medial column arthrodesis. J Foot Ankle Surg. 1993;32(2):180–8.
75. Budny AM, Grossman JP. Naviculocuneiform arthrodesis. Clin Podiatr Med Surg.
2007;24(4):753–63. ix-x
76. Rush SM, Jordan T. Naviculocuneiform arthrodesis for treatment of medial column instabil-
ity associated with lateral peritalar subluxation. Clin Podiatr Med Surg. 2009;26(3):373–84.
77. Ajis A, Geary N. Surgical technique, fusion rates, and planovalgus foot deformity correction
with naviculocuneiform fusion. Foot Ankle Int. 2014;35(3):232–7.
78. O’Malley MJ, Deland JT, Lee KT. Selective hindfoot arthrodesis for the treatment of adult
acquired flatfoot deformity: an in vitro study. Foot Ankle Int. 1995;16(7):411–7.
79. Lombardi CM, et al. Talonavicular joint arthrodesis and Evans calcaneal osteotomy for treat-
ment of posterior tibial tendon dysfunction. J Foot Ankle Surg. 1999;38(2):116–22.
80. Chen CH, et al. Isolated talonavicular arthrodesis for talonavicular arthritis. Foot Ankle Int.
2001;22(8):633–6.
81. Weinheimer D. Talonavicular arthrodesis. Clin Podiatr Med Surg. 2004;21(2):227–40. vi
82. Rammelt S, Marti RK, Zwipp H. Arthrodesis of the talonavicular joint. Orthopade.
2006;35(4):428–34.
83. Kiesau CD, et al. Talonavicular joint fixation using augmenting naviculocalcaneal screw in
modified double hindfoot arthrodesis. Foot Ankle Int. 2011;32(3):244–9.
84. Ma S, Jin D. Isolated Talonavicular arthrodesis. Foot Ankle Int. 2016;37(8):905–8.
85. Cohen BE, Ogden F. Medial column procedures in the acquired flatfoot deformity. Foot
Ankle Clin. 2007;12(2):287–99. vi
86. Yu G, et al. Fusion of talonavicular and naviculocuneiform joints for the treatment of Muller-
Weiss disease. J Foot Ankle Surg. 2012;51(4):415–9.
87. Horton GA, et al. Effect of calcaneal osteotomy and lateral column lengthening on the plantar
fascia: a biomechanical investigation. Foot Ankle Int. 1998;19(6):370–3.
88. Mosier-LaClair S, Pomeroy G, Manoli A 2nd. Operative treatment of the difficult stage 2
adult acquired flatfoot deformity. Foot Ankle Clin. 2001;6(1):95–119.
89. Catanzariti AR, et al. Double calcaneal osteotomy: realignment considerations in eight
patients. J Am Podiatr Med Assoc. 2005;95(1):53–9.
90. Penney NT, et al. Double-calcaneal osteotomy with a unilateral rail external fixator for cor-
rection of pes planus: a case report. Foot Ankle Spec. 2009;2(4):194–9.
91. Guha AR, Perera AM. Calcaneal osteotomy in the treatment of adult acquired flatfoot defor-
mity. Foot Ankle Clin. 2012;17(2):247–58.
92. Chan JY, et al. The contribution of medializing calcaneal osteotomy on hindfoot align-
ment in the reconstruction of the stage II adult acquired flatfoot deformity. Foot Ankle Int.
2013;34(2):159–66.
93. Toullec E. Adult flatfoot. Orthop Traumatol Surg Res. 2015;101(1 Suppl):S11–7.
94. Knupp M, et al. Osteotomies in varus malalignment of the ankle. Oper Orthop Traumatol.
2008;20(3):262–73.
95. Krause FG, et al. Ankle joint pressure changes in a pes cavovarus model after lateralizing
calcaneal osteotomies. Foot Ankle Int. 2010;31(9):741–6.
96. Hamel J. Calcaneal Z osteotomy for correction of subtalar hindfoot varus deformity. Oper
Orthop Traumatol. 2015;27(4):308–16.
97. Lombardi CM, et al. Talonavicular fusion and Evans calcaneal osteotomy for treatment of
PTTD. J Foot Ankle Surg. 1999;38(5):372.
98. Nery C, et al. Combined spring and deltoid ligament repair in adult-acquired flatfoot. Foot
Ankle Int. 2018;39(8):903–7.
99. Haddad SL, et al. Deltoid ligament reconstruction: a novel technique with biomechanical
analysis. Foot Ankle Int. 2010;31(7):639–51.
100. Keefe DT, Haddad SL. Subtalar instability. Etiology, diagnosis, and management. Foot Ankle
Clin. 2002;7(3):577–609.
Localized Osteoarthritis of the Ankle
Emilio Wagner Hitschfeld and Pablo Wagner Hitschfeld
1 Introduction
Arthrosis of the ankle causes pain, dysfunction, and alterations in mobility, limitat-
ing activities and functional evaluations. The classic treatment alternatives for
osteoarthritis of the ankle consist in distraction arthroplasties, total arthroplasties or
ankle arthrodesis. The outcome of distraction arthroplasty is mixed, with satisfac-
tion reported at about 60%, depending on where the results are reported [1, 2]. Total
arthroplasties present a successful outcome in 80% of cases at 10 years (with a high
re-operation rate), so it is not a life-long solution, especially in young patients who
present with post-traumatic arthrosis [3].
It should be remembered that in cases of slight, initial localized osteoarthritis, the
only symptom present is pain at the ankle with no radiological sign of osteoarthritis.
Pain at the ankle plus alterations in the load distribution in the ankle joint constitutes
the diagnosis of localized osteoarthritis of the ankle. We will use this term (i.e., local-
ized osteoarthritis of the ankle, LOA) to characterize the clinical picture of ankle pain
associated with localized overloading for cases with or without visible joint wear.
Since post-traumatic etiology is the most frequent in ankle osteoarthritis, it is
easy to understand the possibility of finding asymmetrical ankle wear in the area
where the greatest damage or impact has occurred. In fact, up to two-thirds of
patients with ankle arthrosis present asymmetrical wear and tear, and may present
greater damage to the anterior, posterior, medial or lateral aspect of the tibiotalar
joint. In the surgical treatment of localized ankle osteoarthritis, given its greater
E. Wagner Hitschfeld (*)

P. Wagner Hitschfeld

Switzerland AG 2022
692 E. Wagner Hitschfeld and P. Wagner Hitschfeld
prevalence in young patients, the use of periarticular osteotomies is the most recom-
mended treatment method given its joint sparing nature [4]. Joint preserving surger-
ies should always include complete ankle and foot rebalancing, considering soft
tissue surgeries such as ligament reconstruction, supra- and inframalleolar osteoto-
mies, tendon transfers, and selective arthrodesis. In cases of failure of these alterna-
tives (patients who persist with symptoms), the realignment surgery is still deemed
beneficial, since a consequent total ankle arthroplasty has better postoperative
results and is technically simpler if it is performed on an aligned ankle [5].
In this chapter, we will analyze in depth the use of periarticular osteotomies for
localized ankle osteoarthritis.
2 Etiology – Pathophysiology
The ankle is formed by the junction of the tibia, talus and calcaneus through the
ankle and subtalar joints. We must not forget the relationship between the ankle and
the rest of the foot, since the talus, not having any tendon or muscle insertion,
behaves as an intercalary segment in the foot. Its position and stability depend on
the neighboring bones and joints, as well as on the stability and strength of the ten-
dons that cross the area.
The etiology of ankle osteoarthritis is estimated to be 70% post-traumatic, 12%
rheumatological and 7% of no demonstrable origin [6]. The post-traumatic etiology
includes mainly ankle fractures, tibial pilon fractures and ankle sprains, as well as
fibular malunions and chronic ankle instabilities. The physiopathology of localized
ankle osteoarthritis (LOA) is easy to understand as the main cause is post-traumatic.
Trauma to the ankle generates asymmetric damage to the joint (see Fig. 1). The bone
resistance of the tibia and talus is not uniform on its surface, with the tibia showing
greater subchondral resistance in its posteromedial aspect than the anterolateral one
[7]. The presence of instability in the ankle is another aggravating factor in localized
osteoarthritis, since subluxation movements and localized loads are produced that
lead to asymmetric wear, which has been observed in biomechanical [8] and clinical
studies [9]. Finally, it is important to note that the load distribution in the ankle is
determined both by its static component, i.e., its skeletal alignment, and by its
dynamic component, composed of the tendon structures. In particular, the Achilles
tendon is an important deforming vector since in varus deformities it increases the
torque in inversion and in valgus deformities it increases the torque in eversion [3].
3 Biomechanical Considerations
In LOA, we must analyze the origin of the joint overload. This is mostly due to limb
malalignment and can be found at the supramalleolar level as in post-traumatic
deformities of the tibia, at the intra-articular level as in cases of asymmetric
Localized Osteoarthritis of the Ankle 693
Fig. 1 Ankle radiograph

of a 28-year-old patient
with an asymmetric
arthrosis of the ankle joint,
due to a previous pilon
fracture treated surgically.
Note the valgus inclination
of the pilon and of the talus
cartilage wear or inframalleolar level as in cases of pes cavus or valgus flatfoot in

which joint instabilities or tendon imbalances of the midfoot and forefoot lead to
overload and subsequent deformities within the ankle.
The alignment is studied with long leg radiographs, analyzing the anatomical
and mechanical axes of the limb. It can also be analyzed by measuring the torque
generated within the ankle, measuring the distance between the mechanical hip-
calcaneal (or tibia-calcaneal) axis and the center of the ankle [10] (see Fig. 2). The
published average distance is −3.2 mm (negative sign indicates varus of the hind-
foot, 95% confidence interval between −18 mm and 12 mm). The hindfoot align-
ment is analyzed with Saltzman’s rearfoot X-ray in which the contribution of the
subtalar joint in the alignment of the hindfoot is discussed. The foot alignment is
analyzed with weight bearing antero-posterior and lateral X-rays by measuring the
angle between the talus and the first metatarsal, which helps to analyze the relative
Fig. 2 Diagram of a bilateral lower limb radiograph, showing both limbs and pelvis. The mechan-
ical axis of the extremities is represented with a line starting on the center of the femoral head and
finishing distally where the calcaneus touches the floor. This line normally intersects the ankle
joint in its middle. The distance between this mechanical axis and the middle of the talus represents
the torque generated inside the ankle joint
abduction or adduction of the foot as well as any medial column insufficiency (see
Fig. 3).
In cases of LOA, we must also differentiate the plane of space in which the osteo-
arthritis is occurring, which will lead to different manifestations in relation to the
general alignment of the limb. Thus, in the coronal plane, when the wear is more
pronounced in the lateral half of the joint, we will speak of valgus arthrosis (see
Fig. 4), and when the wear is more pronounced in the medial half of the joint, we
will speak of varus arthrosis. In the sagittal plane we can find more pronounced
arthrosis in the anterior aspect of the joint which simulates recurvatum deformities
and produces anterior subluxations of the talus. In the opposite case we can find
more pronounced arthrosis in the posterior aspect of the ankle that simulates defor-
mities in procurvatum and leads to posterior subluxations of the talus. The procur-
vatum is better tolerated despite being able to generate anterior ankle impingement.
a b
Fig. 3 Diagram of anteroposterior and lateral weight bearing foot radiographs. (a) shows the
anteroposterior view of the foot, where a line was drawn representing the axis of the first metatarsal
and another one was drawn representing the axis of the talus, allowing to measure the anteropos-
terior talo-first metatarsal angle. (b) shows the lateral view of the foot, where a line was drawn
representing the axis of the first metatarsal and another one was drawn representing the axis of the
talus, allowing to measure the lateral talo-first metatarsal angle
The recurvatum is more damaging to the joint as it leads to a larger “uncovered”

talus surface and therefore a less constrained, unstable joint that is more susceptible
to damage [3]. Supramalleolar alignment should therefore be evaluated in the coro-
nal and sagittal plane using the lateral distal tibial angle or LDTA (average 90°,
range 88–95°) and the anterior distal tibial angle or ADTA correspondingly (aver-
age 81°, range 78–82°) [11, 12]. These angles are measured between a line along the
tibial axis and one tangential to the distal articular tibial joint surface, either in the
coronal (LDTA) or sagittal (ADTA) plane (see Figs. 5 and 6). This measurement
can only be made if the limb has no obvious deformity above the ankle. Intra-
articular alignment can be evaluated with the talar tilt, which should not exceed 4°.
The tilt angle is measured between the distal articular tibial surface and the talar
dome line.
Peritalar stability must be analyzed since in cases of ankle osteoarthritis the talus
loses intrinsic stability due to the decrease in cartilage thickness and consequent
decrease in hindfoot height. The talus is “imprisoned” between the calcaneus and
the tibia and therefore its position is controlled and manipulated by forces applied
from proximal and distal segments (it is an intercalary or sesamoid bone without
tendon attachments). Peritalar instability can manifest itself in various ways, either
Fig. 4 Radiograph of a
patient with a localized
ankle arthrosis, in this case
a valgus arthrosis, with a
lateral mechanical ankle
overload. It must be noted
that there is more
pronounced wear in the
lateral half of the joint
(decreased joint space in
the lateral half of the
ankle)
with deviations in the coronal plane with varus or valgus of the subtalar joint, with
talar external rotation, internal rotation, dorsiflexion, or plantar flexion. In cases of
peritalar instability the talus position should be evaluated using computed tomogra-
phy (CT) under load (WBCT) as it is not predictable through a single radiological
projection [13]. Sometimes when the talus tilts into varus or valgus, the calcaneus
slightly tilts in the opposite direction, compensating the deviation. However, in
cases of peritalar instability, an exaggerated compensatory deviation of the calca-
neus occurs. For example, in a varus ankle, an exaggerated valgus hindfoot is
observed. If a valgus calcaneal osteotomy (any) is performed in these cases (to
compensate the varus ankle), the hindfoot deviation may worsen with more varus at
the tibiotalar joint and no axis correction or symptomatic relief may be obtained. On
Fig. 5 Diagram of an anteroposterior radiograph of the ankle with the whole leg included. A line
is drawn along the mechanical axis of the leg. In the inset picture provided, a magnification shows
where the mechanical axis intersects the talus. The talus is subdivided in quarters with small verti-
cal dotted lines. The alignment is measured by the distance in millimeters between the midpoint of
the talus and the point where the mechanical axis of the leg intersects the talus. The alignment is
measured also by the lateral distal tibial angle (LDTA) which is measured between the mechanical
axis of the leg and a line tangential to the distal articular tibial joint surface
the other hand, a valgus of the ankle, will overcompensate with a varus subtalar
joint. If a varus calcaneal osteotomy is performed, it will lead to an exaggeration of
the ankle valgus due to peritalar instability [3]. In these cases, it is not useful to
perform a calcaneal osteotomy, but a distractive subtalar arthrodesis is recom-
mended instead [14]. It should be remembered that the subtalar joint more likely
will compensate for deviations in the coronal plane when it is found without osteo-
arthritis, i.e., with preserved mobility [15].
Another important point to analyze is the foot, considering its function as a tri-
pod, with the calcaneus, first and fifth metatarsals resting on the floor in static phase.
In valgus deformities, an insufficiency of the medial column leads to a valgus incli-
nation of the hindfoot (called “forefoot-driven hindfoot valgus”). This factor leads
to asymmetrical lateral wear of the ankle cartilage due to overloading of the lateral
aspect of the ankle. The wear of the cartilage leads to a loss of height of the hind-
foot, which secondarily may end in a deltoid insufficiency, which in turn leads to a
talar rotational instability. The talar rotational instability increases the asymmetric
wear of the ankle. In forefoot-driven hindfoot valgus cases, the loading capability of
Fig. 6 Diagram of a lateral radiograph of the ankle. A line is drawn along the mechanical axis of
the leg. This line normally intersects the talocalcaneal joint at the anterolateral process of the talus
(represented by a circle). The alignment is measured by the distance in millimeters between the
mechanical axis of the leg and the anterolateral process of the talus (along an imaginary line paral-
lel to the floor). The alignment is measured also by the anterior distal tibial angle (ADTA) which
is measured between the mechanical axis of the leg and a line tangential to the distal articular tibial
joint surface
the medial column must be restored. The correction of the medial column insuffi-
ciency should be performed at the apex of the deformity. If the apex corresponds to
an unstable or arthritic joint, a fusion is recommended. If no diseased joint is evi-
dent, a plantar flexion osteotomy of the medial column is one option (frequently of
the medial cuneiform or cotton osteotomy), which will reduce the lateral ankle
overload. In cavo-varus deformities, the varus hindfoot is tilted due to the medial
column depression (called forefoot-driven hindfoot varus). In these cases, lateral
and medial ankle instability can be found, as well as a torque increase in inversion
due to the medialized Achilles pull which leads to greater load on the medial aspect
of the ankle. This added to the relative weakness of the peroneal tendons increases
the lateral instability and consequently the asymmetric ankle wear. Treatment for
forefoot-driven hindfoot varus should include medial column elevation to decrease
the inversion and load on the medial aspect of the ankle, for example, through a
metatarsal elevation osteotomy [3].
4 Diagnosis and Analysis
4.1 Clinical Analysis
Patients with LOA initially present with ankle pain associated with changes in phys-
ical activity, changes in the surface where they develop their activity, differences in
footwear, changes in body weight, etc. In other words, any variable that leads to an
increase in the impact or torque that the ankle supports can cause this clinical pic-
ture. The pain may begin immediately after physical activity and subside in the
following hours or persist for hours or days after completing the physical activity.
In more advanced stages of arthrosis, pain may be present even at night [6].
The study of patients with osteoarthritis of the ankle should consider standing
long leg radiographs, in addition to ankle X-rays. Alignment should be analyzed
and evaluated at 3 levels, supramalleolar, intra-articular and infra-malleolar. As
already mentioned, not only should we analyze the maintenance or alteration of the
radiological indices (lateral distal angle of the tibia, talar tilt, anterior distal angle of
the tibia), but we should also measure the leverage generated at the ankle level by
measuring the distance between the calcaneal-hip mechanical axis and the center of
the talus. Patients in early stages of the disease may have joint angles within normal,
but will have ankle pain in the area affected by previous trauma (e.g., a pilon frac-
ture with lateral joint damage) or alterations only visible within the joint on MRI or
nuclear medicine tests such as Single Photon Emission Computed Tomography
(SPECT-CT) (see Fig. 7). In more advanced stages of localized osteoarthritis, radio-
logical alterations will already be seen consisting in changes in the joint space,
angulation of the joint line, sclerosis or osteophytes, bone cysts or already formally
advanced osteoarthritis.
a b
Fig. 7 Images from a patient with right ankle articular pain. (a) shows a bilateral ankle weight
bearing radiograph, where the right ankle side is at the left of the image. Gross normal alignment
can be observed. However, when drawing the mechanical axis of each leg, represented by the verti-
cal dotted yellow line, a lateral overload of the right ankle joint can be suspected, represented by
an increased distance between the midpoint of the talus and the intersection of the mechanical axis
with the talus. (b) shows a SPECT-CT image of the right ankle joint of the same patient, where a
clear increase in marker activity can be seen in the lateral half of the ankle pilon, confirming the
lateral overload of the joint
In the analysis of patients with LOA, we must detect in the radiological study the
apices of deformity. Once the apices are located, preservation surgery can be planned.
It is accepted that the limit for attempting joint preservation surgery is determined by
the amount of remaining cartilage, with up to 50% of the cartilage present in the
ankle being accepted as adequate for joint preservation surgery. This theoretical
limit for indicating joint preservation surgery can be inferred from the wear and tear
on the ankle joint on loaded radiographs. If subchondral tibia-talus contact is already
observed in the medial or lateral space of the ankle joint (gutters), in addition to
subchondral tibia-talus contact being observed in the upper medial or lateral ankle
space, it is no longer considered a candidate for joint preservating surgery. Formal
contraindications for this approach are the presence of diffuse osteoarthritis, unreli-
able patients, bone infection, neurological deficit and neuroarthropathic disorders.
In terms of classifications, there are no generally accepted classifications for val-
gus arthrosis, but there are for varus osteoarthritis. For the latter cases, the Takakura
classification is used, which uses load-bearing AP ankle X-rays, in which symptom-
atic ankle osteoarthritis without joint narrowing is considered a type 1; a type 2
presents with medial tibiotalar joint narrowing; a type 3A considers subchondral
bone contact between the medial malleolus of the tibia and the corresponding talus;
type 3B adds subchondral bone contact between the upper surface of the dome of the
talus and the corresponding tibia (see Fig. 8); finally a diffuse osteoarthritis corre-
sponds to a type 4 [16]. There is also the Knupp classification which can be used for
valgus or varus osteoarthritis, in which stage 1 is diffuse osteoarthritis; stage 2 is
localized osteoarthritis with tilt greater than 4° which is subdivided into: 2A if LOA
has no subchondral bone contact; 2B if there is subchondral bone contact; 2C if there
is talus protrusion through the tibial subchondral bone; and stage 3 is there is an
isolated medial ankle osteoarthritis. This classification also considers whether there
is correct alignment in the sagittal plane or whether there is an anterior extrusion of
the talus, by adding to the main group a letter C (centered) or E (extruded) [17]. With
respect to the use of other imaging modalities, the use of SPECT CT has been useful
since it has been associated with failure of joint preservation treatment when cystic
joint lesions, bipolar lesions, anterocentral tibial, anterocentral and medial talar
uptake are detected on the exam. In isolation, the presence of bipolar lesions on
SPECT CT is significantly associated with failure of joint preservation surgery [18].
4.2 Mechanical Analysis
The authors find the use of pre-operative planning extremely useful, for which sev-
eral computer applications are available (e.g., Bone ninja app). With these applica-
tions, the necessary correction can be more adequately estimated at both the
supra- and infra-malleolar levels and allows for better preparation of supplies and
surgical time. When facing a patient with symptomatic LOA, we must analyze the
type of mechanical overload of the ankle with or without radiological ankle wear,
the talar tilt, the ankle joint congruency or symmetry, the subtalar joint and the foot
alignment. We will analyze each of these characteristics in the following paragraphs.
Fig. 8 Anteroposterior
weight bearing ankle
radiograph of a 52-year-old
patient. Moderate arthrosis
can be seen at the ankle
joint, with tilting of the
talus into varus, and
decreased joint space in the
medial tibio-talar space
and in the upper tibio-talar
space. This can be
classified as a varus ankle
arthrosis Takakura type 3B
4.2.1 Type of Mechanical Overload of the Ankle
We must differentiate whether the patient presents a radiological consequence of his

or her joint overload, that is, a skeletal malalignment with asymmetry of the ankle
joint space. In this way, the following mechanical situations can occur: patients
without radiological wear (without articular asymmetry of the ankle) but with
medial, lateral, anterior or posterior mechanical overload (cavus feet, flat feet, meta-
tarsal adductus, etc.) which we will call neutral ankles; patients with medial or lat-
eral radiological wear of the ankle (medial or lateral overload), which we will call
varus or valgus ankles; and patients with anterior or posterior wear of the ankle
(anterior or posterior overload) that can generate anterior or posterior sublux-
ated ankles.
Neutral Ankles
It should be considered that there are cases with medial, lateral, anterior or posterior
overload of the ankle that, being initial, do not yet present visible wear and defor-
mity in ankle X-rays. In these cases, a long leg mechanical axis deviation could be
observed (congenital limb deformity), associated with ankle symptoms such as
periodic synovitis according to the level of activity of the patient. These cases can
be treated with joint preservation surgery, but it is not always needed to perform
supramalleolar corrections, since the ankle is still preserved. In these cases, we must
plan corrections at the apex of the deformity (called inframalleolar in cases of foot
deformities), either at a subtalar level in isolation or combined with a correction at
a medial column level (flatfoot or pes cavus surgery, for example). In valgus devia-
tions of the hindfoot, if an apex of deformity is found at the medial column (i.e., a
loss of the Meary’s angle or “sag” at a particular joint) an osteotomy or arthrodesis
of the involved joint should be considered to achieve medial column plantar flexion.
The Cotton osteotomy is the most frequently used. In cases of severe subtalar defor-
mities with talonavicular subluxation, peritalar instability cannot be resolved by
medial column plantar flexion. Procedures that attempt to align the talus over the
calcaneus are recommended [19]. This can be achieved through a calcaneal length-
ening osteotomy, with or without a medializing posterior calcaneal osteotomy, pro-
cedures that can be associated or not with a reconstruction of the medial ligament
complex of the ankle (intraoperative decision depending on the resulting alignment
of the hindfoot) [14]. In hindfoot varus cases, it is frequent to find a midfoot cavus
with an increased first metatarsal load, leading to medial ankle overload (forefoot
contribution to the hindfoot varus). In addition, there is a muscular imbalance that
often accompanies cavo-varus feet, with lateral instability and selective loss of
strength (peroneal muscle paresis). The Coleman test is often used to determine the
contribution of the forefoot to the hindfoot varus. It helps to decide whether to per-
form surgery to elevate the medial column if the deformity is flexible (positive
Coleman test). With a negative Coleman test (i.e., none or minimal forefoot contri-
bution to hindfoot varus) a calcaneal osteotomy should be added to a first metatarsal
elevating osteotomy. In more severe cases there is significant equinus and forefoot
adductus. Midfoot osteotomies are recommended for these cases, where the entire
midfoot can be derotated in relation to the hindfoot.
Varus or Valgus Ankles
When analyzing the radiological deformity, we will analyze the deviation of the
extremity mechanical axis (from hip to calcaneus) using the projection called long
leg ray or teleradiography of lower extremities. In addition to the LDTA angle (lat-
eral distal tibial angle) and the talar tilt, importance has been given to the torque or
moment generated at the ankle. The latter is calculated measuring the distance (in
mm) between the hip – calcaneus mechanical axis and the center of the ankle. For
varus ankles with medial osteoarthritis, the load bearing axis will traverse the ankle
joint through its medial half. The opposite will occur for valgus ankles with lateral
LOA. To achieve symptomatic relief, the aim is to unload the diseased half of the
ankle joint and overload the healthier tibiotalar cartilage. This should be performed
by means of a supramalleolar osteotomy (SMOT) that moves the extremity mechan-
ical axis to the healthier joint half. If the talar dome is divided into four quarters in
an anteroposterior radiographic ankle projection, our aim will be to position the
“new” weight bearing axis on the contralateral quarter (see Fig. 5). This mechanical
axis correction corresponds to an LDTA overcorrection of approximately 5° [20].
Ankles with Talar Anterior or Posterior Subluxation
This type of deformity is visible on a lateral ankle or foot X-ray. Generally, the tibial
weight bearing axis intersects the anterolateral process of the talus. The angle mea-
sured is the anterior distal tibial angle (ADTA) with a normal value of 81° on aver-
age. In cases of post-traumatic deformities in which there are supramalleolar
malunions with shortening of the anterior pilon column or anterior ankle wear, the
tibial load axis intersects the talus posterior to the anterolateral process. In these
cases, the ADTA decreases below 80°. The resulting joint load is increased in the
anterior half of the distal tibial joint surface (anterior ankle overload) (see Fig. 9).
Fig. 9 Lateral weight

bearing ankle radiograph
showing posttraumatic
localized arthrosis at the
anterior aspect of the ankle
joint. Please see the
osteophytes on the anterior
aspect of the ankle joint,
besides the decrease in
joint space. The
mechanical axis of the leg
is drawn as a yellow line,
and it can be observed how
the line intersects the
subtalar joint posterior to
the anterolateral process of
the talus, representing an
anterior displacement of
the talus and therefore an
anterior overload of the
ankle joint
This constitutes an ankle with anterior talus subluxation simulating recurvatum

deformities that are poorly tolerated, as previously discussed. In cases of post-
traumatic deformities in which there are supramalleolar malunions with shortening
of the posterior pilon column or posterior wear of the ankle cartilage, the load axis
of the tibia intersects the talus anterior to its anterolateral process. In these cases, the
ADTA increases above 81°. The resulting load is increased in the posterior ankle
half (posterior ankle overload). This deformity presents clinically as an anterior
ankle impingement and is better tolerated than the previously mentioned deformity.
The treatment of both previous situations generally consists of a SMOT that corrects
the anterior distal tibial angle as well as the ankle mechanical alignment.
4.2.2 Analysis of the Talar Tilt
Frequently the deformity is intra-articular, either because of a post-traumatic intra-

articular deformity (for example, after a pilon fracture), or because of an extremity
mal alignment that evolved into localized ankle osteoarthritis. In these cases, there
is a pathological inclination of the talus within its mortise, which leads to an
increased talar tilt. It is important to measure the talar tilt since it has been seen that
in SMOT for localized osteoarthritis in varus ankles, the clinical results are better if
the tilt is less than 10° [21]. In cases where the tilt already exceeds 5°, it is recom-
mended that when performing the SMOT, check under fluoroscopy if the tilt is
manually correctable within its mortise. This is done by stabilizing the distal end of
the tibia with one hand and forcing the hindfoot to the opposite attempting to correct
the talar tilt. If the tilt is corrected, the supramalleolar osteotomy can be performed
in isolation. If the talus persists misaligned, and preoperatively or intraoperatively it
has been detected that there is a severe pilon joint collapse that explains the tilt, an
articular osteotomy or “plafondplasty” can be done. Studies at six years of follow-
up show good results with this technique in which the talar tilt in varus improved
from 19° to 7° [22]. Evidently this surgery is more demanding and needs the use of
double plates for fixation. Another alternative to treat varus talar tilt over 5° that
does not correct with intraoperative manual maneuvers, is to intraoperatively use a
medial or lateral pin distractor (Hintermann’s distractor) or external fixator (should
be positioned depending on where the soft tissue retraction is). This helps reduce the
talar tilt. Good results have been reported with this technique, but with a low num-
ber of cases, with a follow-up of five years [23]. This technique is indicated when
retracted soft tissues are responsible for the talar tilt and not an intra-articular bone
deformity.
4.2.3 Symmetry of the Ankle Join
The purpose of ankle preservation surgery should be to achieve the best possible
alignment, improving balance and load distribution within the ankle. We should be
able to decrease the loads in the damaged or arthritic sector of the ankle, increasing
relatively the load in the healthier segment of the ankle. The final goal is to achieve
symptomatic improvement and prolong the life of the ankle to the maximum. Joint
symmetry means a uniform joint space is present throughout the joint with no (or
minimum) talar tilt. This is very uncommon in cases of LOA, in which a joint asym-
metry is present most of the time. Cadaveric studies have found that SMOT improves
joint congruency and load distribution within the ankle in a more predictable way
when performed in conjunction with a fibula osteotomy [24]. Fibular osteotomies
allow the talus to be repositioned as symmetrically as possible within its mortise after
a SMOT. A relative fibular shortening (together with a valgizating SMOT) helps in
cases of varus deformities [3] (in addition to a medial gutter debridement) by “pull-
ing” the talus into valgus. In cases of valgus deformities, a fibular lengthening oste-
otomy is indicated, working as a lateral talar buttress. The authors always consider
adding a fibular osteotomy to a SMOT to obtain better correction of joint symmetry.
4.2.4 Subtalar Joint
We should try to differentiate how much the subtalar joint is involved in the ankle
overload. In cases of ankle valgus osteoarthritis (lateral LOA), if the subtalar joint
is also in valgus, it will be increasing and worsening the intra-articular overload of
the ankle. The opposite will occur in varus deformities. For the hindfoot alignment
evaluation, a Saltzman axial X-ray or a WBCT is recommended. The WBCT will
help to measure the Foot and Ankle Offset (FAO) as well. The FAO analyzes the
foot as if it were a tripod in which the head of the first metatarsal, the head of the
fifth metatarsal and the point of contact of the calcaneus with the floor form a tri-
angle. The center of the talar dome is then determined. If the talar dome center lies
medial to the triangle axis, the foot is considered to be aligned in valgus. On the
contrary, if the talus center is lateral to the triangle axis, the foot is considered to be
aligned in varus (FAO is expressed as a percentage relative to the foot length, nor-
mal values FAO: 2.3%, varus feet: −11.6%, valgus feet: 11.4%) [25].
Calcaneal osteotomies or subtalar arthrodesis help to increase the SMOT correc-
tion power regarding weight bearing axis location. If the subtalar joint is healthy (no
signs of osteoarthritis), a displacement calcaneal osteotomy can be considered (val-
gus producing for varus ankle osteoarthritis, and varus producing for valgus ankle
osteoarthritis) to improve load distribution at the ankle level (see Fig. 10). The
amount of calcaneal displacement depends directly on the distance in millimeters
that we want to move the limb load axis (see commentary in paragraph entitled
“Type of mechanical overload of the ankle”). When comparing different type of
calcaneal osteotomies, no biomechanical advantage has been found in studies of
varus ankles in terms of decreasing medial intra-articular pressure when doing a
lateralizing calcaneal osteotomy versus a z-osteotomy or a lateralizing osteotomy
plus wedge resection. In varus deformities, a pure lateralizing osteotomy can be
sufficient and is technically simpler [26].
Peritalar instability should be ruled out using a CT or WBCT ensuring that peri-
talar joint relationships are maintained. If this is not the case and peritalar instability
is suspected (a common condition in valgus flat feet), a calcaneal osteotomy is not
recommended, and a subtalar arthrodesis would be more reliable.

bearing ankle radiograph
showing a calcaneal
osteotomy performed in a
medial ankle overload
case. The ankle presented a
varus localized arthrosis,
and therefore a valgizating
calcaneal osteotomy to
improve load distribution
at the ankle joint was
performed and fixed with
two screws
4.2.5 Alignment of the Foot
Finally, we must consider the alignment of the foot. If there is an instability of the
medial column of the foot, characteristic of valgus plane deformities, we must ana-
lyze the foot with concepts of acquired flatfoot. For cases of varus hindfoot with
medial ankle overload, we will analyze the contribution of the foot to the varus
hindfoot using concepts of cavo-varus foot (see commentary in paragraph entitled
“Type of mechanical overload of the ankle”).
5 Treatment
Any treatment that seeks to lessen the symptoms for localized osteoarthritis of the
ankle should decrease the load and impact on the joint. Therefore, weight manage-
ment, physical fitness and healthy living should be promoted. Impact activities
should be avoided as well. The use of insoles and shoes that have cushioning help
decrease ankle joint impact. The use of intra-articular injections with corticoids or
hyaluronic acid achieved partial and temporary symptomatic improvement. They
are helpful but not a lasting option. The use of analgesics and oral anti-inflammatories
is indicated in an intermittent manner for pain crisis. Failure of conservative treat-
ment means that a more radical treatment is needed. A surgical procedure will have
to include actions determined by the previous mechanical analysis. We will analyze
the surgical procedures depending on the type of mechanical overload of the ankle.
5.1 Lateral Mechanical Ankle Overload
5.1.1 Arthroscopy
In general, arthroscopy is the initial procedure used to diagnose medial or lateral

instabilities that may have been in doubt, remove free bodies, remove exostoses that
may be impeding ankle mobility, or perform bone marrow stimulation procedures
on osteochondral lesions which are not validated in the literature but may favor the
SMOT outcome. When removing anterior exostoses of the tibia, the surgeon should
remember that they are part of a biomechanical response to instability and osteoar-
thritis. The surgeon should not be aggressive in removing these exostoses since they
can destabilize the ankle [3]. It should also be confirmed that there is remaining
cartilage in the joint (at least 50%), so that a SMOT is likely to be successful.
5.1.2 Osteotomy Depending on Type of Radiological Wear
1. Neutral ankle
If no alteration is found in the extremity alignment study (hip-calcaneus), the
axis alteration is probably in the foot. In these cases, it is not necessary to perform
supramalleolar osteotomies (SMOT) as already mentioned before. The foot should
be corrected accordingly depending on where the apex of the deformity is located
(go to Sect. 5.1.4 and 5.1.5 of this surgical technique).
2. Ankle with valgus arthritic deviation
In these cases, the hip-calcaneus mechanical load axis intersects the talar dome
through its lateral half. The ankle will have an articular asymmetry (intra-articular
valgus) with alteration of the LDTA (under 90°) and probably an altered talar tilt
(see Fig. 11). The correction should be planned to move the load axis to the medial
half of the ankle joint, which corresponds to an overcorrection of the LTDA by 5°.
This correction should be made through a varus producing SMOT. With a digital
planning app (e.g., Bone ninja), it is easy to evaluate how much supramalleolar cor-
rection is needed to move the mechanical load axis to the desired position. If you do
Fig. 11 Anteroposterior weight bearing ankle radiograph, where a lateral ankle overload can be
suspected. Please see the augmented image on the right side of the figure, where the mechanical
axis is represented by a vertical continuous line. The talus is subdivided in quarters by small,
dashed lines. Please note that the mechanical axis of the leg intersects the talus through its lateral
quarter, representing a lateral mechanical overload. The angle that can be measured is the LDTA
or lateral distal tibial angle, which will measure less than 90°
not have a planning app, the recommendation is to calculate the osteotomy with
respect to the LDTA. If the LDTA is 85° (5° of valgus), it should be brought to 95°
(5° of varus) to achieve the desired overcorrection.
Most of these cases present with an intra-articular apex of deformity and not a
supramalleolar one, because the deformity is generated by a posttraumatic localized
joint arthrosis, rather than by a bone deformity. Cases of malunited tibia fracture or
a long standing congenital tibial deformity (tibia valga) could present with both a
supramalleolar deformity (at the tibial deformity) and an intraarticular deformity (at
the degenerated joint). To avoid overlooking these findings, always start the ankle
evaluation with a long leg x-ray to rule out other causes for the LOA.
The ankle radiological study is performed by drawing the mechanical axis of the
tibia (from center of tibial spines to center of tibial plafond) and a line parallel to the
tibial pilon. The resulting angle is the LDTA and should be 90° in a normal ankle.
For valgus ankles LDTA will be <90°.
When a SMOT is performed for LOA with an intraarticular deformity apex,

since the tibial osteotomy is performed outside the apex, the so-called third rule of
osteotomies occurs. This rule mandates that when angular misalignment is cor-
rected through an osteotomy outside the deformity apex, a secondary translation of
the distal segment occurs [27]. This secondary translation occurs in the direction of
correction (a SMOT in varus medializes the distal segment). This third rule is desir-
able in arthritic cases since it further helps with mechanical axis medialization. The
most frequently used tibial osteotomy is medial wedge resection. As already men-
tioned, the authors recommend always adding a lengthening fibular osteotomy,
which favors adequate replacement of the talus in its mortise. If a supramalleolar
angular correction greater than 10° is necessary, dome osteotomies are preferred.
Supramalleolar Osteotomy Technique: Wedge Osteotomy
Tibial wedge resection uses a trigonometric equation or formula for planning: the
height of the wedge should measure: H = tan α * W, with H being the wedge height
to be resected, α the degrees to be corrected, and W the tibial width at the height of
the osteotomy (32 mm in average). If we take an ankle valgus with an LDTA of 83°,
it has an intra-articular deformity of 7° of valgus (difference to reach 90° of LDTA).
An 5° overcorrection must be achieved in arthritic cases, so the target LDTA is 95°.
In this hypothetical case, a 12° correction must be calculated. Applying the formula
previously shown, a 7 mm wedge should be resected to correct 12°. Because this
formula is easy to forget, there is a simpler rule of thumb which can be followed. If
there is an LDTA of 83°, the difference with a normal LDTA is calculated, e.g., 7°
(difference between 90 and 83° LDTA). Then, the wedge to be resected should be a
7 mm wedge (number of mms equivalent to number of degrees).
A longitudinal medial approach is made at the distal tibial end. The osteotomy is
located under radiographs according to the preoperative planning. In general, the
osteotomy is performed in metaphyseal bone, 3–4 cm proximal to the tibiotalar
joint, in the metaphyseal area where the tibia is concave in its medial aspect. The
osteotomy trajectory should be oblique from proximal medial to distal lateral, so
that it ends at the tibiofibular syndesmosis (about 2 cm proximal to the ankle joint).
This makes the lateral osteotomy exit more stable thanks to the syndesmotic liga-
ments in that area. Two K-wires are used marking the proximal and distal limits of
the wedge to be resected. The wedge height has already been calculated in the pre-
operative planning. The two Kirschner wires must be placed from the medial side,
converging towards the lateral side. An oscillating saw of adequate length is used to
resect the wedge, using frequent cooling and intermittent power (avoiding thermal
osteonecrosis). If we use the previously mentioned example with an LDTA of 83°,
this wedge demarcated by the wires should be of 7 mm height. Once the bone
wedge is resected, the osteotomy should be closed and a Kirschner wire is used for
temporary fixation (see Fig. 12). If correction is adequate, a small fragment locking
plate is used. If talar correction is not adequate, check for calcifications on the
a b
Fig. 12 Anteroposterior ankle radiograph of the same patient shown in Fig. 11. (a) shows the
planned resection of a supramalleolar medial closing wedge, to achieve a varizating effect. (b)
shows the bone wedge already resected, and the osteotomy closed and fixed temporarily
with K wires
anteromedial tibial rim that could prevent talus correction. The position and length
of the fibula should also be monitored (see Sect. 5.1.3 of this surgical technique).
Supramalleolar Technique: Dome Osteotomy
An anterior ankle approach is performed, over the distal metaphysis of the tibia.
Subperiosteal dissection is performed, and the osteotomy site is marked according to
preoperative planning, usually 3–4 cm proximal to the ankle joint line. It is recom-
mended that the osteotomy be planned using a third tube plate by fixing one end of
the plate as subchondral as possible to the distal tibia and rotating the other end of the
plate, using it as a compass. In the third or fourth hole (coinciding with 3–4 cm proxi-
mal to the articular surface), multiple drill holes are made to “draw” the osteotomy at
the distal tibial metaphysis. The fibula should always be included in these cases per-
forming an oblique osteotomy at the same level of the tibial osteotomy (through the
same approach or through a separate lateral approach). The tibial dome osteotomy is
completed with a small osteotome uniting the drill holes previously made.
The amount of rotation needed at the osteotomy should be confirmed with fluo-
roscopy until adequate correction is achieved. An alternative way of estimating cor-
rection is to measure the mms of step formed at the osteotomy level medially; 10 mm
is equivalent to 20° of correction / [28]. A Hintermann’s distractor (pin distractor) is
of great help when performing the rotation. Once the osteotomy has been sufficiently
rotated, it is temporarily fixed with Kirschner wires. If the desired correction has
been achieved, 2 anterior locking plates are recommended for definitive fixation.
5.1.3 Ankle Symmetry
In cases where SMOT has been performed through a medial closing tibial wedge
osteotomy, the general recommendation is to perform a fibular osteotomy when it
prevents adequate correction of the talus in its mortise. This is measured by evaluat-
ing the talar tilt after the SMOT correction. When the desired correction is greater
than 10° or the ankle is congruent (no increased talar tilt, such as in initial LOA with
minimum cartilage wear), fibular osteotomy is necessary to avoid paradoxical load
shifts in the joint [24]. In general, the authors recommend always performing a long
oblique fibular osteotomy, at the level of the tibia osteotomy, through a direct lateral
approach to ensure adequate tibiotalar load transfer, both in cases of varus and val-
gus osteoarthritis. The fibula should always be fixed in the position that allows an
adequate reduction of the mortise, usually by lengthening it minimally. In some
cases (severe valgus) it is necessary to lengthen the fibula by 1 cm or more. For
these cases, a Z osteotomy is recommended, which is very stable and easy to fix
(resembles a “scarf osteotomy”)(see Fig. 13). In cases of valgus LOA, with a preop-
erative tilt greater than 10° in valgus, a plafondplasty or even grafting in the area of
lateral collapse should be considered (see alternative to plafondplasty for osteoar-
thritis varus below).
a b
Fig. 13 Anteroposterior ankle radiograph of the same patient shown in Fig. 12. (a) shows a distal
tibial plate fixing the supramalleolar osteotomy. Please note the slightly shortened fibula, repre-
sented by an increased space between the talus and the distal end of the fibula. (b) shows a length-
ening fibular osteotomy, performed in a “z” fashion, and stabilized by two interfragmentary screws
and a small third tubular plate
5.1.4 Inframalleolar Correction
As noted in the biomechanics paragraph, there are cases of lateral ankle overload
without extremity malalignment. In these cases, the alignment should be analyzed
at the inframalleolar and midfoot level. If there are no signs of subtalar instability,
we will decide whether to add a medializing calcaneal osteotomy. In cases where a
SMOT was performed, it is important to have a complete preoperative planning to
be prepared to add a calcaneal osteotomy if necessary. We must clinically evaluate
the hindfoot axis after completion of the SMOT to assess whether it is slightly varus
or neutral (which is the objective). If the SMOT did not completely correct the lever
arm described above as much as necessary, a medializing calcaneal osteotomy
should be added. The medializing osteotomy of the calcaneus or Koutsogiannis
technique, is performed through a direct lateral approach on the calcaneus, oblique
in 45° from proximal cephalic to distal caudal, accessing the lateral surface of the
calcaneus. After careful dissection two Hohmann-type retractors are placed, one in
the proximal cephalic concave part of the calcaneus, and another is placed in the
lower concave part of the calcaneus. The osteotomy is initiated with an oscillating
saw (with frequent cooling) until it touches the medial cortex of the calcaneus. A
narrow chisel is then used to carefully breach numerous areas of the medial calca-
neal cortex and then completed with a wider osteotome (1 cm or more). This ensures
that no damage is done to the medial neurovascular bundle. The ankle is brought
into plantar flexion to relax the Achilles tendon and the posterior tuberosity is then
moved medially according to preoperative planning. Two axial screws are recom-
mended for fixation (4 mm or more in diameter).
5.1.5 Foot Deformity - Stability of the Medial Column
In cases of valgus LOA, it is common to find instabilities of the medial column

associated with flatfoot. In these cases, the joints that may be unstable include the
talo-navicular, naviculocuneiform, and cuneometatarsal joints. It is beyond the
scope of this chapter to analyze a flatfoot deformity, but a medially unstable foot
should be addressed as an unstable flatfoot and the apex of the medial column
should be located through clinical analysis and AP and lateral X-ray of the patient’s
foot. If an apex is identified in which the medial column presents a plantar sag or
deformity, plantar flexion osteotomies (cotton osteotomy) are recommended in
young patients without arthrosis. If there is severe instability with evident sublux-
ation of a medial column joint, or older patients with associated osteoarthritis, an
arthrodesis of the involved joints is recommended. If there is a symptomatic hallux
valgus, we recommend performing plantar flexion of the first metatarsal through a
cuneometatarsal fusion, thus correcting the medial column insufficiency and the
first metatarsal varus.
5.1.6 Ligament Reconstruction
In a valgus deformity we must consider repairing medial hindfoot-midfoot liga-

ments. Radiographs under varus or valgus stress can help identify these cases. If
ankle instability is identified, bone anchored sutures may be added to the medial or
lateral side of the ankle. Continuing distally, the spring ligament may be damaged
as well as the entire tibiocalcaneonavicular component. In cases of severe instabil-
ity, allograft or synthetic graft reconstruction may be considered.
5.2 Medial Ankle Mechanical Overload
5.2.1 Arthroscopy
As in the case of lateral overloads or ankle valgus, we must begin with an arthros-
copy to confirm there is at least a 50% of remaining cartilage. Intra-articular free
bodies are removed and any exostosis that is believed to be participating in ankle
motion restriction is resected.
5.2.2 Osteotomy Depending on Type of Radiological Wear
1. Neutral ankle
As discussed in the biomechanics paragraph, it is possible to find patients with
ankle pain and clinical ankle synovitis due to medial ankle overload, without yet
presenting with osteoarthritis or loss of cartilage thickness on the medial side of the
ankle. These patients benefit from ankle-sparing surgeries that realign the limb to
correct the medial overload and should be treated as cavo-varus deformities. As
such, osteotomies or arthrodesis that correct the varus hindfoot and medial column
elevations allowing a more plantigrade foot are recommended. These procedures
decrease medial ankle pressure (see Chap. 26 on cavarus feet). It is the authors pref-
erence to correct pronation of the forefoot in relation to the hindfoot through mid-
foot osteotomies rather than isolated osteotomies of the first metatarsal.
2. Ankle with varus arthritic deviation
In cases of varus LOA (LDTA>90°), as we discussed in the biomechanics sec-
tion, there is information that suggests that the more lateral we move the weight
bearing axis, the better functional results can be obtained. The current preference is
to perform a SMOT that moves the weight bearing axis to the lateral central talar
dome quarter [20]. To perform this, the ankle should end up in a slight valgus
(LDTA <90°). As with ankle valgus deviations, most of these cases present an
intra-articular deformity apex, due to ankle cartilage wear. This apex can be evalu-
ated by drawing the mechanical axis of the tibia and a line parallel to the surface of
the tibial pilon (this resulting angle is the LDTA and should be 90° in a normal
ankle). In these cases, since the tibial SMOT is performed proximal to the apex, the
so-called third rule of osteotomies occurs. This rule means that when an angular
correction is performed outside the deformity apex, a secondary translation of the
distal segment occurs [27]. This secondary translation in cases of valgus SMOT,
means there is a distal segment lateralization. Lateral translation is desired since it
favors and strengthens the correction into valgus of the mechanical axis.
The most frequently recommended osteotomy is the opening medial tibial wedge
plus fibular shortening. If the correction needed is greater than 10°, dome osteoto-
mies are preferred.
For medial tibial opening wedge, the same formula already presented is used
(H = tan α * W). The only difference is that the height delivered by the formula cor-
responds to the height of the opening wedge, instead of the wedge to be resected.
The authors use the same rules discussed for closing wedge osteotomies. An easier
technique is to open the wedge the number of mm corresponding to the number of
degrees of deformity (if LDTA = 95°, then open 5 mm).
In cases where the talar tilt exceeds 10°, soft tissue retraction and/or medial tibial
plafond erosion must be suspected. In those cases, some procedure should be added
to improve the talar tilt. Recommended procedures include aggressive releases of
the medial ankle ligament, medial malleolus osteotomy, medial soft tissue distrac-
tion through an external fixator or performing an intra-articular osteotomy - pla-
fondplasty. For cases with tilt under 5° that persist after SMOT, an aggressive
deltoid ligament release is sufficient. In cases where the tilt exceeds 5° after SMOT,
and a change in the curvature of the tibial plafond is observed, the authors recom-
mend adding the previously mentioned intra-articular osteotomy (plafondplasty) to
the supramalleolar osteotomy.
Intraarticular Ankle Osteotomy (Plafondplasty) Technique
This technique is recommended in cases where the talar tilt is over 5° and there are
significant erosions on the medial tibial plafond. Normally, the tibial joint line is
straight. If there is a depression or change in curvature medially at the joint, an intra-
articular osteotomy may be indicated.
The same medial approach is used as for supramalleolar osteotomy. A Kirschner
wire is used to plan the osteotomy. It starts 2 to 2.5 cm proximal to the ankle joint
line. The exit point of the osteotomy should be planned just lateral to the erosion site
or change in the tibial plafond curvature. After placing and confirming under fluo-
roscopy the position of the guide wire, 2 to 3 one mm Kirchner wires are placed
parallel to the tibiotalar joint, in a subchondral position from medial to lateral. These
thin wires help avoiding the osteotomy completion so that the cartilage is not vio-
lated when the osteotomy is performed. The osteotomy is then performed with an
oscillating saw. Check the AP image to make sure that the cut plane is straight. A
distractor or osteotome is then used to open the osteotomy until a straight joint line
is obtained, thus eliminating the joint incongruence. This position is secured with a
structured graft and fully threaded screws. After completing the intra-articular oste-
otomy, the supramalleolar osteotomy is performed [29].
Supramalleolar Osteotomy Technique: Opening Tibial Wedge Osteotomy
This technique is simpler than the closing wedge resection seen previously. A
medial approach is used on the distal tibia. The apex where the osteotomy is to be
performed must be located and marked with a single Kirschner wire. Following the
wire, the osteotomy is performed with an oscillating saw. Then, the osteotomy is
opened, thus correcting the arthritic varus malalignment (see Fig. 14). The calcula-
tions for performing this medial tibial opening are the same as those explained for
the medial tibial closure. If there is a varus deformity with a 97° LDTA (7° defor-
mity), the tibial opening wedge should overcorrect the LDTA to 85° (12° of total
correction). Using the previously explained rule, we would just equal the opening
wedge to the number of degrees of the deformity, which equals 7 mm. It is recom-
mended to use a structural graft to fill the gap, being the authors preference a struc-
tural iliac crest allograft. For fixation, a locking medial tibial plate is recommended.
A very frequent finding for opening tibial wedges of 5 mm or more, is that the lat-
eral tibial cortex does not open as a hinge and distracts. This decreases the angular
correction power and increases the limb length. If this distraction occurs, a lateral
non locking plate should be placed at the lateral tibial osteotomy exit. One screw
above the osteotomy and one below is enough to avoid osteotomy distraction allow-
ing osteotomy angular opening.
Fig. 14 Anteroposterior
ankle fluoroscopic image,
where a medial opening
wedge supramalleolar
osteotomy was performed,
besides a fibular closing
wedge osteotomy. The
tibial osteotomy is shown
being opened with a
lamina spreader, correcting
the ankle varus
Supramalleolar Osteotomy Technique: Dome Osteotomy

A technique similar to the one mentioned for lateral ankle overload is performed for
medial ankle overloads. The difference occurs when the osteotomy is rotated or
moved as it is turned in the opposite direction, valgizating the distal bone segment.
The amount of rotation needed at the osteotomy should be confirmed with fluoros-
copy until adequate correction is achieved. An alternative way of estimating correc-
tion is to measure the mms of step formed at the osteotomy level medially; 10 mm
is equivalent to 20° of correction [28]. Once the osteotomy has been rotated, it is
fixed with 1 or 2 anterior tibial locking plates.
5.2.3 Ankle Symmetry
It is the experience of the authors that a fibula osteotomy should almost always be
performed, to allow an adequate correction of the talus. There are some cases in which
due to dysplasia of the medial malleolus (longstanding varus) the literature does not
recommend performing a fibula osteotomy, so that the medial malleolus pushes and
closes the mortise thus reducing the talus. The authors believe that this is very uncom-
mon and the cases reported that benefit from this alternative are scarce [30]. Usually,
an oblique osteotomy is sufficient to shorten the fibula to pull the talus to its corrected
position and not impede the varus correction. This osteotomy is usually fixed with a
non-locking third tubular plate. It should be kept in mind that in ankles with medial
malleolus dysplasia (in varus, short and rounded malleolus), an additional osteotomy
of the medial malleolus can be considered to achieve medial tibiotalar space closure.
If the preoperative tilt is greater than 10° in varus and there is a medial depression of
the joint, a plafondplasty should be considered in cases of varus osteoarthritis.
5.2.4 Inframalleolar Correction
As noted in the biomechanics paragraph, there are cases of medial ankle overload
without evident ankle malalignment, but it should be noted that this is much rarer
than for lateral ankle overloads. The approach to these cases is seen in the chapter
on cavovarus deformities, and consist of hindfoot valgizating procedures, medial
column elevating techniques and soft tissue procedures to achieve a static (repair of
lateral and/or medial ligaments) and dynamic balance (tendon transfers or tenodesis).
After completion of the supra- and intra-articular phase, the alignment of the hind-
foot should be in neutral or slight valgus, from 2 to 5°. If this is not achieved, con-
sideration should be given to add an inframalleolar correction, consisting of a
lateralizing calcaneal osteotomy or subtalar arthrodesis. The authors recommend
always to combine both lateralizing (Koutsogiannis = translation) and valgus
(Dwyer = wedge resection) methods for calcaneal correction to enhance the weight
bearing axis lateralization. Performing midfoot or medial column elevation osteoto-
mies should also be evaluated on a case-by-case basis. Lateralizing and valgus
osteotomy of the calcaneus is performed in a similar way to the medializing oste-

otomy described in the previous section. The desired effect of the osteotomy is to
lateralize the load axis. The posterior calcaneal tuberosity must be laterally trans-
lated in addition to a lateral calcaneal wall wedge resection of approximately 5 mm.
This technique combination will enhance the valgus effect of the osteotomy. It is
usually fixed with two axially placed screws.
5.2.5 Foot Deformity
In the case of cavovarus feet, we must consider whether the position of the forefoot
can be fully corrected through an elevation osteotomy of the first metatarsal, or if a
midfoot osteotomy is necessary to completely correct the foot. The latter type of
osteotomies is preferred by the authors and have the greatest correction power. The
first metatarsal elevation osteotomy and the midfoot osteotomy are described in
detail in the cavovarus foot section.
5.2.6 Ligament Reconstruction
The lateral and medial ankle ligaments are frequently compromised and must be
evaluated intra-operatively and aggressively reconstructed. The lateral side requires
the use of anchors and sometimes even grafts since after the debridement (necessary
to achieve a reduction of the talus in its mortise), the ligaments can be damaged.
Medially, a deltoid imbrication is generally enough.
Since these are long-standing varus deformities, the peroneal tendons are usually
damaged and must be examined and repaired if necessary. If complete ruptures are
found, autograft or free allograft can be used to reconstruct the peroneus brevis or
longus. If both tendons are completely ruptured, it is recommended to reconstruct
one of them with an auto or allograft and to perform a tenodesis of the remnant
(brevis to longus). It is preferable to keep the longus since it achieves greater ever-
sion leverage in the forefoot.
5.3 nterior or Posterior Mechanical Overload of the Ankle

A
(Sagittal Plane)
Generally, the tibial load axis intersects the anterolateral talus process in the lateral
ankle X-ray. The angle measured is the anterior distal angle of the tibia (ADTA,
normal value 81°) which was mentioned in the mechanical analysis section.
Deformities in the sagittal plane are usually associated with deformities in the coro-
nal plane. Anterior ankle overload (with anterior talar subluxation) is usually cor-
rected with a posterior tibial closing wedge; rarely anterior opening osteotomies are
performed. In cases of posterior ankle overload (with posterior talar subluxations),

correction is achieved through anterior tibial wedge resections. The correction is
achieved through the same calculation commented before, that is, resecting a wedge
that equals the number of degrees in mm. It is common to find fibular or syndes-
motic malunions that contribute to ankle deformities in the sagittal plane. In these
cases, fibular corrective osteotomies or tibiofibular arthrodesis are added to the
SMOT to aid in the correction. When correcting sagittal deformities of more than
10°, a Dome osteotomy can be considered, and we recommend performing it from
a medial approach.
5.3.1 Supramalleolar Osteotomy Technique: Wedge Osteotomy
In the case of combined coronal and sagittal plane deformities that are being cor-
rected through tibial wedge osteotomies, it is quite simple to add a second plane to
the resection. Through the same approach performed for the correction of varus or
valgus, a second plane can be added to the resected wedge, that is, to perform a
biplanar wedge osteotomy. A posterior wedge resection is added if we want to cor-
rect an anterior ankle overload. Vice-versa, an anterior wedge resection is added if
we want to correct a posterior ankle overload. After performing the biplanar wedge,
the tibial osteotomy is usually totally unstable, so it is recommended to add an ante-
rior tibial plate in addition to the medial locking plate.
5.3.2 Supramalleolar Osteotomy Technique: Dome Osteotomy
In the case of dome osteotomies, it is difficult to correct the sagittal plane in addition
to the coronal plane. When the dome osteotomy is done through an anterior approach
and performed primarily to correct coronal plane deformities, only minor correc-
tions in the sagittal plane can be achieved. In these cases, it is recommended to
impact the cancellous bone (to achieve angulation correction) and to translate the
osteotomy (anterior or posterior) to achieve sagittal plane weight bearing axis cor-
rection. If the sagittal plane deformity is more significant than the coronal plane
deformity, or if the sagittal deformity to be corrected exceeds 10°, we recommend
performing a dome osteotomy from a medial approach (see Figs. 15 and 16).
6 Published Results and Complications
The published results of ankle joint preservation surgery refer mainly to surgeries
that correct deformities or malalignments in the coronal plane. The largest pub-
lished series shows 189 patients with valgus LOA, 163 with good results at five
years minimum [5]. In 2016, Krähenbühl published a series of the same group
showing a five-year survival rate of 88%, reporting that patients over 60 years of age

bearing ankle radiograph,
showing a deformed distal
pilon with severely altered
LDTA. Note the anterior
talar subluxation relative to
the pilon, the osteophytes
in the anterior distal tibia
and the reduced joint
space. In this case, the
sagittal deformity to be
corrected exceeds 10° and
therefore we recommend
performing a dome
osteotomy from a medial
approach
and with tilt greater than 7° had the worst results [31]. Patients with LOA in varus,
Takakura 2 and 3A show a five-year survival rate of 88% and 93% respectively. The
Takakura 3B group shows a 47% survival rate. If tilt is considered, survival for tilt
between 4 and 10° is 85%, and for more than 10° it is 65% [21]. Having said this,
there is recent information with a low number of cases that shows the possibility of
treating ankle arthrosis in stage Takakura 3b (varus) with SMOT plus distraction
with external fixation for three months, with follow-up at 3.2 years, with good
results. This information should be confirmed with a greater number of published
cases but could extend the indication for SMOT [32].
In terms of quality of life, patients who undergo joint preservation osteotomies
achieve quality of life scores comparable to healthy controls. In any case, they walk
slower, have less range of sagittal mobility of the hindfoot and have less dorsiflexion
torque in their affected ankle [33]. Bone healing has been reported in closing wedge
osteotomies at 2.3 months and in opening wedge osteotomies at 5.4 months [34].
picture of same patient
presented in Fig. 15. A
medial distal tibia
approach was performed.
Please note the third
tubular plate which was
used to “draw” a dome
osteotomy on the medial
tibia using the plate as a
hinge to guide the drilling
As far as complications are concerned, the percentages published are low, but
considering infection, non-union, delayed consolidation, over- or under-correction,
joint impingement, inadequate fixation or natural progression of the osteoarthritis,
as a whole they can reach up to 22% [34]. In the largest series of osteotomies pub-
lished so far, the most frequent complication reported is progression of osteoarthri-
tis by 10% [35, 36]. The prognostic factors for loss of alignment correction have
been identified as male gender, BMI >26.4 and lateral tibial cortex violation when
performing the opening tibial wedge osteotomies [37].
Finally, in relation to fixation plates, no mechanical differences have been dem-
onstrated between different plates models (anatomical and non-anatomical), but
there are currently no dedicated plates for SMOT [38].
References
1. Wynes J, Kaikis AC. Current advancements in ankle Arthrodiastasis. Clin Podiatr Med Surg.
2018;35(4):467–79. https://doi.org/10.1016/j.cpm.2018.05.006.
2. Nguyen MP, Pedersen DR, Gao Y, Saltzman CL, Amendola A. Intermediate-term follow-
up after ankle distraction for treatment of end-stage osteoarthritis. J Bone Joint Surg Am.
2015;97(7):590–6. https://doi.org/10.2106/JBJS.N.00901.
3. Knupp M. The use of osteotomies in the treatment of asymmetric ankle joint arthritis. Foot
4. Barg A, Saltzman CL. Single-stage supramalleolar osteotomy for coronal plane deformity.
Curr Rev Musculoskelet Med. 2014;7(4):277–91. https://doi.org/10.1007/s12178-014-9231-1.
5. Valderrabano V, Paul J, Monika H, Pagenstert GI, Henninger HB, Barg A. Joint-preserving
surgery of valgus ankle osteoarthritis. Foot Ankle Clin. 2013;18(3):481–502. https://doi.
org/10.1016/j.fcl.2013.06.008. Review. PubMed PMID: 24008214.
6. Barg A, Pagenstert G, Hugle T, Gloyer M, Wiewiorski M, Henninger H, Valderrabano V. Ankle
osteoarthritis etiology, diagnostics, and classification. Foot Ankle Clin N Am. 2013;18:411–26.
7. Jensen, N; Krmer, K; Hvid, I. Distribution of bone strength at the distal tibia and fibula. Clin
Biomech. 1989;4(4):228–31.
8. McKinley TO, Tochigi Y, Rudert MJ, Brown TD. Instability-associated changes in contact stress
and contact stress rates near a step-off incongruity. J Bone Joint Surg Am. 2008;90(2):375–83.
https://doi.org/10.2106/JBJS.G.00127.
9. Sugimoto K, Takakura Y, Okahashi K, Samoto N, Kawate K, Iwai M. Chondral injuries of
the ankle with recurrent lateral instability: an arthroscopic study. J Bone Joint Surg Am.
2009;91(1):99–106. https://doi.org/10.2106/JBJS.G.00087.
10. Saltzman C, El-Khoury G. The Hindfoot alignment view. Foot Ankle Int. 1995;16:572.
11. Paley, D; Herzenberg, J; Tetsworth, K; McKie, J; Bhave, A. Deformity planning for frontal and
sagital plane corrective osteotomies. Orthoped Clin North Am. 1994;25(3):425–65.
12. Lopez M, Wagner P. Analisis y Plan quirúrgico de deformidades en tobillo y retropié del
adulto. Rev Chil Ortop Traumatol, abril. 2019; https://doi.org/10.1055/s-0039-3400508.
13. Nosewicz TL, Knupp M, Bolliger L, Henninger HB, Barg A, Hintermann B. Radiological
morphology of peritalar instability in varus and valgus tilted ankles. Foot Ankle Int.
14. Hintermann B, Knupp M, Barg A. Joint-preserving surgery of asymmetric ankle osteoarthri-
tis with peritalar instability. Foot Ankle Clin. 2013;18(3):503–16. https://doi.org/10.1016/j.
fcl.2013.06.010.
15. Wang B, Saltzman CL, Chalayon O, Barg A. Does the subtalar joint compensate for ankle
malalignment in end-stage ankle arthritis? Clin Orthop Relat Res. 2015;473(1):318–25.
https://doi.org/10.1007/s11999-014-3960-8.
16. Tanaka Y, Takakura Y, Hayashi K, et al. Low tibial osteotomy for varus-type osteoarthritis of
the ankle. J Bone Joint Surg Br. 2006;88(7):909–13.
17. Knupp M, Stufkens SA, Bolliger L, et al. Classification and treatment of supramalleolar defor-
mities. Foot Ankle Int. 2011;32(11):1023–31.
18. Gross CE, Barfield W, Schweizer C, Rasch H, Hirschmann MT, Hintermann B, Knupp M. The
utility of the ankle SPECT/CT scan to predict functional and clinical outcomes in supramalleo-
lar osteotomy patients. J Orthop Res. 2018;36(7):2015–21. https://doi.org/10.1002/jor.23860.
19. Hintermann B, Knupp M, Barg A. Peritalar instability. Foot Ankle Int. 2012;33(5):450–4.
https://doi.org/10.3113/FAI.2012.0450. PubMed PMID: 22735291.
20. Haraguchi N, Ota K, Tsunoda N, Seike K, Kanetake Y, Tsutaya A. Weight-bearing-line analy-
sis in supramalleolar osteotomy for varus-type osteoarthritis of the ankle. J Bone Joint Surg
Am. 2015;97(4):333–9. https://doi.org/10.2106/JBJS.M.01327.
21. Krähenbühl N, Akkaya M, Deforth M, Zwicky L, Barg A, Hintermann B. Extraarticular
Supramalleolar osteotomy in asymmetric Varus ankle osteoarthritis. Foot Ankle Int.
22. Hintermann B, Ruiz R, Barg A. Novel double osteotomy technique of distal tibia for correc-
tion of asymmetric Varus osteoarthritic ankle. Foot Ankle Int. 2017;38(9):970–81. https://doi.
org/10.1177/1071100717712543. Epub 2017 Jul 1. PubMed PMID:28670918.
23. Zhao HM, Wen XD, Zhang Y, Liang JQ, Liu PL, Li Y, Lu J, Liang XJ. Supramalleolar oste-
otomy with medial distraction arthroplasty for ankle osteoarthritis with talar tilt. J Orthop Surg
Res. 2019;14(1):120. https://doi.org/10.1186/s13018-019-1168-z.
24. Knupp M, Stufkens SA, van Bergen CJ, et al. Effect of supramalleolar varus and valgus defor-
mities on the tibiotalar joint: a cadaveric study. Foot Ankle Int. 2011;32(6):609–15. https://doi.
org/10.3113/FAI.2011.0609.
25. Lintz F, Welck M, Bernasconi A, Thornton J, Cullen NP, Singh D, Goldberg A. 3D biometrics
for Hindfoot alignment using Weightbearing CT. Foot Ankle Int. 2017;38(6):684–9. https://
doi.org/10.1177/1071100717690806.
26. Krause FG, Sutter D, Waehnert D, Windolf M, Schwieger K, Weber M. Ankle joint pressure
changes in a pes cavovarus model after lateralizing calcaneal osteotomies. Foot Ankle Int.
2010;31(9):741–6. https://doi.org/10.3113/FAI.2010.0741.
27. Paley D, Herzenberg JE. Principles of deformity correction. In: Chapter 5, Osteotomy con-
cepts and frontal plane realignment. Berlin: Springer-Verlag; 2002. p. 102–9.
28. Wagner P, Colin F, Hintermann B. Distal tibia dome osteotomy. Techniques in Foot & Ankle
Surgery June. 2014;13(2):103–7.
29. Al-Nammari SS, Myerson MS. The use of Tibial osteotomy (ankle Plafondplasty) for joint
preservation of ankle deformity and early arthritis. Foot Ankle Clin. 2016;21(1):15–26. https://
doi.org/10.1016/j.fcl.2015.09.009.
30. Ahn TK, Yi Y, Cho JH, Lee WC. A cohort study of patients undergoing distal tibial osteotomy
without fibular osteotomy for medial ankle arthritis with mortise widening. J Bone Joint Surg
Am. 2015;97(5):381–8. https://doi.org/10.2106/JBJS.M.01360.
31. Krähenbühl N, Zwicky L, Bolliger L, Schädelin S, Hinterman B, Knupp M. Mid- to

long-term results of Supramalleolar osteotomy. Foot Ankle Int. 2016; https://doi.
org/10.1177/1071100716673416.
32. Nozaka K, Miyakoshi N, Kashiwagura T, Kasukawa Y, Saito H, Kijima H, Chida S, Tsuchie
H, Shimada Y. Effectiveness of distal tibial osteotomy with distraction arthroplasty in varus
ankle osteoarthritis. BMC Musculoskelet Disord. 2020;21(1):31. https://doi.org/10.1186/
s12891-020-3061-7.
33. Nüesch C, Huber C, Paul J, Henninger HB, Pagenstert G, Valderrabano V, Barg A. Mid- to long-
term clinical outcome and gait biomechanics after realignment surgery in asymmetric ankle
osteoarthritis. Foot Ankle Int. 2015;36(8):908–18. https://doi.org/10.1177/1071100715577371.
34. Barg A, Saltzman CL. Joint-preserving procedures in patients with Varus deformity: role of
Supramalleolar osteotomies. Foot Ankle Clin. 2019;24(2):239–64. https://doi.org/10.1016/j.
fcl.2019.02.004.
35. Knupp M, Stufkens SA, Bolliger L, et al. Classification and treatment of supramalleolar defor-
mities. Foot Ankle Int. 2011;32:1023–31.
36. Espinosa N. What leads to failure of joint-preserving surgery for ankle osteoarthritis?: when
this surgery fails, what next? Foot Ankle Clin. 2013;18(3):555–69. https://doi.org/10.1016/j.
fcl.2013.06.014.
37. Kim YS, Kim YB, Koh YG. Prognostic factors affecting correction angle changes after
Supramalleolar osteotomy using an opening wedge plate for Varus ankle osteoarthritis. J Foot
Ankle Surg. 2019;58(3):417–22. https://doi.org/10.1053/j.jfas.2018.09.003.
38. Ettinger S, Schwarze M, Yao D, Ettinger M, Claassen L, Stukenborg-Colsman C, Thermann
H, Plaass C. Stability of supramalleolar osteotomies using different implants in a saw-
bone model. Arch Orthop Trauma Surg. 2018;138(10):1359–63. https://doi.org/10.1007/
s00402-018-2981-2.
Diffuse Ankle Osteoarthritis
Markus Knupp
1 Introduction
Arthritis of the ankle joint is common and found in 1% of the world’s population. In
contrast to arthritis of the hip or knee (mainly primary arthritis), the etiology at the
ankle is posttraumatic in a large majority of patients. As a result, the patients become
symptomatic 12–15 years earlier than arthritic hip or knee patients. This underlines
the importance of long-lasting treatment options for this patient group [1].
Surgical treatments for ankle joint arthritis are divided into two categories: pro-
cedures that preserve the joint and those that do not.
This chapter focuses on conservative treatment and joint distraction arthroplasty
for joint preservation and non-joint-preserving treatments, e.g., arthrodesis and total
ankle replacement.
2 Etiology
The ankle joint is less commonly affected by degenerative wear than the hip and the
knee. The reasons for this are the high resistance towards wear of the ankle carti-
lage, the well guided joint motion during flexion/extension (see below), and the
susceptibility of the ankle cartilage to inflammatory mediators [2]. The most com-
mon cause for ankle joint arthritis is trauma (70%). Inflammatory arthritis accounts
for approximately 12% of all cases and primary arthritis for the rest [3].
M. Knupp (*)
University of Basel, Mein Fusszentum Basel, Basel, Switzerland

Switzerland AG 2022
724 M. Knupp
3 Anatomy
The ankle joint is a very congruent joint and comprises the tibia, the fibula, the talus,
the collateral ligaments, the syndesmosis, and the joint bridging tendons. Stability
of the joint is provided by the bony configuration and the surrounding soft tissue
mantle (tendons and ligaments).
3.1 Bony Elements
The talus articulates with the malleolar fork on three articulating surfaces: the talar
dome articulates with the pilon and the medial and the lateral gutter. The articulating
surfaces of the gutters are opened anteriorly creating the gutter angle.
3.1.1 Talus
The talus has a conical shape with the radius of the medial shoulder being smaller
than the radius of the lateral talar shoulder. Sixty percent of the surface is covered
by cartilage and there are no tendons inserting into the talus. The width of the talus
is wider anteriorly than posteriorly, making the bone wedge-shaped in the trans-
verse plane. The radius of the talar dome is slightly smaller than the corresponding
radius of the tibia, which allows for some sagittal motion in the ankle joint.
3.1.2 Tibia
The tibia shares two articulating surfaces with the talus: the pilon and the medial
gutter. In the Caucasian population the angle of the distal tibial articulating surface
is in slight valgus, when measuring it in relation to an axis drawn from the tibial
tuberosity to the center of the ankle joint [1, 4]. Radiologically women tend to have
a joint surface in more varus than men [4].
The strength of the tibia decreases with increasing distance from the joint line:
the bone in the metaphyseal area is 70–90% weaker than in the subchondral area [5].
The subchondral bone is strongest posteromedially and weakest anterolaterally.
3.1.3 Fibula
The fibula is dynamically attached to the tibia (syndesmosis complex). This allows
for a slight diastasis in the distal tibio-fibular joint, proximalization and endorota-
tion of the fibula during dorsiflexion of the ankle. During plantarflexion, the fibula
moves distally and rotates externally [6].
Diffuse Ankle Osteoarthritis 725
3.2 Ligaments
The lateral ankle ligaments comprise the calcaneofibular, the anterior and the poste-
rior talofibular ligament. These three ligaments stabilize the ankle joint in different
positions of the ankle; in dorsiflexion the posterior talofibular ligament is tight
whereas in plantarflexion the anterior talofibular ligament is tight.
The deltoid ligament on the medial side has a superficial portion which stabi-
lizes the ankle, the subtalar and the talonavicular joint with their fibers running
from the medial malleolus to the navicular, the calcaneus and the spring ligament.
The deep portion of the deltoid bridges the ankle joint with stabilizing fibers run-
ning from the medial malleolus to the talus. In its entirety, the deltoid ligament
provides ankle stability against exorotation, lateral translation and valgus forces on
the ankle joint.
4 Biomechanical Considerations
Anatomical and biomechanical studies have shown that the ankle joint is not just a
simple hinge but much more, it provides motion in the sagittal, coronal and the
transverse plane [7–10] with a rotational axis of the talus that varies during flexion
and extension.
4.1 Rotational Axis
The ankle joint is part of a kinematic chain containing the tibiofibular joint, the
tibiotalar joint, the subtalar joint and Choparts jointline. Dorsiflexion of the ankle
leads to internal rotation of the lower leg, eversion/valgization of the hindfoot
and pronation of the mid-/forefoot. Plantarflexion leads to external rotation of
the lower leg, inversion/varization of the hindfoot and supination of the mid-/
forefoot.
4.2 Range of Motion
The normal range of motion of the ankle joint varies from 23–56° in plantarflexion
and 13–33° in dorsiflexion. Walking on even surface requires 10–15° plantarflexion
and 10° dorsiflexion. Climbing stairs has been found to require 37° (upstairs) and
56° (downstairs). For normal daily activities (without climbing of stairs) a range of
motion of 15° in the ankle joint has been described to be sufficient.
726 M. Knupp
4.3 Load Transfer at the Ankle Joint
Walking on even surfaces creates axial forces up to 5.2 times body weight at the
ankle joint. These forces result from ground reaction forces, gravitation and forces
resulting from the muscles/tendons and the ligaments. These forces are transmitted
over the articular surface which is 7 cm2 in size.
5 Diagnosis
A thorough history includes questions on all joints of the lower extremity, a history
of trauma (fractures, osteochondral lesions, ligament/tendon tears), disorders dur-
ing childhood, history of inflammatory or infectious arthropathies, gout, hemo-
philia, metabolic diseases (diabetes), or neuropathy.
Physical examination includes observation of gait and the alignment when stand-
ing. Assessment of hindfoot alignment is done in standing and while standing and
in tip toe position (heel rise). A thorough neurovascular examination is mandatory,
not only to assess the nature of the arthritic process in the ankle joint but also to
determine the necessity of further investigations (angiological and neurological
workup). Motion and stability of the ankle and subtalar joint should be assessed.
The function of the joint bridging tendons is noted.
Radiographic examination includes a full set of weight-bearing radiographs of
the foot and ankle. For the planning of ankle replacement and ankle fusion, a whole
leg length radiograph is recommended. Additional alignment views, as described by
Saltzman, may provide further information in case of deformity [11]. These exami-
nations can be completed with CT and/or Spect-CT in selected cases, e.g., involve-
ment of multiple joints, altered bone quality such as osteonecrosis.
Conservative therapy of ankle osteoarthritis is symptomatic and not curative.

Nonsurgical treatment of ankle arthritis focuses on reduction of inflammation and
pain control. Options include NSAIDs, nutritional supplementation, joint injec-
tions, and bracing/shoe modifications. Indications for conservative therapy include:
initial treatment before surgery, end-stage OA to buy time in the young and active
patient, severe vascular or neurologic deficiency, neuropathic disorders, unstable
soft tissues and ongoing infection of soft tissue, bone or joint [12].
6.1 Viscosupplementation
Viscosupplementation injections in the ankle are discussed controversially. Some

studies showed significant improvement in the short term, however, after 1 year no
difference was found when comparing viscosupplementation with saline injec-
tion [13].
6.2 Platelet-Rich Plasma/Corticosteroids Injections
Platelet-rich plasma (PRP) has gained increasing popularity in the treatment of a

multitude of disorders. While intraarticular injections have shown to be beneficial in
mild to moderate knee osteoarthritis, the literature for the ankle remains
controversial.
Corticosteroids can provide pain relief for a limited amount of time. However,
repetitive injections are not without risks. Corticosteroids can cause damage to the
soft tissue and there are reports on serious deleterious effects on the articular carti-
lage in repeated corticosteroids injections.
Keeping patients with osteoarthritis active has been shown to slow down the degen-
erative wear in the joint with the potential to postpone surgery. The focus is set on
local anti-inflammatory measures, muscle strengthening, ankle and hindfoot joint
mobilization to prevent joint stiffness and gait educations.
6.4 Orthoses and Shoe Modification
Orthoses can provide effective pain reduction and postpone ankle replacement/
ankle fusion in patients with ankle arthritis. The orthoses/shoe modifications aim to
absorb shock, cushion the heel, decrease the peak joint forces (for example correc-
tive wedges in cases with a deformity) and stabilize the affected joints.
Surgical treatment of ankle arthritis is divided into joint preserving surgery (correc-
tive osteotomies, open/arthroscopically debridement, distraction arthroplasty) and
non-preserving options (ankle fusion and arthroplasty).
7.1 Distraction Arthroplasty
The author has only very limited experience with this technique and has not used it
in the last 14 years. Distraction arthroplasty unloads the ankle joint with an external
fixator. Distraction is performed in conjunction with osteophyte removal, micro-
fracture, soft tissue release and deformity correction, where needed. Decreasing the
load on the joint surface for a certain time potentially promotes cartilage repair. The
external fixator is used to mechanically unload the ankle to halt or even partially
reverse the arthritic process in the ankle joint. Patient selection is crucial for success
of distraction arthroplasty. Inclusion criteria are a congruent joint with a preserved
motion of >20° [14].
728 M. Knupp
Distraction is maintained for at least 8 weeks. No added benefit has been seen
beyond 12 weeks [15]. The frames can provide distraction with or without a hinge.
In a randomized study the patients with a hinged framed showed a better outcome
2 years after frame removal [16]. However, with a longer follow up the same authors
reported on better outcomes in the fixed frame group in the same cohort. Some
authors have tried to stimulate hyaline cartilage regeneration by injection of autolo-
gous bone marrow aspirate into the ankle joint. However, no clinical evidence for
this method has been presented.
Considering that most recruited patients in the studies were classified as candi-
dates for ankle arthroplasty or ankle fusion, it is not surprising that the survivorship
analysis of this method shows a high failure rate. Fusion rates within the first year
after frame removal range from 24% to 27% [17, 18]. Long-term follow-up studies
reported fusion rates of 45% at 8 years [16] and 44% at 12 years [19].
7.2 Ankle Fusion
Ankle fusion has for many years been the most reliable treatment in end-stage ankle
arthritis. In contrast to the hip and the knee, which are now rarely fused, ankle
arthrodesis will never be completely replaced by arthroplasty of the ankle joint.
Despite the very promising development of the newest technology in ankle replace-
ment, ankle fusion will remain an important tool in the armamentarium of a foot and
ankle surgeon- not only as a salvage procedure but also as a primary treatment option.
For the indications, please refer to the section “fusion versus ankle replacement.”
Ankle fusion can be done through an anterior, lateral (transfibular or anterolat-
eral), posterior approach or arthroscopically. Traditionally most authors preferred
the lateral approach. In recent years many surgeons increasingly use the same ante-
rior approach for isolated ankle fusions as for ankle arthroplasty.
7.2.1 Anterior Approach
An incision of 10–12 cm is placed anteriorly to the ankle joint, extending to the

level of the talonavicular joint. The extensor retinaculum is exposed and split
between the anterior tibial tendon and the extensor hallucis longus tendon. The dis-
tal tibia is approached through a longitudinal incision along the lateral border of
anterior tendon and exposed subperiosteally. After arthrotomy and partial resection
of the capsule, the exposure is extended to the talar neck. To improve visualization
of the joint, a self-retaining retractor can be used, e.g., Hintermann distractor.
In primary ankle fusion, osteophytes are removed and the tibial and talar joint
surfaces, including the gutters, are cleared from cartilage, fibrous and necrotic mate-
rial. Cartilage removal will lead to a mismatch of the joint surfaces; the radius of the
tibial surface will increase whereas the talar radius decreases. Therefore, the joint
surfaces need to be feathered with a chisel to increase bony contact.
In cases of failed arthroplasty or ankle fusion, the implants are removed, preserv-
ing as much bone stock as possible. Any necrotic bone is removed until healthy,
viable bone is exposed. The void is filled with autologous bone graft from the iliac
bone crest, allograft (e.g., Tutoplast®, Tutogen Medical GmbH, Neunkirchen a.B,
Germany) or – in large defects – vascularized bone grafts from the medial femoral
condyle, pelvis or scapula. Orthobiologics, such as demineralized bone matrix
(DBX®, Synthes, Oberdorf, Switzerland) can be added to stimulate bone healing.
Fixation is done with screws and/or plates. Different techniques for the place-
ment of the screws have been suggested. In primary fusion, two or three cannulated
screws are used. If the screws (for example cannulated 7.0 mm screws) are placed
strictly parallel (usually from the medial tibia into the talus), partially threaded
screws can be used to create compression across the fusion site. If the screws are not
placed parallel (for example one screw from the medial tibia and one screw from the
lateral tibia) only one screw should be used as a compression screw while the sec-
ond screw should be a fully threaded one. An additional third screw can be placed;
however, this has not shown to increase the union rate.
Different plating systems can be used for the anterior approach. When choosing
a plating system, the surgeon must plan the positioning of the plates carefully. In a
primary ankle fusion, the main fusion sites are the two articulating surfaces of the
tibiotalar joint (talar dome/medial gutter). Therefore, the plate(s) should create
compression on the talar dome and in the medial gutter. When using compression
devices with anterior plating systems, the surgeon must avoid anterior subluxation
of the talus. This is prevented by attaching the plates to the talus first, also using a
spacer temporarily between the proximal end of the plate and the anterior tibia,
which will shift the talus posteriorly when the tibial screws are tightened (Fig. 1).
Positioning of the fusion is usually neutral in flexion/extension, neutral or slight
exorotation in the transverse plane and neutral to slight valgus in the coronal plane.
However, the positioning can vary in special indications, e.g., patients with quadri-
ceps weakness, for example in post-polio syndrome, benefit from an ankle fusion in
equinus to stabilize their knee joint.
7.2.2 Lateral Approach
The patient is placed in a lateral decubitus or supine position on the operating table.
An incision is made over the fibula and soft tissue dissection to the bone is directed
anteriorly. With a sagittal saw, an osteotomy of the fibula is created about 10 cm
proximal from the tip of the fibula. Distally, the anterior syndesmosis and the ante-
rior talofibular ligaments are detached to allow for the fibula to be reflected posteri-
orly. Care is taken to preserve the posterior soft tissue. The articular surfaces
between the tibia, the fibula and the talus are removed. The bone is prepared with
multiple drill holes in the subchondral bone und feathered to encourage fusion. The
talus is then reduced and either fixed with as above or a lateral plate. If a plate is
chosen, care is taken not to violate the subtalar joint. Finally, the fibula is reduced
and secured with screws into the tibia/fibula. The retromalleolar groove must be
maintained to preserve peroneal tendon function.
730 M. Knupp
a b
Fig. 1 Fifty-six-year-old male patient with a stage 4 tibialis posterior insufficiency. The patient
has been advised against a total ankle replacement because of a complete incompetence of all
medial soft tissues. (a–c) show the preoperative weight bearing radiographs. (d–f) the postopera-
tive images 9 months after the ankle fusion and a medial displacement calcaneal osteotomy
d f
Fig. 1 (continued)
732 M. Knupp
7.2.3 Posterior Approach
The ankle can be approached through a posteromedial or a posterolateral approach.

The posterolateral approach uses a skin incision posterior to the fibula. To enable
deep dissection, the peroneus longus and brevis muscles/tendons are pulled anteri-
orly. The interval between the flexor hallucis longus tendon and the peroneal tendons
is split bluntly to access the posterior aspect of the ankle. For the posteromedial
approach, the skin incision is made 1 cm medial to the Achilles tendon, extending
from the calcaneal insertion proximally for a length of 10 cm. The Achilles tendon is
retracted laterally, and blunt dissection used to expose the transverse intramuscular
septum. This is opened sharply to expose the FHL muscle belly. The interval between
the FHL and neurovascular bundle is then developed and the FHL is elevated from
the posterior tibia using a periosteal elevator. Hohman retractors are then placed over
the medial and lateral borders of the tibia to fully expose the posterior aspect of the
ankle. Thereafter the ankle joint is freed from the remaining cartilage and prepared
for the fusion analogously to the description above. Fixation usually is achieved with
two cannulated screws entering the tibia dorsally and aiming to the talar neck.
Alternatively, a plate can be used: either a blade-plate, which is inserted posteriorly
into the talar body and then secured to the tibia, or with a standard plate (Fig. 2).
a b
Fig. 2 Sixty-two-year-old male patient with a paralytic foot after spinal surgery. The dorsal plate
was chosen to act as a tension banding device. The images (a, b) show the preoperativeand the
images (c–f) the 6 months postoperative radiographic presentation (g)
c d
Fig. 2 (continued)
734 M. Knupp
Fig. 2 (continued)
g
7.2.4 Arthroscopic Ankle Fusion
Arthroscopic joint preparation can be achieved through either anterior portals

with the patient in a supine position or posterior portals in a prone position. An
abrader is used to remove the cartilage. Care is taken to remove as little of the
subchondral bone as possible while maintaining the joint’s normal contour. A burr
is then used to make multiple holes through the subchondral bone to maximize the
bleeding surface, giving the joint the aspect of a ‘golf ball’. Thereafter the talus is
reduced, and percutaneous cannulated screws used for fixation in the above-
described manner.
7.2.5 Postoperative Treatment
Once the wounds have healed and the swelling has decreased, the preliminary post-
operative splint is replaced by either a below-knee cast or a walker. Patients who did
not receive bone grafting are allowed weight bearing as tolerated after 4 weeks,
whereas patients who receive a bone graft for interposition are allowed only partial
weight bearing during the first 8 weeks after surgery and full weight bearing
thereafter.
7.2.6 Outcomes of Ankle Fusion
Union rates vary from 60% to 100% with larger studies showing 90% union rates
[20]. The nonunion rate dramatically increases in patients with previous subtalar
joint fusion and in varus deformity.
The clinical impact of the altered gait after ankle fusion has not been fully eluci-
dated. While the effect on the knee seems to be very minor, the compensatory
increase of motion in the talonavicular and the subtalar joint increases the risk for
adjacent joint arthritis in these joints [21].
7.3 Ankle Arthroplasty
Total ankle replacement was first attempted in the early 1970s. The initial implants
lead to very poor outcomes with catastrophic failures. The interest was then renewed
in the 1980s and 1990s with new designs. With increasing understanding of the
hindfoot kinematics the surgical techniques and implants for total ankle replace-
ment improved and became more reliable in mimicking the physiological mechan-
ics. This led to more consistent clinical results making ankle arthroplasty a valuable
alternative to ankle fusion.
For the indications, please refer to the section “fusion versus ankle replace-
ment” below.
7.3.1 Technique
All but one implant design (Zimmer TM) use an anterior approach (see above) as
described in the fusion section.
After exposure of the ankle joint as described above, removal of the osteophytes,
synovial tissue and excessive capsule is carried out. In congruent ankles the surgeon
can directly move on to the bony resection. This is carried out with the aim to posi-
tion the tibial and talar components perpendicular to the plumb line of the body. In
tilted ankles (incongruent ankles) two different subgroups need to be distinguished.
In the first group the tilt of the talus results from the loss of joint height and
736 M. Knupp
subsequently leads to slack ligaments. In these cases, intraoperative distraction of

the tibiotalar joint allows for gapping/correction of the joint space. In the second
subgroup, the tilt of the talus results from contract intraarticular deformity and pas-
sive correction of the talus is not possible through traction. While the first subgroup
can be addressed by joint line distalization, using the ankle arthroplasty as a spacer.
Patients in the second subgroup with contract intraarticular deformities a thorough
soft tissue balancing is mandatory. In most cases the latter comprises (cavo-) varus
feet. These are addressed with a medial soft tissue release including the deltoid, the
posterior tibial tendon and the spring ligament (Fig. 3). In rare cases an osteotomy
of the medial malleolus is necessary to balance the joint.
The bony preparation is then continued according to the guidelines of the implant
manufacturer. After implantation of the components the alignment, the ligament
balancing, and the range of motion is reassessed. In case of ligamentous instability,
the ligaments need to be tightened/augmented. In case of lack of dorsiflexion the
posterior joint capsule is resected, and the Achilles’ tendon lengthened.
7.3.2 Postoperative Treatment
The post-operative treatment protocol is determined by the combined bony proce-

dures (fusions, osteotomies) or soft tissue procedures. In isolated ankle arthroplas-
ties most authors immobilize the patients in a cast or walker boot for 6 weeks and
allow for early weight bearing as tolerated.
7.3.3 Outcomes of Ankle Arthroplasty
Reports on the survivorship of the implants vary widely in the literature. Data from
the Cochrane collaborations found an 89% survivorship after 10 years with an
annual failure rate of 1.2% after reviewing 7942 total ankles [22]. This is consistent
with a few multicenter studies showing survivorship rates of 96% at 5 years and
90% at 10 years [23]. Some of the register data from Europe, New Zealand and
Australia show lower survivorships. It is important to note that comparisons of
international registries are very difficult because the implants differ from country to
country. Furthermore, a large majority of the surgeons in these registries implant
less than 20 ankle arthroplasties per year, which has been shown to be a major factor
for a worse outcome [24].
While diabetes (with a good glycemic control), weight and etiology (primary-
rheumatoid-posttraumatic) does not seem to affect the outcome, smoking has been
found to significantly increase the risk for wound complications and a worse out-
come [25].
One of the most feared early complications is an infection. In our own case-
control study we reported an infection rate of 4.7%. This is significantly higher than
in the reported data on ankle arthrodesis. The most common pathogen was a
Staphylococcus aureus, followed by coagulase-negative staphylococci. Risk factors
a b
Fig. 3 Sixty-five-year-old old male patient with idiopathic varus osteoarthritis of the ankle.
Previously attempted supramalleolar osteotomy did not give a lasting effect. The ankle was
addressed with a total ankle replacement. The tight soft tissues on the medial side were released
(superficial deltoid ligament, lengthening of the tibialis posterior tendon and release of the spring
ligament). Preoperative images: (a–c), 4 months postoperative images: (d–f)
738 M. Knupp
e f
Fig. 3 (continued)
for periprosthetic joint infection included previous surgery at the ankle, a long oper-
ative time, and secondary wound-healing problems [26].
7.4 Fusion Versus Arthroplasty
The indication for both, fusion, and ankle arthroplasty, is end-stage ankle arthritis.
Although patient selection has been described to be critical for the outcome, par-
ticularly for ankle arthroplasty, the recommendations in the literature remain con-
troversial. High volume ankle arthroplasty surgeons simplify the indication for
ankle fusion; all cases that do not qualify for joint replacement are fused. The
primary requirements for ankle arthroplasty are a stable joint, a correct alignment
and a sufficient bone stock to guarantee stable implant fixation. If these factors can-
not be established prior or during the implantation of an ankle prothesis, a fusion
should be chosen.
There is an agreement on absolute contraindications for ankle arthroplasty: inad-
equate soft-tissue envelope, Charcot neuroarthropathy, severe malalignment involv-
ing several segments (ankle, midfoot, forefoot), uncorrectable ankle instability/
severe sensomotoric deficits and osteonecrosis of the talus and active infections. For
patients with active infections, a majority of authors recommend ankle fusion after
the infection has been treated.
In the following paragraphs some factors are discussed that help to decide over
one or the other procedure.
7.4.1 Age and Weight
Earlier recommendations stated that the patients subjected to joint replacement sur-
gery should be older than 50 years, non-obese and with low physical demands. The
recent literature shows no difference in the outcome in younger patients or obese
patients. Patients with higher expectations do better with an ankle arthroplasty.
7.4.2 Multiple Joint Involvement
It is generally agreed that the presence of degenerative changes in other joints, such
as the subtalar, midtarsal, knee and the contra-lateral ankle, must be considered
when choosing between ankle arthroplasty and ankle fusion. Patients with multiple
joint involvement show better outcomes with an ankle arthroplasty than with an
ankle fusion. The reason is that an ankle fusion increases the loads in the neighbor-
ing joints and therefore makes them prone to degeneration. It has been shown that
8 years after ankle fusion half of the patients present with hindfoot arthritis [27] and
after 22 years all patients developed hindfoot arthritis [21].The treatment of second-
ary arthritis of the subtalar joint after ankle fusion is demanding. Surgical treatment
options of secondary subtalar joint osteoarthritis are subtalar joint fusion with or
without a takedown of the ankle fusion (desarthrodesis). In isolated subtalar joint
fusions after ankle fusion the non-union rates have been reported to be as high as
38.5%. This is a significantly higher nonunion rate than in the isolated subtalar joint
fusion (8.7%) [28]. The alternative is to combine the subtalar joint fusion with a
conversion of the ankle fusion into an ankle arthroplasty (desarthrodesis). The latter
is a technically demanding procedure with high complication rates and should be
only offered to very selected cases [29].
The concerns about secondary adjacent joint involvement are also true for
patients with systemic diseases, such as rheumatoid arthritis and hemochromatosis.
These patients carry the risk of multiple joint involvement and are prone to develop
adjacent joint arthritis. This is in accordance with observations on rheumatoid
740 M. Knupp
patients who underwent ankle fusion. Cracchiolo et al. reported on 14 fusions in

patients with rheumatoid arthritis with only one patient reporting a functional
improvement [30].
7.4.3 Deformity
Malalignment increases the risk for early implant failure in ankle arthroplasty.
While earlier recommendations limited ankle arthroplasty to patients with less than
10° deformity in any planes, recent publications have shown no difference in the
outcome in patients with greater deformity when comparing them to preoperatively
well aligned ankles, provided the deformity is corrected during or before the
replacement surgery [31]. Deformities of less than 10° can be corrected with the
tibial cut. Larger deformities usually require osteotomies. It is mandatory to elimi-
nate all deforming forces during the time of implantation of an ankle arthroplasty:
the ligaments and the joint crossing tendons must be balanced and deforming forces
resulting from mid-/forefoot must be addressed. If the deformity cannot be cor-
rected in all planes, the surgeon should choose ankle fusion.
To date all studies comparing ankle arthroplasty versus fusion have been obser-
vational and randomized data is sparse. A randomized study has been launched but
the data not yet published [32]. In a meta-analysis by Haddad, TAR and fusions had
a similar intermediate term outcome in terms of clinical scores, patients’ satisfac-
tion and revision rate [33]. The functional scores are higher in the ankle arthroplasty
group than in the ankle fusion [34], however, the risk for a major a complication in
the arthroplasty group is higher than in the fusion group [35, 36].
Acknowledgments The author wishes to thank Jennifer Anderson, M. D. for her support in the
preparation of this chapter.
References
1. Sammarco J. Biomechanics of the ankle: surface velocity and instant centre of rotation in the
sagittal plane. Am J Sports Med. 1977;5:231–4.
2. Huch K, Kuettner KE, Dieppe P. Osteoarthritis in ankle and knee joints. Semin Arthritis
Rheum. 1997;26(4):667–74.
3. Saltzman CL, Salamon ML, Blanchard GM, et al. Epidemiology of ankle arthritis: report
of a consecutive series of 639 patients from a tertiary orthopaedic center. Iowa Orthop
J. 2005;25:44–6.
4. Knupp M, Ledermann HP, Magerkurth O, Hintermann B. The surgical tibiotalar angle: a radio-
logical study. Foot Ankle Int. 2005;26:713–5.
5. Hvid I, Rasmussen O, Jensen NC, Nielsen S. Trabecular bone strength profiles at the ankle
joint. Clin Orthop Relat Res. 1985;199:306–12.
6. Kapandji IA. Das obere Sprunggelenk. In: Kapandji IA, editor. Funktionelle Anatomie der
Gelenke, Band 47. Enke Verlag; 1987. pp. 150–63.
7. Michelson JD, Schmidt GR, Mizel MS. Kinematics of a total arthroplasty of the ankle: com-
parison to normal ankle motion. Foot Ankle Int. 2000;21:278–84.
8. Rasmussen O, Tovberg-Jensen I. Mobility of the ankle joint: recording of rotatory movements
in the talocrural joint in vitro with and without the lateral collateral ligaments of the ankle.
Acta Orthop Scand. 1982;53:155–60.
9. Lundberg A, Goldie I, Kalin B, Selvik G. Kinematics of the ankle / foot complex, part 1: plan-
tar flexion and dorsiflexion. Foot Ankle. 1989;9:194–200.
10. Lundberg A, Svennson OK, Nemeth G, Selvik G. The axis of rotation of the ankle joint. J Bone
Joint Surg Br. 1989;71:94–9.
11. Saltzman CL, el-Khoury GY. The hindfoot alignment view. Foot Ankle Int. 1995;16(9):572–6.
12. Schmid T, Krause FG. Conservative treatment of asymmetric ankle osteoarthritis. Foot Ankle
Clin. 2013;18(3):437–48.
13. Karatosun V, Unver B, Ozden A, Ozay Z, Gunal I. Intra-articular hyaluronic acid compared to
exercise therapy in osteoarthritis of the ankle. A prospective randomized trial with long-term
follow-up. Clin Exp Rheumatol. 2008;26(2):288–94.
14. Saltzman CL, Hillis SL, Stolley MP, Anderson DD, Amendola A. Motion versus fixed distrac-
tion of the joint in the treatment of ankle osteoarthritis: a prospective randomized controlled
trial. J Bone Joint Surg. 2012;94(11):961–70.
15. van Valburg AA, van Roermund PM, Marijnissen AC, et al. Joint distraction in treatment of
osteoarthritis (II): effects on cartilage in a canine model. Osteoarthr Cartil. 2000;8(1):1–8.
16. Nguyen MP, Pedersen DR, Gao Y, Saltzman CL, Amendola A. Intermediate term fol-
low-up after ankle distraction for treatment of end-stage osteoarthritis. J Bone Joint Surg.
2015;97(7):590–6.
17. Marijnissen AC, Van Roermund PM, Van Melkebeek J, et al. Clinical benefit of joint distrac-
tion in the treatment of severe osteoarthritis of the ankle: proof of concept in an open prospec-
tive study and in a randomized controlled study. Arthritis Rheum. 2002;46(11):2893–902.
18. Ploegmakers JJ, van Roermund PM, van Melkebeek J, et al. Prolonged clinical benefit from
joint distraction in the treatment of ankle osteoarthritis. Osteoarthr Cartil. 2005;13(7):582–8.
19. Marijnissen AC, Hoekstra MC, Pré BC, et al. Patient characteristics as predictors of clini-
cal outcome of distraction in treatment of severe ankle osteoarthritis. J Orthop Res.
2014;32(1):96–101.
20. Chalayon O, Wang B, Blankenhorn B, et al. Factors affecting the outcomes of uncomplicated
primary open ankle arthrodesis. Foot Ankle Int. 2015;36(10):1170–9.
21. Coester LM, Saltzman CL, Leupold J, et al. Long-term results following ankle arthrodesis for
post-traumatic arthritis. J Bone Joint Surg. 2001;83A(2):219–28.
22. Zaidi R, Cro S, Gurusamy K, et al. The outcome of total ankle replacement: a systematic
review and meta-analysis. Bone Joint J. 2013;95B(11):1500–7.
23. Mann JA, Mann RA, Horton E. STARankle: long-term results. Foot Ankle Int.
2011;32(05):473–84.
24. Basques BA, Bitterman A, Campbell KJ, Haughom BD, Lin J, Lee S. Influence of surgeon
volume on inpatient complications, cost, and length of stay following total ankle arthroplasty.
Foot Ankle Int. 1987;37(10):1046–51. https://doi.org/10.1177/1071100716664871.
25. Lampley A, Gross CE, Green CL, et al. Association of cigarette use and complication
rates and outcomes following total ankle arthroplasty. Foot Ankle Int. 2016. https://doi.
org/10.1177/1071100716655435.
26. Kessler B, Knupp M, Graber P, Zwicky L, Hintermann B, Zimmerli W, Sendi P. The treatment
and outcome of peri-prosthetic infection of the ankle: a single cohort-centre experience of 34
cases. Bone Joint J. 2014;96-B(6):772–7. https://doi.org/10.1302/0301-620X.96B6.33298.
27. Easley ME, Vertullo CJ, Urban WC, Nunley JA. Review total ankle arthroplasty. J Am Acad
Orthop Surg. 2002;10(3):157–67.
28. Zanolli D, Nunley J, Easley M. Subtalar fusion rate in patients with previous ipsilateral ankle
arthrodesis. Foot Ankle Int. 2015;36(9):1025–8. https://doi.org/10.1177/1071100715584014.
742 M. Knupp
29. Hintermann B, Barg A, Knupp M, Valderrabano V. Conversion of painful ankle arthrodesis

to total ankle arthroplasty. J Bone Joint Surg. 2009;91(4):850–8. https://doi.org/10.2106/
JBJS.H.00229.
30. Cracchiolo A III, Cimino WR, Lian G. Arthrodesis of the ankle in patients who have rheuma-
toid arthritis. J Bone Joint Surg. 1992;74(6):903–9.
31. Hobson SA, Karantana A, Dhar S. Total ankle replacement in patients with significant pre-
operative deformity of the hindfoot. J Bone Joint Surg Br. 2009;91(4):481–6.
32. Goldberg A, Zaidi R, Thomson C, Doré CJ, Skene SS, Cro S, Round J, Molloy A, Davies
M, Karski M, Kim L, Cooke P, TARVA study group. Total ankle replacement versus
arthrodesis (TARVA): protocol for a multicentre randomised controlled trial. BMJ Open.
2016;6(9):e012716. https://doi.org/10.1136/bmjopen-2016-012716.
33. Haddad SL, Coetzee JC, Estok R, et al. Intermediate and long-term outcomes of total ankle
arthroplasty and ankle arthrodesis. A systematic review of the literature. J Bone Joint Surg Am.
2007;89:1899–905.
34. Saltzman CL, Mann RA, Ahrens JE, et al. Prospective controlled trial of STAR total ankle
replacement versus ankle fusion: initial results. Foot Ankle Int. 2009;30(7):579–96.
35. Daniels TR, Younger ASE, Penner M, et al. Intermediate-term results of total ankle replacement
and ankle arthrodesis: a COFAS multicenter study. J Bone Joint Surg. 2014;96(2):135–42.
36. Kim BS, Choi WJ, Kim YS, Lee JW. Total ankle replacement in moderate to severe varus
deformity of the ankle. J Bone Joint Surg Br. 2009;91(9):1183–90.
Part V
Adult Orthopaedics: Tibial Reconstruction
Tibial Post-traumatic Deformity
Arnd F. Viehöfer and Stephan H. Wirth
1 Introduction
Fractures of the tibia reveal an incidence of up to 29 per 100,000 cases per year
including shaft fractures and distal tibia fractures [1]. Malunion is a common com-
plication after conservative and operative treatment and may lead to chronic pain
and disability of the lower limb [2]. The periarticular joints allow compensatory
movements even in the presence of malunited tibiae, which might impair normal
function.
Therefore, simple static assessment of deformity may not be sufficient to show
the whole impact on lower limb function. In addition, plain radiographs have their
limitations when evaluating complex three-dimensional deformities. Currently, the
contemporary literature is still controversially debating the amount of correction
needed with regard to tibial deformities. And most of the recommendations given in
the literature are simple expert opinions without much evidence provided for gen-
eral use in a practical setting.
Although a malunion of the tibial shaft may increases the risk of post-traumatic
arthritis of the ankle and knee joint, there is not much evidence to support a reliable
relationship between tibial malalignment and the development of arthritis of the
adjacent joints [3]. Nevertheless, the main aetiology of ankle arthritis is lower limb
trauma [4] and is often associated with a supramalleolar deformity [5].
The ankle joint has a relatively small contact area (ankle about 350 mm2) when
compared with the knee and hip joints (e.g. knee 1120 mm2) [6]. Thus, load distri-
bution occurs through a comparably small contact area. Post-traumatic malalign-
ment unbalances the load distribution with additional local increase in cartilage
load. In patients with a tibial deformity and consecutive ankle joint degeneration,
A. F. Viehöfer · S. H. Wirth (*)

University Hospital Balgrist, Zurich, Switzerland

Switzerland AG 2022
746 A. F. Viehöfer and S. H. Wirth
restoring the alignment has shown to be an effective treatment option [7–9]. The
following chapter provides an overview of the anatomic background and discusses
operative planning for realignment surgery.
2 Aetiology and Pathophysiology
Post-traumatic deformity may result in translational, rotational and angular defor-

mity [10]. Translational deformity is caused by a translation of the distal tibia in
relation to the proximal tibia. Translation might result in shortening or lengthening
of the tibia. Rotational deformity is defined as rotation of the distal tibia around the
longitudinal axis of the tibia. As a result, the ankle joint is more internal or exter-
nally rotated in relation to the knee joint. Although a rotational deformity is thought
to cause an inferior clinical outcome and might lead to arthritis of the adjacent joints
[11–14], recent studies have shown that moderate rotational deformity (less than
15°) are often well-tolerated [15, 16]. Angular deformity includes a deformity in the
frontal plane (e.g. varus or valgus deformity), sagittal plane (e.g. ante- or retrocur-
vatum) or a combination of both. A special type of long bone deformities are intraar-
ticular malunions. Multiplanar deformities themselves pose major difficulties for
surgeons when attempting an anatomical reconstruction.
3 Anatomy
The anatomical and mechanical axis of the tibia are parallel and in minimal offset
to each other. Therefore, the anatomical axis is often used to plan the realignment
surgery. This is specifically the case in diaphyseal deformities [2]. In healthy indi-
viduals, the distal tibial articular surface is in slightly valgus. This can be verified by
measuring the lateral distal tibial ankle surface angle (LDTA) which averages physi-
ologically 89° (86–92°) [2] (Fig. 1). In the sagittal plane the anterior distal tibia
angle ADTA is defined as the anterior angle between distal tibial articular surface
and the tibia axis (Fig. 1). Normally, the ADTA averages 80° (78–82°) [2].Tibia
rotation is defined as the angle between an axis along the tibia plateau and an axis
through the medial and lateral malleolus. In adults, the tibia is around 20° externally
rotated [17, 18].
4 Diagnosis
Clinical examination reveals an obvious malalignment of the leg. In more distinct

cases, where the peritalar joints are compensating for a supramalleolar deformity
this malalignment could potentially be missed. The subtalar joint allows more
Tibial Post-traumatic Deformity 747
Fig. 1 Left: Anterior distal

tibia angle (ADTA)
(sagittal plane). The angle
is defined as the angle
between the tibia axis and
joint line of the ankle in
the lateral view. It is
measured to the anterior
side. Right: Lateral distal
tibial ankle surface angle
(LDTA) (coronal plane).
The angle is defined as the
angle between the tibia
axis and the joint line of
the ankle in the ap view. It
is measured to the
lateral side
inversion than eversion moment. Thus, a supramalleolar valgus deformity can better
be compensated for than a varus deformity. In some cases, a protrusion and hyper-
trophy of the medial malleolus might be visible as an expression of varus deformity
in the clinical examination. The rotation of the tibia can clinically be determined by
measuring the foot axis or axis through both malleoli in relation to the axis of the
thigh while putting the patient in a prone position with 90° flexion within the knee
joints [12]. However, clinical rotational analysis has a poor sensitivity of 55% and
moderate specifity of 73% compared to methods based on CT scans [16]. Patients
with increased external rotation of the tibia also show an altered stance and gait pat-
tern with a more internally rotated knee [19]. An angular deformity in the sagittal
plane may furthermore lead to ventral ankle impingement and decreased ankle
ROM [2]. Gait analysis helps to detect those changes [20, 21]. Clinical examination
should also include a detailed assessment of the soft tissues (e.g. contracture/joint
stability). Radiographic evaluation is used to determine and quantify the deformity.
Antero-posterior and lateral weightbearing radiographs of the foot and ankle as well
as long leg radiographs reveal any coronal and sagittal plane deformities.
Contralateral radiographs can be used for direct comparison. In addition, a long
axial view, or three-dimensional assessment of the hindfoot [22] axis should be
included to complete the entire assessment. As it is difficult to determine the tibia
rotation on plain radiographs, CT scans are necessary for a more accurate assess-
ment [23].
Conservative treatment includes specific insoles, orthotics and/or orthopaedic shoe

wear. Physical therapy may help to improve the strength of the periarticular mus-
cles/tendons, which may have a positive impact on the gait pattern while potentially
providing adequate relief of pain.
The type of deformity dictates the type of correction: Surgeons can choose among a
wide spectrum of armamentarium to correct the deformity, including open- and
closed wedge-, dome-, single plane osteotomies. The first step of surgical planning
includes the identification of deformity level. This is of major importance because
the assessment of the level influences the type of surgical procedure exerted on the
limb. The method will now be illustrated in detail for an angular deformity in the
frontal plane (e.g. varus or valgus deformity). First, the LDTA and ADTA are mea-
sured (Fig. 1). Especially in deformities, which are found close to the ankle joint and
could easily be missed this assessment is necessary [2]. Second, the mid-diaphyseal
lines of the proximal and distal tibia shaft are outlined. Those lines define the ana-
tomical axes of the proximal and distal segment as well (Fig. 2). In cases, where the
deformity is found close to the ankle joint it is better to use the distal tibial articular
surface as the reference, especially in cases where the apex of deformity lies on the
distal tibial surface. Of note, a comparison to the contralateral side is often helpful.
Notable, inter-individual differences exist and have been described for any defor-
mity assessment. However, available reference standards for healthy individuals
should carefully be used [2]. Vice versa, if the deformity is found close to the knee
joint, the axis can be referred to the proximal tibial joint line. The intersection of
both axes is the apex of the deformity and forms the centre of rotation and angula-
tion (CORA). The angle between both axes is the deformity angle. Once the CORA
is identified an osteotomy can be performed to realign the fragments by rotating
around a centre of rotation at the CORA (osteotomy rule 1 defined by Paley; Fig. 3).
If the osteotomy cannot be performed at the CORA, it is still possible to realign
both segments when the magnitude of correction equals the magnitude of
Fig. 2 Deformity
assessment in the coronal
plane. The mid-diaphyseal
line of the proximal and
distal tibia is marked to
define the anatomical axis
of the proximal and distal
segment. The intersection
point defines the centre of
rotation and angulation
(CORA)
angulation. However, if the rotation is still around a CORA the bone ends will angu-
late and translate to each other at the osteotomy site with a proper aligned end parts
of the fragments (osteotomy rule 2 defined by Paley). If both the osteotomy site and
centre of rotation are shifted proximal or distally both segments will be parallel but
translated to each other (osteotomy rule 3 by Paley). These rules are important when
performing osteotomies as the osteotomy cannot always be performed at the level
of the CORA (e.g. a deformity at the joint level has to be corrected more proxi-
mally). If the centre of rotation is chosen at the level of the osteotomy a translation
of the distal fragment (lateral for varus and medial for valgus correction) will be the
result (osteotomy rule 3). This can be avoided by rotation around the CORA with
subsequent translation and angulation at the osteotomy site (osteotomy rule 2).
To allow translation of the tibia an osteotomy of the fibula might be necessary. It
is recommended to perform the osteotomy of the fibula distal to the osteotomy of
Fig. 3 All CORAs are located on the dotted line. Depending on the chosen centre of rotation an
open (red), neutral (green) or closed (blue) wedge osteotomy can be used to correct the deformity.
In case of neutral wedge osteotomy the wedge can be used to put in the resulting gap after defor-
mity corretion. (Modified from Paley [2])
the tibia. This is in contrast to an osteotomy due to a concomitant malalignment of

the fibula. In this case an osteotomy at the level of the deformity is recommended.
The translation and rotation at the osteotomy site can lead to decreased contact area,
potentially impairing bony healing. This can be avoided if a focal dome osteotomy
with the centre of the dome at the CORA is performed. The dome osteotomy is an
osteotomy with a spherical cut allowing correction around the axis of the cylinder.
The advantages are a larger bone to bone contact area and increased rotational sta-
bility. Therefore, dome osteotomies are suitable for larger deformity corrections
[24]. However, the radius of the dome osteotomy is important as the contact area
decreases if the radius of the osteotomy exceeds a critical level. If the centre of the
dome osteotomy does not fit within the CORA (namely not a focal dome osteot-
omy) additional translation and angulation occur according to the earlier outlined
rules (Paley rule I and II). Technically the dome osteotomy can be performed with
special saw blades or with repetitive K wire penetration. A short 3.5 mm plate,
which is loosely fixed over the CORA (by a 3.5 mm screw) helps to create a nice
radius. It must be kept in mind that additional rotational deformities cannot be
addressed by a dome osteotomy.
Due to minimal soft tissue structures medial over the tibia, a medial osteotomy
(opening wedge for varus and closing wedge for valgus deformity) is preferred in
our clinic. For correction, >10° a lateral approach is performed. Dome osteotomies
are performed through an anterior approach. Disadvantages and advantages of
medial, lateral and dome osteotomies are summarised in Table 1.
6.1 Complex Deformities
If the CORA is not found within the tibia, the deformity cannot be explained by an
angulation through a single apex. In this case multiple CORAs or an additional
translation of the segments is present. If both translational and rotational deformity
are present the translational deformity shifts the CORA proximally or distally to the
fracture level (apparent apex). The CORA is then called a-t CORA [2] (Fig. 4).
Traditionally, this type of deformity can be corrected either at the point of maximal
translational deformity which is usually at the fracture site or the a-t CORA [2].
Correction at the fracture site involves a rotational and translational movement of
the distal fragment (Fig. 4). This can be avoided if correction is performed at the a-t
CORA. As soft tissue and vascularisation at the fracture site might be compromised
correction at the a-t CORA might be beneficially. However, correction at the a-t
CORA leads to a residual bump which might disturb the patients after deformity
correction or hinder intramedullary fixation. Furthermore, depending on the defor-
mity, the a-t CORA might lie proximally or distally to the tibia.
Table 1 Commonly performed osteotomies

Medial Varus to Allows multiplane correction with saw Requires bone grafting
opening valgus blade angulation Increased risk of
wedge (<10 varus) Preserves limb length non-union
Increased risk of
neurovascular
compromise
Medial Valgus to Allows multiplane correction with saw Results in shortening of
closing varus blade angulation limb length
wedge Decreased risk of neurovascular
compromise
Decreased risk of non-union
Lateral Varus to Allows multiplane correction with saw Single-plane correction
closing valgus blade angulation
wedge (>10 varus) Decreased risk of non-union
Focal dome Valgus to Ideal for frontal/ sagittal plane deformity Does not allow axial
varus or with Centre of rotation and angulation at correction
varus to level of the ankle joint or in the talus Always translation of
valgus Preserves limb length bone parts (osteotomy
No thermal necrosis rule 2)
Minimal periosteal dissection
Excellent bone to bone contact
a b c d
Fig. 4 (a) Combined rotational (varus) and translationinal (medial) of the distal tibia. The transla-
tion shifts the CORA distally to the a-t point. (b) Correction of rotational deformity with residual
translation at maximum translation. (c) Additional translational deformity. (d) Deformity correc-
tion at the a-t CORA corrects angulational and translational deformity
The mentioned principles do also apply for correction in the sagittal plane (pro-
or retrocurvatum). After defining the axis of the proximal and distal fragment, the
CORA is identified, and the correction can be planned by an open or closing wedge
osteotomy.
It is obvious that angular deformity is not restricted to the frontal or sagittal plane
but can occur in any plane in between. In most cases, the deformity can be assessed
by using plane, i.e. conventional, radiographs [2, 25]. Of note, three-dimensional
visualisation using CT scan datasets has additionally been described to better address
the three-dimensional deformity including rotation (deformity around the longitudi-
nal axes) [2, 10, 26–28]. Rotational deformity below the tibial tuberosity can be
corrected at any level of the tibia. Soft tissue considerations must be made. As trac-
tion to the peroneus nerve is higher if the correction is performed at the proximal
tibia, the correction is preferred at the level of the distal metaphysis. Restoration of
the tibial anatomy is often limited by the fibula. From our clinical experience this can
already be the case in considerably small corrections as scar tissue or bony bridges
may prevent motion between the tibia and fibula (in post-traumatic condition). If the
centre of rotation is located central over the tibia or even medially, a translation of the
fibula fragment occurs. This can reduce the contact area of the fibula that might com-
promise healing. In this case the centre of rotation might be shifted laterally.
Theoretically, any three-dimensional deformation can be corrected by a rotation in
space and translation [27]. If healthy, the contralateral side can be used as the reference
part for planning [29]. The rotation is thereby around an axis in space. An osteotomy
perpendicular to this axis will correct the rotational deformity (single cut plane).
However, the single cut plane is not always suitable for surgery (small angle to the long
axis of the bone, difficult to approach, located in the diaphysis with inferior biological
healing potential). Modern planning systems help to determine the preferred osteot-
omy (single cut, open wedge with or without translation) by visualising the correction
in a three-dimensional model [10, 27]. Patient-specific instrumentation guides or intra-
operative navigation can guide the osteotomy and reduction during surgery [10, 27].
In our clinic, complex deformities are analysed using three-dimensional triangular
surface models of the tibia and fibula gained from CT data. In a special developed
computer program (CASPA, University Hospital Balgrist, Zurich, Switzerland) three-
dimensional deformity analysis is performed. As outlined earlier the mirrored contra-
lateral side is usually used as a template. Therefore, the proximal part of this reference
template is superimposed to the non-deformed part pathologic tibia or fibula using a
surface registration algorithm. In a next step, the distal part of the deformed bone is
separated and aligned to the reference template. This allows to determine the rotation
and translation of the deformity and to calculate the needed correction through a
given osteotomy. A single cut osteotomy is hereby often an elegant option to correct
a translational and rotational deformity without bone loss maintaining a high contact
area. Depending on the type of deformity and chosen surgical approach alternatively
an opening or a closing wedge or dome osteotomy can be chosen. Once the suitable
osteotomy for the individual deformity and patient is found patient specific instru-
mentation guides are planned. One block is designed to guide the osteotomy with a
slit for the saw blade. A second guide is made to guide the reposition. The guides are
printed in 3D. During surgery the bone is exposed at the level of the planned osteot-
omy. The cutting guide is placed on the bone and fixed with k wires. The osteotomy
is then performed guided through the slit of the cutting guide. In the next step the
reposition is achieved by applying the reposition guide using the k wires in place. A
plate is usually used for fixation. In Fig. 5, a three-dimensional planning and correc-
tion of the earlier illustrated case (Fig. 4) is presented. Postoperative, patients are
mobilised in a lower leg cast for 6 weeks with partial weightbearing of 15 kg. At this
point radiographs are taken and protected weightbearing is gradually increased in a
lower leg cast. Three months after the operation full weightbearing is allowed if con-
solidation is progressed on imaging. Analyses of the three-dimensional planed cases
with a supramalleolar osteotomy showed good restoration of the alignment with rota-
tional error of <3° and translational error <6 mm [30].
7 Complications
General postoperative complications include wound healing problems, infections,

complications due to postoperative immobilisation (e.g. deep vein thrombosis) or
complex regional pain syndrome (CRPS). Specific complications include delayed-/
or non-union as well as injury to the saphenous nerve or posteromedial neurovascu-
lar bundle and tendons. If and extensive correction is performed, traction injury to
the tibial or peroneal nerve can occur [2]. Also, skin closure and/or wound healing
can be demanding after performing extensive corrections, because of scar tissue,
Fig. 5 Example of a three- a b

dimensional model for a
complex deformity. (a)
preoperative ap X-ray shows
severe deformity of the tibia. (b)
From CT scans of both lower
extremities a 3D model of the
pathologic side (red) is
developed and proximally
aligned to the contralateral
healthy side (green) which is
used as template for correction.
(c) Analysis of the deformity is
performed. A single cut plane
allows to correct both rotational
and translational deformity. (d)
The cut is virtually performed,
and the distal part (purple) is
aligned using our algorithm to
the healthy part (green). (e)
According to the calculated
cutting plane a cutting guide
which fits to the unique anatomy
of the patient is designed. The
cutting guide is 3D printed and
will lead the surgeon to perform
the exact cut intraoperatively. (f)
After virtually performed
osteotomy the distal fragment is
repositioned using the c d
reposition guide. Watch the
orientation of the guide wires
which are now parallel and in
one line. The plate used for
internal fixation can also be
simulated to plan proper plate
and guide placement. (g)
Intraoperative picture of cutting
guide and osteotomy. The
cutting guide is fixed using
guidewires in its unique position
to the bone. (h) Reposition of
the distal fragment using the
reposition guide. (i) Final result
with the plate in place
Fig. 5 (continued) e f
g h
Fig. 5 (continued)
post-traumatic adhesions, low blood circulation, etc. Therefore, planning of the

approach is also very important, as choosing the kind of correction (e.g. open, clos-
ing or neutral wedge – see Fig. 3). If wound closure due to extensive correction,
post-traumatic scar tissue or prior plastic surgery such as musculocutaneus flaps is
not possible or only with massive tension of soft tissue, negative pressure dressing
or synthetic skin replacement for temporary wound dressing might be necessary.
This will protect the wound borders and prevent necrosis of prior healthy skin soft
tissue. Painful hardware needing removal is common.
References
1. Court-Brown CM, Caesar B. Epidemiology of adult fractures: a review. Injury.

2006;37(8):691–7.
2. Paley D. Principles of deformity correction. Berlin, Heidelberg: Springer Berlin
Heidelberg; 2002.
3. Merchant TC, Dietz FR. Long-term follow-up after fractures of the tibial and fibular shafts. J
4. Horisberger M, Valderrabano V, Hintermann B. Posttraumatic ankle osteoarthritis after ankle-
related fractures. J Orthop Trauma. 2009;23(1):60–7.
5. Barg A, Pagenstert GI, Hugle T, Gloyer M, Wiewiorski M, Henninger HB, et al. Ankle osteo-
arthritis: etiology, diagnostics, and classification. Foot Ankle Clin. 2013;18(3):411–26.
6. Kimizuka M, Kurosawa H, Fukubayashi T. Load-bearing pattern of the ankle joint. Contact
area and pressure distribution. Arch Orthop Trauma Surg. 1980;96(1):45–9.
7. Meyer DC, Siebenrock KA, Schiele B, Gerber C. A new methodology for the planning of
single-cut corrective osteotomies of mal-aligned long bones. Clin Biomech (Bristol, Avon).
2005;20(2):223–7.
8. Stamatis ED, Cooper PS, Myerson MS. Supramalleolar osteotomy for the treatment of distal
tibial angular deformities and arthritis of the ankle joint. Foot Ankle Int. 2003;24(10):754–64.
9. Pearce MS, Smith MA, Savidge GF. Supramalleolar tibial osteotomy for haemophilic arthrop-
athy of the ankle. J Bone Joint Surg Br. 1994;76(6):947–50.
10. Fürnstahl P, Schweizer A, Graf M. Surgical treatment of long-bone deformities: 3D preopera-
tive planning and patient-specific instrumentation. In: Computational radiology for orthopae-
dic interventions. Cham: Springer; 2016.
11. Weinberg DS, Park PJ, Liu RW. Association between tibial malunion deformity parameters
and degenerative hip and knee disease. J Orthop Trauma. 2016;30(9):510–5.
12. Staheli LT, Corbett M, Wyss C, King H. Lower-extremity rotational problems in children.
Normal values to guide management. J Bone Joint Surg Am. 1985;67(1):39–47.
13. Turner MS. The association between tibial torsion and knee joint pathology. Clin Orthop Relat
Res. 1994;302:47–51.
14. Yagi T. Tibial torsion in patients with medial-type osteoarthrotic knees. Clin Orthop Relat Res.
1994;302:52–6.
15. Boucher M, Leone J, Pierrynowski M, Bhandari M. Three-dimensional assessment of tibial mal-
union after intramedullary nailing: a preliminary study. J Orthop Trauma. 2002;16(7):473–83.
16. Theriault B, Turgeon AF, Pelet S. Functional impact of tibial malrotation following intramed-
ullary nailing of tibial shaft fractures. J Bone Joint Surg Am. 2012;94(22):2033–9.
17. Jakob RP, Haertel M, Stussi E. Tibial torsion calculated by computerised tomography and
compared to other methods of measurement. J Bone Joint Surg Br. 1980;62-B(2):238–42.
18. Jakob RP, Stussi E, Haertel M. [Measurement of tibial torsion-Comparison of various
methods was computerised axial tomography (author’s transl)]. Z Orthop Ihre Grenzgeb.
1981;119(5):525–34.
19. Lampert C, Thomann B, Brunner R. [Tibial torsion deformities]. Orthopade. 2000;29(9):802–7.
20. Chang FM. Gait analysis and intoeing. Instr Course Lect. 1988;37:107–8.
21. Davids JR, Davis RB, Jameson LC, Westberry DE, Hardin JW. Surgical management of
persistent intoeing gait due to increased internal tibial torsion in children. J Pediatr Orthop.
2014;34(4):467–73.
22. Rosskopf AB, Sutter R, Pfirrmann CWA, Buck FM. 3D hindfoot alignment measure-
ments based on low-dose biplanar radiographs: a clinical feasibility study. Skelet Radiol.
2019;48(5):707–12.
23. Puno RM, Vaughan JJ, Stetten ML, Johnson JR. Long-term effects of tibial angular malunion
on the knee and ankle joints. J Orthop Trauma. 1991;5(3):247–54.
24. Knupp M. The use of osteotomies in the treatment of asymmetric ankle joint arthritis. Foot
Ankle Int. 2017;38(2):220–9.
25. Bar HF, Breitfuss H. Analysis of angular deformities on radiographs. J Bone Joint Surg Br.
1989;71(4):710–1.
26. Fucentese SF, Meier P, Jud L, Kochli GL, Aichmair A, Vlachopoulos L, et al. Accuracy of
3D-planned patient specific instrumentation in high tibial open wedge valgisation osteotomy.
J Exp Orthop. 2020;7(1):7.
27. Dobbe JG, Pre KJ, Kloen P, Blankevoort L, Streekstra GJ. Computer-assisted and patient-
specific 3-D planning and evaluation of a single-cut rotational osteotomy for complex long-
bone deformities. Med Biol Eng Comput. 2011;49(12):1363–70.
28. Sangeorzan BP, Judd RP, Sangeorzan BJ. Mathematical analysis of single-cut osteotomy for
complex long bone deformity. J Biomech. 1989;22(11–12):1271–8.
29. Schenk P, Vlachopoulos L, Hingsammer A, Fucentese SF, Furnstahl P. Is the contralateral tibia
a reliable template for reconstruction: a three-dimensional anatomy cadaveric study. Knee
Surg Sports Traumatol Arthrosc. 2018;26(8):2324–31.
30. Weigelt L, Furnstahl P, Hirsiger S, Vlachopoulos L, Espinosa N, Wirth SH. Three-dimensional
correction of complex ankle deformities with computer-assisted planning and patient-specific
surgical guides. J Foot Ankle Surg. 2017;56(6):1158–64.
Septic Ankle Arthritis and Tibial
Osteomyelitis
Pablo Mery and Joaquín Palma
1 Introduction
Osteoarticular infections around the ankle (septic arthritis and acute osteomyelitis)
are a complex group of diseases, with high morbidity and mortality if they are not
diagnosed early or optimal treatment is not carried out. In this chapter we will
address the tools to reduce complications, emphasizing:
• Early diagnosis: a good history and physical examination allow a high clinical
suspicion. The proper use of general laboratory and synovial fluid studies is
essential. There are also new diagnostic tools, such as procalcitonin or presepsin,
which improve our diagnostic threshold in septic arthritis. The use of right
images and their adequate interpretation allows early complication
identification.
• Microbiological analysis: we will discuss proper guidelines and techniques to
optimize synovial fluid and bone tissue cultures. Also, we will discuss the useful-
ness of new technologies such as polymerase chain reaction (or PCR) and other
molecular biology assays.
• Antibiotic therapy: once cultures have been taken, we must initiate appropriate
empirical antibiotic regimens and adjust these according to the results of the
cultures. The optimal duration of this treatment will be discussed.
P. Mery (*)
Pontificia Universidad Católica de Chile, Santiago, Chile
J. Palma
Pontificia Universidad Católica de Chile, Complejo Asistencial Dr. Sótero del Río,
Santiago, Chile

Switzerland AG 2022
760 P. Mery and J. Palma
• We will discuss the role of surgery, both from a diagnostic and therapeutic point
of view.
• We will emphasize the importance of having management protocols adjusted to
our resources and a multidisciplinary team to handle these cases.
2 Septic Ankle Arthritis
2.1 Introduction
Although septic ankle arthritis (SAA) is a relatively rare condition, comprising

between 3.4% to 15% of all joint septic arthritis [1–5], it has high potential of mor-
bidity and mortality. Any delay in its diagnosis and treatment can lead to cartilage
erosion, ligament instability and osteomyelitis [6–8]. It had been reported that irre-
versible loss of joint function develops in 25–50% of patients, and even in expert
hands, case-fatality is generally around 11%. This frequency is raised in poly articu-
lar disease, with estimates as high as 50% [9–12].
2.2 Pathophysiology
SAA can arise via hematogenous spread from other infection site, contiguous spread
from bone or wound infection, or direct inoculation as a result of trauma, puncture
wounds, or medical procedures [13]. Concurrent osteomyelitis adjacent to the
infected ankle is reported to occur in 30% of patients [14].
There have been some important advances to understand pathogenesis of septic
arthritis. A hypothetical scheme of host-bacterium interaction, based on an experi-
mental model of Staphylococcus aureus septic arthritis on murine mice, in which
immune system displays many similarities with to human counterpart, had been
used to identify defense and destruction mechanism of joint infections [49].
2.3 Clinical Presentation
Clinical and laboratory findings are not very constant, so clinical suspicion must be
high. Typical presentation consists of rapid onset of ankle pain, limited joint range
of motion with extreme pain with even slight movements of the joint, warmth and
swelling, but they are variable present. Literature reported sensitivities of joint pain
(85%), swelling (78%), fever (57%), sweats (27%), and chills (19%) are not opti-
mal [15].
Septic Ankle Arthritis and Tibial Osteomyelitis 761
Systemic symptoms are not seen in all cases. For example, fever was present
between 30% to 40% of the cases [9, 12, 13]. Recent trauma around the ankle does
not rule out joint sepsis; this even can be a risk factor for hematogenous spread.
Polyarthritis does not rule out septic involvement, as high as 22% of the cases can
be in context of multiple joint infection [16, 17].
Multiple predisposing risk factors that raised the index of suspicion for joint
sepsis had been described (Table 1) [8, 12, 16]. Patients with any predisposing fac-
tors must be evaluated with a higher level of clinical suspicion [14, 18].
Patients that underwent medical procedures involving the ankle had variable risk
of articular infection. Frequency of SAA after arthroscopic procedures of the ankle
had been reported between 0.15% to 0.6% [19].
In young, sexually active patients with no comorbidities, there should be high
suspicion for disseminated Neisseria gonorrhoeae disease, as well for reactive
arthritis secondary to Chlamydia or Mycoplasma urethritis. Septic arthritis second-
ary to Neisseria gonorrhoeae is the most frequent form of septic joint disease. It is
more frequent in women; it is associated with migratory polyarthralgia, tenosynovi-
tis, and non pruriginous rash in trunk and extremities in almost 60% of patients.
Near 25% of the patients had history of urethritis or cervicitis (many women are had
an asymptomatic genitourinary disease). Knee and wrist joints are the most fre-
quently involved in Neisseria arthritis, followed in frequency by the elbow, metacar-
pophalangeal and ankle joints [11].
Table 1 Risk factor for septic joint arthritis

Local host risk factors Systemic host risk factors
Direct trauma Age (newborns / >80 years old)
Recent articular medical Rheumatoid arthritis & other autoimmune arthritis
procedures
Inflammatory arthritis Gout & pseudogout
Degenerative arthritis Diabetes mellitus
Articular replacement Chronic liver disease
Cutaneous ulceration Chronic renal failure
Hemodialysis
Alcoholism
Intravenous drug addiction
Sickle cell disease
Hemophilia
HVI infection
Hypogammaglobulinemia
Transplant immunosuppression drugs
Autoimmune drug treatment (e.g., corticosteroids, anti TNFa
drugs)
2.4 Laboratory Studies
2.4.1 Traditional Blood Tests
If a SAA is suspected, blood analysis should include complete blood-cell count,

erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). In one study,
elevated peripheral white blood-cell count (WBC) was present in only 47% of the
patients with SAA at their admission [14]. ESR and CRP level are sensitive makers,
although their elevation indicate a nonspecific inflammatory condition and they are
not specific for septic arthritis [13]. Combination of WBC over 10,000/uL, ESR
>30 mm/H and CRP over 100 mg/L exhibit a mildly increased likelihood of septic
arthritis [20, 21]. Although they had poor sensitivity and specificity, WBC, ERS and
CRP should be measured, because they are useful to monitor response to treatment.
Liver, renal and coagulability should be assessed at presentation, because their fail-
ures are linked to poor prognosis and abnormal function could affect antibiotic
selection and dosage [22, 23].
Peripheral blood cultures must be obtained before administration of an antibiotic
treatment to enhance the chance of obtaining causative microorganism [22]. Blood
cultures could be positive in 24–50% of non-Neisseria gonorrhoeae arthritis, while
in gonococcal infection recovery of bacteria in blood samples could be possible in
less than 10% of the cases. In one study, blood cultures were the only source of posi-
tive microbiological diagnosis in 9% of the patients with septic arthritis [24].
2.4.2 New Diagnostic Tools
Serum Procalcitonin. Procalcitonin (PCT) is a protein produced by parafollicular

cells of the thyroid gland and neuroendocrine cells of lung and intestines. In healthy
patients, serum PCT levels are low (<0.11 ng/ml), but it increases rapidly in patients
with severe bacterial or fungal infections, but not in patient with viral infections or
with non-infectious inflammatory conditions. A meta-analysis that comprised 10
studies including 838 patients, with 486 patients with septic arthritis, showed an
overall sensitivity of serum PCT of 54% and a specificity of 95% for the diagnosis
of septic arthritis, when using a cutoff value of 0.5 ng/dl. The positive likelihood
ratio for PCT (index of the ability of PCT to rule in the diagnosis of septic arthritis
with that cutoff value was high (10.97)) [25].
Serum & synovial presepsin Soluble CD14 subtype or presepsin is generated as
a product from CD14 when bacteria are phagocytosed by monocytes. It has been
reported that serum synovial fluid levels of presepsin increased significantly in sep-
sis, but there was no increase in patients with systemic inflammatory response syn-
drome in absence of infection, making it very specific for infection. Using a cutoff
value of 1099 ng/ml, Synovial fluid presepsin exhibited 100% sensitivity and 100%
specificity in septic arthritis patients, which were higher than serum presepsin and
serum procalcitonin. Presepsin can be measured in around 15 minutes with
Pathfast® kit, making it a potential new biomarker of sepsis arthritis [26].
2.4.3 Synovial Fluid Aspiration and Analysis
Synovial fluid aspiration is a key procedure to make the diagnosis of septic arthritis
or confirm other causes of arthritis. A competent physician must know the technique
to perform arthrocentesis of ankle synovial fluid. Aspiration must be done with full
aseptic precautions, with the use of an 18- or 21-gauge needle mounted on a 20 mL
syringe. Physician must avoid the insertion of the needle in an area of skin cellulitis,
to prevent contamination of the joint with bacteria in the case of a non-bacterial
arthritis.
The most used technique for ankle joint aspiration is through anteromedial portal
(Fig. 1). Reference lines are drawn in skin in relation to medial malleolus, anterior
tibialis tendon and ankle joint line. Insertion of the needle is made medial to anterior
tibialis tendon at the lever of the joint line, entering the joint at the superior aspect
of the medial gutter [27]. In case of unsuccessful access through anteromedial
approach, an anterolateral approach can be made (Fig. 2). In this case, needle is
inserted at the joint line between lateral border of peroneus tertius and lateral mal-
leolus. If none of these approaches are successful, ultrasound or fluoroscopy guided
ankle arthrocentesis can be helpful.
Analysis of synovial fluid should include three bedside observations (color,
transparency, and viscosity). Also, general laboratory analysis should include total
synovial white cell count, polymorphonuclear cell count, crystal analysis, gram
stain and aerobic bacterial cultures. In certain situations, specific laboratory analysis
should include bacilloscopy and mycobacterium culture, calcofluor white stain and
Fig. 1 Needle ankle joint fluid aspiration through anteromedial approach

Fig. 2 Anterolateral
approach to ankle joint
fluid aspiration
fungus culture, and polymerase chain reaction. Synovial fluid analysis in different
scenarios is listed in Table 2 [28].
In general, the likelihood of septic arthritis increases as synovial white cell count
rises [15]. Although some authors cite a synovial white cell count as low as 17,500/
mm3 in providing diagnostic sensitivity of 83% for septic arthritis, its specificity is
only 67% [29]. Synovial white cell count >50,000/mm3 is the standard cutoff value
which increases the likelihood of septic arthritis [24]. On the other hand, this mea-
sure cannot distinguish between crystal and septic arthritis; synovial white cell
count can be as high as 100,000/mm3 in crystal arthritis [10, 15, 30].
Crystal analysis is very important, because gout and pseudogout can affect the
ankle joint [13]. They can present with clinical characteristics very similar to septic
arthritis. Also, septic and crystal arthritis can occur simultaneously. One review of
29 patients with septic ankle arthritis reported that 43.5% of the patients also had
presence of monosodium urate crystals in joint fluid analysis [18].
Gram stain and cultures are gold standard to confirm the diagnosis of septic
arthritis, although their sensitivity is not high enough. Gram stain is positive in
60–80% of non-gonococcal arthritis, while in gonococcal arthritis could be positive
in less than 50% of the cases. Synovial fluid cultures had a sensitivity of 75–90% to
detect non gonococcal bacteria in a septic arthritis, and they can guide the selection
of appropriate antibiotic treatment [31]. False negative results in gram stain and
cultures of synovial fluid are possible. Is imperative to obtain sufficient amount of
joint fluid to avoid this situation. Also, is important to inform laboratory if there is
clinical suspicion of fastidious microorganism because in these cases the culture
Table 2 Synovial fluid analysis
WBC count (per PMN cell
Arthritis diagnosis Color Transparency Viscosity mm3) count (%) Gram stain Culture PCR test Crystals
Normal Clear Transparent High/ <200 <25 Negative Negative Negative Negative
thick
Noninflamatory Straw Translucent High/ 200–2000 <25 Negative Negative Negative Negative
thick
Inflammatory – Yellow Cloudy Low/thin 2000 to 100,000 >50 Negative Negative Negative Positive
crystalline disease
Inflammatory – Yellow Cloudy Low/thin 2000 to 100,000 >50 Negative Negative Negative Negative
Septic Ankle Arthritis and Tibial Osteomyelitis
noncrystalline disease
Infectious – Lyme Yellow Cloudy Low 3000 to 100,000 >50 Negative Negative Positive Negative
disease (mean: 25,000) (85%)
Infectious – gonococcal Yellow Cloudy – Low 34,000 to 68,000 >75 Variable Positive Positive Negative
opaque (<50%) (25–70%) (>75%)
Infectious – non Yellow – Opaque Very low >50,000 (>100,000 >75 Positive Positive Variable Variable
gonococcal Yellow green is more specific) (60–80%) (>90%)
Notes: Direct joint fluid observation (color, transparency, and viscosity) are made immediately after joint aspiration. In a normal ankle, with transparent ankle
fluid, the physician can clearly read words through the fluid. With increasing turbidity, words become increasingly obscured. Articular fluid had normal viscos-
ity when a long tail, greater than 3 cm, is formed when a drop of liquid falls from the syringe; the more inflammation, the shorter the tail
WBC white blood cell, PMN polymorphonuclear, PCR polymerase chain reaction
765
samples are observed for more days. Other crucial clinical decision to improve
synovial culture sensitivity is to delay the administration of antibiotic treatment
until joint fluid sample is taken. Other way to improve detection of bacteria in syno-
vial fluid culture is to seed sample in a pediatric blood culture; this is a nutritively
rich media with polymeric beads with the capacity of neutralizing antibiotics. This
can improve the capacity to detect bacteria from 60% in traditional culture media to
88% [32, 33]. As occur in other body joints, staphylococci and streptococci are the
most common causative microorganism of septic arthritis of the ankle joint [14, 18].
Neisseria gonorrhoeae is detected in only 50% of synovial fluid culture samples. In
these cases, the addition of polymerase chain reaction test can detect gonococci
genetic material in over 90% of the cases, although this does not provide informa-
tion about antibiotic sensitivity [34].
In the case gram stain and cultures are negative, but clinical history or/and other
blood and synovial fluid analysis are highly suggestive of septic ankle arthritis, the
physician must not hesitate in taking appropriate measures of treatment.
2.5 Imaging
If septic arthritis of the ankle joint is suspected, radiographs of the ankle must be
obtained. Initially, radiographs may be normal or may show soft tissue swelling and
ankle effusion [35]. If radiographs are done in patients with a delayed diagnosis of
septic ankle arthritis, they can show joint destruction and chondrolysis. Also, radio-
graphs can show the presence of ankle implants (old fixation material, foreign mate-
rial, ankle prosthesis). Additionally, radiographs can help in differential diagnosis,
ruling out fractures, loose bodies, and osteoarthritis. Computed tomography has
better sensitivity than radiographs to detect early bone destruction and abscess for-
mation. Ultrasonography can confirm the presence of joint fluid, synovitis, marginal
bone erosions and adjacent soft-tissue involvement (e.g., soft tissue abscess).
Ultrasound guided ankle joint aspiration can be helpful in the case of difficult
arthrocentesis. The most complete study to address in detail septic ankle arthritis is
magnetic resonance imaging. It can show early changes in periarticular bone com-
patible with osteomyelitis, and it can show soft tissue abscess around the ankle [10].
All these imaging modalities are complementary to clinical and laboratory findings;
they may not accurately differentiate between a septic ankle arthritis and other
cause of ankle effusion.
2.6 Differential Diagnoses
Numerous differential diagnoses should be considered when a patient presents with

a swollen, painful, and erythematous ankle joint. Table 3 shows an extensive list of
differential diagnoses for acute ankle arthritis [15, 36].
Table 3 Differential diagnosis of acute arthritis

Diagnosis Etiology
Septic arthritis Bacteria, fungi, mycobacteria, spirochetes (Lyme disease), virus
Crystal induced Gout (urate), pseudogout (calcium pyrophosphate), calcium oxalate, calcium
arthritis hydroxyapatite, cholesterol crystals
Inflammatory Not usually monoarticular: Rheumatoid arthritis, sarcoidosis, still disease,
arthritis systemic vasculitis
Usually monoarticular: Behçet syndrome, systemic lupus erythematosus,
seronegative spondyloarthropathy (psoriatic arthritis, reactive arthritis,
ankylosing spondylitis, inflammatory bowel disease-related arthritis)
Osteoarthritis Erosive/inflammatory variants
Systemic Bacterial endocarditis, human immunodeficiency virus infection
infection
Tumor Pigmented villonodular synovitis, metastasis
Other causes Amyloidosis, avascular necrosis, anticoagulant therapy, bleeding disorders
(e.g., hemophilia), familiar Mediterranean fever, foreign, fracture,
osteochondral fractures, anterior/posterior impingement, hemarthrosis,
hyperlipoproteinemia, extraarticular infection (e.g., cellulitis), post-
corticosteroid injection flare
Joints that had suffered chronic inflammation secondary to different causes, had
a higher risk for septic arthritis. In these cases, hypertrophic synovial tissue presents
a huge vascular supply, with vessels lacking a basement membrane. This situation
allows blood circulating bacteria an easy entry to the joint. This must be remem-
bered in case of crystal arthritis as it was mentioned before; septic and crystal arthri-
tis can occur simultaneously. Also, patients with articular autoimmune disease, such
as rheumatoid arthritis, had a higher risk for developing septic arthritis due chronic
joint inflammatory process as well the immunosuppressive therapy used in disease
treatment. Always must be remembered the possibility of concurrent septic arthritis
in patients with chronic joint disease who present with one new inflamed joint; in
that group of patients, correct diagnosis is often delayed because it is wrongly
assumed that joint symptoms are related to an exacerbation of the underlying rheu-
matoid arthritis. This situation can lead to poor outcome, with a 30–50% case-
fatality rate [11]. In these cases, it should be assumed the inflamed joint is septic
until proven otherwise.
2.7 Medical and Surgical Management
Two general goals of treatment of septic ankle arthritis include prompt sterilization
and decompression of the joint, with the objective of maximizing function after
treatment and minimize risk of mortality [37]. Management should include hospital
admission, supportive care with pain management and immobilization, prompt ini-
tiation intravenous antibiotic treatment (after peripheral blood and joint fluid cul-
tures had been taken) and irrigation plus debridement of the ankle joint in an urgent
fashion. Any delay in the beginning of the treatment can lead to irreversible destruc-
tion of joint cartilage, joint stiffness, sepsis, and death. Depending on the infective
organism, patient comorbidities, source of infection and time course, aggressive-
ness of infection can be variable. Commonly, Staphylococcus aureus and gram-
negative rod bacteria had an aggressive clinical course and require prompt surgical
intervention, while Neisseria gonorrhoeae joint infection rarely need invasive tech-
niques [13, 34].
2.7.1 Antibiotic Treatment
Antibiotics are key part of the management of septic ankle arthritis. It is important
to remember to start antibiotics not until peripheral blood cultures and joint fluid
cultures have been obtained. No study, as well a large meta-analysis, has been able
to demonstrate an advantage of one therapeutic antibiotic regimen over another for
native joint arthritis.
Empirical intravenous antibiotic treatment should be guided by the organism
found in the gram stain of synovial fluid, patient risk factors and knowledge of the
local prevalence of antibiotic-resistance bacteria patterns [38, 39]. If Gram stain is
negative, and as Staphylococcus aureus is reported as the most common causative
pathogen, followed by Streptococci, first line antibiotic treatment should be
β-lactamase stable penicillins (i.e., cloxacillin or flucloxacillin) or first-generation
cephalosporin, such as cefazolin 1 or 2 g three times a day. In case of a patient aller-
gic to penicillin, cephalosporin could be replaced by clindamycin 600–900 mg three
to four times a day. If local prevalence of community acquired methicillin resistant
Staphylococcus aureus (MRSA) is high, or other risk factors for MRSA are present
(e.g., previous MRSA infection, recent impatient, nursing-home resident, leg ulcers
or catheter), recommendation is to start Vancomycin. If the patient has a high risk of
gram-negative rod bacterial infection (e.g., diabetes mellitus, intravenous drug
addiction, recurrent urinary tract infection), third generation cephalosporin (e.g.,
ceftazidime), fourth generation cephalosporin (e.g., cefepime), piperacillin/tazo-
bactam or carbapenems must be added. In case of high suspicion of Neisseria gon-
orrhoeae infection, ceftriaxone or similar antibiotic must be used intravenously for
24–48 hours, followed by oral therapy with cefixime if clinical response is rapid to
complete 10 days of total antibiotic treatment (ciprofloxacin is not a recommended
option in case of high reported Neisseria gonorrhoeae quinolone resistance fre-
quency). In these cases, azithromycin 2 g po for once time, or doxycycline 100 mg
two times a day for 7 days, must be added to treat eventually associated sexual
transmitted diseases [40]. Fungal arthritis is species dependent; usually includes
parenteral amphotericin B or an oral azole [41, 42]. Lyme arthritis has a good
response to intravenous ceftriaxone or oral doxycycline [43, 44].
Once the causative organism is appropriately identified in cultures and its sus-
ceptibilities are available, antibiotic treatment should be adjusted. At this point, is
recommendable to obtain an Infectious Disease consultation.
Duration of antibiotic treatment is recommended for about 6 weeks; intravenous

treatment usually recommended for the first 2 weeks. There is no actual evidence in
literature to define the optimal duration of total antibiotic treatment in septic ankle
arthritis [13].
2.7.2 Serial Joint Aspiration
Usually, open or arthroscopic surgical drainage are the first option in the case of
septic ankle joint arthritis, but in the case of a medically unstable patient who
could not be a able to endure surgery, serial aspiration of the ankle joint can be
done. Is a safe, simple, and relatively noninvasive procedure. Although it can be
done every day, providing a daily measure of clinical response to antibiotics
through leukocyte count and gram/cultures of the synovial fluid, the physician
cannot look for the damaged ankle tissue and debride it [45]. Also, needle can
be blocked during aspiration by thick debris. An old work by Goldenberg et al.
compared daily needle aspiration versus surgical drainage in a retrospective
series of 59 cases of non-gonococcal septic arthritis. Good results (defined as
absence of flexion deformity of >10°, ankylosis, secondary osteomyelitis or per-
sistent effusion) were achieved in 67% of patients treated with daily needle
aspiration and in 42% of patients treated surgically, although mortality in the
daily aspiration group was 12% versus 5% in the surgical group. Daily aspira-
tion group had a higher prevalence of serious underlying illness and immuno-
suppressive therapy, which may have accounted for their higher overall mortality.
In this series only 4–73 compromised joints were ankle joints [46]. Similar
findings were described by Broy et al.; in an analysis done in 93 patients with
non-gonococcal septic arthritis, daily needle aspiration resulted in a signifi-
cantly greater percentage of good outcomes relative to surgical drainage (73.7%
vs 55.9%, respectively), as well as a significantly higher mortality (5.6% vs
2.1%, respectively). As previously noted, higher mortality in aspiration group
was explained by more frequent comorbid conditions in those patients than in
the surgical resolved patient group.
2.7.3 Arthroscopic Ankle Drainage
Usually done under general anesthesia (septic condition of the patient is a relative
contraindication to neuraxial anesthesia), arthroscopic surgery for ankle drainage
has the advantage of been a minimally invasive procedure. With small incisions,
arthroscopy allows great visualization of the joint, minimizing the risk of surgical
wound dehiscence and articular rigidity. It has a shorter hospitalization period and a
more rapid rehabilitation period when compared to open surgical drainage [13].
Arthroscopic ankle drainage is performed using standard anteromedial and
anterolateral arthroscopy portals. External distraction is not used often. A 4.0 or
2.7 mm 30° camera is introduced via anteromedial portal and a standard 21-point
inspection is performed. It is usually difficult to visualize the joint due high degree
of synovitis, swelling and purulent joint fluid. Shaver is placed via anterolateral
portal. Also, surgeon should anticipate difficult finding of shaver; usually, initial
blind debridement of the anterior ankle joint space with the shaver oriented away
from the articular surface, may be necessary. Biopsy and cultures of the synovial
tissue, synovectomy and debridement of anterior, medial, and lateral aspects of the
ankle joint should be completed [13]. The amount of synovial debridement must be
balanced. Aggressive synovectomy should be avoided as synovial tissue provides
nutrition and protection against infection; on the other side, little debridement can
lead to insufficient infection management [47]. A guide for management of ankle
joint sepsis was proposed by Boffeli et al. based on two retrospective case series
studies, correlating Gaetcher criteria with the extent of debridement that should be
performed (Table 4) [1, 3, 47].
Joint lavage is done using 9 L of lactate Ringer’s solution; in some rare circum-
stances a greater volume should be required. Camera portal used as the inflow portal
and the shaver portal used as the outflow portal. The use of solutions impregnated
with antibiotics or antiseptics us discouraged because there is no evidence of better
outcomes with these solutions and concerns of chondrotoxicity [1]. Portals are usu-
ally left opened to allow drainage of the joint.
In case of persisting clinical signs of infection (persisting cellulitis, persisting
pain) and laboratory alteration (persisting elevated WBC, ESR, or C reactive pro-
tein) after first arthroscopic ankle drainage, another surgery may be required.
Magnetic resonance imaging should be considered in these cases, as adjacent osteo-
myelitis can occur in up to 30% of septic ankle arthritis.
Table 4 Joint sepsis stage-based surgical treatment protocol

Stage Intraoperative findings Proposed surgical tratment
I Minimal synovitis Single arthroscopic irrigation
Fluid opacity Minimal debridement
Petechiae
II Fibrin deposits Irrigation and debridement with local
Purulence synovectomy and fibrinectomy
Severe inflammation & synovitis Posible repeated surgery
III Synovial thickening Multiple irrigation & debridement surgeries
Formation of multiple pouches due Adhesion resection
intraarticular adhesion Partial to subtotal synovectomy
IV Aggressive synovitis Consider magnetic resonance imaging
Radiographic changes & subchondral Consider open surgery via arthrotomy
erosions/cysts Multiple irrigation & debridement surgeries
Removal of loose fragments
Erosion & cyst curettage
2.7.4 Open Surgical Drainage
Open surgical drainage of the ankle should be considered in case of unexperienced

surgeon in arthroscopic procedures and in front of the absence of arthroscopic
equipment. Also, it should be considered in a Gaetcher stage IV ankle joint sepsis
or in case of persistent clinical infection, providing full access to adequate debride-
ment of the ankle joint.
One of the open approaches is the anteromedial approach. Which is done between
the anterior lip of the medial malleolus and the medial border of the anterior tibialis
tendon. This approach has the advantage of minimum risk off nerve and anterior
tibialis tendon sheath injury, but visualization of anterolateral and posterior joint
space is limited. To improve that, surgeon can do an anterolateral ankle arthroscopy
portal or an anterolateral open approach, which has the risk of superficial peroneal
nerve damage.
An alternative is an anterior ankle approach, which is done lateral to anterior tibi-
alis tendon, from the proximal level of superior extensor retinaculum to the level of
the talonavicular joint. In superficial distal dissection, careful must be taken to pro-
tect superficial peroneal nerve. Deep dissection must be careful, to avoid damage to
the neurovascular bundle (anterior tibialis artery and veins, and deep peroneal
nerve) in the anterior aspect of the ankle joint, deep to extensor hallucis longus ten-
don. Violation of the sheaths of anterior tibialis tendon and extensor and extensor
hallucis longus tendon is desirable. This approach provides excellent visualization
to evaluate, to debride and to do surgical lavage of entire ankle joint.
To the moment, there is no evidence to support one open approach over the other.
2.7.5 Postoperative Rehabilitation Protocol
First days after surgery, patient is usually maintained non weight bearing, using a
removable boot. Once surgical wounds have healed, physical therapy is started with
passive and active ankle range of motion, to minimize loss of ankle range of motion,
and progressive weight bearing is initiated.
2.8 Outcomes
There are few studies that evaluate the outcomes of treatment of ankle septic arthri-
tis in the literature, and most of them are retrospective series with few patients [3, 7,
14, 18, 48]. In a retrospective series of 29 ankles, Lee et al. reported that early treat-
ment (symptom duration of less than 5 days) significantly improved the chance to
regain ankle function, but most ankles had residual pain at the time of final follow-
up [18]. In other retrospective series of eight ankles who were treated with
arthroscopic debridement and antibiotics, the authors reported favorable outcomes
in all the patients, without recurrence. There is no information in the literature that
compares the outcome between arthroscopic and open approaches for the treatment
of septic ankle arthritis.
In the case of adjacent osteomyelitis or joint sepsis without response to surgical
debridement and prolonged antibiotic treatment, ankle arthrodesis must be consid-
ered to save the limb. Usually, this can be performed as a staged treatment; the ini-
tial surgical treatment consists in infected bone resection and cement spacer with
antibiotics. Once infection is controlled, fusion is performed using internal fixation
or circular external fixation [47].
3 Tibial Chronic Osteomyelitis
3.1 Introduction
Chronic osteomyelitis is a devastating pathology that poses a major challenge for

the treating team in terms of diagnosis and treatment. The lower extremity is more
susceptible to develop this pathology due to a series of conditions typical of this
region: scarce soft tissue envelope, poor irrigation, existence of bony prominences,
neuropathy, and higher frequency of exposed fractures [50]. Bone infection leads to
high morbidity, with long recovery periods, high economic costs, and high probabil-
ity of loss of function, as well as amputation.
Chronic osteomyelitis is defined as pyogenic infection of the bone characterized
by inflammation and progressive destruction, which can affect the periosteum, cor-
tical and cancellous bone and the endomedullary cavity [51, 52]. Treatment is based
on correct diagnosis, culture-guided antibiotic management, and debridement of
non-viable bone tissue. However, despite its relative frequency, there is no consen-
sus on the best diagnostic tool or treatment protocols.
Chronic osteomyelitis of the lower extremity can be caused by multiple etiolo-
gies, one of the most frequent being those that occur in the context of the diabetic
foot [52]. The present chapter focuses on chronic osteomyelitis of the tibia, whose
main etiology is related to the presence of fractures and their surgical management
via direct inoculation or local bacterial invasion. The frequency depends on the
severity of the initial lesion, soft tissue damage and degree of exposure. Osteomyelitis
rates of up to 44% have been reported in exposed fractures treated with plate [53]
and up to 7% in patients treated with endomedullary nail [54, 55]. In surgically
managed closed fractures, the infection rate is considerably lower, with figures
between 0.5% and 2% [56].
Post-traumatic osteomyelitis occurs in the context of young and active patients,
generating an important personal and socioeconomic cost [57, 58]. Rubins et al.
[59] reported costs close to 35,000 dollars (US) on average per patient in the man-
agement of chronic musculoskeletal infections, which can be much higher in those
patients who require reconstructive procedures.
Therefore, timely diagnosis and effective treatment are essential to lessen the
devastating consequences of chronic osteomyelitis of the tibia. A thorough clinical
examination, supported by diagnostic tests and imaging are basic to diagnosis,
while infection control through culture-based antibiotic therapy and resection of
infected bone tissue are key to successful treatment [60]. However, despite advances
in surgical techniques and antibiotic therapy, the recurrence rate following bone
infection varies between 20% and 30% [61].
3.2 Classification
Multiple classification systems have been proposed for chronic osteomyelitis, with
Cierny-Mader [51] being one of the most widely used given its clinical relevance.
The system stratifies the patient into three categories (A–C), depending on physio-
logical status, and assigns four anatomical stages of infection (I–IV). The objective
of the system is to be a tool to guide treatment in terms of surgical cleaning and
antibiotic therapy [60].
The physiological status of the patient is described as type A, B or C and is based
on systemic (age, diabetes, immunosuppression, smoking, etc.) or local (vascular
disease, chronic edema, radiotherapy, etc.) factors that play a major role in the out-
come of treatment. A type A host is one with an adequate immune system, good
local vascularity and normal physiological response to infection and surgical proce-
dures. Type B is characterized by systemic or local factors that will alter healing or
response to infection. Type C is where the factors are so severe that the anticipated
morbidity of treatment exceeds that of the disease itself, so palliative or definitive
treatment is offered once the risk factors have been controlled.
The system identifies four anatomical types of infection (Fig. 3) medullary (I),
superficial (II), localized (III) and diffuse (IV). The medullary type affects the inter-
nal border of the bone, usually associated with endomedullary implants. Superficial
affects the external region of the bone and is associated with soft tissue infection.
The localized one involves the infection of the full thickness of the bone and is an
extension of a superficial infectious process, whose resection leaves a segment that
does not require stabilization. Diffuse osteomyelitis also affects the full thickness of
the bone, but the resection of the tissue is of such magnitude that it leaves an unsta-
ble segment that requires fixation. A good example of osteomyelitis type IV.
3.3 Etiology
Osteomyelitis is the result of an infection by hematogenous dissemination or by

continuity [60]. The former is more frequent in patients younger than 20 or older
than 60 years of age, usually produced by a single type of microorganism, the most
frequent being Staphylococcus aureus [62]. Chronic osteomyelitis of the tibia in
a b
c d
Fig. 3 Scheme Cierny-Mader classification showing the four anatomic types: medullar (a), super-
ficial (b), localized (c), and diffuse (d)
adults is more frequently produced by exogenous dissemination or by continuity,

either at the time of an exposed fracture or infection secondary to surgical treatment,
particularly with the introduction of prostheses or metallic implants [63].
Additionally, osteomyelitis may occur in a context of vascular insufficiency, as
occurs in soft tissue infection in patients with diabetes mellitus [52].
Chronic osteomyelitis of the tibia secondary to dissemination by continuity is
usually caused by multiple microorganisms, the most frequent being Staphylococcus
Aureus. The presence of anaerobes and Gram-negative bacilli should be considered.
In exposed fractures, there is bacterial contamination in up to 60–70% of cases at
the time of injury [56], which added to soft tissue damage and devitalized bone
tissue, increases the risk of infection [64]. Other predisposing factors are the pres-
ence of inert elements (implants) and those of the patient himself, such as vascular
disease, diabetes, smoking and immunosuppression. In infections associated with
implants, biofilm is produced, a form of bacterial aggregation in colonies protected
by a glycocalyx matrix that adheres to inert surfaces such as devitalized bone tissue
or metallic implants [60, 65]. This form of bacterial growth allows evading the
organism’s own defense systems, as well as decreasing the effectiveness of antibiot-
ics, which do not come into contact with the cell wall of the microorganism.
3.4 Microbiology
As mentioned, most post-traumatic infections are poly microbial [66], where the
most frequently encountered agents are Staphylococcus aureus and Gram-negative
agents such as Pseudomonas aeruginosa. Sheehy et al. [66] described the bacterio-
logical spectrum in 166 patients with chronic osteomyelitis. Of those with an identi-
fied agent, 30% presented a polymicrobial infection. The most frequently identified
was Staphylococcus aureus in 32%, followed by Coagulase negative Staphylococcus
in 16%, enteric gram-negative bacilli in 16%, Streptococcus spp in 7% and
Pseudomonas aeruginosa in 5%.
3.5 Pathophysiology
At the onset of infection in osteomyelitis, vascular changes occur that compromise

bone irrigation. If the infection is not eradicated, the bone tissue necroses and allows
the development of sequestration, a collection of devitalized tissue that acts as struc-
tural support for the biofilm [60, 62]. The necrotic bone is resorbed, taking some
weeks for cancellous bone and some months for cortical bone. The granulatory tis-
sue with its inflammatory cells is responsible for the destruction of the infected bone
tissue. The microorganisms spread through the cavity and new bone formation
occurs around the sequestration, known as involucre, which is an irregular bone tis-
sue with sinuous paths, which may increase in density and thickness over time [67].
3.6 Diagnosis
Diagnosis is not simple; there is no gold standard at present. It is based on a good

clinical examination, laboratory studies, histological study and tissue culture,
and imaging [60, 62]. Symptoms in chronic osteomyelitis are variable and are
not always evident given a high percentage of subclinical infection. Some of the
symptoms are localized chronic pain and low-grade fever, although the latter is
less frequent [67, 68]. In addition, enlargement, erythema, and fistulas with dis-
charge may be present. The physician must have a high clinical suspicion and be
very detailed. Special attention should be paid to the history of previous trauma
such as exposed fracture or the presence of implants. It should also be considered
in those patients who present delayed consolidation times or directly an atrophic
nonunion. A detailed characterization of the initial trauma and type of fracture,
number of surgical interventions and complications in its evolution that could
lead to an infectious etiology should be made. Additionally, it is essential to col-
lect a complete history of morbid antecedents such as chronic pathologies,
immunosuppression, vascular disease, history of radiotherapy, smoking and
medications of habitual use. Acute osteomyelitis, particularly in the pediatric
population, more frequently presents systemic symptoms such as fever, chills,
sweating and more intense pain [60].
3.7 Laboratory Studies
Unfortunately, no isolated blood test can independently diagnose osteomyelitis.

Even in patients with severe local and systemic signs of osteomyelitis, blood test
may not show a lot of alterations in almost half of the patients [69]. This is particu-
larly frequent in patients with diabetes mellitus due peripheral arterial disease and
leukocyte dysfunction, or in patients with any kind of immunosuppression. Even
considering this fact, blood test are useful because elevated inflammatory markers
predict worse clinical outcomes of treatment [70]. Also, they are useful in monitor-
ing treatment of osteomyelitis. Combination of laboratory test work better to help
diagnose in osteomyelitis. Additional to inflammatory blood tests, it is recommend-
able to obtain blood albumin, pre-albumin, 25OH vitamin D, glucose, and creati-
nine, to optimize nutritional status of the patient and monitor renal function.
3.7.1 Traditional Blood Tests
If acute tibial osteomyelitis is suspected, blood analysis should include complete

blood-cell count, erythrocyte sedimentation rate (ESR), and C-reactive protein
(CRP). Unfortunately, elevation in white blood cell count (WBC), ESR y CRP are
absent in up to half of the patient [69].
White Blood Cell Count
WBC can be elevated in the context of acute bone infection, but sensitivity and speci-
ficity of leukocytosis are low to moderate. In patients with diabetes mellitus, sensi-
tivity for diagnosis of osteomyelitis of elevated WBC count was low as 14% [71].
Combining patient and wound characteristics in patients with diabetic foot osteomy-
elitis, with WBC count higher than 11,000/mL and neutrophil percentage higher
than 70%, improved diagnostic accuracy for osteomyelitis [72].
C-reactive Protein
C-reactive protein (CRP) is elevated in acute and chronic inflammatory conditions,

but it lack specificity to diagnose osteomyelitis. Inflammatory tests are usually high
in osteomyelitis and soft tissue infection, and they tend to be higher, as well as CRP,
in osteomyelitis [73]. Multiple studies had been trying to establish a cut-off value
indicative of a higher probability of osteomyelitis. One case-control study in 54
diabetic patients with infected ulcers study by Fleischer et al. found that using a
cut-off level duo 3.2 mg/dL, CRP was the most sensitive and accurate single marker
for osteomyelitis, identifying an impressive 85% of the subjects with underlying
bone infection [72]. Other study by Jeandrot et al. showed that a CRP cut-off value
of 1.7 mg/cl had a sensitivity of 72.7%, a specificity of 100% and a negative predic-
tive value of 79.3% [74].
In general cases, CRP lacks specificity; it can be increased in autoimmune dis-
eases, viral infections, tumors, obesity, and other inflammatory conditions.
CRP had a rapid response to the beginning and the relapse of infection. Therefore,
the peak of CRP can be expected 2 days after the worse clinical setting of infection.
In the monitoring of the response to osteomyelitis treatment, CRP had the advan-
tage of a quicker response than other markers such as ESR, and it should normalize
by day 7 of treatment [74].
Erythrocyte Sedimentation Rate
Erythrocyte sedimentation rate (ESR) is the rate at which erythrocytes settle down
when suspended in a vertical tube. ESR is a reflect of blood plasma viscosity, which
depend on the amount of different acute phase reactants, such as fibrinogen, among
others. ESR will elevate in the context of a bone or soft tissue infection. It cannot
differentiate between both scenarios, but ESR usually tend to be higher in patients
with osteomyelitis than in patients with soft tissue infection [73, 75, 76]. Multiple
studies had been trying to define a cut-off value of a higher probability of osteomy-
elitis, and to define sensitivity and specificity. Some of them proposed an ESR
greater than 70 mm/h as cut-off value, finding a specificity of 100%, but with low
sensitivities ranging from 28% to 50% [77–79]. In a study of 46 patients hospital-
ized with diabetic foot lesions, Ertugrul et al. showed that an ESR ≥60 mm/h had a
sensitivity of 92%, but a specificity of 68%; on the other side, an ESR ≥80% had a
sensitivity of 71% but a very high specificity (91%). Combining an ESR ≥65 mm/h
with a wound size ≥2 cm2, had a sensitivity of 83%, a specificity of 77%, a positive
predictive value of 83% and a negative predictive value of 81% in the diagnosis of
osteomyelitis [75]. In a study including 61 patient with untreated foot infection (34
with soft-tissue infection and 27 with osteomyelitis), Michail et al. used an ESR
≥67 mm/h as the optimal cut-off value, with a sensitivity of 84%, a specificity of
75%, a positive predictive value of 71% and a negative predictive value of 86% [73].
As the same situation with CRP, ESR alone is not an optimal predictor of osteomy-
elitis. It can be elevated in a series of other medical conditions, such as obesity,
advanced age, and anemia. ESR over 100 mm/h can be observed in autoimmune
diseases, cancer disease, chronic renal disease, and severe soft tissue infection with-
out osteomyelitis, among other conditions [80, 81]. If ESR is used, it must be com-
bined with other parameters to improve sensitivity and specificity to diagnose
osteomyelitis.
When used to monitor response to osteomyelitis treatment, is key to remember
that its lowering is slow. ESR can take up to 3 months to normalize.
3.7.2 New Diagnostic Tools
Serum Procalcitonin
Procalcitonin (PCT) is a protein produced by parafollicular cells of the thyroid

gland and neuroendocrine cells of lung and intestines. In healthy patients, serum
PCT levels are low (<0.11 ng/mL), but it increases rapidly in patients with
severe bacterial or fungal infections, but not in patient with viral infections or
with non-infectious inflammatory conditions. In a study of 93 patient with
infected and non-infected foot ulcers, the association between CRP and procal-
citonin resulted in a significantly more effective determination between infected
and non-infected foot ulcers [74]. In a meta-analysis to evaluate the accuracy of
determination of procalcitonin and CRP levels for the diagnosis of bacterial
infection in hospitalized patients, procalcitonin was more sensitive (88%) and
more specific (81%) than CRP for differentiating bacterial from non-infective
causes of inflammation [82]. There are some studies that try to determinate the
optimal cut-off values for procalcitonin to diagnose osteomyelitis. In a study of
82 patients with suspected acute osteomyelitis and septic arthritis, procalcitonin
at a cut-off value of 0.4 ng/mL was 85.2% sensitive and 87.3% specific in diag-
nosing septic arthritis and acute osteomyelitis; conventional cut-off value of
0.5 ng/mL had a sensitivity of 66.7% and a specificity of 91% [83]. In another
study in 49 patients with diabetic foot ulcers, it was determined that procalcito-
nin, at a cut-off value of 0.08 ng/mL had 77% sensitivity and 100% specificity,
and it was a better diagnostic marker than WBC count, ESR and CRP for dia-
betic foot infection [84].
As CRP levels, procalcitonin has a fast elevation with peak values at 2 days form
the onset of acute bone infection. It normalizes its values quickly with proper treat-
ment, usually around 7 days from the beginning of treatment, making it a good
marker of response to treatment.
3.7.3 Blood Cultures
Peripheral blood cultures must be obtained when osteomyelitis is suspected. As in

septic arthritis, they must be taken before administration of an antibiotic treatment
to enhance the chance of obtaining causative microorganism [22]. Although often
are negative, blood cultures could be positive in up to 22% of the patients with
hematogenous osteomyelitis, that is more frequent to see in children [85]. Patients
with bone infection associated with skin tissue infections had positive blood cul-
tures in 19% of cases; patients with osteosynthesis and open or closed fracture had
positive blood cultures in 7% of cases. Only 41% of patients with bacteremia pre-
sented fever; this might suggest that blood cultures should be performed in patients
with peripheral bone infection irrespective of the presence of fever [86].
3.8 Bone Biopsy
Histologic analysis of bone samples are usually considered as the reference stan-
dard in osteomyelitis diagnosis [69, 87–90]. But there are various problems with
bone biopsy that had come into question in published literature [90]:
1. Operational definition of what constitutes a “positive” bone biopsy to diagnose
osteomyelitis has not reached consensus.
2. Histologic examination has a relative subjective criterion for diagnosing osteo-
myelitis. One study to quantify the reliability of the histopathologic diagnosis of
diabetic foot osteomyelitis from 39 consecutive bone tissue specimens from four
certified and experienced pathologists, showed that there was complete agree-
ment of osteomyelitis among all four pathologists in only 13 of the 39 specimens
(33.33%), with a corresponding kappa coefficient of 0.31. A situation of clini-
cally significant disagreement in at least one pathologist diagnoses “no evidence
of osteomyelitis,” but at least one other pathologist diagnosed “findings consis-
tent with osteomyelitis,” occurred in 16 of 39 specimens (41.03%). Also, only
50% of pathologist agreed between acute vs chronic osteomyelitis. Considering
these low inter-observer agreement results, the authors recommended that bone
biopsy should not be the “reference standard” for diagnosing diabetic osteomy-
elitis, and emphasize the need for a more comprehensive diagnostic protocol for
diabetic foot osteomyelitis [88]. In another matched case control study of 44
bone specimens from diabetic patients surgically treated for foot infection,
Weiner at al found that a positive microbiologic and negative histologic result
was just as likely as a negative microbiologic and positive histologic result
(p > 0.05) [89]. On the other side, a study in 165 diabetic patients with foot
ulcers who underwent surgery for bone infection, using a well-defined criteria
for diagnose acute, chronic and chronic acute osteomyelitis endorsed an excel-
lent interobserver reliability ratings, with kappa coefficient of 0.97, 0.95, and
0.92%, respectively [91].
Considering these facts, additional studies and experts’ agreement to determine

method to improve histopathologic diagnosis of osteomyelitis are required. Despite
these drawbacks of bone biopsies, higher quality studies evaluating the diagnosis of
osteomyelitis continue to consider bone biopsy as the gold standard to determine
results. More concerning, practice guidelines for diabetic foot infections and other
type of osteomyelitis recommend using bone culture and/or histology to confirm
diagnose of osteomyelitis. The Infectious Disease Society of America suggests that
osteomyelitis is optimally defined by histology and culture [50], and the International
Working Group on the Diabetic Foot states that “definitive diagnosis usually
requires positive results on microbiological (and, optimally, histological) examina-
tion” [88].
On the other hand, there is a lot of studies on osteomyelitis that do not use bone
biopsy to verify the diagnosis to bone infection. They use a combination of images
(radiographs, magnetic resonance images, scintigraphy), probe to bone test, clinical
history and physical exam as diagnostic criteria to define cases of osteomyelitis
[92–94]. The problem is that these other studies are not perfect, too. Radiographs
would miss subtle cases of acute osteomyelitis before radiographic changes are
detected (it requires cortical destruction or 30–50% of cancellous bone destruction
to be noted in radiographs). Magnetic resonance images (MRI) and single-photon
emission computed tomography (SPECT) are more sensitive to detect early bone
changes in infection, but rates of false positive results are higher (20.6% for MRI
and 26.9% for SPECT); this can lead to over treatment of patients [95].
3.9 Bone Cultures
Treatment failure in osteomyelitis is associated with poor functional outcomes,

increased risk of limb amputation, reduced quality of life and major financial costs
[96, 97]. Empirical antibiotic treatment has been proven unsuccessful due high fre-
quency of antibiotic resistance. In an observational study of 80 patients with dia-
betic foot ulcers and clinically suspected osteomyelitis that were given empiric
antibiotics prescribed by general practitioners, bone cultures in 56 patients (77.8%),
displayed bacterial resistance to the antibiotic that they were taken [98]. Therefore,
identification of pathogen agents and their antibiotic susceptibility is of paramount
importance in osteomyelitis. Microbiological diagnosis allows for specific antibi-
otic therapy, improving outcomes and reducing antibiotic resistance [99–101].
Superficial swab cultures in infected wounds are a common practice, but they are
very inaccurate, due colonization with skin flora [86]. Moreover, cultures of overly-
ing soft tissue infection do not correlate with the bacteria involved in bone infection.
In a study of patients with episodes of foot osteomyelitis by Senneville et al., results
of bone and superficial swab cultures were identical in only 17.4% of the patients,
and bacteria present in bone were isolated from the corresponding superficial swab
culture in 30.4% of the patients [102]. Even when comparing cultures from bone
and deep soft tissue specimens, only 36% bacteria grown from soft tissue cultures
matched the corresponding bone specimen exactly [103]. Hence, recommendation

is to take cultures from bone specimens.
Although gram stain and standard bone cultures are relatively inexpensive,
widely available, and simple to take and process, they had a suboptimal microbio-
logical yield, with series showing as low as 61–90% of pathogen identification in
osteoarticular infection in the best of the cases [102, 104]. We must make a point
here; conventional aerobic cultures in osteomyelitis can leave almost 40% of the
patients without a microbiological diagnosis. This low yield of detection depends
on multiple factors:
• False negative culture due to ongoing antibiotic treatment.
• Usual “contaminant” bacteria from skin flora may cooperate with aggressive
bacteria creating biofilm, making them difficult to culture [105].
• Usual aerobic culture media can detect less obligate anaerobic bacteria than
molecular studies. Usual cultures had a 25–39% detection yield of obligate
anaerobic bacteria, while DNA sequencing testing can detect 87.5–90% of them
[106, 107].
Guidelines had been proposed in the literature to take suitable cultures, hence,
enhancing yield of bacteria detection. These recommendations were made for dia-
betic foot infections, but they are applicable for tibial osteomyelitis [69, 87,
108, 109]:
• Delay beginning of antibiotic treatment or discontinue it for at least a few days
(ideally 2 weeks) before taking bone culture sample, to avoid false-negative cul-
tures. Although this is theoretically sensible, there are some reports from studies
of various types of bone infection suggesting that having receiving antibiotic
therapy before a bone culture does not appear to reduce the percentage go posi-
tive cultures or time to culture positivity [110–113]. Antimicrobial therapy
should not be withheld in patients with impending sepsis or hemodynamic insta-
bility [114].
• Prefer bone tissue to take culture sample. Superficial and deep tissue samples are
not optimal [86, 102, 103].
• Obtain bone tissue samples in an aseptic manner (percutaneously or per-
operative, not through a chronic wound). This provides the most accurate assess-
ment of true pathogens. A prospective direct comparison of 46 paired per-wound
and transcutaneous bone biopsies in patients with suspected diabetic foot osteo-
myelitis found that results were identical in only 42% [110].
• If bone tissue samples had to be taken through a chronic wound, it must be done
after cleansing and debriding the wound. Avoid using fluids with antibacterial
substances in doing the cleansing.
• Prefer to take bone samples through intact skin, either doing a percutaneous
technique or using an open approach.
• Send the collected bone sample promptly to the laboratory.
• Use an appropriate sterile container, to avoid contamination or inappropriate
manipulation.
Better identification of bacteria enables for a more specific antibiotic treatment,

thus avoiding empiric antibiotic treatment. This reduces the risk of antibiotic resis-
tance and reduces treatment costs. Additional benefits of a specific antibiotic treat-
ment are reduced failure of bone infection eradication and hence, better clinical
outcomes.
As conventional aerobic bone cultures had a low sensitivity, some efforts had
been made to improve bone culture detection yield. One work showed that synovial
fluid culture seeded in pediatric blood culture bottles (PBCB) had a higher sensitiv-
ity (88%) than samples seeded in conventional aerobic culture bottles (60%). Based
on this, one study compared paired bone tissue samples (Fig. 4) from a prospective
series of 107 patients with a diagnosis of osteomyelitis of the foot and ankle accord-
ing to clinical, laboratory and imaging findings. One of the samples was processed
using conventional aerobic culture method. The other bone sample was morselized
into small fragments with a gouge, under sterile conditions in the operating room
(Fig. 5), and then diluted in 10 mL of physiological saline solution in a sterile con-
tainer until a homogeneous mix was obtained (Fig. 6). This mix was introduced in
sterile fashion into a 20 mL syringe and then injected with a 14G catheter intro a
PBCB (BacT/ALERT ® PF Plus, bioMérieux, Inc, Durham, North Carolina)
Fig. 4 Samples of bone

tissue representative of
osteomyelitis site were
obtained
Fig. 5 Processing of the

samples. The fragments of
the bone sample were
morselized by sterile
means during surgery
Fig. 6 Fragments were

diluted in 10 mL of
physiological saline
solution in a sterile
container until a
homogeneous mix was
obtained
a b
Fig. 7 (a) This mixture was introduced in a sterile fashion into a 20 mL syringe. (b) The mixture
was injected through a 14G catheter into an aerobic pediatric culture medium bottle
(Fig. 7a, b). Sixty-three samples corresponded to diabetic foot infection and 44 to
non-diabetic osteomyelitis. With the conventional culture method, only 60.7% of
the samples yielded at least one bacterium, while with the new culture method,
97.2% of the samples had at least one identified bacterium; this difference was sig-
nificant (p < 0.001). An interesting fact was the culture in PBCB detected additional
bacterial species in 28 of 65 samples (43.1%) with positive conventional culture
method. Additionally, bone cultures in PBCB allowed significantly better identifica-
tion yield of bacteria detection in non-diabetic and in diabetic osteomyelitis of the
foot and ankle. The samples processed in PBCB significantly detected higher mean
bacterial species than de conventional culture method (1.67 ± 0.92 vs 1.05 ± 10.3;
p < 0.01). A possible explanation of higher bacterial identification yield using bone
samples in PBCB is that this is a nutritional enriched medium, containing polymeric
beads with the capacity of adsorption of antibiotics [115].
Anaerobic cultures, cultures for mycobacteria and fungi should be performed in
patients with clinical and epidemiological features supporting a suspicion for these
etiologies Histopathological analysis is essential for confirming or excluding the
diagnosis of infection. Visualization of granulomatous lesions with positive Ziehl–
Neelsen staining may allow the diagnosis of mycobacterial infection (e.g.,
Mycobacterium tuberculosis) [114].
Despite optimal specimen collection and processing, conventional culture-based

techniques have a bias, selecting bacteria species that grow under standard nutri-
tional conditions of the microbiology laboratory, but potentially not the most clini-
cally important nor the most abundant bacteria on the bone infection site.
Conventional cultures commonly fail to identify anaerobic bacteria or fastidious
(very slow growing) bacteria [87].
Cultures of marginal bone in patients undergoing limb amputation or segmental
bone resection for infection can provide useful information. A negative marginal
bone culture may result in deciding a shorter course of antibiotic therapy to treat
soft tissue infection, opposed to a prolonged treatment of a bone infection. This
approach is very useful, because it can avoid potential adverse effects of prolonged
antibiotics, also leading to lower costs and abbreviated hospitalization [116]. Bone
excision is adequate and successful if resection of all infected bone is accomplished.
Positivity of marginal bone cultures depends directly on the distance of bone resec-
tion margin from the border of the area of osteomyelitis. Visual confirmation of
“healthy bone” with adequate bleeding (“paprika sign” or punctuate bleeding of
bone edges on resection) is a clinical but subjective evaluation for establishing suc-
cessful resection of osteomyelitis. Retrospective studies of cultures of surgical mar-
gins using this intraoperative feature doing resections in diabetic foot osteomyelitis
showed between 35.14% and 40.7% of positive marginal bone culture, which is
unacceptable [117, 118]. Positive bone culture of marginal bone result in increased
morbidity and mortality. In a study from Atway et al., 81% of the patients with posi-
tive bone marginal cultures had poor outcomes compared with 25% poor outcomes
for the group with negative culture at residual bone margins [118].
Some studies based the preoperative planning of resection with magnetic reso-
nance imaging of the affected area. In a study by Bernstein et al. in 24 osteomyelitis
positive metatarsals, bone resection done 5 mm proximal to the area of osteomyeli-
tis (low intensity signals on T1-weighted images) resulted in 50% of positive proxi-
mal margin bone culture. After increasing resection margin to 10 mm, there was
found to be a decrease in positive proximal margin bone culture (9%), reducing the
risk of residual osteomyelitis [119]. Other study from Simpson et al. in a series of
50 patients with chronic osteomyelitis of different sites, showed that wide resection
with a clearance margin of 5 mm or more was linked to no recurrence of infection,
while marginal resection, with a clearance margin of less than 5 mm, had 28% of
recurrence [120].
3.10 Molecular Microbiology Diagnostic Methods
New molecular DNA based techniques that are culture-independent has identified
limitations of traditional culture-dependent methods. Conventional culture tech-
niques (e.g., agar plates), can identify a small percentage of known microorganism
that can grow on common media, limited also by the time required for bacteria to
grow [107].
Molecular diagnostics methods had in general higher sensitivity to detect bacte-

ria. They could be done on patients with ongoing antibiotic treatment, not altering
its sensitivity.
Polymerase Chain Reaction (PCR) This is a method to amplify a genomic region
of interest. When followed by DNA sequencing, the abundance and genetic compo-
sition of a gene of interest can be determined. PCR amplify and sequence the small
subunit ribosomal RNA (16S rRNA) gene, a highly conserved gene present in all
prokaryotes (bacteria) but not eukaryotes (e.g., humans). The 16S rRNA gene is an
ideal target for bacterial analysis given that it possesses nine hypervariable regions
that have considerable sequence diversity between bacterial taxa. The hypervari-
able regions are bordered by stretches of sequences that are highly conserved
between bacteria, ideal for designing universal and species-specific primers to
amplify the hypervariable regions by PCR. This has revealed a vastly more com-
plex array of bacterial communities than those identified by traditional culture-
dependent methods [108].
Broad-range polymerase chain reaction (PCR) followed by sequencing, a molec-
ular method of diagnosis that allows for specific bacterial identification, has also
been used to identify pathogens in bone and joint infections [121, 122]. This tech-
nique has reported a high yield of identifying pathogen agents producing bone
infection in up to 96.7% of cases [104].
Molecular diagnostic methods had some disadvantages:
• They have proneness to contamination.
• They cannot distinguish between genetic material of alive and dead bacteria.
• They cannot deliver information on antibiotic susceptibility and resistance.
• They have high costs.
• They are not available everywhere.
• They depend on limited number of available primers.
For best cost-effectiveness, PCR test should be done for culture negative ortho-
pedic infections [109].
3.11 Imaging
The usual techniques for the diagnosis of osteomyelitis include radiography, com-
puted tomography, magnetic resonance imaging and less frequently radionucleotide
labeled scans. Usually more than one type of study modality is required for an
adequate diagnosis and surgical planning, being often difficult to determine the
most appropriate alternative, especially if there are bone alterations or defects due
to the initial trauma or presence of metallic implants.
In most cases the first tool to be used is radiography due to its low cost. Serial
evaluation of radiographic evolution over time provides a good approximation of
the overall healing process of a fracture but has low sensitivity for detecting changes
caused by chronic infection, especially in cases of post-traumatic deformities or

presence of implants. Tumeh et al. [123] in a radiographic analysis of 104 patients
with active osteomyelitis, found a sensitivity and specificity of 14 and 70%, respec-
tively, the only reliable finding being the presence of bone sequestrations.
Radiographic changes are visible approximately 2 weeks after the onset of the
infection process. Classic signs include periosteal reaction and osteopenia [62]. As
the infection progresses, the radiographic signs in order of appearance are soft tis-
sue enlargement, periostitis, osteolysis and radiolucencies, circumferential sclerosis
and sinuous tracts [124] (Fig. 8).
Computed tomography shows in greater detail the bone anatomy, besides being
a validated instrument with good sensitivity for the evaluation of the consolidation
process [125]. In addition, it is useful in showing defects and helps in preoperative
planning since it clearly identifies areas of sequestration and devitalized bone tissue.
Regarding the diagnosis of chronic osteomyelitis, studies with a low number of
patients have shown sensitivity of 67% and specificity of 50% for its diagnosis
[126]. Currently there are techniques for computed tomography with artifact reduc-
tion that have proven to be quite effective [127], allowing visualization of the bone
anatomy even in the presence of metallic elements. For this reason, its use in con-
junction with the administration of contrast medium becomes especially relevant in
those cases with suspected osteomyelitis in which implants are present, since the
image obtained by magnetic nuclear resonance may be very distorted.
Magnetic resonance imaging is recognized as a useful tool in the diagnosis of
bone infections due to its high anatomical resolution and good capacity to detect
signal alterations in the bone marrow and surrounding soft tissues [56, 128].
However, in cases of post-traumatic osteomyelitis, the presence of metallic
implants, fibrous inflammatory scar tissue and bone marrow edema can cause
difficulties in its interpretation [129]. The use of gadolinium as contrast medium
has made it possible to differentiate between an active infection and a fibrovas-
cular scar or artifact [56]. Comparative studies with other techniques have
Fig. 8 AP and lateral

radiograph of the ankle
with radiographic changes
due to chronic
osteomyelitis: osteopenia,
peripheral sclerosis,
periosteal reaction, and
sequestration
shown sensitivity for MRI associated with the use of gadolinium close to 100%,
but with a specificity of only 60% [128]. Typically, osteomyelitis is observed as
a localized decrease of the signal in the bone marrow in T1 and an increase in
T2 [130], which allows differentiating between osteitis and a chronic infectious
process with devitalization of the bone tissue (Fig. 9). In osteitis there is an
a b
Fig. 9 Coronal MRI coronal section with a partial infected tibial joint. (a) T1 sequence; signal
hypo intensity of the bone marrow is observed. (b) STIR sequence; bone marrow edema due to
inflammatory changes and associated medial fistula
increase of signal in T2 due to edema, without correlation with changes in T1

due to the preservation of the bone structure [130]. Sinuous tracts or fistulas are
also well visualized although they usually require the use of gadolinium [124].
In addition to diagnosis, magnetic resonance imaging is useful in delimiting
infected bone tissue, so it is important in preoperative planning and in determin-
ing the amount of tissue that needs to be resected to obtain infection-free
margins.
Diagnostic nuclear medicine studies, including scintigraphy with different tech-
niques and radiopharmaceuticals and PET with [18F] FDG (18F-fluorodeoxyglucose
positron emission tomography) associated or not with computed tomography
(PECT/CT) have been used with variable results for this type of clinical situations
[131]. Conventional monoplanar scintigraphy or SPECT (single-photon emission
computed tomography) are characterized by acceptable sensitivity, but low specific-
ity. In addition, their low anatomical resolution makes interpretation of the results
difficult. Studies performed with Technetium 99 scintigraphy have shown sensitivi-
ties close to 100%, but with a specificity of 25%, so that a positive result is of little
use [132]. PET/CT with [18F] FDG has shown good results as a screening for fever
of unknown origin of infectious cause with adequate precision as to its localization
[133, 134]. In the study of chronic osteomyelitis, it has shown high sensitivity and
specificity, associated with good anatomical correlation, being able to differentiate
bone involvement from soft tissue involvement and little artifact with metallic
implants [135, 136].
Termaat et al. [126] carried out a systematic review and meta-analysis of a total
of 23 studies on the usefulness of different imaging techniques in the diagnosis of
chronic osteomyelitis. PET/CT had the highest sensitivity (96%), followed by mag-
netic resonance imaging (84%), bone scintigraphy (82%) and leukocyte-labeled
scintigraphy (61%). The specificity of the same techniques was 91, 60, 25, and 77%,
respectively. Demirev et al. [137] retrospectively analyzed the results of 26 patients
with suspected osteomyelitis in whom MRI and [18F] FDG PET/CT were per-
formed simultaneously. With both methods good results were achieved in the diag-
nosis of osteomyelitis, obtaining the PET/CT with [18F] FDG a sensitivity of 82%,
with a specificity of 90% and accuracy of 85%. Magnetic resonance imaging had a
sensitivity of 88%, specificity of 70% and final accuracy of 81%. Despite the slight
differences in the results, both approaches were shown to be effective and comple-
mentary, noting that their sequential use in indeterminate cases would have led to a
definitive result in all but one case.
Apparently, PET/CT with [18F] FDG is less influenced by signal increases
observed by degenerative changes, bone edema, ischemia and fractures [131], how-
ever, the anatomical detail of MRI and its availability for use, continue to make it a
first line tool for the study of musculoskeletal infections.
3.12 Treatment
3.12.1 Generalities
In general terms, the treatment consists of eradicating the infection by resection of

all the infected tissue and the complementary use of antibiotics, to later achieve
consolidation or reconstruction of the affected segment in a second stage [60, 68].
After a complete study with laboratory tests and imaging, factors specific to the
affected segment, the patient and his socioeconomic environment must be consid-
ered. Decision-making is often difficult, multiple aspects must be considered and it
must be done together with the patient, since maximum adherence to a treatment
that is often long, costly, and not free of complications is required. The severity and
prognosis must be explained from the beginning, always bearing in mind the pos-
sibility of amputation. An adequate management involves the integration of multi-
ple specialties such as traumatology, plastic surgery, infectious diseases, internal
medicine, physiatry and psychiatry.
With respect to the patient, it is essential to evaluate the general condition,
comorbidities and habits that may reduce the probability of successful treatment.
The Cierny-Mader classification [51] considers these aspects and guides the
decision-making process, integrating the patient’s physiological condition with the
extent of bone involvement.
In relation to the affected bone segment, the location and extent of the involve-
ment must be evaluated, which determines the therapeutic alternatives. For exam-
ple, a location close to the knee or ankle may limit the stabilization possibilities to
a circular external fixator. Attention should be paid to the soft tissues, as many
patients have undergone multiple previous procedures, presenting extensive areas of
scar tissue, deep plane adhesions and retractions that will condition the possible
approach areas. The eradication of the infection must include collections and fistu-
lous tracts, and there may remain defects of skin coverage that must be foreseen.
The classification according to anatomical involvement proposed by Cierny-Mader
[51] guides local management. Medullary osteomyelitis (type I) associated with a
consolidated fracture requires the removal of implants and reaming of the canal. For
superficial osteomyelitis (II) associated with the presence of consolidated fracture
and plaque, the treatment consists of surgical cleaning, resection of the infected
cortical bone up to bleeding tissue and removal of the implant. In type I and II there
is bone stability, so reconstruction procedures are not necessary. In localized osteo-
myelitis (III), resection of the devitalized bone is required, which produces a bone
defect that does not require stabilization. In contrast, diffuse osteomyelitis (type IV)
there is circumferential involvement of the bone, resulting in an intercalary defect
or infected nonunion.
Faced with type IV osteomyelitis, the two main treatment strategies are limb
salvage or amputation. The latter is an appropriate alternative in case of extensive
bone defects, poor soft tissue coverage, neurovascular involvement of the limb, low
functionality, or presence of significant comorbidities. Before deciding on limb sal-
vage, the patient should be clearly informed of the possible need for multiple proce-
dures, prolonged treatment and rehabilitation, and the eventual failure with the need
for subsequent amputation. If limb salvage is chosen, the stages consist of debride-
ment and resection, stabilization, systemic and local antibiotics, soft tissue coverage
and management of the segmental bone defect by means of reconstruction proce-
dures [68].
3.13 First Stage: Eradication of the Infection
3.13.1 Radical Resection
The extent of surgical resection must be planned prior to surgery, as well as the need
for soft tissue coverage. Traditionally, radical resection consists of the removal of all
devitalized bone tissue until margins with bleeding bone are left, which is observed
macroscopically by a characteristic punctiform bleeding called Paprika’s sign.
Simultaneously, all contaminated metallic implants that perpetuate the infection
through bacterial biofilm should be removed.
Inadequate resection inevitably leads to recurrence of infection. Simpson et al.
[120] demonstrated in a prospective study the importance of wide resection to
healthy tissue margins to decrease recurrence of infection. In their prospective study
of 40 patients with chronic osteomyelitis, those who had wide resection over 5 mm
of healthy tissue did not present recurrence. The group with marginal resection less
than 5 mm had a 28% recurrence at 1 year, while all those with intralesional debride-
ment had recurrence. In an attempt to decrease the rate of positive margins described
in the literature to between 35% and 40%, Bernstein et al. [119] conducted a study
in which they determined the amount of resection necessary based on preoperative
MRI. A resection of 0.5 cm proximal to the T1 signal change had 50% positive
margins, while with a 1 cm resection the positivity dropped to 9%.
Special mention requires resection and biopsy of the drainage fistula, since
0.2–1.6% of patients with chronic fistulas due to osteomyelitis may develop squa-
mous cell carcinoma (Majorlin’s ulcer) [138].
3.14 Systemic Antibiotherapy
Antibiotic treatment in chronic osteomyelitis should be considered as a complemen-

tary therapy to surgical treatment and should not be considered in isolation since it
is not curative.
The concentration of an antibiotic in healthy bone reaches only 20% of the

plasma level [139]. In the case of infected bone, the concentration is considerably
lower due to fibrosis and soft tissue damage, devitalized and necrotic tissue and the
presence of biofilms, so they must be resected, or the infection will persist.
Traditionally, intravenous treatment has been suggested for 4–6 weeks followed
by another oral course for 4–6 weeks more. However, there is no consensus regard-
ing the duration of intravenous treatment. The 4 weeks may have a basis in studies
that have shown that it corresponds to the time of bone revascularization after curet-
tage [62]. However, studies have been published with favorable results with short-
ened intravenous therapy followed by an oral schedule adjusted to the antibiogram
[140, 141].
In a prospective multicenter randomized study, Rombach et al. [142] demon-
strated that oral antibiotic therapy is not inferior to intravenous therapy when used
during the first 6 weeks in the treatment of chronic osteomyelitis using treatment
failure at 1 year as the primary outcome. Additionally, an update of a Cochrane
review [61] regarding the route of antibiotic administration concluded that it does
not affect the rate of disease remission if the bacteria causing the infection are sensi-
tive to the antibiotic used.
3.15 Local Antibiotherapy
To achieve better antibiotic concentrations at the site of infection and to occupy the
dead space left after resection, polymethylmethacrylate (PMMA) spacers mixed
with antibiotics have been used. The configuration can be beads or cylindrical rods,
and the larger the contact surface, the greater the effectiveness, so the configuration
in small-sized beads or fenestrated rods seems to be the one of choice [143–145].
The spacers should be kept in situ for at least 6–8 weeks, time in which the local
concentration of antibiotic begins to decay, and should be withdrawn later; however,
there are reports of cases in which they have been abandoned for years without
harmful effects [146]. Ideally, thermostable antibiotics adjusted by antibiogram
should be used, the most commonly used being vancomycin, gentamicin, or
tobramycin.
The effectiveness of this approach has been demonstrated in animal models and
also in humans [140]. In a rabbit model of chronic osteomyelitis, the frequency of
infection control with gentamicin beads was 79% versus 92% for intravenous anti-
biotic therapy with ceftriaxone. When both therapies were used together, they
achieved 100% infection control [147].
In a clinical trial, Calhoun et al. [67] compared the use of parenteral antibiotic
therapy for 4 weeks with the use of antibiotic beads plus a short course of 2–5 days
of perioperative antibiotic, finding a frequency of infection control of 83 and 89%,
respectively.
3.16 Bone Stabilization
Once the resection has been performed, local antibiotics have been administered
and adequate soft tissue coverage has been achieved, the segment must be stabi-
lized. For this there are multiple alternatives for external fixation, and the choice of
the particular type will depend on the location, size of the defect and proximity to
joints, presence of angular deformities, shortening and the reconstruction technique
chosen. Reconstruction techniques will be discussed in another chapter.
3.17 Conclusion
Chronic osteomyelitis of the tibia in adults generally occurs as a complication sec-

ondary to a traumatic injury such as an exposed fracture or surgical treatment with
the use of metallic implants. It is a devastating complication because of its long
treatment times, need for multiple surgical interventions, high economic costs, and
risk of limb loss. It is the role of the orthopedic surgeon to prevent this type of com-
plications, as well as to make an accurate and timely diagnosis. A two-stage treat-
ment, achieving the eradication of the infection as the first objective, is fundamental
for the success of reconstructive procedures.
References
1. Vispo Seara JL, Barthel T, Schmitz H, Eulert J. Arthroscopic treatment of septic joints: prog-
nostic factors. Arch Orthop Trauma Surg. 2002;122(4):204–11. Epub 2002 Apr 6.
2. Newman JH. Review of septic arthritis throughout the antibiotic era. Ann Rheum Dis.
1976;35(3):198–205.
3. Stutz G, Kuster MS, Kleinstück F, Gächter A. Arthroscopic management of septic arthritis:
stages of infection and results. Knee Surg Sports Traumatol Arthrosc. 2000;8(5):270–4.
4. Esterhai JL Jr, Gelb I. Adult septic arthritis. Orthop Clin North Am. 1991;22(3):503–14.
5. Kang SN, Sanghera T, Mangwani J, Paterson JM, Ramachandran M. The management of
septic arthritis in children: systematic review of the English language literature. J Bone Joint
Surg Br. 2009;91(9):1127–33.
6. Shadrick D, Mendicino RW, Catanzariti AR. Ankle joint sepsis with subsequent osteomy-
elitis in an adult patient without identifiable etiologies: a case report. J Foot Ankle Surg.
2011;50(3):354–60. Epub 2011 Apr 2.
7. Mankovecky MR, Roukis TS. Arthroscopic synovectomy, irrigation, and debridement for
treatment of septic ankle arthrosis: a systematic review and case series. J Foot Ankle Surg.
2014;53(5):615–9. Epub 2013 Dec 15.
8. Boffeli TJ, Thompson JC. Arthroscopic management of the septic ankle joint: case report of
a stage-guided treatment. J Foot Ankle Surg. 2013;52(1):113–7. Epub 2012 Oct 23.
9. Weston V, Coakley G; British Society for Rheumatology (BSR) Standards, Guidelines and
Audit Working Group; British Society for Antimicrobial Chemotherapy; British Orthopaedic
Association; Royal College of General Practitioners; British Health Professionals in
Rheumatology. Guideline for the management of the hot swollen joint in adults with a partic-
ular focus on septic arthritis. J Antimicrob Chemother. 2006;58(3):492–3. Epub 2006 Jul 19.
10. Mathews CJ, Weston VC, Jones A, Field M, Coakley G. Bacterial septic arthritis in adults.
Lancet. 2010;375(9717):846–55.
11. Goldenberg DL. Septic arthritis. Lancet. 1998;351(9097):197–202.
12. Gupta MN, Sturrock RD, Field M. A prospective 2-year study of 75 patients with adult-onset
septic arthritis. Rheumatology (Oxford). 2001;40:24–30.
13. Movassaghi K, Wakefield C, Bohl DD, Lee S, Lin J, Holmes GB Jr, Hamid KS. Septic arthri-
tis of the native ankle. JBJS Rev. 2019;7(3):e6.
14. Holtom PD, Lawrence B, Zalavras CG. Hematogenous septic ankle arthritis. Clin Orthop
Relat Res. 2008;466:1388–91.
15. Margaretten ME, Kohlwes J, Moore D. Does this adult patient have septic arthritis? J Am
Med Assoc. 2007;297(13):1478–88.
16. Kaandorp CJ, Dinant HJ, van de Laar MA, Moens HJ, Prins AP, Dijkmans BA. Incidence and
sources of native and prosthetic joint infection: a community based prospective survey. Ann
Rheum Dis. 1997;56:470–5.
17. Dubost JJ, Fis I, Denis P, Lopitaux R, Soubrier M, Ristori JM. Polyarticular septic arthritis.
Medicine (Baltimore). 1993;72:296–310.
18. Lee CH, Chen YJ, Ueng SW, Hsu RW. Septic arthritis of the ankle joint. Chang Gung Med
J. 2000;23(7):420–6.
19. Bauer T, Boisrenoult P, Jenny JY. Post-arthroscopy septic arthritis: current data and prac-
tical recommendations. Orthop Traumatol Surg Res. 2015;101(8 Suppl):S347–50. Epub
2015 Sep 26.
20. Söderquist B, Jones I, Fredlund H, Vikerfors T. Bacterial or crystal-associated arthritis?
Discriminating ability of serum inflammatory markers. Scand J Infect Dis. 1998;30:591–6.
21. Jeng GW, Wang CR, Liu ST. Measurement of synovial tumor necrosis factor-alpha in diag-
nosing emergency patients with bacterial arthritis. Am J Emerg Med. 1997;15:626–9.
22. Coakley G, Mathews C, Field M, on behalf of the British Society for Rheumatology Standards,
Guidelines and Audit Working Group. BSR & BHPR, BOA, RCGP and BSAC guidelines for
management of the hot swollen joint in adults. Rheumatology (Oxford). 2006;45:1039–41.
23. Mathews CJ, Kingsley G, Field M. Management of septic arthritis: a systematic review. Ann
Rheum Dis. 2007;66:440–5.
24. Weston VC, Jones AC, Bradbury N, Fawthrop F, Doherty M. Clinical features and outcome
of septic arthritis in a single UK health district 1982–1991. Ann Rheum Dis. 1999;58:214–9.
25. Zhao J, Zhang S, Zhang L, Dong X, Li J, Wang Y, Yao Y. Serum procalcitinin levels as a diag-
nostic marker for septic arthritis: a meta-analysis. Am J Emerg Med. 2017;35(8):1166–71.
Epub 2017 Jun 7.
26. Imagama T, Tokushige A, Seki K, Seki T, Nakashima D, Ogasa H, Sakai T, Taguchi T. Early
diagnosis of septic arthritis using synovial fluid presepsin: a preliminary study. J Infect
Chemother. 2019;25(3):170–4. Epub 2018 Nov 23.
27. Tallia AF, Cardone DA. Diagnostic and therapeutic injection of the ankle and foot. Am Fam
Physician. 2003;68(7):1356–62.
28. Horowitz DL, Katzap E, Horowitz S, Barilla ML. Approach to septic arthritis. Am Fam
Physician. 2011;84(6):653–60.
29. Li SF, Cassidy C, Change C. Diagnostic utility of laboratory tests in septic arthritis. Emerg
Med J. 2007;24:75–7.
30. McGillicuddy DC, Shah KH, Friedberg RP, Nathanson LA, Edlow JA. How sensitive is
the synovial fluid white blood cell count in diagnosing septic arthritis? Am J Emerg Med.
2007;25:749–52.
31. Shmerling RH. Synovial fluid analysis: a critical reappraisal. Rheum Dis Clin N Am.
1994;20:503–12.
32. Krisher KK, Gibb P, Corbett S, Church D. Comparison of the BacT/Alert PF pediatric FAN
blood culture bottle with the standard pediatric blood culture bottle, the Pedi-BacT. J Clin
Microbiol. 2001;39(8):2880–3.
33. Garcia P, Irribarra L, Ramirez V, Cervilla V, De la Barra R, Montiel F, Ortiz C, Jacobelli
S. Rendimiento del estudio microbiologico en el diagnostico de la infeccion osteoarticular.
Rev Chilena Infectol. 1999;17(2):101e8. [Spanish].
34. Dalla Vestra M, Rettore C, Sartore P, Velo E, Sasset L, Chiesa G, Marcon L, Scarano L,
Simioni N, Bacelle L, Patrassi GM. Acute septic arthritis: remember gonorrhea. Rheumatol
Int. 2008;29(1):81–5. Epub 2008 May 24.
35. Wilkinson VH, Rowbotham EL, Grainger AJ. Imaging in foot and ankle arthritis. Semin
Musculoskelet Radiol. 2016;20(2):167–74. Epub 2016 Jun 23.
36. Schumacher HR, Chen LX. Musculoskeletal signs and symptoms: mono-articular joint dis-
ease. In: Klippel JH, editor. Primer on the rheumatic diseases. 13th ed. New York: Springer;
2008. p. 42–6.
37. Goldenberg DL, Cohen AS. Acute infectious arthritis. A review of patients with nongonococ-
cal joint infections (with emphasis on therapy and prognosis). Am J Med. 1976;60(3):369–77.
38. Sharff KA, Richards EP, Townes JM. Clinical management of septic arthritis. Curr Rheumatol
Rep. 2013;15(6):332.
39. Stengel D, Bauwens K, Sehouli J, Ekkernkamp A, Porzsolt F. Systematic review and
meta-analysis of antibiotic therapy for bone and joint infections. Lancet Infect Dis.
2001;1(3):175–88.
40. Workowski KA, Berman SM. Sexually transmitted diseases treatment guidelines, 2006. In:
Centers for Disease Control and Prevention. https://www.cdc.gov/mmwr/PDF/rr/rr5511.pdf.
Accessed 16 Nov 2010.
41. Ytterberg SR. Infectious disorders: mycobacterial, fungal, and parasitic arthritis. In: Klippel
JH, Stone JH, Crofford LJ, White PH, editors. Primer on the rheumatic diseases. 13th ed.
New York: Springer; 2008. p. 290–5.
42. Kohli R, Hadley S. Fungal arthritis and osteomyelitis. Infect Dis Clin N Am.
2005;19(4):831–51.
43. Hu L. Lyme arthritis. Infect Dis Clin N Am. 2005;19(4):947–61.
44. Steere A. Borrelia burgdorferi (Lyme disease, Lyme borreliosis). In: Mandell GL, Douglas
RG, Bennett JE, Dolin R, editors. Mandell, Douglas, and Bennett’s principles and practice of
infectious diseases. 7th ed. Philadelphia: Churchill, Livingstone/Elsevier; 2010. p. 3071–81.
45. Manadan AM, Block JA. Daily needle aspiration versus surgical lavage for the treatment of
bacterial septic arthritis in adults. Am J Ther. 2004;11(5):412–5.
46. Goldenberg D, Brandt K, Cohen A. Treatment of septic arthritis: comparison of needle aspi-
ration and surgery as initial modes of joint drainage. Arthritis Rheum. 1975;18:83–90.
47. Boffeli TJ, Thompson JC. Diagnosis and Management of the Septic Joint. In: Boffeli TJ,
editor. Osteomyelitis of the foot and ankle: medical and surgical management. 1st ed.
Switzerland: Springer; 2015. p. 91–8.
48. Thordarson DB, Ahlmann E, Shepherd LE, Patzakis MJ. Sepsis and osteomyelitis about the
ankle joint. Foot Ankle Clin. 2000;5(4):913–28, vii–viii.
49. Tarkowski A, Collins LV, Gjertsson I, Hultgren OH, Jonsson IM, Sakiniene E, Verdrengh
M. Model systems: modeling human staphylococcal arthritis and sepsis in the mouse. Trends
Microbiol. 2001;9(7):321–6.
50. Shank CF, Feibel JB. Osteomyelitis in the diabetic foot: diagnosis and management. Foot
Ankle Clin. 2006;11(4):775–89.
51. Cierny G, Mader JT, Penninck JJ. A clinical staging system for adult osteomyelitis. Clin
52. Lindbloom BJ, James ER, McGarvey WC. Osteomyelitis of the foot and ankle. Foot Ankle
Clin. 2014;19(3):569–88.
53. Clifford RP, Beauchamp CG, Kellam JF, Webb JK, Tile M. Plate fixation of open fractures of
the tibia. J Bone Jt Surg Br. 1988;70(4):644–8.
54. French B, Tornetta P. High-energy tibial shaft fractures. Orthop Clin North Am.
2002;33(1):211–30.
55. Giannoudis PV, Papakostidis C, Roberts C. A review of the management of open fractures of
the tibia and femur. J Bone Joint Surg Br. 2006;88(3):281–9.
56. Gross T, Kaim AH, Regazzoni P, Widmer AF. Current concepts in posttraumatic osteomyeli-
tis: a diagnostic challenge with new imaging options. J Trauma. 2002;52(6):1210–9.
57. Bondurant FJ, Cotler HB, Buckle R, Miller-Crotchett P, Browner BD. The medical and eco-
nomic impact of severely injured lower extremities. J Trauma. 1988;28(8):1270–3.
58. Poultsides LA, Liaropoulos LL, Malizos KN. The socioeconomic impact of musculoskeletal
infections. J Bone Joint Surg Am. 2010;92(11):e13.
59. Rubin RJ, Harrington CA, Poon A, Dietrich K, Greene JA, Moiduddin A. The economic
impact of Staphylococcus aureus infection in New York City Hospitals. Emerg Infect Dis.
1999;5(1):9–17.
60. Sanders J, Mauffrey C. Long bone osteomyelitis in adults: fundamental concepts and current
techniques. Orthopedics. 2013;36(5):368–75.
61. Conterno LO, Turchi MD. Antibiotics for treating chronic osteomyelitis in adults. Cochrane
Database Syst Rev. 2013;(9):CD004439.
62. Lazzarini L, Mader JT, Calhoun JH. Osteomyelitis in long bones. J Bone Joint Surg Am.
2004;86(10):2305–18.
63. Zimmerli W. Clinical presentation and treatment of orthopaedic implant-associated infection.
J Intern Med. 2014;276(2):111–9.
64. Tsukayama DT. Pathophysiology of posttraumatic osteomyelitis. Clin Orthop Relat Res.
1999;360:22–9.
65. Costerton JW, Stewart PS, Greenberg EP. Bacterial biofilms: a common cause of persistent
infections. Science. 1999;284(5418):1318–22.
66. Sheehy SH, Atkins BA, Bejon P, Byren I, Wyllie D, Athanasou NA. The microbiology of
chronic osteomyelitis: prevalence of resistance to common empirical anti-microbial regi-
mens. J Infect. 2010;60(5):338–43.
67. Calhoun J, Manring MM, Shirtliff M. Osteomyelitis of the long bones. Semin Plast Surg.
2009;23(2):59–72.
68. Patzakis MJ, Zalavras CG. Chronic posttraumatic osteomyelitis and infected nonunion of the
tibia: current management concepts. J Am Acad Orthop Surg. 2005;13(6):417–27.
69. Lipsky BA, Berendt AR, Cornia PB, Pile JC, Peters EJ, Armstrong DG, Deery HG, Embil
JM, Joseph WS, Karchmer AW, Pinzur MS, Senneville E. 2012 Infectious Diseases Society
of America clinical practice guideline for the diagnosis and treatment of diabetic foot infec-
tions. Clin Infect Dis. 2012;54(12):e132–73.
70. Lipsky BA, Sheehan P, Armstrong DG, Tice AD, Polis AB, Abramson MA. Clinical predic-
tors of treatment failure for diabetic foot infections: data from a prospective trial. Int Wound
J. 2007;4:30–8.
71. Armstrong DG, Lavery LA, Sariaya M, Ashry H. Leukocytosis is a poor indicator of acute
osteomyelitis of the foot in diabetes mellitus. J Foot Ankle Surg. 1996;35(4):280–3.
72. Fleischer AE, Didyk AA, Woods JB, Burns SE, Wrobel JS, Armstrong DG. Combined clini-
cal and laboratory testing improves diagnostic accuracy for osteomyelitis in the diabetic foot.
J Foot Ankle Surg. 2009;48(1):39–46.
73. Michail M, Jude E, Liaskos C, Karamagiolis S, Makrilakis K, Dimitroulis D. The perfor-
mance of serum inflammatory markers for the diagnosis and follow-up of patients with osteo-
myelitis. Int J Low Extrem Wounds. 2013;12(2):94–9.
74. Jeandrot A, Richard JL, Combescure C, Jourdan N, Finge S, Rodier M. Serum procalcitonin
and C-reactive protein concentrations to distinguish mildly infected from non-infected dia-
betic foot ulcers: a pilot study. Diabetologia. 2008;51(2):347–52.
75. Ertugrul BM, Sack O, Ozturk B, Cobanoglu M, Oncu S, Sakarya S. The diagnosis of dia-
betic foot osteomyelitis: examination findings and laboratory values. Med Sci Monit.
2009;15(6):CR307–12.
76. Rabjohn L, Roberts K, Troiano M, Schoenhaus H. Diagnostic and prognostic value of eryth-
rocyte sedimentation rate in contiguous osteomyelitis of the foot and ankle. J Foot Ankle
Surg. 2007;46(4):230–7.
77. Newman LG, Waller J, Palestro CJ, Schwartz M, Klein MJ, Hermann G. Unsuspected osteo-
myelitis in diabetic foot ulcers. Diagnosis and monitoring by leukocyte scanning with indium
in 111 oxyquinoline. JAMA. 1991;266(9):1246–51.
78. Game FL. Osteomyelitis in the diabetic foot: diagnosis and management. Med Clin North
Am. 2013;97(5):947–56.
79. Eneroth M, Larsson J, Apelqvist J. Deep foot infections in patients with diabetes and foot
ulcer: an entity with different characteristics, treatments, and prognosis. J Diabetes Complicat.
1999;13(5–6):254–63.
80. Fincher RM, Page MI. Clinical significance of extreme elevation of the erythrocyte sedimen-
tation rate. Arch Intern Med. 1986;146(8):1581–3.
81. Yudkin JS, Stehouwer CD, Emeis JJ, Coppack SW. C-reactive protein in healthy subjects:
associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for
cytokines originating from adipose tissue? Arterioscler Thromb Vasc Biol. 1999;19(4):972–8.
82. Simon L, Gauvin F, Amre DK, Saint-Louis P, Lacroix J. Serum procalcitonin and C-reactive
protein levels as markers of bacterial infection: a systematic review and meta-analysis. Clin
Infect Dis. 2004;39(2):206–17.
83. Maharajan K, Patro DK, Menon J, Hariharan AP, Parija SC, Poduval M. Serum Procalcitonin
is a sensitive and specific marker in the diagnosis of septic arthritis and acute osteomyelitis.
J Orthop Surg Res. 2013;8:19.
84. Uzun G, Solmazgul E, Curuksulu H, Turhan V, Ardic N, Top C. Procalcitonin as a diagnostic
aid in diabetic foot infections. Tohoku J Exp Med. 2007;213(4):305–12.
85. Goergens ED, McEvoy A, Watson M, Barrett IR. Acute osteomyelitis and septic arthritis in
children. J Paediatr Child Health. 2005;41(1–2):59–62.
86. Peters EJ, Lipsky BA. Diagnosis and management of infection in the diabetic foot. Med Clin
N Am. 2013;97(5):911–46.
87. Lipsky BA, Aragon-Sanchez J, Diggle M, Embil J, Kono S, Lavery L, Senneville E,
Urbancic-Rovan V, Van Asten S, Peters EJG, International Working Group on the Diabetic
Foot. IWGDF guidance on the diagnosis and management of foot infections in persons with
diabetes. Diabetes Metab Res Rev. 2016;32(suppl 1):45–74.
88. Meyr AJ, Singh S, Zhang X, Khilko N, Mukherjee A, Sheridan MJ. Statistical reliabil-
ity of bone biopsy for the diagnosis of diabetic foot osteomyelitis. J Foot Ankle Surg.
2011;50(6):663–7.
89. Weiner RD, Viselli SJ, Fulkert KA, Accetta P. Histology versus microbiology for accuracy in
identification of osteomyelitis in the diabetic foot. J Foot Ankle Surg. 2011;50(2):197–200.
90. Lavery LA, Crisologo PA, La Fontaine J, Bhavan K, Oz OK, Davis KE. Are we misdiagnosing
diabetic foot osteomyelitis? Is the gold standard gold? J Foot Ankle Surg. 2019;58(4):713–6.
91. Cecilia-Matilla A, Lazaro-Martinez JL, Aragon Sanchez J, Garcia-Morales E, Garcia- Alvarez
Y, Beneit-Montesinos JV. Histopathologic characteristics of bone infection complicating foot
ulcers in diabetic patients. J Am Podiatr Med Assoc. 2013;103:24–31.
92. Shone A, Burnside J, Chipchase S, Game F, Jeffcoate W. Probing the validity of the probe-to-
bone test in the diagnosis of osteomyelitis of the foot in diabetes. Diabetes Care. 2006;29:945.
93. Valabhji J, Oliver N, Samarasinghe D, Mali T, Gibbs RG, Gedroyc WM. Conservative man-
agement of diabetic forefoot ulceration complicated by underlying osteomyelitis: the benefits
of magnetic resonance imaging. Diabet Med. 2009;26:1127–34.
94. Vouillarmet J, Moret M, Morelec I, Michon P, Dubreuil J. Application of white blood cell
SPECT/CT to predict remission after a 6 or 12 week course of antibiotic treatment for dia-
betic foot osteomyelitis. Diabetologia. 2017;60:2486–94.
95. La Fontaine J, Bhavan K, Lam K, Van Asten S, Erdman W, Lavery LA, Oz OK. Comparison
between Tc-99m WBC SPECT/CT and MRI for the diagnosis of biopsy-proven diabetic foot
osteomyelitis. Wounds. 2016;28:271–8.
96. Lavery LA, Armstrong DG, Wunderlich RP, Mohler MJ, Wendel CS, Lipsky BA. Risk factors
for foot infections in individuals with diabetes. Diabetes Care. 2006;29(6):1288–93.
97. Uckay I, Gariani K, Pataky Z, Lipsky BA. Diabetic foot infections: state-of-the-art. Diabetes
Obes Metab. 2014;16(4):305–16.
98. Tardaguila-Garcia A, Lazaro-Martinez JL, Sanz-Corbalan I, Garcia-Alvarez Y, Alvaro-
Afonso FJ, Garcia-Morales E. Correlation between empirical antibiotic therapy and bone
culture results in patients with osteomyelitis. Adv Skin Wound Care. 2019;32(1):41–4.
99. Berendt AR, Peters EJ, Bakker K, Embil JM, Eneroth M, Hinchliffe RJ, Jeffcoate WJ, Lipsky
BA, Senneville E, The J, Valk GD. Specific guidelines for treatment of diabetic foot osteomy-
elitis. Diabetes Metab Res Rev. 2008;24(Suppl 1):S190–1.
100. Zhang J, Chu Y, Wang P, Ji X, Wang C, Peng Y. Clinical outcomes of multidrug resistant pseu-
domonas aeruginosa infection and the relationship with type III secretion system in patients
with diabetic foot. Int J Low Extrem Wounds. 2014;13(3):205–10.
101. Lipsky BA, Berendt AR, Deery HG, Embil JM, Joseph WS, Karchmer AW, LeFrock JL, Lew
DP, Mader JT, Norden C, Tan JS. Diagnosis and treatment of diabetic foot infections. Clin
Infect Dis. 2004;39(7):885–910.
102. Senneville E, Melliez H, Beltrand E, Legout L, Valette M, Cazaubiel M, Cordonnier M,
Caillaux M, Yazdanpanah Y, Mouton Y. Culture of percutaneous bone biopsy specimens for
diagnosis of diabetic foot osteomyelitis: concordance with ulcer swab cultures. Clin Infect
Dis. 2006;42(1):57–62.
103. Lavery LA, Sariaya M, Ashry H, Harkless LB. Microbiology of osteomyelitis in diabetic foot
infections. J Foot Ankle Surg. 1995;34(1):61–4.
104. Fihman V, Hannouche D, Bousson V, Bardin T, Liote F, Raskine L, Riahi J, Sanson-Le Pors
MJ, Berçot B. Improved diagnosis specificity in bone and joint infections using molecular
techniques. J Infect. 2007;55(6):510e7.
105. Glaudemans AW, Uckay I, Lipsky BA. Challenges in diagnosing infection in the diabetic
foot. Diabet Med. 2015;32(6):748–59.
106. Smith K, Collier A, Townsend EM, O’Donnell LE, Bal AM, Butcher J, Mackay WG, Ramage
G, Williams C. One step closer to understanding the role of bacteria in diabetic foot ulcers:
characterizing the microbiome of ulcers. BMC Microbiol. 2016;16:54.
107. Malone M, Gosbell IB, Dickson HG, Vickery K, Espedido BA, Jensen SO. Can molecular
DNA-based techniques unravel the truth about diabetic foot infections? Diabetes Metab Res
Rev. 2017;33(1):e2834.
108. Spichler A, Hurwitz BL, Armstrong DG, Lipsky BA. Microbiology of diabetic foot infec-
tions: from Louis Pasteur to “crime scene investigation”. BMC Med. 2015;13(1):2.
109. Lipsky BA, Senneville E, Abbas ZA, Aragón-Sanchez J, Diggle M, Embil JM, Kono S, Lavery
LA, Malone M, Van Asten S, Urbancic-Rovan V, Peters EJG, on behalf of the International
Working Group on the Diabetic Foot (IWGDF). Guidelines on the diagnosis and treatment
of foot infection in persons with diabetes (IWGDF 2019 update). Diabetes Metab Res Rev.
2020;36(S1):e3280.
110. Couturier A, Chabaud A, Desbiez F, Descamps S, Petrosyan E, Letertre-Gilbert P, Mrozek N,
Vidal M, Tauveron I, Maqdasy S, Lesens O. Comparison of microbiological results obtained
from per-wound bone biopsies versus transcutaneous bone biopsies in diabetic foot osteomy-
elitis: a prospective cohort study. Eur J Clin Microbiol Infect Dis. 2019;38(7):1287–91.
111. Beroukhim G, Shah R, Bucknor MD. Factors predicting positive culture in CT-guided bone
biopsy performed for suspected osteomyelitis. AJR Am J Roentgenol. 2019;212:620–4.
112. Wu JS, Gorbachova T, Morrison WB, Haims AH. Imaging-guided bone biopsy for osteomy-
elitis: are there factors associated with positive or negative cultures? AJR Am J Roentgenol.
2007;188:1529–34.
113. Anagnostopoulos A, Bossard DA, Ledergerber B, Zingg PO, Zinkeragel S, Gerber C,
Achermann Y. Perioperative antibiotic prophylaxis has no effect on time to positivity and
proportion of positive samples: a cohort study of 64 Cutibacterium acnes bone and joint
infections. J Clin Microbiol. 2018;56
114. Glaudemans AW, Jutte PC, Cataldo MA, Cassar-Pullicino V, Gheysens O, Borens O, Trampuz
A, Wörtler K, Petrosillo N, Winkler H, Signore A, Sconfienza LM. Consensus document fot
the diagnosis of peripheral bone infection in adults: a joint paper by the EANM, EBJIS, and
ESR (with ESCMID endorsement). Eur J Nucl Med Mol Imaging. 2019;46(4):957–70.
115. Ledermann G, Klaber I, Urrutia J, Mery P. A novel intraoperative technique seeding mor-
selized bone tissue into pediatric blood culture bottles improves microbiological diagnosis in
patients with foot and ankle osteomyelitis. J Orthop Sci. 2020;25(3):492–6.
116. Shiraev TP, Lipsky BA, Kwok TMY, Robinson DA. Utility of culturing marginal
bone in patients undergoing lower limb amputation for infection. J Foot Ankle Surg.
2019;58(5):847–51.
117. Kowalski TJ, Matsuda M, Sorenson MD, Gundrum JD, Agger WA. The effect of residual
osteomyelitis at the resection margin in patients with surgically treated diabetic foot infec-
tion. J Foot Ankle Surg. 2012;50:171–5.
118. Atway S, Nerone V, Springer K, Woodruff D. Rate of residual osteomyelitis after partial foot
amputation in diabetic patients: a standardized method for evaluating bone margins with
itnraoperstaive culture. J Foot Ankle Surg. 2012;51:749–52.
119. Bernstein B, Stouder M, Bronfenbrenner E, Chen S, Anderson D. Correlating pre-operative
MRI measurements of metatarsal Osteomyelitis with surgical clean margins reveals the need
for a one centimeter resection margin. J Foot Ankle Res. 2017;10:40.
120. Simpson AH, Deakin M, Latham JM. Chronic osteomyelitis. The effect of the extent of surgi-
cal resection on infection-free survival. J Bone Joint Surg Br. 2001;83(3):403–7.
121. Fenollar F, Levy PY, Raoult D. Usefulness of broad-range PCR for the diagnosis of osteoar-
ticular infections. Curr Opin Rheumatol. 2008;20(4):463–70.
122. Fisher TK, Wolcott R, Wolk DM, Bharara M, Kimbriel HR, Armstrong DG. Diabetic foot
infections: a need for innovative assessments. Int J Low Extrem Wounds. 2010;9(1):31–6.
123. Tumeh SS, Aliabadi P, Weissman BN, McNeil BJ. Disease activity in osteomyelitis: role of
radiography. Radiology. 1987;165(3):781–4.
124. Pineda C, Vargas A, Rodríguez AV. Imaging of osteomyelitis: current concepts. Infect Dis
Clin N Am. 2006;20(4):789–825.
125. Bhattacharyya T, Bouchard KA, Phadke A, Meigs JB, Kassarjian A, Salamipour H. The accu-
racy of computed tomography for the diagnosis of tibial nonunion. J Bone Joint Surg Am.
2006;88(4):692–7.
126. Termaat MF, Raijmakers PGHM, Scholten HJ, Barker FC, Patka P, Haarman HJTM. The
accuracy of diagnostic imaging for the assessment of chronic osteomyelitis: a systematic
review and meta-analysis. J Bone Joint Surg Am. 2005;87(11):2464–71.
127. Link TM, Berning W, Scherf S, Joosten U, Joist A, Engelke K, Daldrup-Link HE. CT of
metal implants: reduction of artifacts using an extended CT scale technique. J Comput Assist
Tomogr. 2000;24(1):165–72.
128. Kaim A, Ledermann HP, Bongartz G, Messmer P, Müller-Brand J, Steinbrich W. Chronic
post-traumatic osteomyelitis of the lower extremity: comparison of magnetic resonance
imaging and combined bone scintigraphy/immunoscintigraphy with radiolabelled monoclo-
nal antigranulocyte antibodies. Skelet Radiol. 2000;29(7):378–86.
129. Mason MD, Zlatkin MB, Esterhai JL, Dalinka MK, Velchik MG, Kressel HY. Chronic
complicated osteomyelitis of the lower extremity: evaluation with MR imaging. Radiology.
1989;173(2):355–9.
130. Ma LD, Frassica FJ, Bluemke DA, Fishman EK. CT and MRI evaluation of musculoskeletal
infection. Crit Rev Diagn Imaging. 1997;38(6):535–68.
131. Gemmel F, Rijk PC, Collins JMP, Parlevliet T, Stumpe KD, Palestro CJ. Expanding
role of 18F-fluoro-d-deoxyglucose PET and PET/CT in spinal infections. Eur Spine
J. 2010;19(4):540–51.
132. Al-Sheikh W, Sfakianakis GN, Mnaymneh W, Hourani M, Heal A, Duncan RC. Subacute and
chronic bone infections: diagnosis using in-111, Ga-67 and Tc-99m MDP bone scintigraphy,
and radiography. Radiology. 1985;155(2):501–6.
133. Dong MJ, Zhao K, Liu ZF, Wang GL, Yang SY, Zhou GJ. A meta-analysis of the value of
fluorodeoxyglucose-PET/PET-CT in the evaluation of fever of unknown origin. Eur J Radiol.
2011;80(3):834–44.
134. Glaudemans AWJM, Signore A. FDG-PET/CT in infections: The imaging method of choice?
Eur J Nucl Med Mol Imaging. 2010;37(10):1986–91.
135. Sarda L, Crémieux AC, Lebellec Y, Meulemans A, Lebtahi R, Hayem G. Inability of 99mTc-
ciprofloxacin scintigraphy to discriminate between septic and sterile osteoarticular diseases.
J Nucl Med. 2003;44(6):920–6.
136. Basu S, Chryssikos T, Moghadam-Kia S, Zhuang H, Torigian DA, Alavi A. Positron emission
tomography as a diagnostic tool in infection: present role and future possibilities. Semin Nucl
Med. 2009;39(1):36–51.
137. Demirev A, Weijers R, Geurts J, Mottaghy F, Walenkamp G, Brans B. Comparison of
[18 F]FDG PET/CT and MRI in the diagnosis of active osteomyelitis. Skelet Radiol.
2014;43(5):665–72.
138. McGrory JE, Pritchard DJ, Ilstrup D, Rowland CM. Malignant lesions arising in chronic
osteomyelitis. Clin Orthop Relat Res. 1999;362:181–9.
139. Lew PDP, Waldvogel PFA. Osteomyelitis. Lancet. 2004;364(9431):369–79.
140. Haidar R, Der BA, Atiyeh B. Duration of post-surgical antibiotics in chronic osteomyelitis:
empiric or evidence-based? Int J Infect Dis. 2010;14(9):e752–8.
141. Swiontkowski MF, Hanel DP, Vedder NB, Schwappach JR. A comparison of short- and long-
term intravenous antibiotic therapy in the postoperative management of adult osteomyelitis.
J Bone Joint Surg Br. 1999;81(6):1046–50.
142. Li H-K, Rombach I, Zambellas R, Walker AS, McNally MA, Atkins BL. Oral versus intrave-
nous antibiotics for bone and joint infection. N Engl J Med. 2019;380(5):425–36.
143. Greene N, Holtom PD, Warren CA, Ressler RL, Shepherd L, McPherson EJ. In vitro elution
of tobramycin and vancomycin polymethylmethacrylate beads and spacers from Simplex and
Palacos. Am J Orthop (Belle Mead NJ). 1998;27(3):201–5.
144. Holtom PD, Patzakis MJ. Newer methods of antimicrobial delivery for bone and joint infec-
tions. Instr Course Lect. 2003;52:745–9.
145. Holtom PD, Warren CA, Greene NW, Bravos PD, Ressler RL, Shepherd L. Relation of sur-
face area to in vitro elution characteristics of vancomycin-impregnated polymethylmethacry-
late spacers. Am J Orthop (Belle Mead NJ). 1998;27(3):207–10.
146. Henry SL, Hood GA, Seligson D. Long-term implantation of gentamicin-
polymethylmethacrylate antibiotic beads. Clin Orthop Relat Res. 1993;295:47–53.
147. Evans RP, Nelson CL. Gentamicin-impregnated polymethylmethacrylate beads compared
with systemic antibiotic therapy in the treatment of chronic osteomyelitis. Clin Orthop Relat
Res. 1993;295:37–42.
Tibial Bone Defect Reconstruction
Techniques
Gonzalo F. Bastías and Gregorio Verschae
1 Introduction
The management of tibial bone defects at the level of the leg and ankle is complex
and involves the use of diverse strategies to achieve the preservation of the limb,
especially in cases of massive deficits [1]. Technological advances in terms of
innovation in methods of both external and internal osteosynthesis, development
of microsurgical techniques of soft tissue coverage, and advances in biological
coadjuvants for consolidation have allowed an increase in successful results
while also reducing the number of complications during treatment. Despite the
above, the salvage process continues to be long-lasting and not without
difficulties.
2 Etiology
Segmental defects of the tibia have three main origins [2]:

(a) Infection: Chronic osteomyelitis has a preferential location to the tibia and usu-
ally requires extensive resection of devitalized bone tissue to achieve infection
eradication. They are usually associated with nonunion infection as a result of
high-energy trauma [3, 4].
G. F. Bastías (*)
Clínica las Condes, Santiago, Chile
Hospital del trabajador de Santiago, Santiago, Chile
G. Verschae
Clinica Redsalud, Santiago, Chile

Switzerland AG 2022
802 G. F. Bastías and G. Verschae
(b) Trauma: In this context, loss of tibial bone stock can occur due to large com-
minution, segmental loss from exposed fractures, firearm injuries, and resection
secondary to massive contamination [5]. It is usually accompanied by severe
soft tissue damage and neurovascular injury [6].
(c) Bone Tumors: The bone–block resection of aggressive malignant or benign
bone tumors usually results in associated bone defects or no coverage deficit.
The increase in associated survival in the management of this type of neoplastic
lesions has made it necessary to establish new objectives for salvage and recov-
ery of function [7, 8].
3 General Considerations
The definition of a segmental defect is diverse in the literature, and the precise limit
to be considered critical is not clear [9]. In general, there is some agreement that a
critical bone defect is one that, without intervention, will not consolidate spontane-
ously [10]. Several reports define a loss of 1–2 cm and 50% of the circumference of
the tibia as an intercalary defect [2, 11–13].
The ideal conditions for the patient who will undergo bone reconstruction are as
follows: an informed and cooperative patient, stable coverage of surrounding soft
tissue, adequate nutritional status, and absence of active infection and smoking [2].
Multidisciplinary management in those patients who do not meet these conditions
is essential to optimize the patient’s previous condition and increase the chances of
success in the reconstruction process.
An important factor in the management of tibial bone defects for the foot and
ankle surgeon is the involvement of the distal tibia and the tibiotalar joint. In the
event that this epiphyseal segment is not part of the defect, all efforts should be
directed at salvaging the tibial plafond in order to maintain ankle function. In defects
involving the distal tibia, a tibial arthrodesis must usually be performed as a manda-
tory part of limb salvage [14].
The choice of the method of reconstruction of tibial segmental defects depends
significantly on the patient’s characteristics, the etiology of the defect, and the sur-
geon’s experience. We will describe below the most commonly used methods for
their management and treatment.
3.1 Distraction Osteogenesis
Distraction osteogenesis (DO) is a biological process by which the generation of

high-quality bone tissue is produced, in relation to the gradual distraction of a cor-
ticotomy performed at low speed. The bone that originates through DO has biologi-
cal and mechanical qualities similar to native bone [13]. This technical concept was
devised by Gavriil Ilizarov in the Soviet Union in the 1950s and popularized since
Tibial Bone Defect Reconstruction Techniques 803
then as “the Ilizarov method” to refer indistinctly to both DO and fixation methods
used today in a myriad of orthopedic applications [15, 16].
An important aspect regarding DO is the fact that besides bone growth, other
tissues of the limb must also respond to gradual distraction such as muscles, nerves,
ligaments, tendons, and skin. Given the above has also begun to use the term dis-
tractive histogenesis, refer to the process [13, 16].
There are multiple devices generated from the Ilizarov apparatus for the manage-
ment of segmental defects using ODs such as monoplanar external fixators with rails,
classic circular or hexapod external fixators, and more recently motorized internal fixa-
tion devices such as endomedullary nails or bone transport plates [15, 17–19].
The preoperative evaluation with long leg X-rays of both extremities in two pro-
jections is fundamental for the correct planning and estimation of the defect to be
reconstructed. Regardless of the device and type of fixation to be used, the technique
used to perform the corticotomy should be done with low energy, privileging the use
of drills and osteotomes to reduce heat damage and preserve the periosteal lining [2].
The location of the corticotomy should be metaphysial whenever possible. This
area has a greater proportion of cancellous bone tissue associated with greater vas-
cularization so that the quality of regeneration is considerably better than that pro-
duced by DO in diaphyseal segments. However, in some cases, it may not be
possible to perform a metaphyseal corticotomy due to defects located in this area.
In such cases, it should be performed in the immediately adjacent diaphyseal seg-
ment. There is an initial latency period (10–14 days) after corticotomy during which
the soft callus forms, the surgical approaches heal, and the hydroxyapatite pins are
osseointegrated. DO also consists of two other phases, the transport phase during
which one or more bone segments are moved to the area of the bone defect and the
consolidation phase during which the bone regeneration must mature and ossify
until it has the necessary conditions to support physiological loads.
Once the latency phase is finished, the transport phase begins at a suggested rate
of between 0.75 and 1 mm per day, separated into movements of 0.25 mm every
6–8 hours [8]. In those cases in which retrograde transport is being done from distal
to proximal and in diaphyseal corticotomies of the tibia, we recommend performing
distraction at a rate of 0.5 mm per day, separated into two movements per day [20].
Once the transported segment reaches the far end of the defect, compression or
docking is performed. This step can be performed in a closed way or surgically
associating bone graft in a secondary way. Generally, the consolidation phase lasts
approximately two to three times the duration of the transport phase [3, 21].
The most commonly used DO strategies for managing tibial bone defects are as
follows.
3.1.1 Classic Bone Transport
The classic bone transport consists of one or more bone segments that move in an
anterograde or retrograde manner and in a controlled way toward the farthest end of
the bone defect [4, 13]. Usually, monolateral or circular external fixators are used,
a b c d
Fig. 1 Classic bone transport. (a) Distal metaphyseal bone defect. (b) Frame configuration with a
middle mobile ring and proximal corticotomy. (c) Docking site and mature regenerate. (d)
Post external fixation removal appearance
using rails and bars, respectively, for the displacement of the segment to be trans-
ported (Figs. 1 and 2).
Among the advantages of bone transport is the fact that it allows the patient to
perform progressive loading with the external fixator, produces excellent quality
bone tissue from the biological point of view, and stimulates local blood flow whilst
it can be used for all defect sizes to be reconstructed [2, 22]. Disadvantages include
the need for patient cooperation and participation, long treatment times and psycho-
logical burden, joint stiffness, delayed healing, and insertion site infections.
More than one corticotomy (bifocal or tandem bone transport) has been described
to reduce the consolidation time in massive bone defects. In addition, transport
through endomedullary nails and early transition to internal fixation once transport
is completed are strategies used to decrease external fixator time, improving func-
tional outcomes without associated infectious complications [23, 24].
Fig. 2 Bone transport to ankle arthrodesis. (a) 67-year-old patient with an 8-cm defect secondary
to infection from an exposed tibial pylon fracture. (b) Spacer removal, circular tutor installation,
and proximal metaphyseal osteotomy. (c) Post-docking radiological control with adequate proxi-
mal bone regeneration. (d) Final radiological control 3 months after the removal of the external
fixator corticalized mature proximal regeneration and consolidated ankle arthrodesis
a b
c d
a b c d
Fig. 3 Shortening–Lengthening using a hexapod external fixator. (a) Distal metaphyseal defect.
(b) Programming in two levels with an upper level of lengthening and a lower level of progressive
shortening associated with fibular ostectomy. (c) Finished programs with proximal bone regenerate
and early docking site at lower level. (d) Post external fixator removal appearance
3.1.2 Shortening–Lengthening
The shortening–lengthening strategy consists in performing a shortening at the

defect level, while another independent proximal segment performs bone lengthen-
ing in order to avoid limb length discrepancy (Fig. 3) [3].
In tibial defects smaller than 3 cm, it is possible to perform acute shortening to
privilege early consolidation, decrease dead space, increase stability of the fixation
construct, and achieve adequate soft tissue closure [25, 26]. Vascular alterations,
edema, distal perfusion deficit, and surgical wound complications have been
reported with shortenings greater than 3 cm so we do not recommend their routine
use [2, 20, 22]. In these cases, it is advisable to perform a gradual or combined
shortening in order to avoid these complications (Fig. 4).
Fig. 4 Lengthening technique with double-level hexapod circular fixator. (a) Post-traumatic
defect of 6.5 cm of tibial diaphysis with massive contamination. (b) Installation of a circular exter-
nal fixator, proximal corticotomy, and installation of distal cement spacer for 6 weeks. The proxi-
mal segment initiates distractive osteogenesis at 14 days post-surgery. (c) Removal of cement
spacer and progressive compression of the distal bone defect. (d) Radiological follow-up 3 months
after fixator removal
a b
c d
3.1.3 Transport with Motorized Endomedullary Nail
In recent years, the development of motorized endomedullary nail lengthening tech-

nology has been a breakthrough in the field of limb salvage without the discomfort
and complications of external fixation [27]. Applications have been increasing
including the management of limb length discrepancy, compression at nonunion of
long bones, and recently also the bone transport nail [28]. This device allows
through an electromagnetic mechanism the management of bone defects of the tibia
completely internally (Fig. 5). Although there are still no studies in the literature
that support its efficacy with respect to conventional management of tibial defects,
its results to date are promising [18].
3.2 Induced Membrane Technique (Masquelet)
The induced membrane technique or “Masquelet” technique has gained adherence

and popularity in recent years as an alternative to OD because of its good clinical
results [29, 30]. Described in 1986 by Alain Masquelet, this procedure consists of
two stages (Fig. 6). The first is the radical resection of macroscopically compro-
mised tissue, both bone and soft tissue. In some cases, repeated cleaning and
debridement are necessary in order to be sure to resect all devitalized tissue. This
resection must be associated with the installation of a polymethylmethacrylate
(PMMA) cement spacer. It is essential to have a multidisciplinary team and plastic
surgery support to achieve adequate skin coverage in those cases with associated
soft tissue defects [31].
The second stage is performed 6–8 weeks later and already when complete heal-
ing of the soft tissues is found. In this stage, the membrane must be carefully opened
with the use of a scalpel, removing the spacer and taking care not to damage the
cement-induced membrane. The defect is then filled with morselized autologous
cancellous bone obtained from the iliac crest, or from the medullary canal of long
bones [32]. In those cases in which a greater volume is required or it is not possible
to have a sufficient amount of autologous graft, a mixture with allograft or synthetic
graft can be made in a proportion no greater than 1:3 of the total. This is due to the
fact that morcellated autologous cancellous bone has physical properties (porosity)
and biological properties (biocompatibility, growth factors, and stem cells) that are
fundamental to favor consolidation capacity [1, 30].
There are four key factors in the process of bone consolidation, known as the
“diamond concept” [31]: presence of osteogenic cells, formation of the osteoinduc-
tive membrane, growth factors, and mechanical stability.
The mechanism by which the hypervascularized membrane is generated and the
subsequent consolidation of the defect has not been completely elucidated and is a
matter of extensive research and development. The four fundamental points of the
mechanism of action of the induced membrane are as follows:
a b
c d
Fig. 5 Bone transport with a motorized transport nail. (a) Post-traumatic diaphyseal defect of
9 cm with cement spacer. (b) Installation of transport nail and proximal corticotomy. (c)
Radiological control during bone transport with adequate excursion and early formation of
bone regenerate. (d) Radiological control 3 months post-docking with regenerate in advanced con-
solidation stage. (Case courtesy of Austin T. Fragomen MD, NY, USA)
• Protection against the environment and prevention of bone resorption.

• Production of osteoinduction growth factors.
• Recruitment of adult stem cells and promotion of osteogenesis.
• Revascularization of the graft from the internal zone of the membrane.
a b c d e
Fig. 6 Induced membrane technique. (a) Metaphyseal defect of the distal tibia. (b) Installation of
polymethylmethacrylate cement spacer. (c) Formation of hypervascularized membrane. (d)
Careful resection of the cement spacer taking care not to damage the induced membrane.
Contribution of bone autografting and definitive fixation. (e) Final aspect after bone
consolidation
There is controversy regarding the importance of the spacer and its physical,
morphological, and compositional characteristics. The formation of the membrane
would be related to irritation and response to foreign body of the surrounding tissue,
being benefited by the rough surface of the bone cement. It is recommended the use
of monoblocks in diaphysial defects, which also help with the stability of the seg-
ment. In metaphyseal segments, the use of beads should be privileged to achieve an
adequate filling of cavities and optimize their rescue once the membrane is formed.
The use of antibiotics helps the local control of the infection and would not have
relation with the quality of the formed membrane.
Another relevant factor for the consolidation of bone defects treated with the
Masquelet technique is mechanical stability [33]. This fixation should be as rigid as
possible using both plates and an endomedullary nail or external fixator in cases
associated with infection and osteomyelitis (Fig. 7) [34].
Fig. 7 Induced membrane technique. (a) Comminuted fracture of the distal tibia associated with
infection. (b) Resection of devitalized metaphyseal segment associated with circular tutorial fixa-
tion. (c) and (d) Radiological controls after spacer removal and autograft contribution. Healing
progress is observed. (e) Fixator removal and installation of internal osteosynthesis plates. (f) Final
control after plate removal. Complete consolidation of the bone defect is observed. (Case courtesy
of Pablo Wagner MD, Santiago, Chile)
a b
c d
e f
In relation to the results, there are multiple studies that show a good rate of con-
solidation with the strict use of the previously described protocol. One factor that
could diminish the good results of this technique has to do with recurrent infection.
Emphasis should be placed on completely drying out all infected or devitalized tis-
sue in the area in the first stage in order to optimize local management of the infec-
tion and improve results [1, 29, 31].
3.3 Structural Allograft
The use of intercalary allografts has been widely reported in the literature, espe-
cially in the context of tibial bone defects secondary to tumor resection [22, 35]. The
most frequently used frozen structural allograft alternatives in the tibia are the tibial
diaphysis allograft, distal tibia, and femoral head [36].
The advantages of this type of treatment include immediate restoration of limb
length without donor site morbidity or limitation of the length of the defect to be
reconstructed. On the other hand, the main disadvantages are nonunion at one or
both interfaces, slow incorporation of the allograft to the host, and potential collapse
or subsequent fractures [2]. The combined use of allografts associated with vascu-
larized fibular grafting has had acceptable results reported in the literature either as
a primary outcome or as rescue from allograft nonunion [37, 38].
3.4 Vascularized Fibular Graft
The vascularized fibular graft has been reported both as free and as pediculated
transfer for the management of diaphyseal defects in the upper and lower extremi-
ties having Approximately 25 cm of fibula can be harvested and a size of at least
4 cm above the size of the defect is recommended in order to have at least 2 cm of
proximal and distal overlap [22].
Because of its inherent vascularity, it tends to attach earlier to native bone tissue
and is more resistant to infection. However, it requires prolonged unloading and a
subsequent hypertrophy process in order to withstand cyclic physiological loads
and be functionally comparable to the tibia [39, 40]. Other disadvantages include
the following: donor site morbidity, limited availability, and risk of stress fractures,
in addition to requiring a highly trained surgeon to increase the chances of success-
ful vascular anastomosis (Fig. 8).
4 Comparative Results
The choice of the reconstruction method for tibial segmental defects does not cur-
rently have evidence to establish a clear management algorithm. Despite multiple
reports in the literature on the subject, comparative studies are scarce and there are
Fig. 8 Free vascularized

fibular graft with skin
island
no randomized prospective studies that allow defining the superiority of one method
over another. The vast majority of studies include defects of other long bones asso-
ciated with diverse protocols of infection and soft tissue management, making the
results not comparable.
However, there is literature that may be useful in guiding the treatment strategy
and adapting it on a case-to-case basis, pending higher levels of evidence that
include new technologies and standardized management protocols.
Tong and colleagues retrospectively evaluated 39 patients who underwent seg-
mental defect reconstruction (26 tibias/13 femurs) of which 20 were managed using
the induced membrane technique and 19 were reconstructed with monofocal bone
transport using a monopolar tutor [41]. The average defect in this series was 6.7 cm
in induced membrane and 6.9 cm in bone transport being comparable groups. The
bone defect results were defined in terms of union, limb length discrepancy, and
residual angular deformities. The functional results were measured in relation to the
degree of activity, joint stiffness, pain, and presence or not of reflex sympathetic
dystrophy. The bone defect results were excellent/good in 15/20 patients (75%) in
induced membrane and 16/19 (82.2%) in bone transport. From a functional point of
view, 17/20 patients (85%) had excellent/good results in the induced membrane
group versus 9/19 (31.6%) of the patients in the bone transport group. The authors
conclude that both methods have satisfactory bone results, while the induced mem-
brane technique has better functional results, especially at the femoral level.
In a recent meta-analysis, 37 studies were evaluated in which bone transport was
used for the management of bone defects of 6.9 cm on average (range 3.5–11.1 cm)
and their results were compared with 41 studies in which the induced membrane
technique was used for defects of 6.32 cm (range 2–25 cm) [29]. There were no
significant differences in the rate of attachment, deep infection, poor attachment,
and amputation. However, the rate of refractures was 8.5 times more frequent in the
group treated with bone transport.
The role of defect size in the choice of reconstruction technique is not clear. A
recently published animal study revealed that for minor defects (4 mm in rat tibia
model) distractive osteogenesis has a higher bone regeneration rate associated with
better bone quality and shorter treatment time [42]. However, in major defects
(8 mm) the results reversed favoring the induced membrane. In the medium range
(6 mm), no differences were found between the two methods. This study concludes
that the reconstruction method should be guided by the size of the defect; however,
both techniques would have the capacity to regenerate quality bone tissue. The role
of tandem or multifocal transports has not been studied or compared with induced
membrane techniques and theoretically could take advantage of reducing treatment
times of transports with a single focus of distractive osteogenesis or the induced
membrane.
There are studies that have compared the results of bone transport and free vas-
cularized fibula with comparable results in terms of reconstruction success rate [40,
43, 44]. However, other studies have results that favor bone transport in defects
smaller than 12 cm, while in those cases with superior defects the vascularized fib-
ula would present better functional results [44]. Bone transport is superior in terms
of surgery hours, less hospitalization time and associated costs [43].
References
1. Masquelet AC, Begue T. The concept of induced membrane for reconstruction of long bone
defects. Orthop Clin North Am. 2010;41(1):27–37; table of contents.
2. Mauffrey C, Barlow BT, Smith W. Management of segmental bone defects. J Am Acad Orthop
Surg. 2015;23(3):143–53.
3. Tetsworth K, Paley D, Sen C, et al. Bone transport versus acute shortening for the management
of infected tibial non-unions with bone defects. Injury. 2017;48(10):2276–84.
4. Zhang S, Wang H, Zhao J, Xu P, Shi H, Mu W. Treatment of post-traumatic chronic osteomy-
elitis of lower limbs by bone transport technique using mono-lateral external fixator: follow-up
study of 18 cases. J Orthop Sci. 2016;21(4):493–9.
5. Battiston B, Santoro D, Baido RL, Pasquero F. Treatment of acute bone defects in severe lower
limb trauma. Injury. 2019;50(Suppl 5):S40–5.
6. Southam BR, Archdeacon MT. “Iatrogenic” segmental defect: how i debride high-energy open
tibial fractures. J Orthop Trauma. 2017;31(Suppl 5):S9–S15.
7. Yang Z, Tao H, Ye Z, Jin L, Lin N, Yang D. Bone transport for reconstruction of large bone
defects after tibial tumor resection: a report of five cases. J Int Med Res. 2018;46(8):3219–25.
8. Demiralp B, Ege T, Kose O, Yurttas Y, Basbozkurt M. Reconstruction of intercalary bone
defects following bone tumor resection with segmental bone transport using an Ilizarov circu-
lar external fixator. J Orthop Sci. 2014;19(6):1004–11.
9. Aktuglu K, Erol K, Vahabi A. Ilizarov bone transport and treatment of critical-sized tibial bone
defects: a narrative review. J Orthop Traumatol. 2019;20(1):22.
10. Schemitsch EH. Size matters: defining critical in bone defect size! J Orthop Trauma.
2017;31(Suppl 5):S20–2.
11. Nauth A, McKee MD, Einhorn TA, Watson JT, Li R, Schemitsch EH. Managing bone defects.
J Orthop Trauma. 2011;25(8):462–6.
12. Sanders DW, Bhandari M, Guyatt G, et al. Critical-sized defect in the tibia: is it critical?
Results from the SPRINT trial. J Orthop Trauma. 2014;28(11):632–5.
13. Quinnan SM. Segmental bone loss reconstruction using ring fixation. J Orthop Trauma.
2017;31(Suppl 5):S42–6.
14. Matsubara H, Watanabe K, Takata M, Nomura I, Tsuchiya H. A new classification for
ankle arthrodesis when using an external fixator. Strategies Trauma Limb Reconstr.
2019;14(3):148–54.
15. Gubin A, Borzunov D, Malkova T. Ilizarov method for bone lengthening and defect manage-
ment review of contemporary literature. Bull Hosp Jt Dis. 2016;74(2):145–54.
16. Gubin AV, Borzunov DY, Marchenkova LO, Malkova TA, Smirnova IL. Contribution of
G.A. Ilizarov to bone reconstruction: historical achievements and state of the art. Strategies
Trauma Limb Reconstr. 2016;11(3):145–52.
17. Zeckey C, Ehrl D, Kammerlander C, Böcker W, Neuerburg C. [All internal segmental trans-
port in tibial bone defects: first experiences with the PRECICE bone transport system].
Unfallchirurg 2020;123(10):816–21.
18. Olesen UK, Herzenberg JE. Bone transport with internal devices. Tech Orthop.
2020;35(3):219–24.
19. Shannon C, Paley D. Extramedullary internal limb lengthening. Tech Orthop.
2020;35(3):195–200.
20. Spiegl U, Pätzold R, Friederichs J, Hungerer S, Militz M, Bühren V. Clinical course, complica-
tion rate and outcome of segmental resection and distraction osteogenesis after chronic tibial
osteitis. Injury. 2013;44(8):1049–56.
21. Oh C-W, Apivatthakakul T, Oh J-K, et al. Bone transport with an external fixator and a locking
plate for segmental tibial defects. Bone Joint J. 2013;95-B(12):1667–72.
22. Ashman O, Phillips AM. Treatment of non-unions with bone defects: which option and why?
Injury. 2013;44(Suppl 1):S43–5.
23. Sheridan GA, Fragomen AT, Rozbruch SR. Integrated limb lengthening is superior to classical
limb lengthening: a systematic review and meta-analysis of the literature. J Am Acad Orthop
Surg Glob Res Rev. 2020;4(6):e20.00054. https://doi.org/10.5435/JAAOSGlobal-D-20-00054.
24. Bernstein M, Fragomen AT, Sabharwal S, Barclay J, Rozbruch SR. Does integrated fixation
provide benefit in the reconstruction of posttraumatic tibial bone defects? Clin Orthop Relat
Res. 2015;473(10):3143–53.
25. Pierrie SN, Hsu JR. Shortening and angulation strategies to address composite bone and soft
tissue defects. J Orthop Trauma. 2017;31(Suppl 5):S32–5.
26. Rigal S, Merloz P, Le Nen D, Mathevon H, Masquelet A-C, French Society of Orthopaedic
Surgery and Traumatology (SoFCOT). Bone transport techniques in posttraumatic bone
defects. Orthop Traumatol Surg Res. 2012;98(1):103–8.
27. Keshet D, Addar A, Bernstein M. Principles of motorized internal lengthening of long bones.
Tech Orthop. 2020;35(3):158–63.
28. Fragomen AT. Motorized intramedullary lengthening nails: outcomes and complications. Tech
Orthop. 2020;35(3):225–32.
29. Mi M, Papakostidis C, Wu X, Giannoudis PV. Mixed results with the Masquelet technique: a
fact or a myth? Injury. 2020;51(2):132–5. https://doi.org/10.1016/j.injury.2019.12.032.
30. Masquelet AC. The induced membrane technique. Orthop Traumatol Surg Res.
2020;106(5):785–7. https://doi.org/10.1016/j.otsr.2020.06.001.
31. Andrzejowski P, Masquelet A, Giannoudis PV. Induced membrane technique (Masquelet) for
bone defects in the distal tibia, foot, and ankle: systematic review, case presentations, tips, and
techniques. Foot Ankle Clin. 2020;25(4):537–86.
32. Siboni R, Joseph E, Blasco L, et al. Management of septic non-union of the tibia by the
induced membrane technique. What factors could improve results? Orthop Traumatol Surg
Res. 2018;104(6):911–5. https://doi.org/10.1016/j.otsr.2018.04.013.
33. Klein C, Monet M, Barbier V, et al. The Masquelet technique: current concepts, animal mod-
els, and perspectives. J Tissue Eng Regen Med. 2020;14(9):1349–59.
34. Aurégan J-C, Bégué T. Induced membrane for treatment of critical sized bone defect: a
review of experimental and clinical experiences. Int Orthop. 2014;38(9):1971–8. https://doi.
org/10.1007/s00264-014-2422-y.
35. Liu Q, He H, Duan Z, et al. Intercalary allograft to reconstruct large-segment diaphy-
sis defects after resection of lower extremity malignant bone tumor. Cancer Manag Res.
2020;12:4299–308.
36. Escudero MI, Poggio D, Alvarez F, Barahona M, Vivar D, Fernandez A. Tibiotalocalcaneal
arthrodesis with distal tibial allograft for massive bone deficits in the ankle. Foot Ankle Surg.
2019;25(3):390–7.
37. Houben RH, Rots M, van den Heuvel SCM, Winters HAH. Combined massive allograft and
intramedullary vascularized fibula as the primary reconstruction method for segmental bone
loss in the lower extremity: a systematic review and meta-analysis. JBJS Rev. 2019;7(8):e2.
38. Friedrich JB, Moran SL, Bishop AT, Wood CM, Shin AY. Free vascularized fibular graft sal-
vage of complications of long-bone allograft after tumor reconstruction. J Bone Joint Surg Am.
2008;90(1):93–100.
39. Yazar S, Lin C-H, Wei F-C. One-stage reconstruction of composite bone and soft-tissue defects
in traumatic lower extremities. Plast Reconstr Surg. 2004;114(6):1457–66.
40. Kovoor CC, Jayakumar R, George V, Padmanabhan V, Guild A, Viswanath S. Vascularized
fibular graft in infected tibial bone loss. Indian J Orthop. 2011;45(4):330–5.
41. Tong K, Zhong Z, Peng Y, et al. Masquelet technique versus Ilizarov bone transport for
reconstruction of lower extremity bone defects following posttraumatic osteomyelitis. Injury.
2017;48(7):1616–22.
42. Shen Z, Lin H, Chen G, et al. Comparison between the induced membrane technique and dis-
traction osteogenesis in treating segmental bone defects: an experimental study in a rat model.
PLoS One. 2019;14(12):e0226839. https://doi.org/10.1371/journal.pone.0226839.
43. Cierny G 3rd, Zorn KE. Segmental tibial defects. Comparing conventional and Ilizarov meth-
odologies. Clin Orthop Relat Res. 1994;(301):118–23.
44. El-Gammal TA, Shiha AE, El-Deen MA, et al. Management of traumatic tibial defects
using free vascularized fibula or Ilizarov bone transport: a comparative study. Microsurgery.
2008;28(5):339–46.
Below-Knee Amputations
Roberto Muñoz Molina and Octavio Polanco Torres
Introduction: Below-knee amputation techniques were first described in the late

eighteenth century. Until the end of the nineteenth century, amputation in the case
of tumors, infections, or injuries at the level of the leg or foot was used to maintain
life; at the beginning of the twentieth century, the need for a strong and functional
residual limb with improved soft tissue covering techniques for the subsequent fit-
ting of prostheses or orthoses was established. Today, the increase in life expectancy
associated with the pandemic of diabetes mellitus generates a high number of cases
that are complicated and end in amputations. In this chapter, we describe the differ-
ent types of below-knee procedures, each with its advantages and disadvantages
according to the needs of the case.
Causes: Nowadays, the main cause of below-knee amputation is diabetes (with
the dreaded diabetic foot, which includes neuropathic ulcers, Charcot neuroarthrop-
athy, soft tissue infections, and osteomyelitis) followed by occlusive arterial pathol-
ogy without leaving aside high-energy trauma. Other causes are tumors, deformities
(acquired such as severe hallux valgus, rheumatoid foot, or congenital such as poly-
dactyly), infected orthopedic surgeries, frostbite injuries, electrical burns, and oth-
ers [1, 2].
Evaluation: Whatever the cause or indication for amputation, a multidisciplinary
evaluation is always necessary and advisable, which, in addition to the orthopedic
surgeon, includes an internist (compensation and management of pathologies such
as diabetes mellitus, chronic renal disease, and occlusive vascular pathology), infec-
tious disease specialist (in case of chronic infection, osteomyelitis, or any infectious
complication), psychiatrist [3] (or psychologist), the orthotist or prosthetist, and
finally the rehabilitation team. Since amputation as such is a terminal and definitive
R. Muñoz Molina (*)

Clínica Bupa Antofagasta, Universidad de Antofagasta, Antofagasta, Chile
O. Polanco Torres
Hospital Regional Talca, Universidad Católica del Maule, Talca, Chile

Switzerland AG 2022
818 R. Muñoz Molina and O. Polanco Torres
procedure, the quality of the tissue, the extent of the lesion or infection, the vascular
flow capacity, the nutritional condition, and the immunological capacity must be
properly evaluated. It is also pertinent to request a preoperative evaluation from the
vascular surgeon. Usually, along with the clinical examination that includes evalua-
tion of distal pulses, evaluation of skin condition, capillary filling, and others, the
clinician can also rely on partial measurement of transcutaneous oxygen, an echo-
Doppler, or, if the case warrants it, an angio-CT (or angio-MRI). There are cases in
which the vascular specialist indicates a perfusion surgery prior to the amputation,
thus increasing and improving the healing options and viability of the segment
under treatment.
Conditions for Below-Knee Amputation: The conditions are as follows: (1) sta-
bilization of the patient’s medical conditions in severe acute situations (ATLS,
hypovolemic shock, septic shock, etc.) or in patients with chronic comorbidities
(glycemia, electrolyte disturbances, renal function, anemia, etc.); (2) adequate qual-
ity of life for the patient (e.g., glycemia, electrolyte disturbances, renal function,
and anemia); (3) adequate quality of soft tissue and bone to allow proper closure of
the amputation stump; dehiscence and ulceration of the stump will lead to a higher
risk of more proximal amputations; (4) adequate nutritional and immunological sta-
tus in non-emergency amputations; and (5) adequate arterial blood supply to allow
adequate perfusion of the amputation stump.
Pinzur et al. [4] proposed clinical and laboratory parameters that determine the
evolution of Syme disarticulation.
Preoperative requirements are as follows:
• Ankle brachial arterial index >0.5
• Transcutaneous oxygen >30 mm Hg
• Total lymphocytes >1500 ul
• Serum albumin >3 g/dl
• Prealbumin >16–35 mg/dl
• Glycosylated hemoglobin <8 mg/dl
• Plasma glucose <250 mg/dl
• Renal function (plasma creatinine) <2.0 mg/dl
Other factors are as follows:
• Palpable posterior tibial and pedial pulses
• Body mass index <30 kg/m2
• Stop smoking habit
• High patient motivation
In the study by Sayiner et al, they correlated comorbidities and amputation [5].
Male sex, coronary artery disease, peripheral arterial disease (PAD), proteinuria,
Wagner 3–4 ulcers, smoking, history of diabetic ulcers, and previous amputations
were the effective predictors of the need for amputation. The most significant deter-
minants were PAD with histories of diabetic ulcer.
Types of below–knee amputation are as follows: transtibial, Syme (disarticula-
tion at ankle level), Pirogoff–Boyd, Chopart or tarsal, Lisfranc or tarsal metatarsal,
Below-Knee Amputations 819
transmetatarsal, ray (1 or several), and finally of the toes, which can be partial or
complete (disarticulation at metatarsal phalangeal level).
1 Transtibial Amputation
Guillotine: It is undoubtedly the oldest type of transtibial amputation recorded. In

remote times of medicine, it was very common to observe the “Turkish” or “guil-
lotine” amputation, which was performed as an emergency to save the life of a
patient in the face of a major aggression such as war injuries, firearms, explosions,
traumatic amputations, and infections. The surgery was performed at any level or
area of an injured limb according to the needs of the particular case (forearm, arm,
thigh, leg, hand, wrist, etc.) leaving the soft tissues and bone exposed at the same
level of the cut, always requiring a new procedure for proper closure and coverage
of the stump, which necessarily included further shortening the bony end to achieve
a closure without tension. The great surgeons of those times boasted of performing
the amputation in less than 30 seconds, for which they used large and sharp curved
knives that allowed maneuvering by quickly turning the circumference of the limb
in 360°. It should be noted that this technique did not observe an adequate manage-
ment of the nervous vascular tissue nor a minimum planning of flaps, leaving the cut
of all the exposed planes at the same level of the amputation. Today, it is anecdotal
that in any modern hospital or clinic a salvage amputation like this is performed,
since even in the most serious case with the need for immediate amputation to save
the life of a patient, current standards oblige the surgeon not to perform guillotine
amputations (Fig. 1).
Fishmouth: It is the most common transtibial technique nowadays, being the
standard in tibial amputations, very easy to perform, and with excellent results as
long as certain rules are respected. It is advisable to place an ischemia cuff on the
proximal thigh, which can be inflated if the bleeding warrants it. The vitality and
bleeding of the tissues should always be observed, which in some cases may force
the surgeon to go to a higher level than planned. The amputation level should be
drawn, calculating an adequate flap length to cover the defect. A full-thickness pos-
terior flap including calf and soleus is recommended and should be calculated to
cover from posterior to anterior, ideally 3 times the length of the anterior flap. This
ensures adequate closure without tension. The tibial cut level for prosthetic utility is
a minimum of 15 cm from the anterior tuberosity of the tibia [6]. The tibial osteot-
omy is performed with an oscillating saw. The fibula is not completely resected as
it was established some years ago [7], but an osteotomy of the fibula is preferred
about 2 cm more proximal to the level of the tibial cut, thus avoiding the classic
lateral bony prominence. The sharp and cutting edges of both the tibia (anterior) and
fibula (lateral) should be rounded, thus achieving a cylindrical residual limb, ideally
with homogeneous coverage and without hyperpressure points that could cause
future support ulcers or pressure injuries in contact with the prosthesis. Currently, it
is recommended to suture the deep muscular flap (fascia) and also the Achilles
Fig. 1 Photograph shows a case file of a patient who underwent a “Turkish style” amputation.
Note that with the passage of time, along with the appearance of gratulatory tissue, retraction of
the soft tissues is also observed, revealing the exposure of the tibia and fibula at the same level.
Subsequently, it had to be converted to a classic amputation with a “fish mouth” technique as
shown in the sequence. (Courtesy of Dr. Lobos)
tendon, to achieve a point of anchorage and traction of the flap, thus avoiding retrac-
tion and muscular atrophy with consequent weakening and thinning of the muscular
cushion of the residual limb. The closure should be without dead spaces to avoid
hematomas. It is always prudent and advisable to identify the nervous vascular bun-
dle, which is temporarily marked with colored vascular tapes. The arteries (poste-
rior tibial, anterior tibial, and fibular) should be ligated. The nerves should be
identified and sectioned with a scalpel under gentle traction to achieve retraction
into the soft tissues (minimum 5 cm). A nerve should never be left in direct contact
with the bone because of the risk of generating painful neuroma. The use of drain-
age is at the surgeon’s discretion depending on the patient’s own characteristics and
bleeding observed. In case it is used, it is usually removed in 12 hours. The aponeu-
rotic muscle plane is sutured with separate stitches using resorbable suture 2.0,
achieving the closure of the stump. The subcutaneous is sutured with separate total
stitches. Finally, the closure of the cutaneous plane is performed, always avoiding
tension in the closing stitches (separate stitches, monofilament suture 3.0, or brack-
ets according to the surgeon’s preference). It is not uncommon to generate “dog
ears” on both edges of the operative wound. Its resection and plasty are at the sur-
geon’s discretion. The use of plaster is not recommended. It should be kept in mind
that in spite of all the care and precautions taken, not all amputations evolve well, a
situation that increases in cases of diabetic patients or with previous occlusive arte-
rial pathology. An amputated patient should remain hospitalized (at least one week
after surgery) until it is certain that the operative wound is on the right track and
shows adequate signs of healing. If suffering or necrosis of the soft tissues is
observed, the patient should not hesitate to undergo a surgical cleaning with even-
tual revision of the amputation level if necessary. In diabetic patients or with periph-
eral vascular pathology, cryotherapy is not recommended as postoperative support
because it can generate cold burns and borderline vasoconstriction that could nega-
tively affect the evolution of the operative wound. If the evolution is satisfactory and
healing is adequate, the patient can be discharged within 5–7 days, ideally with 2
canes or a walker. It may be necessary to leave oral antibiotics for 5–7 days as
needed. The postoperative check-up is fixed between 7 and 10 days and may be
done earlier if there are any complications. The classic recommendations for any
operative wound are also valid in this case: Do not wet the wound and do not manip-
ulate it. In case healing is required, it should be performed only by trained personnel
and ideally coordinated with the treating physician. Compressive bandaging [8] for
molding and preparation of the residual limb for its future prosthesis can be started
from the first postoperative week if the conditions allow it, always by trained per-
sonnel, avoiding excessive or ischemic compression [8]. The stitches are usually
kept for about 5 weeks after which they are removed, and an appointment is made
with the rehabilitation team to prepare the patient (and his residual limb) for his
future prosthesis. More than half of amputee patients present depression and
increased levels of distress [3]. Psychological support is ideally initiated before sur-
gery and will continue in parallel for as long as the patient needs it and may even
continue after the orthopedic surgeon has discharged the patient. In cases of severe
acute trauma, and considering that amputation is a definitive procedure, it is not
recommended as entry management, and however, there are situations in which the
viability of the segment is null and the patient’s life is at risk. The ideal recom-
mended height of the osteotomy cannot always be respected if the lesion is very
proximal, since it will depend in great part on what the damage and viability of the
tissues allow. That is why the surgical consent should always mention the possibil-
ity of complication, cleanliness, revision in the ward, or even a new amputation if
the evolution warrants it. According to the study by Low and collaborators [9],
lower extremity amputees secondary to traumatic causes present a high rate of com-
plications “considering the appearance of a compartment syndrome a risk predictor
for greater complications, increasing hospital stay as well as the amputation revi-
sion rate” (Fig. 2).
Tennis Ball Stump: To avoid thick scars in the prosthetic loading zone and the
annoying “dog ears,” Lobos [10] modified the classic “fish mouth” technique, devel-
oping a technique that can be extended to any amputation of a cylindrical extremity
(arm, forearm, thigh, leg) in which, to achieve a perfect cylindrical closure, he emu-
lated the sutures of a tennis ball where the flaps embrace and generate a rounded
closure. According to Lobos, a typical tennis ball “has two hulls at a 90° angle, the
length of the hulls being three quarters of a circumference at its equator and the width
Fig. 2 Classic fishmouth technique. Note the exact measurement and marking on the skin of the
minimum 15 cm from the tibial tuberosity that must be respected before proceeding with the
amputation. The prominent anterior edge of the tibia should be rounded with a saw to achieve a
blunt edge. Subsequently, the muscle flap is dorsalized and anchored to the bony plane, completely
covering the defect and creating a cushion for prosthetic support. (Courtesy of Dr. Jara)
of one quarter of a circumference.” According to this, he calculated and developed the

flaps in such a way that in the tibia, the superior flap (or short flap) must circumscribe
three quarters of the perimeter circumference of the leg and whose length corre-
sponds to a quarter of the calculated length. Likewise, the posterior flap (which would
correspond to the long mouth of the fishmouth technique) must have a width corre-
sponding to one quarter, but its length must be three quarters of the previous calcula-
tion. It is required that the aponeurotic muscle plane be kept attached to the skin (full
thickness) to avoid necrosis. Both flaps should end in rounded edges allowing the
skin edges to be accurately confronted. This technique respects the recommended
bone length of 15 cm from the tibial tuberosity modifying only the drawing and shape
of the arms of both flaps allowing a perfect coaptation of the edges minimizing the
scar that will be located outside the area of support, also avoiding the classic and
annoying “dog ears.” According to Lobos, drains are rarely necessary (Fig. 3).
2 Hindfoot Amputation
The first line of hindfoot amputation is the Chopart joint, which consists of the talo-
navicular and calcaneus cuboid joint, which corresponds to the transition from the
hindfoot to the midfoot. It is named after the French surgeon François Chopart
(1743–1795). Osteoplastic hindfoot amputation with partial retention of the calca-
neus after talectomy was first described by the Russian surgeon Nikolai Ivanovich
Pirogoff (1810–1881). In the original technique, only the calcaneal tuberosity is
retained, rotated 90° cranially, and fused with the distal tibia, resulting in a consid-
erable shortening of the hindfoot by about 5 cm. The Pirogoff amputation has
Fig. 3 Case of a man, with an advanced soft tissue sarcoma in which transtibial amputation was
decided as the definitive solution. The drawing of the dorsal arm can be seen, which surrounds the
leg in ¾ of the perimeter, leaving the long flap toward the posterior, which will have the same ¾ of
length measured in the perimeter. Both distal edges must be cylindrical and full thickness, allowing
a perfect closure. (Courtesy of Dr. Lobos)
undergone many other modifications over the past 100 years (including Spitzy and
Boyd), some of which allow for even greater length preservation. With the described
modification, the shortening of the leg is only 2–2.5 cm. Amputation at the level of
the ankle joint was first described in 1831 by the Scottish surgeon James Syme
(1799–1870) and later modified by the author himself with resection of the malleoli.
Syme amputation, which leaves a stump on the lower leg, is still counted as a hind-
foot amputation because it is covered with the heel pad. These amputations are
indicated when there are necrotic and inflammatory processes of bone and soft tis-
sues of the foot secondary to medical conditions such as diabetes mellitus, severe
deformities due to Charcot neuroarthropathy, immunological vascular diseases,
necrosis or gangrene due to obstructive arterial disease, tumor diseases, uncorrect-
able neurological or post-ischemic deformities (Volkmann’s syndrome), and com-
plex trauma with non-vital or non-reconstructible forefoot. Partial or total calcaneal
resection is indicated for osteomyelitis, tumors, talectomy due to septic or complete
aseptic talar necrosis, and, in exceptional cases, combined resection of the talus,
calcaneus, and malleoli. The ultimate goal is to achieve loading of the injured limb
with minimal or no loss of leg length along with a stable soft tissue covered by the
sensitive skin of the sole of the foot above the heel.‑
Chopart’s Amputation: Chopart’s disarticulation was first described by François
Chopart in 1792. It corresponds to the disarticulation performed at the level of the
talonavicular joint and the calcaneocuboid joint. It is the first line of rear foot disar-
ticulation and is mostly caused by vascular damage secondary to diabetes (80%),
trauma, or tumors. Its advantage over more proximal amputations is that it preserves
the ankle, and the plantar skin allows full-body weight bearing and does not create
a length discrepancy with the contralateral limb. The disadvantages are that subjects
are more prone to develop severe equinus of the hindfoot over time due to the imbal-
ance generated between the gastrocnemius soleus complex and the weakness or
absence of reconstruction of the dorsiflexor musculature; in addition, the absence of
the forefoot prevents the lever arm that generates heel lift-off in the propulsion
phase of gait [11]. The Chopart joint is made up of 2 essential joints: the articular
facet of the anterior process of the calcaneus and the proximal articular facet of the
cuboid laterally; and the articular facet of the head of the talus together with the
proximal articular facet of the navicular medially. As primary stabilizers, there are
specific ligaments joining the calcaneus with the navicular (third functional joint of
Chopart). In the plantar area, there are three ligaments that go from the medial facet
of the subtalar of the calcaneus to the navicular, the inferior calcaneal navicular liga-
ment, superomedial calcaneal navicular ligament, and the third ligament. These
ligaments are the floor of a fibrocartilaginous structure that corresponds to the
spring ligament and are part of the acetabulum or coxa pedis. Superolaterally, in
relation to the sinus of the tarsus, we find the superomedial branch of the arcuate or
arcuate ligament, joining the anterior process of the calcaneus with the lateral tuber-
osity of the navicular; the inferior branch is part of the calcaneocuboid articular
capsule. Prior to the procedure, a percutaneous lengthening of the Achilles tendon
should be performed with three or four hemi-sections. A dorsal line is marked join-
ing a medial point on the head of the talus 2 cm distal to the medial malleolus and a
lateral point 2 cm distal to the fibula in relation to the end of the anterior process of
the calcaneus; it is continued plantarly with a circular line that reaches the base of
the metatarsals (longest plantar flap) and joins these two points plantarly. From the
dorsal side, the extensor retinaculum is sectioned, the pedis artery is ligated, and the
extensors are sectioned as distally as possible to prepare them for their reinsertion.
The anterior tibial tendon is located and sectioned as distal as possible to prepare it
for reinsertion. The capsule of the talus, navicular joint, is identified and opened.
The posterior tibial tendon is identified, and according to preoperative planning, it
can be used to reinsert in the head of the talus and increase the dorsiflexor force of
the ankle after transfer from posterior to anterior through the passage through the
interosseous membrane of the distal leg. Laterally, the arcuate ligament and superior
capsule of the calcaneocuboid joint are transected and the peroneus longus and
brevis are identified in preparation for reinsertion. At this time, the plantar capsule
and the spring ligament under the head of the talus and capsule of the calcaneocu-
boid joint are sectioned. The medial and lateral plantar artery is identified and
ligated. It is dissected distally, and at the level of the base of the metatarsals, plantar
musculature, plantar fascia, and skin are sectioned. Through bony tunnels, extensors
and tibialis anterior are reinserted in the head of the talus and peroneus longus in the
lateral wall of the calcaneus. Plantar fascia is closed with extensor retinaculum and
skin. The reconstruction of the dorsiflexor musculature in Chopart amputation is
performed by inserting the tendons of the common extensor of the toes and the ten-
don of the anterior tibial in the head of the talus; and the long and short peroneal in
the lateral wall of the calcaneus to avoid the equinus and varus of the rear foot [12].
This would prevent displacement of plantar fat posteriorly by maintaining the axis
of loading from the tibia, through the talus and anterior process of the calcaneus.
However, without the presence of the forefoot, the Achilles tendon lever arm is
stronger than the reinserted dorsiflexors, so functional walking is only achieved
with external prostheses. The results in diabetics with Chopart amputation and dor-
siflexor reconstruction show recurrence of plantar skin ulceration with no improve-
ment in gait function or residual stump pain [13]. To improve standing and gait,
prosthetic devices that restore the loss of biomechanical foot leverage are required.
High-profile prostheses (cover prosthetic devices) are the best option to restore level
walking through the combination of a rigid construction with a ventral cover. This
prosthesis prevents ankle motion and shifts the load center to the forefoot, while the
ankle is in the major dorsiflexion position caused by body weight. Conversely, low-
profile Chopart prostheses do not allow limitation of ankle motion, which prevents
adequate residual foot leverage. The effective lever arm of the foot is at the expense
of ankle dorsiflexion limitation [14, 15]. For the reasons already explained, this
amputation does not generate much acceptance among ankle and foot orthopedic
surgeons, since the great majority of patients who require it present concomitant
pathology that prevents the transposed musculature from maintaining adequate
ankle mobility and prevents them from walking short distances without an orthosis.
Good results have been reported in cases of post-traumatic Chopart amputation
through tibiotalocalcaneal arthrodesis with retrograde nail, screws, or external fix-
ators. This avoids plantar cushion migration, secondary progressive equinus varus,
imbalance between the gastrocnemius–soleus–Achilles system, and reinserted dor-
siflexors. It maintains the normal length of the amputated limb, which improves
function and body image, fundamental for quality of life [12, 16].
Amputation of Pirogoff, Boyd, Modified Pirogoff: This technique was first
described by the Russian surgeon Nicolai Pirogoff in 1854, modified by Boyd and
Spitzy in 1939 and again modified by several authors in the last 20 years [12, 17,
18]. It corresponds to amputation of the foot with removal of the talus and osteo-
plasty of the calcaneus to the surface of the distal tibia. The objective is to preserve
the fat pad of the heel and avoid height discrepancy in both extremities to allow
short distance walking without requiring external prostheses. In the original tech-
nique, the greater calcaneal tuberosity was preserved, rotated through 90°, and fixed
to the distal tibia, resulting in a shortening of 4.5–5 cm; the Boyd technique resects
the anterior process of the calcaneus, at the level of the subchondral bone of the
calcaneocuboid joint, and the tali sustentaculum to fit the verticalized calcaneus into
the mortise. The modified Pirogoff technique makes an oblique cut from the anterior
process of the calcaneus directed 60° to 70° from distal plantar to dorsal proximal
including the posterior, medial, and anterior subtalar facets fusing to the distal tibia
(Fig. 4). The latter two techniques shorten 2–2.5 cm.
To perform the modified Pirogoff technique, the devitalized tissue of the forefoot
to be removed must be clearly delimited and the skin and bone tissue of the calca-
neus must be confirmed to be adequate to perform osteosynthesis or to tolerate
external fixators as a form of stabilization. Two points should be marked medial and
Fig. 4 1–2 Boyd technique. Anterior process cuts, subtalar facet of the calcaneus, and sustentacu-
lum tali. 3–4 Lateral and anterior view of tibiocalcaneal fusion. 5 Modified Pirogoff technique,
anterior and subtalar process cut at 60° from distal plantar to proximal dorsum. 6–7 Lateral and
frontal view of tibiocalcaneal fusion
lateral to the ankle, one centimeter distal to the malleoli, where the dorsal incision
is drawn joining these two points and the plantar incision is drawn with a 5–6 cm
distal circular flap in the shape of a fishmouth joining these two points. The extensor
retinaculum, which is essential for closure, must be identified dorsally. The pedis
artery is identified and ligated and the 2 branches of the superficial peroneal nerve
are tracted and sectioned so that they retract into the proximal soft tissues. The ten-
dons of the anterior tibialis, extensor hallucis longus, extensor digitorum longus,
and the peroneus tertius are identified; they are tractioned and cut at the level of the
myotendinous junction if possible. Laterally, the extensor digitorum brevis muscle
is identified, which is disinserted from its insertion in the cuboid and the dorsal
capsule of the talonavicular and calcaneus cuboid joint is opened. Lateral dissection
is continued by traction and sectioning both peroneal tendons. The sural nerve is
identified, and it is also sectioned with previous traction. It is directed again medi-
ally, the posterior tibial tendon is identified, and flexor digitorum longus and the
nervous vascular bundle of the posterior tibial artery and tibial nerve are identified.
The artery is ligated, and the tibial nerve is sectioned with traction. This step is vital
for the calcaneal irrigation. Once the navicular, talus, and the cuboid are disarticu-
lated from the calcaneus, the talus is tractioned to disarticulate it from the ankle (a
Steinman pin is passed through the neck of the talus to allow traction). The removal
of the talus is performed from posterior to anterior, being the release of the posterior
ligaments critical to avoid injury to the posterior circulation, the deep peroneal
artery posterior to the tibiofibular ligament must be ligated, the interosseous liga-
ment was sectioned, and the talus was removed. The surgical technique of calcaneal
preparation varies depending on whether it is the Boyd or modified Pirogoff tech-
nique already indicated. Osteosynthesis can usually be performed with cannulated
screws; however, if the conditions of the bone tissue do not allow sufficient stability,
it can be stabilized with a circular fixator of the Ilizarov type [19, 20]. It is advisable
to resect the medial and lateral malleolus, since it should maintain the cylindrical
shape of the amputation stump, which will allow a better adaptation of the amputa-
tion stump to the external prosthesis. In the literature review study of 2020 by
Andronic et al. [21], the review of 123 cases showed that the patency of the poste-
rior tibial artery is the main requirement to perform this technique and neuropathy
is not a contraindication since the loading surface of the stump is fixed given by the
osteosynthesis of the calcaneus to the tibia, which avoids the risk of new ulcers
(failure of the procedure with more proximal amputation). The limb shortening is
1.6–2.8 cm, and the functional result is 69% of very good results and 31% of bad
results with no significant differences between the Boyd and modified Pirogoff
technique. These results are reinforced in the work of Nather et al. [22] in which
they conclude that the modified Pirogoff technique has a role in the management of
diabetic foot problems.
Syme amputation: This amputation technique has had its historical indication
with neuropathic diabetic patients who generate plantar ulcers that end in bone
infections and in patients with arterial insufficiency that cause necrotic tissue due to
arterial deficit. It was described by Scotsman James Syme in 1831 and has had mul-
tiple variations up to the present day. The objective of the Syme amputation is to
avoid transtibial amputation, which generates a discrepancy of the limb that pre-
vents it from walking without an orthosis and causes a higher metabolic expense; it
is also associated with a 30% increase in mortality. The other major benefit of Syme
amputation is to preserve the heel cushion or pad without the preservation of the
calcaneus requiring fusion to the tibial plafond, which allows walking short dis-
tances without a prosthesis and allows the fabrication of more comfortable external
prostheses. The publication by Pinzur et al. [4] describes the current surgical tech-
nique, its indications, and results. Patient in supine position, excising area is isolated
with occlusive seal of the compromised extremity prior to presurgical cleaning.
Ischemia cuff is placed at thigh level for bleeding management. Two points are
marked one centimeter anterior to the lateral malleolus, and one centimeter anterior
to the medial malleolus, a line is drawn dorsally and a circular line plantar is fish-
mouth-shaped. The dorsal cut should be direct to the talus and the plantar cut direct
to the calcaneus to create a vital flap. The dorsal skin is opened, branches of the
superficial peroneal nerve are identified, tractioned, and cut, and the saphenous vein
magna is ligated. The extensor retinaculum is identified, dissected, and sectioned
across its entire width (fundamental structure for closure). The retinaculum is
opened and the dorsiflexor tendons, anterior tibial, extensor hallucis longus, exten-
sor digitorum longus, and peroneus tertius are exposed. They are tractioned and cut
at the myotendinous level. Once the anterior tibial artery is identified, it is ligated.
Opening the capsule, proceed alternately with the section of the lateral and medial
ligaments of the ankle. In the medial area of the talus, opening the tibionavicular
ligament of the deltoid, the tendon of the tibialis posterior to plantar is identified, it
is tractioned, and the most proximal part is sectioned, and immediately, the tendon
of the flexor digitorum longus is identified and sectioned. At this point, the vascular
nerve bundle that is intimately related to the flexor hallucis longus tendon should be
identified. The posterior tibial artery is dissected and ligated, and the tibial nerve is
identified, tractioned, and cut. This step is important since the irrigation of the cal-
caneal plantar cushion is through the calcaneal branch of the posterior tibial. Once
the vascular bundle is secured, we proceed to traction of the talus with a bone hook
being careful not to severe the interosseous talocalcaneal ligament so that the trac-
tion of the talus mobilizes the calcaneus anteriorly. This step is the most difficult
and important since a subperiosteal dissection of the calcaneus must be performed,
and this can injure the plantar skin. Before removing the calcaneus from its tendon,
the peroneal tendons and the sural nerve are identified, tractioned, and cut. Care
must be taken when sectioning the posterior talar fibular ligament with the presence
of the deep peroneal artery that runs posterior to the posterior tibial fibular ligament.
Since this ligament is not sectioned, its section may go unnoticed. Once the piece is
removed, it should be checked carefully. Prior to dissection of the calcaneus, the
plantar skin is sectioned and the deep plantar intrinsic musculature is sectioned; in
this step, the sectioned plantar fascia, which is essential for closure, must be
respected. The last osseous procedure is the resection of the fibular malleolus and
the medial malleolus at the level of the articular surface of the tibial plafond. Prior
to closure, hemostasis should be thoroughly checked, and if there is any doubt of
correct hemostasis, a drain should be left through a counter opening. To avoid dis-
placement of the plantar cushion, the Achilles tendon should be fixed to the poste-
rior border of the tibia with transosseous stitches. Anterior closure should include
the plantar fascia with the extensor retinaculum or transosseous stitches between the
plantar fascia and the anterior border of the tibia. The skin is closed with separate
homeostatic stitches. In the systematic review by Braaskma et al. [23] after Syme
amputation in children, bone remodeling and migration of the fat pad of the residual
limb were the most frequent problems, followed by skin problems. In adults, infec-
tions, ulcerations, skin necrosis, wound dehiscence, and painful residual limb were
most frequent. Higher-level amputations were performed in 0% of children and
20% of adults during the follow-up periods of the included studies. The 23-year
review of the Syme technique by Finkler et al. [24] shows lower energy costs com-
pared to below knee amputation, required less rehabilitation, and achieved better
levels of functional independence. The postoperative period of rear foot amputa-
tions should be directed to the preparation of the residual limb to receive the socket
of the external prosthesis. The surgeon applies a plaster or resin bandage (plastic
plaster) over 2 prosthetic socks covering the residual limb. This prevents postopera-
tive edema. After 48 hours, the cast is removed and a removable rigid bandage is
placed after placing a soft gauze as a barrier to protect the skin. A compressible
tubular layer is placed over this padding. This system reduces the edema and pre-
pares the shape of the limb for the prosthesis and protects the residual limb from any
trauma. After three weeks, the stitches are removed, and at the fourth week, the
Fig. 5 1–2. Bedding and anatomical piece in Syme’s amputation. 3–4 Stump closure with drain-
age and healed stump. 5–6. Chopart amputation stump
prosthesis fabrication can begin. In Syme amputation, there are 3 types of amputa-
tion socket designs (Fig. 5): small cover (pelite liner) when the circumference of the
residual limb is between 0 and 0.75 inches; medial gate with circumference between
0.75 and 1.5 inches; and posterior gate with circumference greater than 1.5
inches [25].
3 Transmetatarsal Amputation
This amputation level is reached in those cases in which the damage or compromise
of the forefoot is advanced or irrecoverable, or in those patients who have already
undergone amputations of several successive toes (or partial amputations of a meta-
tarsal) resulting in re-infected ulcers or unmanageable painful support areas. The
transmetatarsal offers an adequate and even level for the amputation, biomechani-
cally balanced since the insertions of the peroneals, anterior and posterior tibialis
are respected [26], although it is true that the power of the push-off is lost, it has in
its favor that the surface on which the load is distributed is more than 50% of that of
the original foot, which must be taken advantage of avoiding generating unbalanced
areas or that could generate new support ulcers, especially in some diabetic patients
or those with peripheral vascular disease. Special attention should be paid to the
shortening of the plantar gastro soleus–soleus complex, which could lead to a ten-
dency to equinus, which associated with an inadequately aligned metatarsal (or with
some residual plantar exostosis or prominence) can lead to new areas of ulcers and/
or infection. The patient should be positioned in the supine position, ideally with the
lower extremity free to move it at will during the surgical procedure, even if intra-
operative support X-rays are needed. It is advisable to have an ischemia cuff posi-
tioned at thigh level, although not inflated, so that the bleeding and vitality of the
tissues can be evaluated, which in some cases may determine to go to a more proxi-
mal level than originally planned. As always, it is recommended to draw with a
marking pencil before using the scalpel. The typical horizontal fishmouth incision
is the easiest and most useful in these cases.
A plantar flap three times the length of the dorsal should be planned, allowing it
to eventually retract dorsally and cover the defect loosely and free of tension. If
there is excess tissue, it can always be resected, but if coverage is lacking or we are
left with a tight closure, it is better to go back and perform the osteotomy at a more
proximal level. The scalpel should be presented at 90° directly to the bone [2],
avoiding beveled cuts and obtaining a full-thickness flap along the entire length of
the incision. The flexor and extensor tendons at this level do not need to be rein-
serted. The vessels of the intermetatarsal spaces should be identified and ligated.
Once the bony plane is reached, the osteotomy should be performed at the most
distal level possible, as far as the case allows (a more distal amputation counteracts
more efficiently the tendency to equinus that the Achilles tendon will exert and vice
versa [27]), always under direct vision and seeking to recreate the metatarsal parab-
ola. The bone is cut with an oscillating saw at 45° from distal to proximal and from
dorsal to plantar [28]. This should be done with careful detail, making sure that no
bony protrusions are left in the new region of metatarsal support. The full-thickness
flap is rotated from plantar to dorsal and firmly sutured with separate stitches of 2.0
resorbable suture until the entire osteotomy is covered, avoiding leaving dead spaces
that could cause hematoma and/or re-infection. During closure, remembering that
the cuff is positioned but not inflated, bleeding is easily evaluated in situ, so that
hemostasis is usually sufficient to not need drains, although if the surgeon deems it
necessary, he can leave it and remove it after 12 hours. The skin is sutured with
nylon 3.0 at separate stitches, always avoiding tension. According to the surgeon’s
discretion, this surgical technique offers the possibility of performing the osteotomy
at 3 levels: in the neck of the metatarsals, in the middle third, or in the proximal
region of these, in which case the insertions of the tibialis anterior and peroneus
must always be protected to maintain the biomechanics of the ankle and foot, being
the transmetatarsal the last level of amputation that allows the patient an acceptable
gait mechanics [26]. It must be kept in mind that the more proximal the amputation
is performed, the greater the deforming power that the Achilles tendon will exert, so
it is recommended to evaluate case by case, being necessary in some cases to add at
the end a transfer of the anterior tibial to the lateral cuneiform (or cuboid) associated
with a tenotomy of lengthening of the Achilles (or gastro release according to the
surgeon’s preference) to ensure a plantigrade foot [27]. The patient’s discharge is
with oral antibiotics for 10–14 days (according to culture and antibiogram). It can
be prolonged in diabetic patients or with peripheral vascular pathology. Unloading
is recommended with 2 crutches for 3–4 weeks according to healing and evolution
of the soft parts. After this, partial loading is authorized until complete closure of
the operative wound is achieved, which usually takes between 5 and 6 weeks, after
which the stitches are removed, and full loading is authorized. It should be kept in
mind that in diabetics the evolution may be slower. They should be referred to the
orthotist to make shoes with spacer padding and also to the kinesiologist to re-
educate and optimize the gait. Psychological support may also be necessary [3]
(Fig. 6).
Tarsometatarsal Amputation: Originally described by Lisfranc from whom it
acquired its name [29], the tarsometatarsal amputation is reserved for injuries whose
damage or severity make it impossible to perform a more distal amputation. Due to
the anatomical level of the cut, the eversion power of the peroneus brevis (base of
the fifth metatarsal) and the dorsiflexor and supinator arm of the tibialis anterior
(inferior and medial region of the medial wedge and base of the first metatarsal) are
lost, leaving the foot with a short lever arm and without opposition to the Achilles
or the posterior tibial, which translates into a stump that will slowly deform in equi-
nus varus, resulting in a vicious gait, with new areas of hyper pressure and infected
ulcers that will end in a more proximal or definitive amputation [30]. That is why in
this amputation, it is mandatory to plan an adequate balancing with tendon
Fig. 6 Transmetatarsal amputation. The net scalpel cut can be seen, with full thickness up to the
bony plane, both dorsally and plantar. The length of the plantar flap is clearly greater than its oppo-
nent, which allows a dorsal rotation of the same giving complete coverage of the defect. It is
important to evaluate and rule out a shortened Achilles, which could generate distal overload and
future pressure ulcers. (Courtesy of Dr. Jara)
reinsertion and augmentation. The surgical technique described is very similar to

the trans metatarsal amputation, ideally with a fishmouth incision of the long plantar
arm to allow dorsalization and closure of the defect. The entire Lisfranc line must
be identified and disarticulated along with all the metatarsals. The novelty here is
the necessary tendon balancing. According to the technique proposed by Greene &
Bibbo [30], the cuboid is drilled 4.0 from dorsal lateral dorsal to lateral plantar pass-
ing the peroneus longus, which is secured in situ, with a loop on itself or with a
biotenodesis screw, and then, the brevis is tightened in a neutral position of the
stump. Then, in the lateral cuneiform, a new tunnel is drilled from dorsal to plantar
and from proximal to distal (4.0 drill), tunneled, and anastomosed on itself the
extensor hallucis longus. The procedure is repeated with the anterior tibial, which
was previously disinserted from the first metatarsal (respecting its insertion in the
first cuneiform) and tunneled with drill 4.0 from dorsal to plantar and from lateral
to medial in the first cuneiform. Finally, an Achilles lengthening should be added to
ensure that the Achilles tension is reduced. From here on, the surgical procedure
does not differ from the previously described transmetatarsal technique, being nec-
essary an exhaustive cleansing with physiological saline, closure by planes avoiding
dead spaces, and then assuring an adequate coaptation of the plantar flap. Drainage
is optional. At discharge, the control is weekly to closely monitor the soft parts, at
the sixth week begins passive rom and partial load with boot, at 8 weeks full load.
As in the transmetatarsal, it will be necessary to consider footwear with forefoot
spacer. Due to the aggressiveness of the amputation and considering the tendon
transfers, the support of a kinesiologist is mandatory for an adequate gait re-educa-
tion. Psychological support is also necessary for prolonged periods of time [3].
Partial or total foot ray amputation is not a technique usually recommended
because it is not able to generate a stump with homogeneous load that allows a gait
with firm support. It is highly probable that it generates a vicious and unstable gait,
with support ulcers and that in a high percentage, will need care, cures, antibiotics
and with time, perhaps a more proximal amputation. It must be taken into account
that the great majority of patients requiring a ray amputation correspond to diabetics
complicated with peripheral vascular pathology who also present a severe infection
or unmanageable necrosis that can only be solved with amputation. On the other
hand, it is necessary to remember that the complete amputation of the first ray will
lose the insertions of the tibialis anterior and peroneus longus, and the amputation
of the fifth ray will lose the insertion of the peroneus brevis, generating an imbal-
ance per se that will increase the risk of transfer ulcers. Some authors suggest a
surgical management as conservative as possible, preferring to resect only the com-
promised metatarsal but respecting the toes [28] of the respective ray, which eventu-
ally translates into multiple and future accommodative procedures. The argument in
favor is that despite the amputation of a metatarsal, the patient does not feel ampu-
tated because he can see his entire foot. However, perhaps a more definitive proce-
dure such as a transmetatarsal amputation is better, avoiding subjecting the patient
to several successive surgeries with associated ulcerative infections that will not
always be easy and simple to manage. According the surgical principles for amputa-
tion recommended by Ramczykowski and Schildhauer [26] who established that the
stump should be as distal as possible, as long as possible, with the largest possible
bearing surface, with a homogeneous load distribution in the bearing zone, with-
stand the most significant possible load and ideally have preserved plantar sensibil-
ity, it will be moderately clear that the amputation of rays as an elective procedure
is not a good solution, less in a diabetic patient or a patient with compromised distal
circulation. Despite the above, if the surgeon decides to perform a first ray amputa-
tion, he can do it with a tennis racket incision (Fig. 7), with the handle proximal to
the metatarsal axis and the head of the racket distal, planning previously the oste-
otomy area so that the flap (full thickness) of the head of the racket can rotate and
cover the defect area loosely. It can be dorsal or medial, depending on the particular
case. The second metatarsal can also be reached through this same incision. For the
fourth and fifth metatarsal, the procedure is similar but with a lateral approach. For
Fig. 7 This sequence shows the versatility of the tennis racket incision for amputation of toes,
metatarsals, or complete rays. The first line shows the handle of the racket on the axis of the
metatarsal(s) and the ball of the racket distally according to the desired level, always keeping in
mind the circular flap that will allow closure of the defect dorsally, medially, or laterally according
to need. Note that for the central toes, it is sufficient to make a single wider “racket.” The first and
fifth metatarsals also allow the racket to be drawn medially or laterally. To resect one/more rays, it
is enough to perform the racket incision more proximal
the third metatarsal, the tennis racket incision is drawn on the dorsum of the foot,
following its axis with the head of the racket distally, which will also allow resection
of the toe(s) in the same procedure if necessary. If the resection of the first or fifth
metatarsal is complete (including the base), it will be necessary to think about trans-
ferring the respective tendons to maintain the adequate balance of the stump. At the
level of the osteotomy, care should be taken to palpate the edges, not leaving in situ
bony prominences or sharp edges in support areas, which should be rounded with
rugina or fine saw if necessary. A sample of bone tissue from the proximal end of
the osteotomy (free margin) should always be sent for biopsy and culture [2], and
the closure should avoid dead spaces. The use of drainage is optional. The postop-
erative management does not differ from that described for transmetatarsal amputa-
tion. In this type of amputation, the use of accommodative padded shoes is
mandatory. Surveillance and patient education regarding the appearance of hyper-
pressure zones should be stricter and closer.
4 Amputation of the Toes
The reasons for amputating a toe can be varied, without a doubt the most frequent is
to observe them secondary to diabetic foot complications (neuropathic ulcers, distal
angiopathy, and deformities due to Charcot neuroarthropathy, infections), trauma
(high-energy accidents, vehicular trauma, exposed fractures), or due to occlusive
arterial disease. Among the less frequent are tumors (malignant such as melanomas,
spine cell cancer, or benign as enchondromas), burns (electrical or freezing), com-
plications of orthopedic surgery, severe infections of soft tissue or involving the
bone, infected onychomycosis with secondary osteomyelitis, irreconstructible
deformities (congenital, severe hallux valgus, rheumatoid foot), etc. This type of
amputation can be partial including only part of the distal phalanx (distal Syme), at
the level of the middle third (middle phalanx), or total which would correspond to a
disarticulation of the toe. How proximal (or distal) the procedure is performed will
depend on the cause or state of the injury, coexistence of ischemia or necrosis, vital-
ity of the soft tissues, possibility of coverage, and/or presence of infection or bone
involvement. It is the surgeon who must evaluate in situ, always trying to be as
conservative as possible, but always keeping in mind that it is better to have a “defin-
itive surgery” than to have to perform several “touch-ups” due to necrosis, infection,
or complications of closure. It is advisable, as long as the conditions of the case
allow it, to leave a minimum bony remnant of the first phalanx [26] to avoid devia-
tion of the other toes. This is especially valid when amputating the second toe, since
if at least the proximal phalanx is preserved, we avoid hallux valgus deviation [2].
However, there are authors who always prefer to disarticulate the toe, since they
argue that by leaving part of the first or second phalanx, there could be deviation in
elevation of the remnant [31]. If the case warrants it and metatarsophalangeal disar-
ticulation of one or more toes is necessary, it will be necessary to send the patient to
the orthotist to make shoes with a spacer for the defect area (filling). Surgical
technique for disarticulation: The ischemia cuff should be placed on the proximal
thigh, but not inflated to allow careful observation of soft tissue viability and perfu-
sion, especially in cases of critical or insufficient perfusion. The tennis racket inci-
sion is recommended, with the handle toward the proximal (metatarsal neck)
achieving complete closure of the defect from plantar to dorsal. Ideally, the flap
should be of full thickness, including from skin to bone, passing through the joint
capsule, thus achieving complete excision of the toe. If amputation of 2 or more toes
is required, a sufficiently wide incision should be drawn to allow for an adequate
tension-free closure flap. The flexor and extensor tendons should be severed without
reattachment. It is also recommended to leave in situ the metatarsal head cartilage,
which presents a natural barrier to bacterial dissemination, while avoiding endo-
medullary bone bleeding. A deep tissue (soft tissue and bone) sample from the most
proximal healthy region of the amputated toe should always be submitted for culture
and biopsy. If the whole toe was infected including the first phalanx, culture and
biopsy should be taken from the remaining metatarsal head. According to Roll and
collaborators [31], the revision rate of the lesser toes is 15%, so that a new surgical
cleaning or an eventual amputation can never be ruled out a priori, which should be
previously warned to the patient and recorded in the informed consent. It is not rec-
ommended to suture the deep planes, preferring only a full-thickness closure, with-
out tension, with separate stitches, and with non-absorbable 2–0 suture, avoiding
leaving spaces that could generate hematomas. It is not usually necessary to use
drains. The dressing should not be tight or compressive.
Surgical Technique for Partial Amputation of a Toe: A classic fishmouth incision
is recommended, calculating the length of the dorsal and plantar flap adequately to
always achieve a tension-free closure. It is ideal to leave the plantar flap slightly
longer, avoiding the future scar to be located in the support area. The incision can be
made at the phalangeal or interphalangeal level according to need. The tendons do
not require additional handling and should not be sutured. If only part of the last
phalanx needs to be resected, it should be considered that the fact of leaving a rem-
nant of the nail can generate more problems than benefits, since the scar tissue that
will be generated could cause a deformed, thickened, or painful nail to grow in
contact with footwear or neighboring toes, so in this case the possible need to com-
pletely resect the nail bed instead of leaving only a portion in situ should be evalu-
ated. Although in the past it was common to leave wounds open for closure by
secondary intention (or while waiting to delimit tissue necrosis), nowadays we do
not recommend such conduct. The authors always prefer complete closure of the
operative wound, avoiding tension in the closure, which could lead to future necro-
sis and/or complications. If the evolution determines the presence of ischemic tis-
sue, frank necrosis, or remaining infection, a new surgical cleaning (and eventual
revision of the amputation level) should be planned. Depending on the adequate
evolution of soft tissues, ruling out ischemic or infectious complications of closure,
the patient can be discharged with oral antibiotics (according to culture and antibio-
gram), using 2 canes and partial loading until complete closure of the operative
wound is achieved, which can usually take between 3 and 5 weeks, after which the
stitches are removed and full loading is authorized. The orthotist should be referred
to make an insole or padded shoe if necessary. Usually, these patients require train-
ing and instruction in self-care of the skin and vigilance for future injuries, espe-
cially at the level of the residual limb, which could eventually generate complications,
ending again in an amputation.
Amputation of the Great Toe: The reasons for amputating the hallux are practi-
cally the same as those for amputating the lesser toes. If only the distal phalanx
needs to be amputated, a fishmouth incision is sufficient. As far as possible, it is
advisable to respect the first phalanx in order to preserve the insertion of the short
flexor as well as the plantar fascia, thus avoiding greater repercussions in the
mechanics and push-off after the loss of the long flexor of the hallux, as well as
overload by transfer to the remaining metatarsal heads [2]. If what we need is to
perform a hallux disarticulation, a tennis racket incision with the handle proximal
(metatarsal shaft) would be useful. The position or pattern of the racket (dorsal,
medial, lateral, or plantar) will depend on how we need to perform the disarticula-
tion. Before making the incision, it is always advisable to draw the racket with a
marker pencil, thus planning the exact location where the flap or “head of the racket”
will be, which should be rotated to dorsal, plantar, or lateral according to the need,
allowing to cover the defect generated (Fig. 7). It should be noted that there are situ-
ations in which disarticulation of the hallux is not enough and partial amputation of
the first metatarsal is necessary. In these cases, a medial tennis racket approach will
allow us a better view and management of the first metatarsal as well as the metatar-
sophalangeal joint of the hallux. Techniques for amputating the first toe, in particu-
lar, can vary depending on the location and extent of the injury, sometimes requiring
accommodation as the soft tissue remnant allows. The idea is to plan and draw the
flap at the skin level, which often needs to include the dorsal plantar skin of the hal-
lux itself to achieve adequate coverage. Personally, we prefer (as long as the lesion
allows it) to leave a remnant of the first phalanx for reasons already explained. Also,
if possible, we leave the cartilage of the first metatarsal head in situ. Once the
infected or injured tissue has been removed, closure is performed, which may some-
times require dorsiflexion of the plantar flap to achieve coverage of the dorsum. The
postoperative management of a hallux amputation does not differ from that described
for the lesser toes with respect to antibiotic management and discharge times. More
than 50% of hallux amputations will generate new ulcers and require a new amputa-
tion at a more proximal level [2].
References
1. Wallace GF. Indications for amputations. Clin Podiatr Med Surg. 2005;22(3):315–28.
2. Boffeli TJ, Thompson JC. Partial foot amputations for salvage of the diabetic lower extremity.
Clin Podiatr Med Surg. 2014;31(1):103–26.
3. Pedras S, Carvalho R, Pereira MG. A predictive model of anxiety and depression symptoms
after a lower limb amputation. Disabil Health J. 2018;11:79–85.
4. Pinzur MS, Stuck R, Sage R, Hunt N, Rabinovich Z. Syme ankle disarticulation in patients
with diabetes. J Bone Joint Surg. 2003;85-A(9):1667–72.
5. Sayiner ZA, et al. Patients' clinical charecteristics and predictors for diabetic foot amputation.
Prim Care Diabetes. 2019;13:247–51.
6. Molina CS, Faulk J. Lower extremity amputation. In: StatPearls [Internet]. Treasure Island:
StatPearls Publishing; 2020.
7. Stahel PF, et al. Concepts of transtibial amputation: Burgess technique versus modified
Brückner procedure. ANZ J Surg. 2006;76:942–6.
8. Ramczykowski T, Schildhauer TA. Amputation of the lower limb - treatment and management.
Z Orthop Unfall. 2017;155(4):477–98. German.
9. Low EE, Inkellis E, Morshed S. Complications and revision amputation following trauma-
related lower limb loss. Injury. 2017;48(2):364–70.
10. Muñón de amputación con extremo redondeado: diseño de colgajos. Lobos Bermudez, Luis.
LXXXIX Congreso Chileno e Internacional de Cirugía; 2006.
11. Dillon MP, Fatone S, Hodge MC. Biomechanics of ambulation after partial foot amputation: a
systematic literature review. J Prosthet Orthot. 2007;19:2–35.
12. Rammelt S, Olbrich A, Zwipp H. Oper Orthop Traumatol. 2011;23:265–79.
13. Brodell Jr JD, et al. Chopart amputation: questioning the clinical efficacy of a longstanding
surgical option for diabetic foot infection. J Am Acad Orthop Surg. 2020;28:684–91.
14. Aldridge Whitehead JM, Russell Esposito E, Wilken JM. Stair ascent and descent biomechani-
cal adaptations while using a custom ankle-foot orthosis. J Biomech. 2016;49(13):2899–908.
15. Kaib T, Block J, Heitzmann DWW, Putz C, Alimusaj M, Wolf SI. Prosthetic restoration of the
forefoot lever after Chopart amputation and its consequences onto the limb during gait. Gait
Posture. 2019;73:1–7.
16. Chiu Y-C, Chung T-C, Wu C-H, Tsai K-L, Jou I-M, Tu Y-K, Ma C-H. Chopart amputation with
tibiotalocalcaneal arthrodesis and free flap reconstruction for severe foot crush injury. Bone
Joint J. 2018;100-B(10):1359–63.
17. Zwipp H. Chirurgie des Fußes. Wien – New York: Springer; 1994.
18. Rijken AM, Raaymakers ELFB. The modified Pirogoff amputation for traumatic partial foot
amputations. Eur J Surg Acta Chirurgica. 1995;161(4):237–40.
19. Bilgehan Tosun, MD. Foot & Ankle International. November 2011;32(11).
20. Langeveld ARJ, et al. The Pirogoff amputation for necrosis of the forefoot: surgical technique.
Bone Joint Surg Am. 2011;93(Suppl 1):21–9.
21. Andronic O, et al. Modifications of the pirogoff technique in adults: A retrospective analysis
of 123 cases. J Orthop. 2020;18:5–12.
22. Abdul Aziz Mohd Nather, et al. Results of the modified Pirogoff amputation with cannulated
screws for diabetic foot infection. Singapore Med J. 2019;60(7):339–42.
23. Braaksma R, Dijkstra PU, Geertzen JHB. Syme amputation: a systematic review. Foot Ankle
Int. 2018;39:284–91.
24. Finkler ES, Marchwiany DA, Schiff AP, Pinzur MS. Long-term outcomes following Syme’s
amputation. Foot Ankle Int. 2017;38(7):732–5.
25. Philbin, et al. Syme Amputation and Prosthetic Fitting Challenges. Techniques in Foot and
Ankle Surgery. 2007;6(3):147–55.
26. Cano DP, Elvira RG. Amputaciones de la extremidad inferior en el paciente diabetico. Mon
Act Soc Esp Med Cir Pie Tobillo. 2018;10:57–65.
27. Clark GD, et al. Tendon balancing in pedal amputations. Clin Podiatr Med Surg.
2005;22:447–67.
28. Baumgartner R. Forefoot and midfoot amputations. Oper Orthop Traumatol.
2011;23(4):254–64. German.
29. LisFranc J. Nouvelle methode operatoire pour l’amputation partielle dans so articulation tar-
sos- metatarsienne. Paris7 Sabon; 1815.
30. Greene CJ, Bibbo C. The Lisfranc amputation: a more reliable level of amputation with proper
intraoperative tendon balancing. J Foot Ankle Surg. 2017;56(4):824–6.
31. Roll C, Forray M, Kinner B. Amputation and exarticulation of the lesser toes. Oper Orthop
Traumatol. 2016;28(5):345–51.
Part VI
Adult Orthopaedics: Tendinopathy, Soft
Tissue Pathology and Systemic Diseases
Insertional Achilles Tendinopathy:
Diagnosis and Treatment
Giovanni Carcuro and Manuel J. Pellegrini P.
1 Introduction
Pain in relation to the Achilles tendon is a relatively frequent symptom, both in the
general population and in those who practice sports. In general, this condition
occurs in the context of repetitive activities and overuse. It may be related to an
increase in the performance of sports activities, but it may also be related to intrinsic
conditions of the patient, such as overweight and hindfoot deformities. Given the
transversality with which this pathology affects the population, it is estimated that it
produces a considerable impact in lost working days and in expenses for the health
system. As epidemiological data, Achilles tendinopathy in general has an incidence
in the population that ranges between 7% and 9% [1] and approximately one third
of them correspond to pathology in its insertion [1–4].
The most characteristic symptom is pain, which may be associated with decreased
mobility or difficulty in loading and dorsal flexion of the ankle. This is particularly
frequent after prolonged periods of rest and may lead to difficulty in wearing con-
ventional footwear.
Pathophysiologically, diseased tendons have three essential differences with
healthy tendons that could explain the pain and dysfunction associated with this
pathology: (1). Vascularization, rarely in healthy tendons the presence of blood ves-
sels, is observed in the insertion of the Achilles tendon, and on the contrary, studies
with echo-Doppler have shown the presence of vessels in pathological tendons
instead of connective tissue in the periphery of the insertion. (2). Healthy tendons
G. Carcuro (*)
University of the Andes Clinic, Las Condes, Chile
M. J. Pellegrini P.
University of the Andes Clinic, Las Condes, Chile
Clinical Hospital of the University of Chile, Santiago, Chile

Switzerland AG 2022
842 G. Carcuro and M. J. Pellegrini P.
are aneuronal. Only in pathological tendons, hypersensitivity has been observed in

the area as a consequence of the innervation of the area and increase in local noci-
ceptors. (3). Degenerative changes occur in the tendinous insertion, which means
alteration in the order and disposition of the collagen fibers, partial rupture of fibers,
and fatty infiltration.
From the anatomical point of view, the Achilles tendon originates in the myoten-
dinous junction of the gastrocnemius–soleus complex and plantaris [5], to descend
and insert 2 cm distal to the posterior tuberosity of the calcaneus in a crescent shape
[6, 7]. This particular arrangement allows the dissipation of the loads to which the
tendon is exposed [7–9]. In the vicinity of this insertion, the presence of two bursae
is described: the first between the Achilles and the calcaneus; and the second
between the tendon and the skin [6, 7]. This anatomical disposition determines that
three pathological entities can be established in the area: (1). insertional tendinopa-
thy, (2). retrocalcaneal bursitis, and (3). superficial bursitis. In addition, Dickinson
et al. [10] added a fourth possibility known as the “pump bump” and refer to an
overgrowth of the posterolateral region of the calcaneal tuberosity [11]. The pump
bump is often confused with Haglund’s disease or deformity, and it is worth clarify-
ing that the latter is the prominence found on the dorsum of the calcaneus anterior
to the insertion of the tendon and that the literature has shown that its presence or
size has no direct relationship with the development of insertional disease. From the
clinical point of view, it is not easy to differentiate these entities, the three are char-
acterized by pain in relation to the greater tuberosity of the calcaneus, differentiat-
ing element is the presence of increased volume and erythema in superficial bursitis
and “pump bump,” and acute local inflammatory changes are rare to see in retrocal-
caneal bursitis and insertional tendinopathy itself.
In images, it is considered normal if the tendon insertion has a thickness of less
than 6 mm. This measurement has generated a graduation based on the study in the
axial slice of the T1 MRI, differentiating three degrees: (1). posterior antero-anterior
diameter between 6 and 8 mm without tendon degeneration, (2). diameter >8 mm
with degeneration <50%, and (3). diameter >8 mm with degeneration greater than
50%. This differentiation has a relevant prognostic implication, since grades 2 and
3 are more frequently related to failure of conservative treatment [4].
The presence of posterior osteophytes by traction is not a reflection of the sever-
ity of the lesion, but it is described that the larger their size, the greater the possibil-
ity of presenting symptoms in relation to the area and it would also be related to the
failure of conservative therapeutic measures [12–14]. Additionally, there is no sup-
port in the literature to demonstrate that the shape of the calcaneus and Haglund’s
deformity are related to the development of insertional pathology [15, 16].
From this information, it can be extracted that the imaging study of this pathol-
ogy considers fundamentally 2 examinations, the lateral weight bearing ankle radio-
graph, where the presence and size of enthesophytes or calcifications in the area are
evaluated and this is complemented with an MRI that will allow grading the dam-
age, with which the prognosis of the pathology and possibilities of success of the
conservative treatment can be established [12, 17]. In our opinion, ultrasonography
is not a useful test, since it does not provide useful information for therapeutic deci-
sions and it is operator dependent, making it an unreliable tool.
Insertional Achilles Tendinopathy: Diagnosis and Treatment 843
The available evidence for the treatment of this pathology is poor, generating
long periods of treatment in our patients with uncertain clinical results.
Most studies suggest that treatment at an initial stage should be conservative,
reserving surgical management for patients in whom it fails. Surgical alternatives
include minimally invasive techniques, endoscopic techniques, and open surgery. In
this chapter, we will try to show these different alternatives and our vision of the
therapeutic approach to this pathology.
2 Therapeutic Measures
Together with the diagnosis and grading of the lesion, our first indication is conser-
vative treatment. This is based, as in all overuse pathology, on the control of the
extrinsic and intrinsic factors that produce it. Within the extrinsic factors, the first
thing will be the modification of the sports activities or of the daily life that are
considered deleterious for this pathology, and in this sense, the sportsmen will have
to modify the loads of training and to suspend the activities of impact and rebound,
in addition to pay attention in the surfaces in which they are training and in the cor-
rect use of the sport footwear in relation to the sport that he/she practices. Among
the intrinsic factors that should be evaluated and corrected are leg length asymme-
tries, malalignments, foot deformities, joint stiffness, muscular imbalances, and
neurological deficits should be considered. Once these factors are controlled, we
base our conservative treatment on physical therapy.
Physical therapy (PT) will be based on the use of exercise routines that fundamen-
tally use eccentric contraction as a therapeutic measure. These routines have evi-
dence that supports them but with dissimilar results. The published series report
from 30% of success to 67% of good and excellent results [18–20]. Recent publica-
tions have added to these protocols the importance of maximum load, contraction
speed, and number of repetitions as useful elements to improve the results of these
exercises as a treatment for this pathology [21, 22]. From the point of view of
evidence-based medicine, this treatment has a grade B recommendation.
2.3 Shock Wave Therapy
Shock wave therapy (SWT) has some support in evidence-based medicine, and in
the review carried out by Irwin et al. in 2010 [23], it appears with a grade B recom-
mendation because there are several reports in the literature that show that its use is
more effective in reducing pain than medical–kinetic therapy. We use SWT as a

second line once isolated physical therapy has failed. SWT is always accompanied
by an eccentric exercise protocol [24]. We do not use it as a first option because a
percentage of patients, around 20% [24], do not tolerate this therapy due to the pain
it produces in the area, which leads them to abandon the treatment or to the use of
anesthetics in order to be able to apply it.
2.4 Corticosteroid Infiltration
We do not use infiltration as therapy. We only consider the use of local corticoste-
roids in the case that the predominant condition is retrocalcaneal or superficial bur-
sitis, in which case we indicate it after noninvasive conservative measures have
failed and we perform it under ultrasound vision to avoid degeneration and eventual
tendon rupture that could cause the placement of intra-tendinous corticosteroids
[25]. The use of other substances, such as sclerosing agents (e.g., polidocanol) or
PRP, has poor support in the literature and in our experience has not shown to be
useful in insertional pathology of the Achilles tendon (AT). For these reasons, we do
not indicate it as treatment [26–28].
We consider conservative treatment failure when it has been well performed for at
least 6 months, and there has been no decrease in pain with the performance of
therapeutic exercise protocols associated with the use of shock waves. We also con-
sider suspending conservative treatment if after performing it correctly for 4 months
the symptoms have worsened. If this happens, we indicate surgical treatment, in
which our surgical alternatives are limited to three options: (1). endoscopic or mini-
mally invasive techniques, (2). debridement and Achilles reinsertion surgery, and
(3). transfer of the flexor hallucis longus.
3 Endoscopic and Minimally Invasive Techniques
The advantage of endoscopic and minimally invasive procedures is the low or no

rate of soft tissue or operative wound complications associated with them [15], but
they have not proven to be effective in the treatment of this pathology. Only two
publications of case series show good results in the treatment of this pathology with
endoscopic calcaneoplasty and they are prior to 2010 [29–31]. We reserve the use of
this technique for patients with retrocalcaneal bursitis refractory to medical treat-
ment who have a prominent Haglund’s and MRI images suggestive of
Achilles–Calcaneal impingement, and this refers to the presence of fluid and thick-
ening of the retrocalcaneal bursa and degenerative signs on the ventral aspect of the
tendon insertion. In this case, we performed Haglund’s resection plus debridement
of the pre-Achilles bursa under endoscopic visualization using the arthroscopic
shaver or the MIS burr. We consider a sufficient resection when in the intraoperative
radioscopic control we achieve that the dorsum of the calcaneus is flat.
4 Debridement and Achilles Reinsertion
For all cases where the pathology is centered on the Achilles insertion itself and is
associated with tendon degenerative phenomena, presence of osteophytes, with or
without intratendinous calcifications, and bursitis, our preference is for open
surgery.
5 Surgical Technique
We perform it through a central longitudinal approach (Fig. 1) that completely

exposes the Achilles insertion. The midline incision is preferred because it produces
the least vascular damage to the branches of the tibial and peroneal arteries in addi-
tion to having a low risk of damage to the sural nerve [32]. In the same way, we open
the paratendon and tendon to resect all the damaged tissue, calcifications, and pre-
Achilles bursa preserving only the medial and lateral borders at the insertion (2–3 mm
on each side), which will serve as a reference point for the posterior Achilles reinser-
tion and thus ensure the equinus and physiological tone of the tendon [33] (Fig. 2). If
the insertion has to be completely resected, because the pathology compromises the
AT it in its full width, we use the healthy extremity equinus position as a guide to
know the appropriate tension of the tendon reinsertion. Through the midline approach,
we perform the decompression of the tendon insertion through the resection of
Haglund’s deformity under direct visualization (Figs. 3 and 4). Finally, we proceed
with the reinsertion of the Achilles tendon, which we do with a double row with four
anchors (Figs. 5, 6, and 7), which has shown better results than other single-row
anchor systems, with statistically superior AOFAS scores postoperatively [23, 34].
This treatment strategy has good results; the literature reports success rates of
around 87% [32, 34–40] with complication rates ranging from 6% to 30%, mainly
associated with operative wound complications (hematoma, dehiscence, and infec-
tion), but DVT and Achilles disinsertion have also been reported [32, 34, 37, 39,
40]. To avoid soft tissue complications, we make a careful closure by planes and use
simple stitches with resorbable suture in the deep planes and non-resorbable suture
in the skin. In case of wound dehiscence, we consider the use of advanced healing
techniques, local negative aspiration systems, and finally grafting with microsurgi-
cal free flaps, when the other options have failed.
Fig. 1 Midline incision
6 Flexor Hallucis Longus Transfer
We reserve FHL transfer for cases in which the insertional Achilles pathology is
associated with extensive degenerative tendon damage that prevents adequate reat-
tachment or the resection of the damaged tissue is so extensive that there is no
residual tendon tissue to allow adequate functionality. In these cases, together with
the treatment of the underlying pathology, we reinforce the construct with the trans-
fer of the FHL to the calcaneal tuberosity [23, 41, 42]. This technique is preferably
performed endoscopically, to avoid the soft tissue complications involved in an
open approach, through the standard medial and lateral portals posterior ankle
arthroscopy portals. The FHL is identified and harvested, and then, the insertion
point is prepared, and under mixed endoscopic and fluoroscopic vision, we make
the tunnel where we finally introduce the tendon and fix it with an interference screw.
Fig. 2 Opening of the

peritenon and Achilles
tendon in midline,
preserving the medial and
lateral insertions
7 Postoperative Care
We pay special attention to the operative wound care, with stitches removal not
before 20 days. We do not use immobilization (boot). The high resistance offered by
the double row anchors allows us to indicate a weight bearing of 10% of body
weight from the first week and increasing by 20% per week, achieving the complete
removal of crutches between the fourth and sixth weeks. We indicate passive mobi-
lization and start the rehabilitation program after the first postop week, but without
going beyond neutral dorsiflexion during the first month. We emphasize the man-
agement of postoperative edema, indicating partial rest with the foot elevated, use
of compression stockings, and massage therapy. We usually indicate physical ther-
apy for the first 3 months and then start a progressive sports reintegration program,
to achieve sports restart around the sixth postoperative month.
Fig. 3 Dissection and

resection of Haglund’s
deformity with an
oscillating saw
Fig. 4 View after resection

of Haglund’s deformity
Fig. 5 Placement of the

two anchors of the
proximal row of the
Achilles reinsertion system
with four anchors in
double row
Fig. 6 Placement of the

second distal row of
anchors
Fig. 7 Final image of the

Achilles tendon new
insertion with four double
row anchors
References
1. Kujala UM, Sarna S, Kaprio J. Cumulative incidence of Achilles tendon rupture and tendi-
nopathy in male former elite athletes. Clin J Sport Med. 2005;15(3):133–5.
2. Karjalainen PT, Soila K, Aronen HJ, et al. MR imaging of overuse injuries of the Achilles
tendon. Am J Roentgenol. 2000;175(1):251–60.
3. Khan KM, Forster BB, Robinson J, et al. Are ultrasound and magnetic resonance imaging of
value in assessment of Achilles tendon disorders? A two year prospective study. Br J Sports
Med. 2003;37(2):149–53.
4. Nicholson CW, Berlet GC, Lee TH. Prediction of the success of nonoperative treatment of
insertional Achilles tendinosis based on MRI. Foot Ankle Int. 2007;28(4):472–7.
5. Phisitkul P. Endoscopic surgery of the Achilles tendon. Curr Rev Musculoskelet Med.
2012;5(2):156–63.
6. Benjamin M, Theobald P, Suzuki D, Toumi H. The Achilles tendon. London: Springer; 2007.
7. Benjamin M, Toumi H, Ralphs JR, et al. Where tendons and ligaments meet bone: attachment
sites (entheses) in relation to exercise and/or mechanical load. J Anat. 2006;208(4):471–90.
8. Lohrer H, Arentz S, Nauck T, Dorn-Lange NV, Konerding MA. The Achilles tendon
insertion is crescent-shaped: an in vitro anatomic investigation. Clin Orthop Relat Res.
2008;466(9):2230–7.
9. Syed TA, Perera A. A proposed staging classification for minimally invasive manage-
ment of Haglund’s syndrome with percutaneous and endoscopic surgery. Foot Ankle Clin.
2016;21(3):641–64.
10. Dickinson PH, Coutts MB, Woodward EP, et al. Tendo Achillis bursitis. Report of twenty-one
cases. J Bone Joint Surg Am. 1966;48(1):77–81.
11. Van Dijk CN, Van Starkenburg MN, Wiegerinck JL, et al. Terminology for Achilles tendon
related disorders. Knee Sure Sports Traumatol Arthrosc. 2011;19(5):835–41.
12. Chimenti RL, Chimenti PC, Buckley MR, Houck JR, Flemister AS. Utility of ultrasound
for imaging osteophytes in patients with insertional Achilles tendinopathy. Arch Phys Med
Rehabil. 2016;97(7):1206–9.
13. Mellado J, Rosenberg ZS, Beltran J. Low incorporation of soleus tendon: a potential diagnostic
pitfall on MR imaging. Skeletal Radiol. 1998;27(4):222–4.
14. Sundararajan PP, Wilde TS. Radiographic, clinical, and magnetic resonance imaging analysis
of insertional Achilles tendinopathy. J Foot Ankle Surg. 2014;53(2):147–51.
15. Leitze Z, Sella EJ, Aversa JM. Endoscopic decompression of the retrocalcaneal space. J Bone
Joint Surg Am. 2003;85(8):1488–96.
16. Shibuya N, Thorud JC, Agarwal MR, Jupiter DC. Is calcaneal inclination higher in patients
with insertional Achilles tendinosis? A case-controlled, cross-sectional study. J Foot Ankle
Surg. 2012;51(6):757–61.
17. van Sterkenburg MN, Muller B, Maas M, Sierevelt IN, van Dijk CN. Appearance of the
weight-bearing lateral radiograph in retrocalcaneal bursitis. Acta Orthop. 2010;81(3):387–90.
18. Fahlstrom M, Jonsson P, Lorentzon R, Alfredson H. Chronic Achilles tendon pain treated with
eccentric calf-muscle training. Knee Surg Sports Traumatol Arthrosc. 2003;11(5):327–33.
19. Rompe JD, Furia J, Maffulli N. Eccentric loading versus eccentric loading plus shock-wave
treatment for midportion Achilles tendinopathy: a randomized controlled trial. Am J Sports
Med. 2009;37(3):463–70.
20. Jonsson P, Alfredson H, Sunding K, Fahlstrom M, Cook J. New regimen for eccentric calf-
muscle training in patients with chronic insertional Achilles tendinopathy: results of a pilot
study. Br J Sports Med. 2008;42(9):746–9.
21. Couppe C, Svensson RB, Silbernagel KG, Langberg H, Magnusson SP. Eccentric or concentric
exercises for the treatment of tendinopathies? J Orthop Sports Phys Ther. 2015;45(11):1–25.
22. Malliaras P, Barton CJ, Reeves ND, Langberg H. Achilles and patellar tendinopathy load-
ing programmes: a systematic review comparing clinical outcomes and identifying potential
mechanisms for effectiveness. Sports Med. 2013;43(4):267–86.
23. Irwin TA. Current concepts review: insertional Achilles tendinopathy. Foot Ankle Int.
2010;31(10):933–9.
24. Wei M, Liu Y, Li Z, Wang Z. Comparison of clinical efficacy among endoscopy-assisted radio-
frequency ablation, extracorporeal shockwaves, and eccentric exercises in treatment of inser-
tional Achilles tendinosis. J Am Podiatr Med Assoc. 2017;107(1):11–6.
25. Coombes BK, Bisset L, Vicenzino B. Efficacy and safety of corticosteroid injections and other
injections for management of tendinopathy: a systematic review of randomised controlled tri-
als. Lancet. 2010;376(9754):1751–67.
26. Ohberg L, Alfredson H. Sclerosing therapy in chronic Achilles tendon insertional pain—
results of a pilot study. Knee Surg Sports Traumatol Arthrosc. 2003;11(5):339–43.
27. Murawski CN, Newman H, Kennedy JG. Platelet-rich plasma injection for the treatment of
chronic insertional Achilles tendinopathy. Paper presented at: American Orthopaedic Foot &
Ankle Society Annual Meeting, Keystone, CO; 2011.
28. O’Malley MJ. PRP shows potential for treating Achilles tendinosis. New Orleans, LA:
American Academy of Orthopaedic Surgeons; 2010.
29. Jerosch J, Schunck J, Sokkar SH. Endoscopic calcaneoplasty (ECP) as a surgical treatment of
Haglund’s syndrome. Knee Surg Sports Traumatol Arthrosc. 2007;15(7):927–34.
30. Ortmann FW, McBryde AM. Endoscopic bony and soft tissue decompression of the retrocalca-
neal space for the treatment of Haglund deformity and retrocalcaneal bursitis. Foot Ankle Int.
2007;28(2):149–53.
31. van Dijk CN, van Dyk GE, Scholten PE, Kort NP. Endoscopic calcaneoplasty. Am J Sports
Med. 2001;29(2):185–9.
32. Gillis CT, Lin JS. Use of a central splitting approach and near complete detachment for inser-
tional calcific Achilles tendinopathy repaired with an Achilles bridging suture. J Foot Ankle
Surg. 2016;55(2):235–9.
33. DeOrio MJ, Easley ME. Surgical strategies: insertional Achilles tendinopathy. Foot Ankle Int.
2008;29(5):542–50.
34. Ettinger S, Razzaq R, Waizy H, et al. Operative treatment of the insertional Achilles tendinopa-
thy through a transtendinous approach. Foot Ankle Int. 2016;37(3):288–93.
35. Ahn JH, Ahn CY, Byun CH, Kim YC. Operative treatment of Haglund syndrome with central
Achilles tendon-splitting approach. J Foot Ankle Surg. 2015;54(6):1053–6.
36. Elias I, Raikin SM, Besser MP, Nazarian LN. Outcomes of chronic insertional Achilles tendi-
nosis using FHL autograft through single incision. Foot Ankle Int. 2009;30(3):197–204.
37. Greenhagen RM, Shinabarger AB, Pearson KT, Burns PR. Intermediate and long-term out-
comes of the suture bridge technique for the management of insertional Achilles tendinopathy.
Foot Ankle Spec. 2013;6(3):185–90.
38. Johnson KW, Zalavras C, Thordarson DB. Surgical management of insertional calcific Achilles
tendinosis with a central tendon splitting approach. Foot Ankle Int. 2006;27(4):245–50.
39. Lim S, Yeap E, Lim Y, Yazid M. Outcome of calcaneoplasty in insertional Achilles tendinopa-
thy. Malay Orthop J. 2012;6(suppl A):28–34.
40. Lin HA, Chong HA, Yeo W. Calcaneoplasty and reattachment of the Achilles tendon for inser-
tional tendinopathy. J Orthop Surg (Hong Kong). 2014;22(1):56–9.
41. Hunt KJ, Cohen BE, Davis WH, Anderson RB, Jones CP. Surgical treatment of insertional
Achilles tendinopathy with or without flexor hallucis longus tendon transfer: a prospective,
randomized study. Foot Ankle Int. 2015;36(9):998–1005.
42. McGarvey WC, Palumbo RC, Baxter DE, Leibman BD. Insertional Achilles tendinosis: surgi-
cal treatment through a central tendon splitting approach. Foot Ankle Int. 2002;23(1):19–25.
Non-insertional Achilles Tendinopathy
Rocco Aicale and Nicola Maffulli
1 Anatomy of the Tendon
The Achilles tendon is formed by the confluence of the gastrocnemius and soleus
muscles. The soleus lies deep to the gastrocnemius muscle, arising from the poste-
rior surface of the upper tibia. The Achilles tendon inserts on the posterior surface
of the calcaneus, distal to the postero-superior calcaneal tuberosity, not encased in a
true synovial sheath, the Achilles tendon is surrounded by paratenon, which is com-
posed of a single layer of cells. The paratenon is highly vascularized, and it is
responsible for the tendon’s blood supply [1] through a series of transverse vincula
which reach the tendon and act as passageways for vessels. Another source of blood
comes from vessels arising at the musculo-tendinous and osteo-tendinous junctions
[2, 3]. Healthy tendons are brilliant white, with a fibroelastic texture. The rotation of
the tendon begins about 12–15 cm proximal to its insertion, becoming more marked
in the distalmost 5–6 cm. The tendon spirals approximately 90°, with the medial
R. Aicale (*)
Department of Musculoskeletal Disorders, Faculty of Medicine and Surgery, University of
Salerno, Baronissi, Italy
N. Maffulli
Department of Musculoskeletal Disorders, Faculty of Medicine and Surgery, University of
Salerno, Baronissi, Italy
Queen Mary University of London, Barts and the London School of Medicine and Dentistry,
Centre for Sports and Exercise Medicine, Mile End Hospital, London, UK
Keele University, Faculty of Medicine, School of Pharmacy and Bioengineering, Guy Hilton
Research Centre, Hartshill, Stoke-on-Trent, UK

Switzerland AG 2022
856 R. Aicale and N. Maffulli
fibers rotating posteriorly, and the posterior fibers rotating laterally. Angiographic
injection techniques have demonstrated a zone of hypovascularity 2–7 cm proximal
to the tendon insertion.
Within the extracellular matrix network, tenoblasts and tenocytes constitute
90–95% of the cellular elements of tendons [4]. The remaining 5–10% consists of
fibrochondrocytes, synovial cells of the tendon sheath, and endothelial cells and
smooth muscle cells [5]. Collagen type 1 accounts for 65–80%, while elastin
accounts for about 2% of the dry mass of tendons. Tenocytes and tenoblasts lie
between the collagen fibers along the long axis of the tendon [5].
The innervation of the Achilles tendon originates from 3 main sources:
• Cutaneous nerve trunks
• Muscular nerve trunks
• Peritendinous nerve trunks
Nerve fibers cross and enter the endotenon septa at the musculo-tendinous junction.
Nerve fibers penetrate the epitenon from plexuses in the paratenon. Most nerve fibers do
not actually enter the main body of the tendon, but they terminate as nerve endings on
its surface. Nerve endings of myelinated fibers function as specialized mechanorecep-
tors to detect changes in pressure or tension. Unmyelinated nerve endings act as noci-
ceptors, sensing and transmitting pain. Both sympathetic and parasympathetic fibers
have been identified in tendons [6]. Autonomic peptides such as neuropeptide Y and
vasoactive intestinal peptide, which regulate vasoactivity, are present in tendons [6, 7].
Tendons transmit forces generated by muscle to bone. They also act as a buffer, by
absorbing external forces to limit muscle damage: This function requires mechanical
strength, flexibility, and elasticity [5]. As collagen fibers deform, they respond lin-
early to increasing tendon loads [8]. The configuration is initially lost when the
stretch exceeds 2% but is re-gained if the strain placed on the tendon remains at less
than 4%. If strain exceeds 8%, macroscopic rupture will occur [9, 10]. The tensile
strength of tendons is related to their dimensions and collagen content: A tendon with
a cross-sectional area of 1 sq. cm is capable of supporting 500–1000 kg. Loading of
the Achilles tendon reaches up to 9 kN during running (corresponding to 12.5 times
the body weight), 2.6 kN during slow walking, and less than 1 kN during cycling [11].
2 Introduction
Non-insertional Achilles tendinopathy is the most common condition, representing

between 55% and 65% of disorders [9, 12, 13]. The term “Tendinosis” was used by
Puddu et al. [14] in 1976 to describe the histological changes, which include loss of
the normal collagenous architecture and replacement with an amorphous mucinous
material, hypercellularity, increased glycosaminoglycans, and neovascularization
evident in tendinopathy [15–17]. It was previously thought that inflammation was
not an important factor in the condition [15, 18]; however, recently the importance
of inflammation in the pathological process has been re-evaluated: Inflammation
may be a contributory factor to the development of tendinopathy [19, 20].
Non-insertional Achilles Tendinopathy 857
The term “tendinopathy” is preferred to the previously used term “tendinitis”

because it does not convey the concepts of inflammation or degeneration [21, 22].
In tendinopathy, the essential lesion is failed healing response [23, 24].
The incidence of Achilles tendinopathy has been reported to be as high as 37.3
per 100,000 in some European populations [25–27]. This condition is the result of
intrinsic and extrinsic factors which contribute to the development of non-insertional
Achilles tendinopathy [28]. The first ones are age, body habitus, nutrition, meta-
bolic diseases, genetics, lower limb malalignment, leg length discrepancy, [29, 30]
limited ankle dorsiflexion [31, 32]; the others are training errors and drugs including
steroids and fluoroquinolones [33–35], compression, disuse, and excess loading [2].
Another retrospective study also found various statistically significant associations
between tendinopathy and diabetes mellitus, obesity, and hypertension [36]. Among
the metabolic diseases, the most important is dyslipidemia, but measurement of
cholesterol in patients presenting Achillodynia does not seem to be justified. The
literature nevertheless suggests that it should probably be considered in patients
with bilateral extensive disease or those who give a history of intermittent episodes
of severe Achilles tendon pain lasting a few days [37].
Achilles tendinopathy has been associated with different sporting activities, but mid-
dle and long-distance runners have the greatest susceptibility to it [13, 28, 38–40].
The annual incidence in high-level club runners was between 7% and 9% [41].
Typically, it occurs between 2 cm and 6 cm from the insertion of the Achilles tendon
into the calcaneus [23]. Pain is the major symptom, which can interfere with function,
athletic, and daily activity. The pain is common on first moving after a period of rest.
The origin of pain in tendinopathy of the main body of the Achilles tendon is, how-
ever, controversial [42–44]. Abnormal neoinnervation often accompanies the neovas-
cularization and is thought to play a central role in the development of pain [17,
45–47]. A 2014 meta-analysis concluded that the most appropriate clinical reference
standard for diagnosis of Achilles tendinopathy needed further investigation [48].
4 Diagnosis
4.1 Clinical Diagnosis
Beyond swelling on the tendon posteromedial aspect and palpation pain, some clini-
cal tests have been described for non-insertional Achilles tendinopathy diagnosis.
They can be divided into palpation tests (tendon thickening, crepitus, pain on palpa-
tion, the Royal London Hospital (RLH) test [49], the painful arc sign), and tendon
loading tests (pain on passive dorsiflexion, pain on single heel raise, and pain on
hopping).
The painful arc sign, in which a painful swelling moves with ankle movement,
indicates tendinopathy rather than paratendonitis [50]. Less pain of the swelling in
ankle dorsiflexion is indicative of tendinopathy with the RLH test [51]. Maffulli
et al. studied sensitivity, specificity, reproducibility, and predictive value of palpa-
tion of the painful arc sign and of the Royal London Hospital test in 10 patients with
Achilles tendinopathy and in 14 asymptomatic subjects and found no evidence of a
difference of the three assessment methods (p > 0.05); when the test was combined,
the overall sensitivity was 0.586, and the overall specificity was 0.833 [52].
Hutchinson et al. in 2013 studied the ten clinical tests mentioned above and found
that two tests (location of pain and pain to palpation) are sufficient and accurate for
clinical use [51].
4.2 Instrumental Diagnosis
Ultrasound (US) and magnetic resonance imaging (MRI) scans can occasionally be
useful to identify nature, location, and size of the lesion [53, 54]. The first one may
be useful with the addition of power Doppler, given the correlation of neovascular-
ization areas and area of pain in Achilles tendinopathy [17, 47, 55]. Furthermore,
US may also be used to guide the various injection therapies available. Few studies
compared US with MRI, showing that MRI is better for characterizing degeneration
in Achilles tendon [56, 57], but later research demonstrated better accuracy with US
when compared with MRI scans in the detection of tendinopathy [58]. Newer imag-
ing modalities such as ultrasound tissue characterization and sono-elastography
have yielded promising initial results in improving sensitivity, specificity, and accu-
racy in diagnosis [59, 60]. Further studies may be needed to investigate their role
and application in the management of Achilles tendinopathy.
5 Treatment
5.1 Conservative Management
First-line management is conservative, and different treatments such as nonsteroidal

anti-inflammatory drugs (NSAIDs), physical therapy, taping, cryotherapy, shock-
wave therapy, hyperthermia, and various peritendinous injections have been used
with varying success. However, there is lack of evidence-based support, because
few treatment modalities have been investigated in randomized controlled trials [61,
62], and approximately 25% of patients do not respond to conservative manage-
ment [63].
Good results have been reported with eccentric exercises [64–66], which are the
most effective conservative treatment for non-insertional Achilles tendinopathy, but
they alone may not work in all patients [67]; also, their mechanism of action is not
clear [65].
The most commonly used protocol is Alfredson’s protocol: The exercises are
performed in three sets of 15 repetitions, twice a day for 12 weeks [68]. This regime
was demonstrated to be effective in a recent meta-analysis, which outlined the best
pooled data supporting eccentric exercises, with the majority of the studies adopting
Alfredson’s protocol [69]. Hailing this as “probably the greatest single advance in
the management of this condition in the past 20 years,” [70] Alfredson and other
Scandinavian authors have reported excellent results in prospective RCTs [71, 72].
However, the proportion of good and excellent results in other studies using eccen-
tric exercises is definitely lower [67, 73]; this can result from many factors, and the
protocol requires motivated and compliant patients.
A prospective randomized controlled study [74] showed that eccentric strength-
ening plus repetitive low-energy shock-wave therapy (ESWT) was better than
eccentric strengthening alone in terms of Victorian Institute of Sports Assessment—
Achilles (VISA-A) scores and pain ratings at 4 months. The proportion of patients
who were “completely recovered” or “significantly improved” on the Likert scale
was significantly better in the combined therapy group (82%) compared with the
strengthening alone group (56%).
When compared with eccentric strengthening, ESWT showed comparable out-
comes, with 60% of the patients completely recovered in both groups and signifi-
cantly better than the “wait and see” control group [73]. However, success rate was
lower than that seen in other studies, possibly because one third of patients in this
study were not athletes [67]. ESWT works on tissue healing and pain transmission,
modulating both central and peripheral nervous system inducing long-term analge-
sia [75]. Regarding tendon healing, ESWT increases levels of tissue healing factors,
such as TGF-β1 and IGF-I in rat tendinopathy model [76] and significantly decreases
some interleukins [77] and matrix metalloproteinases (MMPs) on cultured teno-
cytes [78].
Generally, first-line management is conservative treatment, with satisfactory
results in 25–45% of cases [79]. In the last few decades, several non-operative treat-
ments modalities have been introduced, with an increasingly relevant role of local
drug injections such as blood products, hyaluronic acid, botulin toxin, polidocanol,
protease inhibitors, corticosteroids, and high-volume image-guided injections
(HVIGI) [62, 80].
Autologous blood products have been used in the management of different mus-
culoskeletal disorders [81, 82],, providing in situ release of molecules able to pro-
mote healing through the stimulation of chemotactic, proliferative, and anabolic
cellular responses [75, 83]. When associated with appropriate physical therapy, PRP
did not produce any additional benefit in terms of clinical outcome [84] or in terms
of restoration of the tendon structure [85].
HA is a novel treatment for tendinopathies, and some studies have demonstrated
that HA injections can lead to better clinical results than corticosteroid injections in
patients suffering from various tendinopathies [86, 87].
The use of HAHyaluronic acid (HA) in tendinopathy is still debated, but, In

vitro studies shown the cells viability and proliferation are increased, counteract-
ing apoptosis in tendon-derived cell [88]. The results of its use in Achilles and
patellar tendinopathy [89] are encouraging, comparable with the effects of PRP in
Level I studies [90]. When HA injections were compared with PRP, there was no
increase in isokinetic strength, and no difference in pain outcomes: more studies
with longer follow-up should be carried out.
HVIGI aim to produce local mechanical effects stretching, breaking or occluding
neo-vessels, and, probably, damaging the accompanying nerve supply, thus decreasing
pain. The effect of decreased pain in patients with AT may result from a possible overlap
effect for the presence of corticosteroids in HVIGI [91]. Indeed, in combination with
eccentric exercises, HVIGI with corticosteroid showed a better short-term improvement
than HVIGI without corticosteroid, though in the longer term, there was no clinically
relevant difference. More studies are needed to define the role of this therapeutic option.
Interesting results have been reported for prolotherapy, consisting in the injec-
tion of hypertonic solution, mainly glucose, which may stimulate an acute inflam-
matory response, followed by collagen deposition, which should strengthen the
suffering structure. This modality has shown potential improvement in pain and
function, but no improvements in long-term results compared with those achieved
following a typical physical therapy program [92].
If conservative management fails, surgical intervention is indicated [93]. Open sur-

gery has shown varying success rates between 50% and 100% [94–97] with removal
of intratendinous lesions, and late-presenting lesions showing significantly fewer
good to excellent results [98, 99]. In particular, for non-insertional Achilles tendinopa-
thy, surgery traditionally involved a large incision and excision of all of the pathologi-
cal tissue, with or without augmentation with a tendon transfer [100] (Figs. 1 and 2).
The main concern of open surgery is the risk of complications: A series of 432
consecutive patients reported an overall complication rate of 11% [101], including
skin-edge necrosis, wound infection, seroma formation, hematoma, fibrotic reac-
tions or excessive scar formation, sural nerve irritation or injury, tendon rupture, and
thromboembolic disease. Complication rate may decrease adopting a minimally
invasive approach [61].
Minimally invasive technique which strips the paratenon from the tendon, either
directly [102] (Fig. 3) or indirectly with high-volume fluid injection [103], has
shown good initial results in relieving symptoms [61, 104]. Multiple percutaneous
longitudinal tenotomies, performed under US guidance, produce good results, with
the further advantage of being able to perform the procedure under local anesthesia
in an outpatient setting [105, 106]. Minimally invasive open debridement with
resection of the plantaris tendon has also shown promising results with minimal
complications in elite athletes and regular patients with non-insertional Achilles
tendinopathy [107–111]. However, there are no comparative studies between these
Fig. 1 The Achilles

tendon is incised sharply in
line with the tendon fiber
bundles, according to
preoperative imaging
studies
Fig. 2 The tendinopathic

tissue must be identified
and sharply excised
a b c d e
Fig. 3 Patient in prone position with a calf tourniquet. Four skin incisions are made (a, b). The
first two incisions are longitudinal the proximal origin of the Achilles tendon; the other two inci-
sions are 1 cm distal to the distal end of the tendon insertion on the calcaneus. A Number 1
unmounted Ethibond (Ethicon, Somerville, NJ) suture thread is inserted proximally, passing
through the two proximal incisions (b). The Ethibond is retrieved from the proximal incisions in a
X-fashion (c, d). Using a gentle see-saw motion, similar to using a Gigli saw, the Ethibond suture
thread is made to distally to the tendon (e). The same steps are repeated for the posterior aspect of
the Achilles tendon which is stripped and freed from the fat of Kager’s triangle
different minimally invasive approaches, and it is unclear when longitudinal tenoto-

mies might be preferred to excise plantaris tendon. Minimally invasive surgical
approach appears to be a useful intermediate step between failed conservative treat-
ment and formal open surgery [61].
Recently, more importance has been given to Achilles tendoscopy to manage this
condition, in particular, for mid-term results in patients with chronic painful due to
non-insertional Achilles tendinopathy are satisfactory with rapid rehabilitation and
reporting that this procedure is safe and has a low complication rate [112]; further-
more, the addition of PRP did not improve outcomes compared with endoscopic
debridement alone [113].
7 Conclusion
Non-insertional Achilles tendinopathy is an activity-limiting condition arising from

failed healing response and may affect both athletes and non-athletes. The majority
of patients will respond to conservative treatment, but when it fails, minimally inva-
sive techniques and tendoscopy show promising results with low complication rates
and may be a good option before open surgery.
References
1. Carr AJ, Norris SH. The blood supply of the calcaneal tendon. J Bone Joint Surg Br.
1989;71:100–1.
2. Aicale R, Tarantino D, Maffulli N. Basic science of tendons. In: Bio-orthopaedics. Berlin,
Heidelberg: Springer. p. 249–73.
3. Aicale R, Tarantino D, Maffulli N. Non-insertional Achilles tendinopathy: state of the art. In:
Canata GL, d’Hooghe P, Hunt KJ, et al., editors. Sports injuries of the foot and ankle. Berlin,
Heidelberg: Springer Berlin Heidelberg. p. 359–67.
4. Aicale R, Tarantino D, Maffulli N. Surgery in tendinopathies. Sports Med Arthrosc Rev.
2018;26:200–2.
5. Kirkendall DT, Garrett WE. Function and biomechanics of tendons. Scand J Med Sci Sports.
1997;7:62–6.
6. Ackermann PW, Li J, Finn A, et al. Autonomic innervation of tendons, ligaments and joint
capsules. A morphologic and quantitative study in the rat. J Orthop Res Off Publ Orthop Res
Soc. 2001;19:372–8.
7. Ljung BO, Forsgren S, Fridén J. Sympathetic and sensory innervations are heterogeneously
distributed in relation to the blood vessels at the extensor carpi radialis brevis muscle origin
of man. Cells Tissues Organs. 1999;165:45–54.
8. Kleiner DM. Human tendons: anatomy, physiology and pathology. J Athl Train.
1998;33:185–6.
9. Kvist M. Achilles tendon injuries in athletes. Sports Med Auckl NZ. 1994;18:173–201.
10. Leppilahti J, Orava S, Karpakka J, et al. Overuse injuries of the Achilles tendon. Ann Chir
Gynaecol. 1991;80:202–7.
11. Komi PV, Fukashiro S, Järvinen M. Biomechanical loading of Achilles tendon during normal
locomotion. Clin Sports Med. 1992;11:521–31.
12. Fahlström M, Lorentzon R, Alfredson H. Painful conditions in the Achilles tendon region in
elite badminton players. Am J Sports Med. 2002;30:51–4.
13. Järvinen TAH, Kannus P, Maffulli N, et al. Achilles tendon disorders: etiology and epidemi-
ology. Foot Ankle Clin. 2005;10:255–66.
14. Puddu G, Ippolito E, Postacchini F. A classification of Achilles tendon disease. Am J Sports
Med. 1976;4:145–50.
15. Khan KM, Cook JL, Bonar F, et al. Histopathology of common tendinopathies. Update and
implications for clinical management. Sports Med Auckl NZ. 1999;27:393–408.
16. Xu Y, Murrell GAC. The basic science of tendinopathy. Clin Orthop. 2008;466:1528–38.
17. Alfredson H, Ohberg L, Forsgren S. Is vasculo-neural ingrowth the cause of pain in chronic
Achilles tendinosis? An investigation using ultrasonography and colour Doppler, immu-
nohistochemistry, and diagnostic injections. Knee Surg Sports Traumatol Arthrosc Off J
ESSKA. 2003;11:334–8.
18. Rolf C, Movin T. Etiology, histopathology, and outcome of surgery in achillodynia. Foot
Ankle Int. 1997;18:565–9.
19. Battery L, Maffulli N. Inflammation in overuse tendon injuries. Sports Med Arthrosc Rev.
2011;19:213–7.
20. Abate M, Silbernagel KG, Siljeholm C, et al. Pathogenesis of tendinopathies: inflammation
or degeneration? Arthritis Res Ther. 2009;11:235.
21. Maffulli N, Khan KM, Puddu G. Overuse tendon conditions: time to change a confusing ter-
minology. Arthrosc J Arthrosc Relat Surg Off Publ Arthrosc Assoc N Am Int Arthrosc Assoc.
1998;14:840–3.
22. Khan KM, Cook JL, Kannus P, et al. Time to abandon the ‘tendinitis’ myth.
BMJ. 2002;324:626–7.
23. Longo UG, Ronga M, Maffulli N. Achilles tendinopathy. Sports Med Arthrosc Rev.
2009;17:112–26.
24. Maffulli N, Aicale R. Update on non-insertional Achilles tendinopathy. Fuß Sprunggelenk.
2019;17:248–56.
25. Leppilahti J, Puranen J, Orava S. Incidence of Achilles tendon rupture. Acta Orthop Scand.
1996;67:277–9.
26. Levi N. The incidence of Achilles tendon rupture in Copenhagen. Injury. 1997;28:311–3.
27. Nyyssönen T, Lüthje P, Kröger H. The increasing incidence and difference in sex distribution
of Achilles tendon rupture in Finland in 1987–1999. Scand J Surg. 2008;97:272–5.
28. Wilder RP, Sethi S. Overuse injuries: tendinopathies, stress fractures, compartment syn-
drome, and shin splints. Clin Sports Med. 2004;23:55–81. vi
29. Waldecker U, Hofmann G, Drewitz S. Epidemiologic investigation of 1394 feet: coincidence
of hindfoot malalignment and Achilles tendon disorders. Foot Ankle Surg Off J Eur Soc Foot
Ankle Surg. 2012;18:119–23.
30. Lersch C, Grötsch A, Segesser B, et al. Influence of calcaneus angle and muscle forces on
strain distribution in the human Achilles tendon. Clin Biomech Bristol Avon. 2012;27:955–61.
31. Gurdezi S, Kohls-Gatzoulis J, Solan MC. Results of proximal medial gastrocnemius release
for Achilles tendinopathy. Foot Ankle Int. 2013;34:1364–9.
32. Rabin A, Kozol Z, Finestone AS. Limited ankle dorsiflexion increases the risk for mid-
portion Achilles tendinopathy in infantry recruits: a prospective cohort study. J Foot Ankle
Res. 2014;7:48.
33. Fleisch F, Hartmann K, Kuhn M. Fluoroquinolone-induced tendinopathy: also occurring with
levofloxacin. Infection. 2000;28:256–7.
34. Corps AN, Harrall RL, Curry VA, et al. Ciprofloxacin enhances the stimulation of matrix
metalloproteinase 3 expression by interleukin-1beta in human tendon-derived cells. A poten-
tial mechanism of fluoroquinolone-induced tendinopathy. Arthritis Rheum. 2002;46:3034–40.
35. Bisaccia DR, Aicale R, Tarantino D, et al. Biological and chemical changes in fluoroquinolone-
associated tendinopathies: a systematic review. Br Med Bull. 2019;130:39–49.
36. Holmes GB, Lin J. Etiologic factors associated with symptomatic Achilles tendinopathy.
37. Singh D. Cholesterol level in non-insertional Achilles tendinopathy. Foot Edinb Scotl.
2015;25:228–31.
38. Järvinen M. Epidemiology of tendon injuries in sports. Clin Sports Med. 1992;11:493–504.
39. Knobloch K, Yoon U, Vogt PM. Acute and overuse injuries correlated to hours of training in
master running athletes. Foot Ankle Int. 2008;29:671–6.
40. Kujala UM, Sarna S, Kaprio J. Cumulative incidence of Achilles tendon rupture and ten-
dinopathy in male former elite athletes. Clin J Sport Med Off J Can Acad Sport Med.
2005;15:133–5.
41. Lysholm J, Wiklander J. Injuries in runners. Am J Sports Med. 1987;15:168–71.
42. Tol JL, Spiezia F, Maffulli N. Neovascularization in Achilles tendinopathy: have we been
chasing a red herring? Knee Surg Sports Traumatol Arthrosc. 2012;20:1891–4.
43. van Sterkenburg MN, van Dijk CN. Mid-portion Achilles tendinopathy: why pain-
ful? An evidence-based philosophy. Knee Surg Sports Traumatol Arthrosc Off J
ESSKA. 2011;19:1367–75.
44. Via AG, Papa G, Oliva F, et al. Tendinopathy. Curr Phys Med Rehabil Rep. 2016;4:50–5.
45. Knobloch K. The role of tendon microcirculation in Achilles and patellar tendinopathy. J
Orthop Surg. 2008;3:18.
46. Kristoffersen M, Ohberg L, Johnston C, et al. Neovascularisation in chronic tendon injuries
detected with colour Doppler ultrasound in horse and man: implications for research and
treatment. Knee Surg Sports Traumatol Arthrosc Off J ESSKA. 2005;13:505–8.
47. Ohberg L, Lorentzon R, Alfredson H. Neovascularisation in Achilles tendons with painful
tendinosis but not in normal tendons: an ultrasonographic investigation. Knee Surg Sports
Traumatol Arthrosc Off J ESSKA. 2001;9:233–8.
48. Reiman M, Burgi C, Strube E, et al. The utility of clinical measures for the diagnosis of
Achilles tendon injuries: a systematic review with meta-analysis. J Athl Train. 2014;49:820–9.
49. Maffulli N, Oliva F, Loppini M, et al. The Royal London Hospital test for the clinical diagno-
sis of patellar tendinopathy. Muscles Ligaments Tendons J. 2017;7:315–22.
50. Williams JG. Achilles tendon lesions in sport. Sports Med Auckl NZ. 1993;16:216–20.
51. Hutchison A-M, Evans R, Bodger O, et al. What is the best clinical test for Achilles tendi-
nopathy? Foot Ankle Surg Off J Eur Soc Foot Ankle Surg. 2013;19:112–7.
52. Maffulli N, Kenward MG, Testa V, et al. Clinical diagnosis of Achilles tendinopathy with
tendinosis. Clin J Sport Med Off J Can Acad Sport Med. 2003;13:11–5.
53. Wijesekera NT, Calder JD, Lee JC. Imaging in the assessment and management of Achilles
tendinopathy and paratendinitis. Semin Musculoskelet Radiol. 2011;15:89–100.
54. Aström M, Gentz CF, Nilsson P, et al. Imaging in chronic achilles tendinopathy: a compari-
son of ultrasonography, magnetic resonance imaging and surgical findings in 27 histologi-
cally verified cases. Skelet Radiol. 1996;25:615–20.
55. Andersson G, Danielson P, Alfredson H, et al. Nerve-related characteristics of ventral para-
tendinous tissue in chronic Achilles tendinosis. Knee Surg Sports Traumatol Arthrosc Off J
ESSKA. 2007;15:1272–9.
56. Neuhold A, Stiskal M, Kainberger F, et al. Degenerative Achilles tendon disease: assessment
by magnetic resonance and ultrasonography. Eur J Radiol. 1992;14:213–20.
57. Movin T, Kristoffersen-Wiberg M, Shalabi A, et al. Intratendinous alterations as imaged by
ultrasound and contrast medium-enhanced magnetic resonance in chronic achillodynia. Foot
Ankle Int. 1998;19:311–7.
58. Khan KM, Forster BB, Robinson J, et al. Are ultrasound and magnetic resonance imaging of
value in assessment of Achilles tendon disorders? A two year prospective study. Br J Sports
Med. 2003;37:149–53.
59. van Schie HTM, de Vos RJ, de Jonge S, et al. Ultrasonographic tissue characterisation of
human Achilles tendons: quantification of tendon structure through a novel non-invasive
approach. Br J Sports Med. 2010;44:1153–9.
60. Docking SI, Ooi CC, Connell D. Tendinopathy: is imaging telling us the entire story? J
Orthop Sports Phys Ther. 2015;45:842–52.
61. Maffulli N, Oliva F, Maffulli GD, et al. Minimally invasive Achilles tendon stripping for the
management of tendinopathy of the main body of the Achilles tendon. J Foot Ankle Surg Off
Publ Am Coll Foot Ankle Surg. 2017;56:938–42.
62. Aicale R, Bisaccia RD, Oliviero A, et al. Current pharmacological approaches to the treat-
ment of tendinopathy. Expert Opin Pharmacother. 2020:1–11.
63. Silbernagel KG, Brorsson A, Lundberg M. The majority of patients with Achilles tendinopa-
thy recover fully when treated with exercise alone: a 5-year follow-up. Am J Sports Med.
2011;39:607–13.
64. Weinreb JH, Sheth C, Apostolakos J, et al. Tendon structure, disease, and imaging. Muscles
Ligaments Tendons J. 2014;4:66–73.
65. Maffulli N, Via AG, Oliva F. Chronic Achilles tendon disorders: tendinopathy and chronic
rupture. Clin Sports Med. 2015;34:607–24.
66. Aicale R, Tarantino D, Maffulli N. Overuse injuries in sport: a comprehensive overview. J
Orthop Surg. 2018;13. Epub ahead of print https://doi.org/10.1186/s13018-018-1017-5.
67. Sayana MK, Maffulli N. Eccentric calf muscle training in non-athletic patients with Achilles
tendinopathy. J Sci Med Sport. 2007;10:52–8.
68. Alfredson H, Pietilä T, Jonsson P, et al. Heavy-load eccentric calf muscle training for the
treatment of chronic Achilles tendinosis. Am J Sports Med. 1998;26:360–6.
69. Sussmilch-Leitch SP, Collins NJ, Bialocerkowski AE, et al. Physical therapies for Achilles
tendinopathy: systematic review and meta-analysis. J Foot Ankle Res. 2012;5:15.
70. Rees JD, Maffulli N, Cook J. Management of tendinopathy. Am J Sports Med.
2009;37:1855–67.
71. Silbernagel KG, Thomeé R, Thomeé P, et al. Eccentric overload training for patients with
chronic Achilles tendon pain--a randomised controlled study with reliability testing of the
evaluation methods. Scand J Med Sci Sports. 2001;11:197–206.
72. Roos EM, Engström M, Lagerquist A, et al. Clinical improvement after 6 weeks of eccentric
exercise in patients with mid-portion Achilles tendinopathy -- a randomized trial with 1-year
follow-up. Scand J Med Sci Sports. 2004;14:286–95.
73. Rompe JD, Nafe B, Furia JP, et al. Eccentric loading, shock-wave treatment, or a wait-and-
see policy for tendinopathy of the main body of tendo Achillis: a randomized controlled trial.
Am J Sports Med. 2007;35:374–83.
74. Rompe JD, Furia J, Maffulli N. Eccentric loading versus eccentric loading plus shock-wave
treatment for midportion Achilles tendinopathy: a randomized controlled trial. Am J Sports
Med. 2009;37:463–70.
75. Rompe JD, Furia JP, Maffulli N. Mid-portion Achilles tendinopathy--current options for
treatment. Disabil Rehabil. 2008;30:1666–76.
76. Chen Y-J, Wang C-J, Yang KD, et al. Extracorporeal shock waves promote healing of
collagenase-induced Achilles tendinitis and increase TGF-beta1 and IGF-I expression. J
Orthop Res Off Publ Orthop Res Soc. 2004;22:854–61.
77. Rees JD, Wilson AM, Wolman RL. Current concepts in the management of tendon disorders.
Rheumatol Oxf Engl. 2006;45:508–21.
78. Han SH, Lee JW, Guyton GP, et al. J.Leonard Goldner Award 2008. Effect of extracorporeal
shock wave therapy on cultured tenocytes. Foot Ankle Int. 2009;30:93–8.
79. Maffulli N, Sharma P, Luscombe KL. Achilles tendinopathy: aetiology and management. J R
Soc Med. 2004;97:472–6.
80. Maffulli N, Papalia R, D’Adamio S, et al. Pharmacological interventions for the treatment
of Achilles tendinopathy: a systematic review of randomized controlled trials. Br Med Bull.
2015;113:101–15.
81. de Albornoz PM, Aicale R, Forriol F, et al. Cell therapies in tendon, ligament, and musculo-
skeletal system repair. Sports Med Arthrosc Rev. 2018;26:48–58.
82. Andia I, Sánchez M, Maffulli N. Platelet rich plasma therapies for sports muscle injuries: any
evidence behind clinical practice? Expert Opin Biol Ther. 2011;11:509–18.
83. Maffulli N, Longo UG, Loppini M, et al. Current treatment options for tendinopathy. Expert
Opin Pharmacother. 2010;11:2177–86.
84. de Jonge S, de Vos RJ, Weir A, et al. One-year follow-up of platelet-rich plasma treatment
in chronic Achilles tendinopathy: a double-blind randomized placebo-controlled trial. Am J
Sports Med. 2011;39:1623–9.
85. de Vos RJ, Weir A, Tol JL, et al. No effects of PRP on ultrasonographic tendon structure
and neovascularisation in chronic midportion Achilles tendinopathy. Br J Sports Med.
2011;45:387–92.
86. Lynen N, De Vroey T, Spiegel I, et al. Comparison of peritendinous hyaluronan injections
versus extracorporeal shock wave therapy in the treatment of painful Achilles’ tendinopathy:
a randomized clinical efficacy and safety study. Arch Phys Med Rehabil. 2017;98:64–71.
87. Gorelick L, Gorelick AR, Saab A, et al. Lateral epicondylitis injection therapy: a safety
and efficacy analysis of hyaluronate versus corticosteroid injections. Adv Tech Biol Med.
2015;3:2379–1764.1000130.
88. Gallorini M, Berardi AC, Berardocco M, et al. Hyaluronic acid increases tendon derived cell
viability and proliferation in vitro: comparative study of two different hyaluronic acid prepa-
rations by molecular weight. Muscles Ligaments Tendons J. 2017;7:208–14.
89. Frizziero A, Oliva F, Vittadini F, et al. Efficacy of ultrasound-guided hyaluronic acid injec-
tions in Achilles and patellar tendinopathies: a prospective multicentric clinical trial. Muscles
Ligaments Tendons J; 9.
90. Kaux J-F, Bornheim S, Dardenne N, et al. Comparison between platelet-rich plasma injec-
tions and hyaluronic acid injections in the treatment of patellar tendinopathies: a randomized
trial. Muscles Ligaments Tendons J. 2019;9:322–7.
91. Boesen AP, Langberg H, Hansen R, et al. High volume injection with and without corticoste-
roid in chronic midportion achilles tendinopathy. Scand J Med Sci Sports. 2019;29:1223–31.
92. Yelland MJ, Sweeting KR, Lyftogt JA, et al. Prolotherapy injections and eccentric loading
exercises for painful Achilles tendinosis: a randomised trial. Br J Sports Med. 2011;45:421–8.
93. Paavola M, Kannus P, Paakkala T, et al. Long-term prognosis of patients with achilles tendi-
nopathy. An observational 8-year follow-up study. Am J Sports Med. 2000;28:634–42.
94. Lohrer H, David S, Nauck T. Surgical treatment for achilles tendinopathy – a systematic
review. BMC Musculoskelet Disord. 2016;17:207.
95. Kvist H, Kvist M. The operative treatment of chronic calcaneal paratenonitis. J Bone Joint
Surg Br. 1980;62:353–7.
96. Schepsis AA, Leach RE. Surgical management of Achilles tendinitis. Am J Sports Med.
1987;15:308–15.
97. Snook GA. Achilles tendon tenosynovitis in long-distance runners. Med Sci Sports.
1972;4:155–8.
98. Paavola M, Kannus P, Orava S, et al. Surgical treatment for chronic Achilles tendinopathy: a
prospective seven month follow up study. Br J Sports Med. 2002;36:178–82.
99. Maffulli N, Binfield PM, Moore D, et al. Surgical decompression of chronic central core
lesions of the Achilles tendon. Am J Sports Med. 1999;27:747–52.
100. Maffulli N, Aicale R, Tarantino D. Autograft reconstruction for chronic achilles tendon dis-
orders. Tech Foot Ankle Surg. 2017;16:117–23.
101. Paavola M, Orava S, Leppilahti J, et al. Chronic Achilles tendon overuse injury: complica-
tions after surgical treatment. An analysis of 432 consecutive patients. Am J Sports Med.
2000;28:77–82.
102. Longo UG, Ramamurthy C, Denaro V, et al. Minimally invasive stripping for chronic Achilles
tendinopathy. Disabil Rehabil. 2008;30:1709–13.
103. Chan O, O’Dowd D, Padhiar N, et al. High volume image guided injections in chronic
Achilles tendinopathy. Disabil Rehabil. 2008;30:1697–708.
104. Alfredson H. Ultrasound and Doppler-guided mini-surgery to treat midportion Achilles ten-
dinosis: results of a large material and a randomised study comparing two scraping tech-
niques. Br J Sports Med. 2011;45:407–10.
105. Testa V, Capasso G, Benazzo F, et al. Management of Achilles tendinopathy by ultrasound-

guided percutaneous tenotomy. Med Sci Sports Exerc. 2002;34:573–80.
106. Maffulli N, Testa V, Capasso G, et al. Results of percutaneous longitudinal tenotomy
for Achilles tendinopathy in middle- and long-distance runners. Am J Sports Med.
1997;25:835–40.
107. Pearce CJ, Carmichael J, Calder JD. Achilles tendinoscopy and plantaris tendon release and
division in the treatment of non-insertional Achilles tendinopathy. Foot Ankle Surg Off J Eur
Soc Foot Ankle Surg. 2012;18:124–7.
108. Alfredson H. Midportion Achilles tendinosis and the plantaris tendon. Br J Sports Med.
2011;45:1023–5.
109. Calder JDF, Freeman R, Pollock N. Plantaris excision in the treatment of non-insertional
Achilles tendinopathy in elite athletes. Br J Sports Med. 2015;49:1532–4.
110. Masci L, Spang C, van Schie HTM, et al. Achilles tendinopathy-do plantaris tendon removal
and Achilles tendon scraping improve tendon structure? A prospective study using ultrasound
tissue characterisation. BMJ Open Sport Exerc Med. 2015;1:e000005.
111. van Sterkenburg MN, Kerkhoffs GMMJ, Kleipool RP, et al. The plantaris tendon and a poten-
tial role in mid-portion Achilles tendinopathy: an observational anatomical study. J Anat.
2011;218:336–41.
112. Wagner P, Wagner E, Ortiz C, et al. Achilles tendoscopy for non insertional Achilles tendi-
nopathy. A case series study. Foot Ankle Surg Off J Eur Soc Foot Ankle Surg. 2020;26:421–4.
113. Thermann H, Fischer R, Gougoulias N, et al. Endoscopic debridement for non-insertional
Achilles tendinopathy with and without platelet-rich plasma. J Sport Health Sci. Epub ahead
of print 30 June 2020. https://doi.org/10.1016/j.jshs.2020.06.012.
Achilles Lengthening
1 Introduction
The gastrocnemius-soleus complex, or triceps surae, is the most powerful muscle

complex influencing the ankle and subtalar joints. The more superficial gastrocne-
mius muscle takes origin from the posterior femoral condyles, while its anterior
counterpart, the soleus muscle, originates more inferiorly from the posterior tibia,
fibula, and interosseous membrane. Distally, the tendon fibers of both muscles con-
verge to become the Achilles tendon that attaches to the calcaneal tuberosity. This
muscle tendon unit spans three joints and has a paramount impact on foot and ankle
pathology. In short, the gastrocnemius muscle tendon unit has effectively tightened
in humans by having to stretch across a straightened knee, ankle, and subtalar joint
during upright stance.
Contracture of the gastrocnemius-soleus complex is often referred to as ankle
equinus. It is a common clinical finding, often associated with a wide variety of foot
and ankle conditions, and its surgical treatment is common in conjunction with
other treatments [1].
M. Resende Sousa (*)

Foot and Ankle Unit at Hospital da Luz, Lisbon, Portugal
D. Ribeiro Mendes
Foot and Ankle Unit at Hospital Cuf Tejo, Lisbon, Portugal
J. Vide
Foot and Ankle Surgeon at Hospital da Luz, Lisbon, Portugal

Switzerland AG 2022
While gastrocnemius recession has long been used as part of the treatment for
spastic equinus due to neurological conditions, such as cerebral palsy, only recently
it has begun to be used to manage foot pain in neurologically healthy adults. A tight
gastrocnemius is a common trait in adult-acquired flatfoot, metatarsalgia, diabetic
forefoot ulceration, plantar fasciitis, Achilles tendinitis, Charcot neuropathic
arthropathy, recurrent ankle sprains, and many others [2–4]. Gastrocnemius reces-
sion for isolated foot pain due to midfoot–forefoot overload syndrome, non-
insertional Achilles tendinopathy, and plantar ulcers of the diabetic foot is evidence
supported as a therapeutic intervention [5].
Equinus is defined as an ankle joint passive dorsiflexion of less than 5 degrees
with the knee extended for gastrocnemius equinus and a dorsiflexion of less than 10
degrees with a flexed knee for gastrocnemius-soleus equinus [6], but the important
parameter to be measured is the dorsiflexion achievable in stance, where the anterior
muscles are silent and the gastrocnemius resting tone is relevant [1]. Additional
clinical signs of ankle equinus include genu recurvatum, hip flexion, lumbar hyper-
lordosis, and forefoot overload.
This chapter highlights the multitude of factors that contribute to ideal procedure
selection including positioning for adjunctive procedures (supine or prone), site of
incision/visibility of scar, postoperative weight-bearing status, proximity to the
sural nerve, the desired degree of lengthening, and complications. Our approach is
to incorporate all of these factors along with patient-specific indications for optimal
procedure selection.
2 Indications
Achilles surgical lengthening is indicated in ankle equinus, either isolated or associ-

ated with other lower extremity disorder, that has not responded to conservative care
[7]. Typically, the equinus correction is an adjunctive gesture to other procedures,
which has implications regarding patient positioning and postoperative ambula-
tory status.
The surgeon may choose between a tendo-Achilles lengthening (TAL), a
gastrocnemius-soleus recession (GSR), or a gastrocnemius recession (GR) [7]. TAL
is performed on level I [8], either with an open, a minimally invasive or a percutane-
ous approach. GSR and GR can be performed more proximally at different levels (II
to V), either through an open or an endoscopic approach (Fig. 1).
The Silfverskiöld test is used to differentiate between gastrocnemius equinus and
combined gastrocnemius-soleus equinus, which has implications for procedure
selection [9]. In a positive Silfverskiöld test, an ankle equinus is present when the
knee is extended but disappears when the knee is flexed, indicating a gastrocnemius-
driven equinus. Combined gastrocnemius-soleus equinus does not improve with
flexion of the knee.
Achilles Lengthening 871
Anatomic Eponymous
Level
Origin of the
gastrocnemius
Barouk
V
Silfverskiold
Origin of the
soleus
IV Baumann
Distal extent of
gastroc muscle
belly III Strayer
Gastroc
aponeurosis Vulpius
joins soleus Baker
fascia II Modified
tongue in
groove
Proper tendon
Z-lengthening
I Hoke
White
Fig. 1 Surgical procedures and anatomic levels
3 Surgical Techniques
Level I—Tendo-Achilles Lengthening (TAL)

(a) Z-lengthening.
(b) Hoke.
(c) White.
Level II— Gastrocnemius-Soleus Recession (GSR)
(a) Vulpius.
(b) Baker.
(c) Modified Tongue-In-Groove.

Level III—Distal Gastrocnemius Tenotomy
(a) Strayer.
Level IV—Deep Gastrocnemius-Soleus Recession
(a) Baumann.
Level V—Proximal Gastrocnemius Tenotomy
(a) Barouk.
(b) Silfverskiold.
While all approaches may work, procedure selection beyond TAL/GSR versus
GR lacks established patient-centered guidelines. The majority of the literature
involving equinus procedure selection is level 3 or 4 evidence [10].
The goal is to achieve a minimum of 0° of ankle dorsiflexion up to 15°, with the
knee extended [1, 11]. Corrections of more than 30° should be avoided to prevent
tendon rupture [1]. Whenever found, the plantaris tendon is usually an active com-
ponent of the equinus deformity and should be sharply transected.
The amount of required lengthening is important for procedure selection, with
power increments from level V to level I. Expected lengthening for different proce-
dures has been evaluated in cadaver: Baumann 2.1 mm, Strayer 9.7 (14.3 with
soleus aponeurosis release), Baker 20.7 mm, Vulpius 23.2 mm, White 30 mm, and
Hoke 32.9 mm [12]. Despite these results, ankle dorsiflexion improvements in vivo
are variable among the different procedures, ranging from 6° to 22.8°, depending on
the technique and the pathology [13].
Additionally, the most powerful procedures will have a greater effect in reducing
the muscle strength. This balance is of particular importance in athletes and neuro-
logical patients. Thus, there is probably more than one correct procedure for a given
patient but some factors are worthy of consideration (Table 1).
3.1 Level I—Tendo-Achilles Lengthening (TAL)
In patients with Achilles tendon contracture, the tendon can be lengthened open or
percutaneously (Fig. 2). In all procedures, the patient can be placed prone or supine
with the leg crossed in a figure of four position. Level I procedures are the most
Table 1 Factors for consideration and goals

Factors for consideration Goals
Age Optimize positioning to adjunctive procedures
Desired level of activity Avoid excessive tendon lengthening
Underlying medical conditions Minimize scar tissue
Associated surgical procedures Avoid sural injury
Planned postoperative rehabilitation
a b c d
Fig. 2 Level I procedures: (a)—open Z-lengthening; (b)—Hoke; (c)—White; (d)—Paley. In

Paley’s technique: 1—first incision; 2—second incision
powerful, with considerable risk of overlengthening. After all procedures, a poste-

rior splint is placed with the ankle at 90° for 2 weeks. Sutures are removed and the
patient can start weight-bearing on a cast or cast boot. By 8 weeks, the patient can
start walking on a regular shoe.
For the open “Z-Lengthening” procedure, a posterior longitudinal incision is
made, medial to the tendon. The tendon sheath is opened. Two strategies can be
used. A long longitudinal split is performed down the center of the tendon. The
tendon is then divided by cutting in either direction at the top and bottom of the
split, medially and laterally or anteriorly and posteriorly. The ankle is dorsiflexed to
neutral with the knee extended, and the foot is placed in neutral. Otherwise, the
transverse cuts can be performed first and the ankle forced dorsiflexion will make
the tendon fibers slide for the desired amount. The tendon is sutured in tension with
multiple horizontal mattress sutures. The paratenon and the skin are sutured care-
fully and separately, to minimize adhesions.
The percutaneous Achilles tendon lengthening is a less invasive option. The
patient can also be placed supine with the leg held up by the surgeon’s assistant. The
foot is maximally dorsiflexed by the assistant. The tendon insertion is identified by
palpation. For the Hoke’s technique or triple hemisection (1931) [1, 10], 3 equidis-
tant incisions are preformed along the tendon, each separated a minimum of 3 cm.
The blade perforates the midline of the tendon and rotates transversely, and the cut
is completed medially or laterally. About 50% of the tendon is incised with each cut.
To minimize the risk of sural nerve injury, the proximal and distal cuts are per-
formed medially and the middle cut is performed laterally. White’s technique or
double hemisection (1943) [2] is based on the rotation of tendon’s collagen fibers.
Using the DAMP mnemonic, a distal incision releases the anterior half of the tendon
fibers and another medial half is released by a proximal incision. In both incisions,
the blade enters the skin just medial to the tendon, to avoid sural nerve injury. For
Paley’s percutaneous Z-lengthening (2005) [8], a distal central incision is performed

through the skin and the tendon, creating a short split through the tendon, longitudi-
nally. A Smillie knife is inserted in the tendon and pushed proximally for 4 cm. A
second, proximal central incision is performed over the blade. Each half of the ten-
don is cut transversely at the level of the split incisions. When a varus hindfoot is
present, cuts are performed distal medial and proximal lateral, and the opposite is
true for a valgus hindfoot. The tendon slides on itself with dorsiflexion of the foot.
The open technique is associated with an increased risk of tendinosis due to
increased scar tissue formation, an increased operating time, and a larger skin inci-
sion. However, the amount of lengthening is easier to control.
3.2 Level II—Gastrocnemius-Soleus Recession
For level II techniques (Fig. 3), the patient is usually placed prone and is submitted
to an open procedure. At this location, the risk of sural nerve injury is higher and
scar formation is most visible. After surgery, the extremity is incorporated in a
below knee cast, with the foot placed in slight dorsiflexion. Walking is encouraged
at four weeks. Around 6 to 8 weeks after surgery, the patient can start walking on a
regular shoe.
In the Vulpius procedure (1913) [11, 14], a straight longitudinal incision is per-
formed on the lower third of the calf. The fascia is divided in line with the skin
a b c d
Fig. 3 Level II procedures: (a)—Vulpius; (b)—transverse Vulpius; (c)—Baker; (d)—modified

tongue-in-groove
a b c d
Fig. 4 Vulpius procedure: (a)—incision planning; (b)—gastrocnemius aponeurosis; (c)—aponeu-

rosis incision planning; (d)—aponeurosis cut with underlying soleus muscle
incision. The aponeurosis of the gastrocnemius-soleus complex is identified and cut

sharp in an inverted “V,” apex pointing proximal (Fig. 4). The ankle is dorsiflexed 10°
to 15° with the knee extended. The median septum of the soleus is cut with fine dis-
section. Occasionally, two septa are also found on the soleus and must also be divided.
Care must be taken to ensure the muscle fibers are left intact. The deep fascia is
sutured and the skin is closed. A cast is applied with the foot in neutral position for
4 weeks. If only this procedure is performed, the patient is allowed to walk weight-
bearing. If there is active voluntary ankle dorsiflexion, further bracing may not be
necessary.
The transverse Vulpius procedure [15, 16] is a modification of the original tech-
nique that may be performed through a smaller incision. The gastroc-soleus fascia
is divided with a transverse cut, resulting in a similarly controlled and predictable
lengthening of the muscle tendon unit. Division at a more distal level results in an
average larger lengthening that significantly increases after the division of the mid-
line raphe.
In the Baker technique (1956) [17, 18], a longitudinal midline incision extends
from the lower border of the belly of the gastrocnemius muscle to the proximal end
of the Achilles tendon. An inverted “U” incision is made through the aponeurosis.
Lateral and medial horizontal extensions of this incision are performed distally,
with division of the underlying soleus muscle fibers. The middle portion, or tongue,
is dissected from the soleus, so no muscle fibers remain attached to the distal portion
of the lengthened structure. As the ankle is placed in dorsiflexion, the distal tendon
slides and the four corners of the overlapping aponeurosis are held with one suture
each. Following closure of the deep fascia and the subcutaneous tissue, the skin is
closed with intradermal suture. Baker advocates that when lengthening is performed
for postpoliomyelitic contractures, the soleus muscle fibers must not be dissected
from the distal tongue, unless necessary for achieving the desired lengthening.
The modified tongue-in-groove technique, by Fulp and McGlamry (1974) [19],

is an alternative to the Baker procedure. A non-inverted “U” is made through the
aponeurosis. Although possible, no suturing is mandatory where the tendon fibers
overlap. Some authors close the defect distal to the end of the tongue.
3.3 Level III—Distal Gastrocnemius Tenotomy
For level III techniques, the patient can be placed prone or supine, if additional pro-
cedures are performed. Surgery can be performed open or through endoscopy (Fig. 5).
At this location, there is considerable risk of sural nerve injury and skin puckering.
After surgery, the extremity is incorporated in a below knee cast, with the foot placed
in slight dorsiflexion for at least 4 weeks and weight-bearing is allowed. There is a
considerable risk of deformity recurrency if the postoperative care is insufficient.
The Strayer resection (1950) [20–22] separates the gastrocnemius from the
soleus, just proximal to the gastrocnemius-soleus aponeurosis, allowing the first one
to retract. The gastrocnemius-soleus junction is located about 2 cm distal to the vis-
ible indentation of the gastrocnemius muscle and the Achilles tendon, which
a b c
A A
B B
Fig. 5 Level III: (a)—level of open or percutaneous Strayer; (b)—Strayer; (c)—Strayer plus
soleus fascial lengthening (SFL). A—gastrocnemius muscle body; B—soleus muscle body
corresponds to half the length of the fibula [20]. A longitudinal incision is per-
formed, just distal to the indentation. This incision can be performed, depending on
different authors, laterally, medially (the authors’ option), or over the midline.
Dissection is carried through the subcutaneous tissue to the deep fascia. The saphe-
nous vein and nerve may be found in the subcutaneous tissue. The sural nerve may
be found superficial or deep to the fascia [20] so its identification and protection are
important. The deep fascia is opened longitudinally. If a medial or lateral approach
is performed, the soleus muscle can be visualized anteriorly. Transverse blunt dis-
section separates the gastrocnemius-soleus interval, exposing the gastrocnemius
aponeurosis posteriorly. Distinction between the gastrocnemius fascia and the
soleus fascia is best appreciated on the medial side. If the posterior approach is
chosen, the gastrocnemius muscle body is visualized, and blunt dissection reveals
the gastrocnemius aponeurosis. Through either approach, the gastrocnemius tendon
is cut transversely, with tendon edges separating 1 to 2 cm, as the soleus tendon will
prevent further retraction. After the release and with the ankle in neutral position,
the gastrocnemius fascia can be sutured back to the soleus fascia, adding strength to
the calf muscles. This reattachment is not performed by some surgeons, including
the authors. The deep fascia is closed, preventing tendon to skin adhesions.
The additional resection of the soleus aponeurosis is commonly performed by
many surgeons, in what is usually referred to as the “Modified Strayer Procedure”
or the “Strayer procedure plus Soleus Fascial Lengthening (SFL)“ [23] (Fig.6). This
modification is possible through all the before-mentioned incisions. The soleus fas-
cia release should be complete, including the soleus middle raphe.
Sural nerve neuropraxia is common, either due to nerve retraction during surgery
or more likely to increased stretch of the calf muscles, but nerve laceration is rare.
A frequent hypertrophic scar tissue pushed the development of the endoscopic
gastrocnemius release, possible with a two-portal technique, first described by
Saxena [24]. A 1- to 2-cm-longitudinal incision is performed distal to the medial
gastrocnemius muscle belly, 10 to 15 cm proximal to the medial malleolus. Blunt
a b
Fig. 6 (a)—Modified Strayer procedure through medial incision: release of soleus fascia; (b)—
Strayer resection: gastrocnemius fascia and plantaris tendon release
dissection is carried to the level of the deep fascia. The subcutaneous tissue is sepa-
rated from the gastrocnemius aponeurosis, and the endoscope is inserted. If possible,
the sural nerve is visualized, and its position is confirmed. A lateral portal may help
to reveal any potential sural nerve branches. The endoscope is replaced by a cannu-
lated camera-mounted knife. The foot is dorsiflexed to aid in transection. The knife
cuts the aponeurosis as it is pushed through the cannula. In younger patients with a
wider gastrocnemius fascia, the lateral fibers are often transected through the second
portal. Saxena et al. reported 15% of lateral foot dysesthesia [24]. Other possible
complications are superficial infection and uncompleted aponeurosis release [25].
3.4 Level IV—Deep Gastrocnemius-Soleus Recession
The Baumann procedure (1989) [26] first described the release of the anterior apo-
neurosis of the central gastrocnemius muscle belly for the treatment of patients with
cerebral palsy (Fig. 7). Patient is supine, with the limb in a figure of four position.
a b c
Fig. 7 Level IV / Baumann: (a)—gastrocnemius divisions; (b)—soleus divisions; (c)—incisions

on sagittal plane represented by dotted lines
A 5 cm medial longitudinal incision is performed at the transition of the proximal to

the middle third of the leg, 2 finger breaths posterior to the posterior edge of the
tibia. The deep fascia is opened. Careful medial to lateral blunt dissection separates
gastrocnemius and the soleus muscle bellies [27], while avoiding damage to the
greater saphenous vein and the saphenous nerve. The plantaris tendon is resected
[12]. With the knee extended and the foot dorsiflexed, the gastrocnemius fascia is
divided from medial to lateral, sparing the muscle fibers. The intramuscular septum
between the medial and lateral heads of the gastrocnemius muscle is identified and
carefully incised [28]. If inadequate ankle dorsiflexion results, several additional
fascia divisions are performed, separated 2 cm from each other. If necessary, the
soleus aponeurosis can also be divided, distally to the gastrocnemius fascia inci-
sions. Closure is performed in separated layers and a posterior splint is applied in
maximum dorsiflexion. At 2 weeks, patients start weight-bearing as tolerated on a
walker boot and calf stretches and isometric exercises are allowed [29]. For the first
postoperative month, a night splint is used to maintain the ankle at 90 degrees. At
around 6 weeks after surgery, patients may transition to a supportive shoe.
Baumann procedure allows a selective lengthening of the gastrocnemius [30] pre-
serving muscle strength secondary to the intramuscular lengthening, but also provides
the ability to correct GSE deformities. The risk of neurologic complication is low [28]
but a large skin incision in a proximal and visible area of the calf is required [12].
3.5 Level V—Proximal Gastrocnemius Tenotomy
The Silfverskiöld procedure (1923) [31] first described the proximal gastrocnemius
lengthening in cases of cerebral palsy (Fig. 8). The initial technique released both
medial and lateral heads transferring the proximal insertions of the gastrocnemius
to the tibia. The patient is prone, with a pillow under the ankles to relax the gastroc-
nemius. A transverse incision is made through skin, subcutaneous tissue, and deep
fascia at the popliteal crease. The tibial nerve is identified. Historically, half of its
motor branches to the proximal gastrocnemius bellies were sacrificed to decrease
their innervation [12]. An excessively lateral incision can place neurovascular struc-
tures at risk (e.g., common fibular nerve, lateral and medial sural cutaneous nerve,
tibial nerve, and lesser saphenous vein). The medial and lateral heads of the gastroc-
nemius muscle are isolated and transected from the posterior aspect of the femoral
condyles. Closure is performed in separated layers. The patient is placed in a walk-
ing boot for 6 weeks and allowed to weight bear as tolerated [28]. Barouk and col-
leagues [25] suggested dividing only the aponeurosis of each muscle head without
disrupting the underlying muscle tissue.
In their study on muscle balance, Silver and colleagues [32] found the soleus to
be the main plantar-flexor muscle of the foot and the most powerful muscle crossing
the ankle. The soleus provides more than twice the plantar-flexor force of the gas-
trocnemius, whose medial head provides 71% of its force and has 2.4 times the
cross-sectional area of the lateral head. After experiencing equivalent results,
Fig. 8 Level V: (a)— a b

Silfverskiold; (b)—Barouk
Barouk now favors the Isolated medial gastrocnemius release. This approach is less
invasive, less risky, and offers a more aesthetically pleasing surgical scar while pro-
viding similar results. The patient is prone. A 2- to 3-cm transverse incision is made
1 cm lateral to the medial fovea of the popliteal flexion crease. No neurovascular
structures are routinely encountered. The deep fascia is incised in line with the skin
incision (Fig. 9). The pes anserinus is retracted, exposing the medial gastrocnemius
head. All the white fibers are cut; the muscle fibers are left intact. When effective,
no muscle tension is present while moving the ankle into dorsiflexion. No immobi-
lization is recommended. The rehabilitation program consists of passive dorsiflex-
ion of the ankle with the knee in extension and weight-bearing in a shoe without a heel.
Complications are rare; no loss of muscle strength occurs. Releasing the lateral
head is rarely necessary but may increase ankle dorsiflexion. Bilateral procedures
are possible without any postoperative weight-bearing restriction and no loss of
strength.
a b
Fig. 9 Barouk procedure: (a)—medial incision, medial gastrocnemius head; (b)—medial head
released
4 Final Remarks
If surgery is considered for the treatment of a calf contracture, it is essential that the
chosen technique is appropriate to the type of contracture. The Silfverskiold test
allows the surgeon to determine whether the contracture affects both the gastrocne-
mius and the soleus or just the gastrocnemius.
The surgical lengthening of the triceps surae can be performed at 5 different
anatomic levels. Mastering the anatomy of every level is the basis of these surgical
procedures.
Determining which method to use should be based on surgeon comfort with the
particular procedure/anatomy, anticipated patient position, the need for additional
reconstructive procedures, potential complications, and cosmetic concerns. Table 2
summarizes the previously discussed techniques.
The current trend is to propose minimally invasive open procedures in addition
to endoscopic procedures. It is possible that proximal medial gastrocnemius length-
ening developed by L.S. Barouk and P. Barouk in France will be the gastrocnemius
lengthening procedure of choice for the isolated gastrocnemius contracture after
failed conservative treatment because it directly addresses the contracted gastrocne-
mius, the degree of release is controlled, and it allows for immediate weight-bearing
[33]. Surgical release of the Achilles tendon is associated with a risk of weakness
caused by overlengthening and a lengthy rehabilitation period.
882
Table 2 Decision factors for procedure selection

Procedure Position Incision Level WB PROS CONS Patient selection
Barouk/ Prone Popliteal fossae Level V WB Aesthetic incision Tibial neurovascular Positive Silfverskiold w/
Silfverskiold without Preserves muscle bundle and pes mild equinus
boot mass and strength anserinus at risk
Baumann Supine Proximal medial Level IV isolated WB with Preserves muscle Bleeding Positive Silfverskiold w/
calf gastroc or or without mass and strength Need proper incision mild equinus
combined gastroc boot; positioning
soleus Night Mild lengthening
splint
Strayer Supine Mid leg, medial Level III WB with Simple procedure Release on the lateral Multiple supine
Isolated gastroc or boot Good balance of side is hard procedures with a
combined gastroc lengthening—Power Risk of recurrence if moderate equinus
soleus loss postoperative care is
insufficient
Baker / Prone Posterior midline Level II WB with Suture at desired Visible scar Isolated moderate/severe
Vulpius with most visible Isolated gastroc or boot length Most risk of sural nerve equinus or multiple
scar combined gastroc injury procedures in prone
soleus
Open Z TAL Either Posterior distal Level I NWB Suture at desired Risk of overlengthening Neuromuscular disease
midline with True Achilles length Healing issues Severe equinus
potential healing
issues
Hoke Either 3 stab incisions Level I NWB Best healing Risk of overlengthening Neuromuscular disease
True Achilles Powerful procedure Blind procedure with poor skin
Severe equinus
M. Resende Sousa et al.
For the general adult population, gastrocnemius lengthening is often performed

in conjunction with other reconstructive foot and ankle procedures. In most cases,
therefore, postoperative immobilization and weight-bearing restrictions will be pri-
marily dictated by these additional procedures.
References
1. Chen L, Greisberg J. Achilles lengthening procedures. Foot Ankle Clin N Am. 2009;14:627–37.
2. Mueller MJ, Sinacore DR, Hastings MK, Strube MJ, Johnson JE. Effect of Achilles tendon
lengthening on neuropathic plantar ulcers. A randomized clinical trial. J Bone Joint Surg Am.
2003;85(8):1436–45.
3. Deland JT. Adult-acquired flatfoot deformity. J Am Acad Orthop Surg. 2008;16(7):399–406.
4. Cheung JT-M, Zhang M, An K-N. Effect of Achilles tendon loading on plantar fascia tension
in the standing foot. Clin Biomech Bristol Avon. 2006;21(2):194–203.
5. Cychosz CC, Phisitkul P, Belatti DA, Glazebrook MA, DiGiovanni CW. Gastrocnemius reces-
sion for foot and ankle conditions in adults: evidence-based recommendations. Foot Ankle
Surg Off J Eur Soc Foot Ankle Surg. 2015;21(2):77–85.
6. DiGiovanni CW, Kuo R, Tejwani N, Price R, Hansen ST, Cziernecki J, et al. Isolated gastroc-
nemius tightness. J Bone Joint Surg Am. 2002;84(6):962–70.
7. DeHeer PA. Equinus and lengthening techniques. Clin Podiatr Med Surg. 2017;34:207–27.
8. Lamm BM. Paley D; Herzemberg J; gastrocnemius soleus recession: a simpler, more limited
approach. J Am Podiatr Med Assoc. 2005;95(1):18–25.
9. Barouk P, Barouk LS. Clinical diagnosis of gastrocnemius tightness. Foot Ankle Clin.
2014;19(4):659–67.
10. Hoke M. An operation for the correction of extremely relaxed flat feet. JBJS. 1931;13(4):773–83.
11. Javors JR, Klaaren HE. The Vulpius procedure for correction of equinus deformity in cerebral
palsy. J Pediatr Orthop. 1987;7(2):191–3.
12. Firth GB, McMullan M, Chin T, Ma F, Selber P, Eizenberg N, et al. Lengthening of the
gastrocnemius-soleus complex: An anatomical and biomechanical study in human cadavers. J
Bone Jt Surg. 2013;95(16):1489–96.
13. Hsu RY, VanValkenburg S, Tanriover A, Christopher W, DiGiovanni CW. Surgical techniques
of gastrocnemius lengthening. Foot Ankle Clin N Am. 2014;19:745–65.
14. Takahashi S, Shrestha A. The Vulpius procedure for correction of equinus deformity in patients
with hemiplegia. J Bone Joint Surg Br. 2002;84(7):978–80.
15. Tinney A, Khot A, Eizenberg N, Wolfe R, Graham HK. Gastrocsoleus recession techniques: an
anatomical and biomechanical study in human cadavers. Bone Jt J. 2014;96-B(6):778–82.
16. Tinney A, Thomason P, Sangeux M, Khot A, Graham HK. The transverse Vulpius gastrocso-
leus recession for equinus gait in children with cerebral palsy. Bone Jt J. 2015;97-B(4):564–71.
17. Baker LD. Triceps surae syndrome in cerebral palsy; an operation to aid in its relief. AMA
Arch Surg. Feb. 1954;68(2):216–21.
18. Baker LD. A rational approach to the surgical needs of the cerebral palsy patient. J Bone Joint
Surg Am. 1956;38-A(2):313–23.
19. Fulp MJ, McGlamry ED. Gastrocnemius tendon recession. Tongue in groove procedure to
lengthen gastrocnemius tendon. J Am Podiatry Assoc. 1974;64(3):163–71.
20. Pinney SJ, Sangeorzan BJ, Hansen ST. Surgical anatomy of the gastrocnemius recession
(Strayer procedure). Foot Ankle Int. 2004;25(4):247–50.
21. Strayer LM. Recession of the gastrocnemius; an operation to relieve spastic contracture of the
calf muscles. J Bone Joint Surg Am. 1950;32-A(3):671–6.
22. Strayer LM. Gastrocnemius recession; five-year report of cases. J Bone Joint Surg Am.
1958;40-A(5):1019–30.
23. Firth GB, McMullan M, Chin T, Ma F, Selber P, Eizenberg N, et al. Et al., lengthening of the
gastrocnemius-soleus complex, An anatomical and biomechanical study in human cadavers. J
Bone Joint Surg Am. 2013;95:1489–96.
24. Saxena A, Widtfeldt A. Endoscopic gastrocnemius recession: preliminary report on 18 cases. J
Foot Ankle Surg Off Publ Am Coll Foot Ankle Surg. 2004;43(5):302–6.
25. Barouk P. Technique, indications, and results of proximal medial gastrocnemius lengthening.
Foot Ankle Clin N Am. 2014;19:795–806.
26. Baumann JU, Koch HG. Lengthening of the anterior aponeurosis of the gastrocnemius muscle.
Oper Orthop Traumatol. 1989;1:254–8.
27. Amis J. The gastrocnemius a new paradigm for the human foot and ankle. Foot Ankle Clin N
Am. 2014;
28. Anderson JG, Bohay DR, Eller EB, Witt BL. Gastrocnemius Recession. Foot Ankle Clin N
Am. 2014;19:767–86.
29. Cortina RE, Morris BL, Vopat BG. Gastrocnemius Recession for Metatarsalgia. Foot Ankle
Clin N Am. 2018;23:57–68.
30. Slullitel G. Calvi JP. Gastrocnemius Recession in the Setting of Metatarsalgia The Baumann
Procedure Foot Ankle Clin N Am. 2019;24:649–55.
31. Silfverskiold N. Reduction of the uncrossed two-joints muscles of the leg to one- joint muscles
in spastic conditions. Acta Chir Scand. 1924;56:315–30.
32. Silver RL, Garza J, Rang M. The myth of muscle balance. A study of relative strengths and
excursions of normal muscles about the foot and ankle. J Bone Joint Surg Br. 1985;67(3):432–7.
33. Solan MC, Davies MS. Gastrocnemius shortening and heel pain. Foot Ankle Clin N Am.
2014;19:719–38.
Plantar Fasciitis
Mario Abarca and Jorge Filippi
1 Introduction
Plantar fasciitis is the most frequent cause of heel pain and the main reason for con-
sultation in relation to the foot. In the United States, 10% of the population has
presented this symptom generating more than one million consultations per year
[1]. It is also known that over 90% of those affected will improve before 1 year [2].
For this reason, it is essential to understand the physiology of plantar fasciitis and
also to apply the best available evidence to treat this major public health problem
proportionately and efficiently.
When talking about plantar fasciitis, a clinical entity is recognized that is associ-
ated with anatomopathological findings that evidence the presence of thickened
degenerative tissue, more related to a chronic process than to an acute one, which is
what alludes to the original designation of the problem; that is why the concept of
“plantar fasciopathy” (PF) appears as a term more consistent with the physiopatho-
logical processes found in the literature.
This chapter will deal with the physiopathology, diagnosis, and treatment of PF,
emphasizing the available evidence in this regard.
M. Abarca
Hospital Sótero del Río, Santiago, Chile
J. Filippi (*)
Clínica Las Condes, Santiago, Chile
Hospital del Trabajador, Santiago, Chile

Switzerland AG 2022
886 M. Abarca and J. Filippi
2 Anatomy
The plantar fascia is a thick and specialized ligament structure that extends from the
calcaneus from proximal through the plantar arch and extending as digital bands
toward distal to end up forming a fibrous network in the deep intermetatarsal liga-
ments. Three portions are recognized: the central, medial, and lateral bands. In the
origin of the plantar fascia exists a strong union to the internal, external, posterome-
dial, and posterolateral intermuscular septa of the inferior face of the calcaneus.
From here, this aponeurotic tensor element of the sole of the foot is extended and it
is arranged in two layers, in which the muscular partitions are inserted next to the
sagittal partitions, forming the “functional plantar dermo-aponeurotic system.” In
the forefoot, the plantar fascia forms sagittal partitions joined together surrounding
the flexor tendons that end up joining the deep intermetatarsal ligaments. The parti-
tions arrange the flexor tendons centered under the metatarsal heads during the load-
ing position, which is key to the support of the metatarsal heads and the windlass
effect of the plantar fascia [3, 4] (Fig. 1).
3 Epidemiology
At least 1 in 10 people will suffer from PF at some point in their lives; and it is
estimated that about two million people are treated for this diagnosis in the United
States each year [1]. A high percentage of acute cases will resolve spontaneously
Fig. 1 Diagram of plantar

fascia anatomy
Superficial Transverse
metatarsal ligaments
Anterior arm of inferior

extensor retinaculum
Plantar
aponeurosis
Medial process of
calcaneal tuberosity
Plantar Fasciitis 887
without medical consultation, and the rest are treated initially by primary health
care or general medicine. In general, when the symptoms have already had a
greater impact on the patient’s quality of life, they are evaluated by the subspecial-
ist orthopedist. The peak incidence of the disease occurs between 45 and 65 years
of age [1]. In a systematic review of the disease, it was found that nearly 90% of
patients with PF resolve their symptoms within 12 months with conservative treat-
ment [5].
4 Risk Factors
The literature is not clear on the etiopathogenesis of PF, although it is accepted that
the etiology is multifactorial. Historically, risk factors have been identified, some
without scientific evidence, divided into intrinsic and extrinsic. Most of them are
listed below, describing whether or not there is evidence for their association
with PF.
4.1 Intrinsic Factors
Age: this factor is associated with a process of tissue degeneration with age, decreas-
ing the elasticity of the tissues that absorb the impacts of walking, predisposing
the plantar fascia to be more vulnerable to damage. Older athletes suffer more
from PF than younger ones [6–8].
Weight: Overweight and obesity would be related to a 1.4 times risk of developing
chronic PF [9, 10].
Gender: There would be no gender difference [6].
Calcaneal Spur: This originates in the insertion of the flexor digitorum brevis mus-
cle and not in the insertion of the plantar fascia. This concept evidences an insuf-
ficient causality of the development of PF at least as the only main determinant.
Neither shape nor size correlates with pain in PF after treatment [11].
Nerve Entrapment: Patterns of entrapment of plantar nerves such as the first branch
of the lateral plantar nerve (Baxter’s nerve) are considered a risk factor for simu-
lating pain similar to that of PF. These two conditions can coexist. Altered sensi-
tivity and pain irradiation are characteristic of this situation. It could be the cause
of non-resolution of symptoms after surgical treatment [12].
Systemic Disease: Spondyloarthropathy should be suspected and ruled out in the
context of young patients at atypical ages of presentation with bilateral symp-
toms [7].
Genetics: The genetic influence could be associated with a progressive loss of elas-
ticity of the connective tissue. Genetic interaction with other risk factors may
explain the predisposition of some patients to have more muscle contractures and
tendon diseases [6].
4.2 Extrinsic Factors
Lifestyle and work: Recreational jogging, military activities, and “Irish dancing” are
all related to PF [13–15]. Prolonged standing at work has also been seen as an
association with PF, although with a low quality of evidence [16].
Biomechanical dysfunction: Deformities of the lower extremities and alterations in
their biomechanics may be associated with recalcitrant PF.
It is currently described that the common denominator between intrinsic and
extrinsic factors is gastrocnemius contracture [17]. Thus, it can be found that most
of the risk factors studied are associated with increased gastrocnemius contracture.
It is important to note that the risk factors listed are associated with recalcitrant PF
[18] and that it is very difficult to isolate the influence of the treatment of each of
them separately [16].
5 Pathomechanics
Patel and DiGiovanni described that up to 83% of patients with recalcitrant PF had
limited ankle dorsiflexion. Most of them depend on contracture or shortening of the
gastrocnemius [19]. There are several publications that also associate PF with this
condition [20–23]. The shortening or contracture of gastrocnemius generates an
increase in the tension of the Achilles tendon in the forced dorsiflexion of the ankle,
which leads to an increase in the tension of the plantar fascia in loading activities.
Damage forces appear with the transmission of the leverage force from the foot and
ankle to the tibia (and body) when it passes over the plantigrade foot. Gastrocnemius
shortening, whether congenital or acquired, is the main cause of ankle dorsiflexion
limitation. In the second late rocker gait (just before heel elevation), the knee is
extended by coupling with the dorsiflexion of the ankle; in this situation, with a
contracted gastrocnemius, an antagonistic combination of hindfoot plantarflexion
and forefoot dorsiflexion that elevates the passive tension of the plantar fascia to
counteract the arch flattening due to the gastrocnemius contracture (Fig. 2).
The average patient walks about 6000–7000 steps a day. In an individual with a
shortening of the gastrosoleus complex, a repetitive overload is produced that can
generate micro-damage to the plantar fascia. In the presence of PF with gastrocne-
mius shortening, an antalgic position is evidenced by limiting the dorsiflexion of the
ankle with an external rotation of the leg/foot resulting in a characteristic gait of
early heel elevation (Bouncy Gait).
6 Clinical Presentation—Diagnosis
The diagnosis is made with a medical history compatible with PF that is character-
ized by a puncture-type morning pain at the medial plantar aspect of the heel, and
when walking again after prolonged periods of rest; this pain improves after a while
Weigth-bearing loading
ACHILLES TENDON
PLANTAR FASCIA
Fig. 2 Effect of the tension or shortening of the Achilles tendon on the plantar fascia. The red
arrows indicate the transmission of axial load on the foot at the end of the second Rocker. The yel-
low arrow represents the tension toward proximal of the Achilles tendon. With a shortening of the
Achilles tendon, more load is transmitted toward the plantar fascia, generating an overload result-
ing in the tissue damage that characterizes PF (blue arrow)
of walking. The picture worsens at the end of the day and in physical activities of
impact. The typical age of presentation is between 45 and 65 years, and about one-
third of the patients have bilateral symptomatology of PF. At the physical examina-
tion, it is frequent the presence of pain to the palpation in the medial plantar aspect
of the tuberosity of the calcaneus in relation to the insertion of the plantar fascia [2],
although in some cases the pain also can be non-insertional at level of the plantar
arch or in the lateral portion of the plantar fascia.
It should always be asked for associated neuropathic symptoms, as plantar par-
esthesia, or night pain irradiated toward the distal portion of the foot. In these cases,
one can be in the presence of a syndrome of the inferior tarsal tunnel that corre-
sponds to a neuropathy by entrapment of the lateral plantar branch of the tibial nerve
(Baxter’s nerve). Tinel’s sign on the tarsal tunnel and alterations of sensation in the
path of the tibial nerve are also compatible with peripheral nerve entrapment. The
role of the physical examination and the anamnesis is irreplaceable for the suitable
diagnosis of a syndrome of the inferior tarsal tunnel because the findings of an elec-
tromyography are variable and sometimes, confusing. In the presence of a picture of
chronic plantar fasciopathy associated with neurologic symptoms, it is necessary to
consider a liberation of the branches of the tibial nerve when deciding on surgical
treatment.
The diagnosis of gastrocnemius contracture is based on the Silfverskjöld test
[24]. The correct way to do this is to place the forefoot in supination to block the
influence of movement in the sagittal plane of the joints in the mid-tarsus. A positive
Silfverskjöld sign consists in a greater dorsiflexion of the foot at the ankle joint with
the knee flexed than extended. Despite its widespread use, there is no consensus to
date on the absolute definition of gastrocnemius contracture, and a low interob-
server correlation has been seen in the Silfverskjöld test when it has been studied
[25–27].
7 Imaging Study and Complements
The vast majority of PF only require an adequate history and physical examination
for proper diagnosis and treatment. The use of imaging is necessary in the face of
atypical presentations or concomitant conditions associated with PF.
In loaded radiographs, the presence of associated deformities must be analyzed,
as well as the presence of tumors or fractures. The presence of heel spur presents a
high frequency in asymptomatic population (almost a third) so its presence or size
does not condition the prognosis or the severity of the PF [28]. Besides the calcaneal
spur corresponds mainly to the zone of insertion of the flexor digitorum brevis and
not to an enthesopathy of the plantar fascia.
The use of ultrasound and magnetic resonance is useful to rule out other patholo-
gies in the context of atypical signs of heel pain (tumors, fat atrophy, fractures by
stress of the calcaneus, etc.). The measurement of the thickness of the plantar fascia
is achieved in these exams; however, the thickness of the plantar fascia is not related
to the presence of pain [29].
Cases of heel pain of bilateral synchronous presentation can be associated with
inflammatory diseases (pelvic-spondyloarthropathies for example) or endocrine
diseases. In these cases, a study by rheumatology and/or endocrinology is indicated.
8 Treatment
Over 90% of patients can be managed without surgery. Multiple treatment schemes
have been described, but there are a limited number of high-quality publications
(American Academy of Orthopedic Surgeons—AAOS level 1–2) that support opti-
mal treatment of recalcitrant PF.
Most recommendations are based on lower quality studies (AAOS level 3–4). In
the DiGiovanni et al. study, which surveyed conservative and surgical treatment
among foot and ankle surgeons in recalcitrant PF, they noted that at 4 months of
symptoms, most surgeons preferred plantar fascial stretching exercises. At
10 months, most indicated surgery or shock waves. When surgery was indicated,
there was a wide variety of options, indicating the need for a higher level of evi-
dence at this point [30].
8.1 Non-Surgical Treatment
A fundamental part of the management of PF is to identify the patient’s expectations

and explain that the discomfort will most likely pass spontaneously over time under
conditions favorable to the biomechanics of the foot. The options for non-surgical
management of PF are divided into two focuses: those that focus on the insertional
origin of the plantar fascia and those that take as the origin of the problem to treat
gastrocnemius contracture and tension of the plantar fascia during standing
activities.
Orthoses: The most described alternatives are the use of insoles as they correct the
excess of pronation and insertional overload of the plantar fascia; and the use of
night orthoses to stretch the fascia and prevent morning contracture and its pain.
In the first case, a randomized study to see the cost-effectiveness of the use of
custom-made templates for PF showed no justification for discomfort control at
12 months of follow-up [31]. In the case of night splints, there are several studies
that show improvement in PF symptoms, but tolerance to these devices is poor,
which makes it difficult to apply them regularly as a treatment [32, 33].
Infiltrations: The use of corticosteroids and local anesthetic injections has a very
variable effect on pain in clinical practice. The repeated use of this resource
increases the risk of plantar fascia rupture and fat degeneration by steroids in the
area of administration. Low-quality clinical studies have shown a benefit at
1 month in the use of steroids versus placebo [5, 34]. Other types of infiltrations
have been studied, including the use of hyperosmolar dextrose, autologous
blood, and the use of botulinum toxin A [35–38]. In this last alternative, a ran-
domized study with 50 patients can be mentioned, which showed that the use of
botulinum toxin A would have a sustainable improvement at 6 and 12 months of
follow-up in electromyographically guided infiltrations to recognize the flexor
digitorum brevis (FDB) muscle. This study opens a door to consider as a possible
participant the intrinsic musculature of the foot such as the FDB in the complex
pathomechanics of PF [39].
Platelet-Rich Plasma (PRP): At some point, it was widely accepted within the com-
munity as it was offered as a promising therapeutic alternative. To date, there are
few quality studies that support its use, one of them showing an improvement in
FP symptoms over the use of steroids at 3 months of follow-up, but the cost and
adverse effects would not be comparable. However, the cost and adverse effects
would not be comparable [40].
Extracorporeal Shock Waves (ESW): There are several quality studies that demon-
strate the usefulness of this therapy in PF [41–44]. The effectiveness among the
different types of ECS was evaluated in a meta-analysis and the utility of focused
ECS was shown to be inconclusive with radial ECS [45]. Other researchers have
pointed out that this therapy would be of little use in patients with gastrocnemius
shortening [28]. Another problem with the application of this treatment strategy
is the lack of coverage by health insurance and its high cost.
Elongation and Strengthening Exercises: Weakness of the intrinsic musculature has
been seen as an associated factor in joggers associated with a destabilization of
the medial arch of the foot [45]. Strengthening studies have been performed with
different protocols compared with stretching exercises and all had effects in
decreasing the symptoms of patients with PF [46]. However, it has not been pos-
sible to identify which strengthening measures are performed that decrease the
risk of developing PF.
In the case of stretching exercises, it is known that increased tension in the calf
is associated with increased tension in the plantar fascia [47]. In non-insertional
Achilles tendinopathy, it is widely accepted that eccentric calf stretching exercises
are effective and may have a role in the management of recalcitrant PF [48, 49].
Several publications, including randomized clinical trials, evidence the usefulness
of home Achilles and plantar fascia stretching exercises [49–51].
In a recent review of the topic [52], a meta-analysis is reported that evaluated
various non-surgical therapies such as those described above, with low or moderate
quality and with small short-term benefits for each [53]. However, current evidence
supports the idea of first-line use in the non-surgical treatment of PF with eccentric
calf stretching and plantar fascia elongation exercises [48, 49, 53, 54].
In 90% to 95% of patients with PF, remission of symptoms occurs within 12 months
with non-surgical measures [55]. For this reason, surgical treatment is not recom-
mended before 6 months. As noted above, when planning a surgical procedure for
recalcitrant PF, symptomatology should be actively sought to indicate neuropathic
involvement that leads to suspicion of entrapment in the distal tarsal tunnel. The
most popular procedure in the mid-80s and 90s was open fasciotomy with release of
the lateral plantar nerve. In recent years, with a better understanding of the physio-
pathology of PF, the release of the medial gastrocnemius (gastroc-release) has posi-
tioned itself as a valid alternative.
8.2.1 Plantar Fasciotomy
Plantar fasciotomy (PFA) is the most common type of surgery performed by PF, and
there is controversy as to the best way to perform it: open, minimally invasive or
endoscopic. There are also different opinions about the amount of fascia to be cut.
Open Plantar Fasciotomy
The open surgery option is widely used as a first option against recalcitrant PF. It is
especially useful in patients with motor and sensory neurological symptoms; to
which a lateral plantar nerve release is added (the first branch: Baxter’s nerve)
(Fig. 3).
In studies from the 90s, it was indicated to cut the total plantar fascia, the same
line of authors later pointed out that it should only be two-third of the fascia [56,
57]. Finishing the series of publications with recommendations of only cutting one-
third of the plantar fascia [58]. This can be explained by the involvement of the
biomechanics of the foot destabilizing the lateral column in the calcaneocuboid
joint and also the windlass mechanism of the foot [59].
a b c
Fig. 3 Open fasciotomy with Baxter’s nerve release (a): Modified approach to visualize plantar
fascia and inferior tarsal tunnel. (b): Hallucis Abductor (AH) muscle belly (c): Release of plantar
fascia and AH muscle aponeurosis
The total fasciotomy was a common indication until before the 90s, it is recog-
nized that in normal feet there is no loss of the plantar arch evident as a consequence
of this intervention; however, it does alter the mobility of the tarsal joints [52]. This
has an impact on feet with previous instability, such as the flexible flat foot; and it is
in these types of feet where the complications feared by the biomechanical altera-
tions of a total plantar fascia cutting procedure develop, so this point should always
be considered in those patients with this condition before deciding on a total or
partial fasciotomy.
In open plantar fasciotomy, the medial plantar approach for proximal release of
one-third of the plantar fascia is currently the most accepted. A plantar approach to
access the plantar fascia that has been reported to have good results without involve-
ment of sensory nerves or plantar fat is also described [60]. In long-term follow-up
studies, it refers to up to 76% resolution of symptoms with the open procedure [61].
As for the satisfaction of the procedure, the literature describes from 48 to 90%
depending on the series cited [59].
Endoscopic Plantar Fasciotomy
The endoscopic option allows direct visualization of the plantar fascia, with smaller
incisions, maintaining results similar to the open procedure, approaching 75% reso-
lution of PF symptoms [62, 63]. One of the reasons that have limited the extended
use of this option is that when considering lateral plantar nerve release, the tradi-
tional open technique is preferred.
The procedure is performed with a small incision along the medial side of the
heel, after a blunt dissection that separates the subcutaneous fat from the fascia
underneath and a trocar cannula from medial to lateral is used above. Several sur-
geons choose to make a second incision along the lateral aspect of the heel at the tip
of the trocar. Depending on the number of portals, the endoscope and cutting device
are inserted separately or together and a fasciotomy is performed [64]. In a recent
review of the subject [65] that sought to evaluate the safety and effectiveness of the
endoscopic procedure for the management of recalcitrant PF, it was concluded that
there were 11% of total complications including persistent pain (5.6%), paresthesias
or dysesthesias (4.3%), problems with wound healing (1.7%), and superficial
infection (0.4%). As for the effectiveness against non-surgical interventions such as

the use of shock waves, there was no quality evidence to demonstrate a superiority
of the surgical intervention; on the other hand, the need for randomized studies
considering other surgical interventions compared with PFA, to assess its cost-
effectiveness, is raised.
Resection of the heel spur was commonly associated with surgical treatment of
PF several decades ago [56, 61, 66]. However, there are descriptions of stress frac-
ture of the calcaneus after extensive spur removal. (66) For this reason, and because
it would not be related to the etiology of PF, removal of the heel spur is not
recommended.
The complications of the plantar fasciotomy are related to the instability of the
lateral column that entails the appearance of symptoms for its commitment, altera-
tion of the plantar arch generating flat foot, pain in the sinus of the tarsus, metatar-
salgia, stress fractures for stress, besides persistent pain for compression of the
lateral plantar nerve that can be caught in scar tissue and hypertrophic-painful oper-
ative wounds [60, 67, 68]. With all this, 10 to 50% of patients have been published
who are not satisfied after plantar fasciotomy [61]. On the other hand, the average
recovery time from the operation should be informed to the patient, which can be up
to 7 months [57, 61, 69].
8.2.2 Gastrocnemius Release (Gastroc-Release)
As explained in the pathomechanics of PF, the shortening of gastrocnemius is evi-

dently present in a great majority of patients affected by recalcitrant PF, and some
authors even point out that it is a “sine qua non” condition, although it cannot be
evidenced by physical examination and the Silfverskjöld test [59]. Since 2000, sev-
eral works have appeared relating gastrosoleus contracture and its implication in the
development of PF [19, 70, 71], in addition to other pathologies associated with the
Achilles-calcanean-plant system, such as Achilles tendinopathy and metatarsalgia
for example [72]. Barouk et al. published the safety and simplicity of performing
proximal release of the medial head of the gastrocnemius (GRM) for the manage-
ment of recalcitrant PF [73]. There are several ways to perform the procedure from
local anesthesia and sedation to neuroaxial anesthesia. There are several options for
lengthening the gastrocnemius complex (Fig. 4); however, the GRM option is
favored because there is evidence that it rules out the problem of over-lengthening
the gastrocnemius complex as a result of loss of strength, as would be the case with
the Strayer procedure, for example [74–78]. On the other hand, it has been shown
that the medial head of the gastrosoleus complex makes the greatest relative contri-
bution to effective release [79]. The incision is made in a safe area of the popliteal
fossa (Fig. 5).
Recent studies show good results in the use of GRM for recalcitrant PF with a
percentage of satisfaction ranging from 80 to 89% at one year of follow-up [74, 78].
In one of the studies, with retrospective data collection, GRM and PFA for
Fig. 4 Gastrocnemius-
soleus complex elongation
levels: 1 (red) Barouk
medial Gastroc-release, 2
(orange) Silfverskiöld, 3
(green) Baumann, 4 (blue)
Strayer
recalcitrant PF were compared, demonstrating better results and faster recovery

with GRM, with 80% improvement before 8 weeks in the GRM group [78]. In the
most recent study to date, Gamba C. et al. published a prospective randomized trial
for recalcitrant PF patients with PFA and GRM interventions, which found no dif-
ference in patient satisfaction, AOFAS scale, or health-related quality of life out-
comes at one year of patient follow-up. No significant differences in complications
were reported; however, the same authors point out their position on managing
recalcitrant PF with PFA as a second line of management. All this is supported by
the simplicity and safety of performing GRM, which would also serve as a thera-
peutic alternative for other pathologies that may be concomitant with PF, such as
Achilles tendinopathy [59].
Fig. 5 Surgical technique for the release of the proximal medial gastrocnemius head (Barouk’s
technique)
9 Conclusions and Recommendations of the Authors
The management of PF is non-surgical in 95% of patients. An adequate anamnesis

and physical examination allow the diagnosis to be made without performing imag-
ing tests. The initial treatment is an exercise protocol of elongation of the plantar
fascia and gastrosoleus complex for at least 2 months.
In case of diagnostic doubt or duration of symptoms for more than 1 to 2 months,
we recommend a foot X-ray plus an ultrasound scan. If the diagnosis of PF is con-
firmed by imaging studies, we indicate orthoses with plantar arch support and heel
padding, plus a kinesiologist-guided exercise regimen.
If after 4 to 6 months the symptoms persist (or in patients with atypical symp-
toms such as progressive claudication), we recommend requesting magnetic reso-
nance imaging to rule out tumors or stress fractures.
We recommend performing shock waves (if available) after 4 to 6 months of
treatment failure.
Surgical treatment is indicated no earlier than 6 months of conservative treat-
ment. If there are neurological symptoms that make suspect compression of lateral
plantar branch, we recommend performing tarsal tunnel release plus open partial
plantar fasciotomy. In cases of insertional pain of plantar fascia (recalcitrant PF), we
recommend performing proximal medial gastrocnemius release because it has
shown similar results to plantar fasciotomy, but with less comorbidity and with a
simpler postoperative for the patient.
References
1. Riddle DL, Schappert SM. Volume of ambulatory care visits and patterns of care for
patients diagnosed with plantar fasciitis: a national study of medical doctors. Foot Ankle Int.
2004;25:303–10.
2. Lareau CR, Sawyer GA, Wang JH, DiGiovanni CW. Plantar and medial heel pain: diagnosis
and management. J Am Acad Orthop Surg. 2014;22:372–80.
3. Hicks JH. The mechanics of the foot. I The joints J Anat. 1953;87:345–57.
4. Hicks JH. The mechanics of the foot II. The plantar aponeurosis and the arch. J Anat.
1954;88:25–30.
5. Crawford F, Thomson CE. Interventions for treating plantar heel pain. Cochrane Database Syst
Rev. 2003; https://doi.org/10.1002/14651858.cd000416.
6. Beeson P. Plantar fasciopathy: revisiting the risk factors. Foot Ankle Surg. 2014;20:160–5.
7. Barouk P. Introduction to gastrocnemius tightness. Foot Ankle Clin. 2014;19:xv.
8. Petraglia F, Ramazzina I, Costantino C. Plantar fasciitis in athletes: diagnostic and treatment
strategies. A systematic review. Muscles Ligaments Tendons J. 2017;7:107–18.
9. Frey C, Zamora J. The effects of obesity on orthopaedic foot and ankle pathology. Foot Ankle
Int. 2007;28:996–9.
10. van Leeuwen KDB, Rogers J, Winzenberg T, van Middelkoop M. Higher body mass index is
associated with plantar fasciopathy/“plantar fasciitis”: systematic review and meta-analysis of
various clinical and imaging risk factors. Br J Sports Med. 2016;50:972–81.
11. Ahmad J, Karim A, Daniel JN. Relationship and classification of plantar heel spurs in patients
with plantar fasciitis. Foot Ankle Int. 2016;37:994–1000.
12. Ferkel E, Davis WH, Ellington JK. Entrapment neuropathies of the foot and ankle. Clin Sports
Med. 2015;34:791–801.
13. Scher DL, Belmont PJ Jr, Bear R, Mountcastle SB, Orr JD, Owens BD. The incidence of plan-
tar fasciitis in the United States military. J Bone Joint Surg Am. 2009;91:2867–72.
14. Sobhani S, Dekker R, Postema K, Dijkstra PU. Epidemiology of ankle and foot overuse inju-
ries in sports: a systematic review. Scand J Med Sci Sports. 2013;23:669–86.
15. Noon M, Hoch AZ, McNamara L, Schimke J. Injury patterns in female Irish dancers. PM
R. 2010;2:1030–4.
16. Waclawski ER, Beach J, Milne A, Yacyshyn E, Dryden DM. Systematic review: plantar fasci-
itis and prolonged weight bearing. Occup Med. 2015;65:97–106.
17. Amis J. The gastrocnemius: a new paradigm for the human foot and ankle. Foot Ankle Clin.
2014;19:637–47.
18. Riddle DL, Pulisic M, Pidcoe P, Johnson RE. Risk factors for plantar fasciitis: a matched case-
control study. J Bone Joint Surg Am. 2003;85:872–7.
19. Patel A, DiGiovanni B. Association between plantar fasciitis and isolated contracture of the
gastrocnemius. Foot Ankle Int. 2011;32:5–8.
20. Labovitz JM, Yu J, Kim C. The role of hamstring tightness in plantar fasciitis. Foot Ankle
Spec. 2011;4:141–4.
21. Bolívar YA, Munuera PV, Padillo JP. Relationship between tightness of the posterior muscles
of the lower limb and plantar fasciitis. Foot Ankle Int. 2013;34:42–8.
22. Harty J, Soffe K, O’Toole G, Stephens MM. The role of hamstring tightness in plantar fasciitis.
Foot Ankle Int. 2005;26:1089–92.
23. Barouk P, Barouk LS. Clinical diagnosis of gastrocnemius tightness. Foot Ankle Clin.
2014;19:659–67.
24. Silfverskiold N. Reduction of the uncrossed two-joints muscles of the leg to one-joint muscles
in spastic conditions. Acta Chir Scand. 1924;56:315–30.
25. Baumbach SF, Braunstein M, Seeliger F, Borgmann L, Böcker W, Polzer H. Ankle dorsiflexion:
what is normal? Development of a decision pathway for diagnosing impaired ankle dorsiflex-
ion and M. gastrocnemius tightness. Archives Orthopaedic Trauma Surg. 2016;136:1203–11.
26. Jastifer JR, Marston J. Gastrocnemius contracture in patients with and without foot pathology.
Foot Ankle Int. 2016;37:1165–70.
27. Molund M, Husebye EE, Nilsen F, Hellesnes J, Berdal G, Hvaal KH. Validation of a new
device for measuring isolated gastrocnemius contracture and evaluation of the reliability of the
Silfverskiöld test. Foot Ankle Int. 2018;39:960–5.
28. Solan MC, Carne A, Davies MS. Gastrocnemius shortening and heel pain. Foot Ankle Clin.
2014;19:719–38.
29. Toomey EP. Plantar heel pain. Foot Ankle Clin. 2009;14:229–45.
30. DiGiovanni BF, Moore AM, Zlotnicki JP, Pinney SJ. Preferred management of recalcitrant
plantar fasciitis among orthopaedic foot and ankle surgeons. Foot Ankle Int. 2012;33:507–12.
31. Rasenberg N, Fuit L, Poppe E, Kruijsen-Terpstra AJA, Gorter KJ, Rathleff MS, van Veldhoven
PLJ, Bindels PJ, Bierma-Zeinstra SM, van Middelkoop M. The STAP-study: the (cost) effec-
tiveness of custom made orthotic insoles in the treatment for plantar fasciopathy in general
practice and sports medicine: design of a randomized controlled trial. BMC Musculoskelet
Disord. 2016;17:31.
32. Roos E, Engström M, Söderberg B. Foot orthoses for the treatment of plantar fasciitis. Foot
Ankle Int. 2006;27:606–11.
33. Probe RA, Baca M, Adams R, Preece C. Night splint treatment for plantar fasciitis. A prospec-
tive randomized study. Clin Orthop Relat Res. 1999:190–5.
34. David JA, Sankarapandian V, Christopher PR, Chatterjee A, Macaden AS. Injected corticoste-
roids for treating plantar heel pain in adults. Cochrane Database Syst Rev. 2017;6:CD009348.
35. Ryan M, Hartwell J, Fraser S, Newsham-West R, Taunton J. Comparison of a physiotherapy
program versus dexamethasone injections for plantar fasciopathy in prolonged standing work-
ers: a randomized clinical trial. Clin J Sport Med. 2014;24:211–7.
36. Babcock MS, Foster L, Pasquina P, Jabbari B. Treatment of pain attributed to plantar fasciitis
with botulinum toxin a: a short-term, randomized, placebo-controlled, double-blind study. Am
J Phys Med Rehabil. 2005;84:649–54.
37. Kalaci A, Cakici H, Hapa O, Yanat AN, Dogramaci Y, Sevinç TT. Treatment of plantar fasciitis
using four different local injection modalities: a randomized prospective clinical trial. J Am
Podiatr Med Assoc. 2009;99:108–13.
38. Wheeler P. Autologous blood injections for chronic plantar fasciitis – a pilot case-series study
shows promising results. Inter Musculoskeletal Med. 2013;35:3–7.
39. Ahmad J, Ahmad SH, Jones K. Treatment of plantar fasciitis with botulinum toxin. Foot Ankle
Int. 2017;38:1–7.
40. Singh P, Madanipour S, Bhamra JS, Gill I. A systematic review and meta-analysis of
platelet-rich plasma versus corticosteroid injections for plantar fasciopathy. Int Orthop.
2017;41:1169–81.
41. Buchbinder R, Ptasznik R, Gordon J, Buchanan J, Prabaharan V, Forbes A. Ultrasound-
guided extracorporeal shock wave therapy for plantar fasciitis: a randomized controlled trial.
JAMA. 2002;288:1364–72.
42. Ogden J, Alvarez RG, Lee Cross G, Jaakkola JL. Plantar Fasciopathy and Orthotripsy®: the
effect of prior cortisone injection. Foot Ankle Int. 2005;26:231–3.
43. Gerdesmeyer L, Frey C, Vester J, et al. Radial extracorporeal shock wave therapy is safe and
effective in the treatment of chronic recalcitrant plantar fasciitis: results of a confirmatory
randomized placebo-controlled multicenter study. Am J Sports Med. 2008;36:2100–9.
44. Aqil A, Siddiqui MRS, Solan M, Redfern DJ, Gulati V, Cobb JP. Extracorporeal Shock
wave therapy is effective in treating chronic plantar fasciitis: a meta-analysis of RCTs. Clin
Orthopaedics Relat Res. 2013;471:3645–52.
45. Sun J, Gao F, Wang Y, Sun W, Jiang B, Li Z. Extracorporeal shock wave therapy is effective in
treating chronic plantar fasciitis: a meta-analysis of RCTs. Medicine. 2017;96:e6621.
46. Kamonseki DH, Gonçalves GA, Yi LC, Júnior IL. Effect of stretching with and without muscle
strengthening exercises for the foot and hip in patients with plantar fasciitis: a randomized
controlled single-blind clinical trial. Man Ther. 2016;23:76–82.
47. Carlson RE, Fleming LL, Hutton WC. The biomechanical relationship between the
Tendoachilles, plantar fascia and metatarsophalangeal joint dorsiflexion angle. Foot Ankle Int.
2000;21:18–25.
48. Digiovanni BF, Nawoczenski DA, Lintal ME, Moore EA, Murray JC, Wilding GE, Baumhauer
JF. Tissue-specific plantar fascia-stretching exercise enhances outcomes in patients with
chronic heel pain. J Bone Joint Surg Am Vol. 2003;85:1270–7.
49. Digiovanni BF, Nawoczenski DA, Malay DP, Graci PA, Williams TT, Wilding GE, Baumhauer
JF. Plantar fascia-specific stretching exercise improves outcomes in patients with chronic
plantar fasciitis. A prospective clinical trial with two-year follow-up. J Bone Joint Surg Am.
2006;88:1775–81.
50. Porter D, Barrill E, Oneacre K, May BD. The effects of duration and frequency of Achilles ten-
don stretching on dorsiflexion and outcome in painful heel syndrome: a randomized, blinded,
control study. Foot Ankle Int. 2002;23:619–24.
51. Flanigan RM, Nawoczenski DA, Chen L, Wu H, DiGiovanni BF. The influence of foot position
on stretching of the plantar fascia. Foot Ankle Int. 2007;28:815–22.
52. Monteagudo M, de Albornoz PM, Gutierrez B, Tabuenca J, Álvarez I. Plantar fasciopathy: a
current concepts review. EFORT Open Rev. 2018;3:485–93.
53. Salvioli S, Guidi M, Marcotulli G. The effectiveness of conservative, non-pharmacological
treatment, of plantar heel pain: a systematic review with meta-analysis. Foot. 2017;33:57–67.
54. Alfredson H, Pietilä T, Jonsson P, Lorentzon R. Heavy-load eccentric calf muscle training for
the treatment of chronic Achilles tendinosis. Am J Sports Med. 1998;26:360–6.
55. Thomas JL, Christensen JC, Kravitz SR, Mendicino RW, Schuberth JM, Vanore JV, Weil LS,
Zlotoff HJ, Bouché R, Baker J. The diagnosis and treatment of heel pain: a clinical practice
guideline–revision 2010. J Foot Ankle Surg. 2010;49:S1–S19.
56. Barrett SL, Day SV. Endoscopic plantar fasciotomy for chronic plantar fasciitis/heel spur syn-
drome: surgical technique--early clinical results. J Foot Surg. 1991;30:568–70.
57. Barrett SL, Day SV. Endoscopic plantar fasciotomy: two portal endoscopic surgical tech-
niques--clinical results of 65 procedures. J Foot Ankle Surg. 1993;32:248–56.
58. Barrett SL, Day SV, Pignetti TT, Brian Robinson L. Endoscopic plantar fasciotomy: a multi-
surgeon prospective analysis of 652 cases. J Foot Ankle Surg. 1995;34:400–6.
59. Gamba C, Serrano-Chinchilla P, Ares-Vidal J, Solano-Lopez A, Gonzalez-Lucena G, Ginés-
Cespedosa A. Proximal medial gastrocnemius release versus open plantar fasciotomy for the
surgical treatment in recalcitrant plantar fasciitis. Foot Ankle Int. 2020;41:267–74.
60. Brown JN, Roberts S, Taylor M, Paterson RS. Plantar fascia release through a transverse plan-
tar incision. Foot Ankle Int. 1999;20:364–7.
61. Davies MS, Weiss GA, Saxby TS. Plantar fasciitis: how successful is surgical intervention?
62. Hofmeister EP, Elliott MJ, Juliano PJ. Endoscopic plantar fascia release: an anatomical study.
Foot Ankle Int. 1995;16:719–23.
63. Bader L, Park K, Gu Y, O’Malley MJ. Functional outcome of endoscopic plantar fasciotomy.
64. Healey K, Chen K. Plantar fasciitis: current diagnostic modalities and treatments. Clin Podiatr
Med Surg. 2010;27:369–80.
65. Malahias M-A, Cantiller EB, Kadu VV, Müller S. The clinical outcome of endoscopic plantar
fascia release: a current concept review. Foot Ankle Surg. 2020;26:19–24.
66. Kinley S, Frascone S, Calderone D, Wertheimer SJ, Squire MA, Wiseman FA. Endoscopic
plantar fasciotomy versus traditional heel spur surgery: a prospective study. J Foot Ankle Surg.
1993;32:595–603.
67. Kitaoka HB, Luo ZP, An KN. Mechanical behavior of the foot and ankle after plantar fascia
release in the unstable foot. Foot Ankle Int. 1997;18:8–15.
68. Thordarson DB, Kumar PJ, Hedman TP, Ebramzadeh E. Effect of partial versus complete
plantar fasciotomy on the windlass mechanism. Foot Ankle Int. 1997;18:16–20.
69. Sammarco GJ, Helfrey RB. Surgical treatment of recalcitrant plantar fasciitis. Foot Ankle Int.
1996;17:520–6.
70. Digiovanni CW, Kuo R, Tejwani N, Price R, Hansen ST, Cziernecki J, Sangeorzan BJ. Isolated
gastrocnemius tightness. J Bone Joint Surg Am Vol. 2002;84:962–70.
71. Huerta JP. The effect of the gastrocnemius on the plantar fascia. Foot Ankle Clin.
2014;19:701–18.
72. Maceira E, Monteagudo M. Functional hallux rigidus and the Achilles-calcaneus-plantar sys-
tem. Foot Ankle Clin. 2014;19:669–99.
73. Barouk LS, Barouk P, Toullec E. Brièveté des muscles gastrocnémiens et pathologie de l’avant-
pied La libération proximale chirurgicale. Médecine et Chirurgie du Pied. 2005;21:143–52.
74. Abbassian A, Kohls-Gatzoulis J, Solan MC. Proximal medial gastrocnemius release in the
treatment of recalcitrant plantar fasciitis. Foot Ankle Int. 2012;33:14–9.
75. Brugh AM, Fallat LM, Savoy-Moore RT. Lateral column symptomatology following plantar
fascial release: a prospective study. J Foot Ankle Surg. 2002;41:365–71.
76. Chimera NJ, Castro M, Manal K. Function and strength following gastrocnemius recession for
isolated gastrocnemius contracture. Foot Ankle Int. 2010;31:377–84.
77. Gianakos A, Yasui Y, Murawski CD, Kennedy JG. Effects of gastrocnemius recession on ankle
motion, strength, and functional outcomes: a systematic review and national healthcare data-
base analysis. Knee Surg Sports Traumatol Arthrosc. 2016;24:1355–64.
78. Monteagudo M, Maceira E, Garcia-Virto V, Canosa R. Chronic plantar fasciitis: plantar fasci-
otomy versus gastrocnemius recession. Int Orthop. 2013;37:1845–50.
79. Hamilton PD, Brown M, Ferguson N, Adebibe M, Maggs J, Solan M. Surgical anatomy of the
proximal release of the gastrocnemius: a cadaveric study. Foot Ankle Int. 2009;30:1202–6.
Foot and Ankle Tendon Transfers: Surgical
Techniques
Jose Carlos Cohen
1 Introduction
Tendon transfers around the foot and ankle play a fundamental role in the surgical
management of deformities. They are especially useful for the correction of flexible
deformities caused by dynamic muscular imbalance. Neuromuscular diseases, cen-
tral and peripheral neural lesions (post-traumatic, iatrogenic, and infectious), and
intrinsic tendon alterations (tendinopathies and postcompartment syndrome
sequelae) often require tendon transpositions to replace the action of the lost func-
tion. Some basic principles for the proper functioning of the transfer: the tendon to
be transferred must be healthy (adequate strength and excursion), restoration of the
relationship between tendon and tendon sheath, a good tissue bed for tendon slid-
ing, proper tension, and creating an effective traction line [1].
In cases of neurological origin, the determination of whether the pathology is
progressive (e.g., Charcot-Marie-Tooth’s disease, syringomyelia, and spinal dysra-
phism) or static is imperative (e.g., cerebral palsy and polio), since progressive neu-
ropathies have a worse prognosis and additional surgeries are often necessary as
muscle weakness and imbalance advance during the natural course of the disease.
The differentiation between spastic or flaccid paralysis should be appreciated.
Spastic deformities in the adult foot are observed after traumatic brain injury (TBI)
or stroke from the injury of the first motor neuron. In children, they are observed in
cases of cerebral palsy. The use of transfers in the presence of tendon spasticity are
less predictable and with variable results, because they depend on factors such as
spasticity and muscle activation, the presence or degree of motor control, sensory
function, and cognitive skills [2].
J. C. Cohen (*)
Foot and Ankle Surgery, Federal University Hospital of Rio De Janeiro/Brazil (UFRJ/
HUCFF), Rio De Janeiro, Brazil

Switzerland AG 2022
902 J. C. Cohen
Tendon transfers can be used in combination with bone procedures (osteotomies

or arthrodesis) to correct deformities, instability or joint degeneration, depending on
the underlying pathology and severity of the deformity. In practically all neurogenic
cases and commonly in non-neurogenic deformities (PTC sequelae, traumatic or
degenerative tendon ruptures) with muscle imbalance, tendon transfers are required
as part of surgical correction [3].
The objective of tendon transfer is often not only to replace the lost action of the
previous tendon, but also to redirect the tendon traction line and improve the bal-
ance, eliminating deforming forces and in some situations delaying the progression
of joint degeneration. Thus, in some cases, the re-balancing achieved with tendon
transposition is more important than the force performed by the tendon itself at its
new insertion site.
In addition to the requirements already mentioned for tendon transfer to correct
the deformity and improve motor function, the presence of joint stability and the
absence of fixed deformity in the joint on which the tendon will exert its action are
imperative conditions. Other theoretically desirable characteristics of the transfer
are: synergistic action (isophase contraction with the tendon being replaced), donor
tendon function will be replaced by another tendon (or other tendons), and finally,
single function performed by transferred tendon. In practice, many times we are not
able to meet these last requirements, but they do not prevent a satisfactory result.
After a tendon transfer, there will be some loss of strength played by the donor ten-
don in its original insertion. This loss of strength will be acceptable as long as there
is sufficient residual function to perform the desired action. Those tendons who
primarily perform essential functions should not be sacrificed [4].
The patient’s expectations after the tendon transfer should be understood by the
surgeon, who in turn should explain the objectives of the surgery and the possible
consequences due to the loss of donor tendon function. For example, after surgical
correction of drop foot with transposition of the posterior tibialis tendon (PTT),
some ankle plantar flexion strength is lost (as a consequence of the PTT transfer and
that Achilles tendon is weakened through lengthening) so that the patient can per-
form an adequate dorsiflexion. Moreover, the elimination of the use of orthoses after
surgery is expected with the restoration of motor function of the paralyzed tendon,
but we must guide the patient that this does not occur in all cases.
2 Preoperative Planning
2.1 Anamnesis and Physical Examination
Preoperative planning is crucial for effective correction of foot deformities. The

anamnesis is important to recognize the underlying pathology and should include
detailed information on the development of the deformity, previous history of
trauma, neurological disease (cerebral palsy, stroke, TBI), genetic causes (e.g.,
Foot and Ankle Tendon Transfers: Surgical Techniques 903
Charcot Marie Tooth), and other concomitant diseases (e.g., leprosy, diabetes mel-
litus). During the physical examination, we must observe the mobility of the foot
during walking, alignment of the feet and lower limbs in orthostatic position, and
inspection of shoes, movement arc of the ankle joints, subtalar and Chopart joint,
noting the presence of fixed deformities or instability. The differentiation of static
and dynamic deformities can be difficult, being many times better evaluated with
the anesthetized patient. Occasionally, the use of selective peripheral neural blocks
or botulinum toxin can be used in the differentiation of a joint block caused by joint
contracture (stiffness) or spasticity. Muscle strength tests to detect symmetric or
asymmetric dorsiflexors, plantar flexors, inverters, and evertors are performed.
Specific tests such as the Coleman block test (Figs. 1 and 2) and Silfverskjöld
maneuver are very useful during the surgical decision. Deep patellar tendon and
Achilles reflexes are graduated in absent, normal, hypoactive (diseases of the sec-
ond motor neuron and muscular dystrophies) or hyperactive (diseases of the first
motor neuron). The presence of ulcers in areas of plantar support indicate loss of
protective sensitivity.
3 Methods of Tendon Transfer Fixation
The fixation of the tendon to the receiving site can be done to the bone or to another
tendon. The fixation of the tendon to the bone can be done in different ways. When
there is an adequate length of the tendon, it can be passed through a bone tunnel and
sutured into it. When it is not possible to suture it back into itself, we can fix it to the
bone tunnel by using special implants such as metal anchors or bio-absorbable
interference screws made of poly-lactic acid. A recent study showed a higher fixa-
tion strength using an interference screw compared to a metal anchor in an in vitro
model in a split-type transfer of the anterior tibial tendon [5].
Fig. 1 Patient with CMT

with bilateral cavo-
varus foot
904 J. C. Cohen
Fig. 2 Coleman test

demonstrating correction
of the hindfoot indicating
that plantarflexion of the
first ray is a major
component of deformity
In Pulvertaft’s technique, the transferred tendon is interlaced over the receiver

tendon through small cuts and then the tendons are sutured. The tendons can be
joined in a spiral, where the donor tendon is twisted around the recipient tendon and
then sutured. This technique is the author’s preference in cases of PTT transposition
to the dorsum of the foot as we will see below.
The adjustment of the transfer tension is important to obtain a satisfactory result.
A loose tensioning may compromise the function of the tendon in its new insertion
site, while excessive tensioning could produce a tenodesis effect, thus reducing the
capacity of active contraction of the transferred tendon. Thus, it is up to the surgeon
to choose the correct tensioning during the transference, being generally performed
an intermediate tensioning between the point of maximum and minimum tension
during the anchorage of the donor tendon. The author recommends that in cases of
tendon-tendon fixation, the adjustment (suture) be done in a higher degree of ten-

sion, because the muscle-tendon unit has the capacity to stretch naturally, thus
potentiating the capacity of contraction of the transferred tendon. While in cases of
tendon-bone fixation, the transference is performed at a degree of tension strong
enough that at the end of the surgery the foot is slightly overcorrected in favor of the
direction of movement that the donor tendon proposes to act (for example, slight
dorsiflexion in cases of PTT transfer for dropfoot).
The advantages of tendon-tendon insertion are easier fixation, better control, and
adjustment of tension at the moment of suturing, and no need for anchors or screws
(biotenodesis or poles). Bone insertion is often used because it provides, at least in
theory, a stronger fixation without the possibility of loosening the tendon transfer,
but it presents as disadvantages a greater difficulty of fixation and tensioning of the
suture, besides the need for special implants. Rodeo et al. [6] demonstrated in a
biomechanical and histological study in dogs that the maturation of the tendon-bone
interface occurs around 12 weeks, and therefore a considerable immobilization
period is recommended so that there is no risk of fixation failure. Wagner E et al. [7]
in a biomechanical study using different side-to-side tenorrhaphies configurations
in porcine tendons, demonstrated that all four commonly used techniques (running
locked, simple eight, vertical mattress, and pulley suture) sustained the physiologi-
cal expected loads to occur in tendons in foot and ankle, although the vertical mat-
tress configuration showed the least resistance. The authors concluded that
immediate loading or motion after tendon-to-tendon fixation was safe.
4 Imaging Tests
AP/lateral weight-bearing X-rays of the foot and ankle and the axial incidence of
Cobey modified by Saltzman are indispensable for the evaluation and planning of
the deformity correction (Figs. 3 and 4). The advent of weight-bearing computed
tomography (WBCT) brought new perspectives for a better understanding of defor-
mities, but it is not yet widely available. Conventional computed tomography can be
useful in cases of suspected joint degeneration, thus helping in the surgical decision
between arthrodesis or osteotomy and nonunion after previous arthrodesis. Nuclear
magnetic resonance imaging is not routinely performed, being used in cases of
infection, tumors or tendon ruptures. Dynamic baropodometry can be useful in
measuring the pattern of pressure distribution during walking.
5 Transfer of the Posterior Tibial Tendon
Initially described by Watkins [8], anterior transposition of the posterior tibialis is

used to restore ankle dorsiflexion. Common fibular nerve lesion is the most frequent
cause of dropfoot, being also indicated for a variety of conditions (neurogenic and
906 J. C. Cohen
Figs. 3 and 4 Weight-bearing AP and lateral X-rays demonstrate a typical CMT cavo-varus with
talar external rotation, medial subluxation of the talonavicular caused by overpull of PTT. On the
lateral view, tibial external rotation and plantar flexed first metatarsal
non-neurogenic) such as cerebral palsy, spina bifida, hemiplegia after brain injury
(stroke or TBI), Duchenne muscular dystrophy or polyneuropathies such as ex
Charcot Marie Tooth.
In cases of paralysis after traumatic injury of the common fibular nerve, an elec-
troneuromyography test can determine if the peripheral neural lesion is transient
(neuropraxia), where we should wait about 1 year for its improvement, or an axo-
notmesis with the complete section of the nerve, with little possibility of recovery
of muscle function.
Some aspects of PT transfer are still controversial [9]: the route of transposition
(subcutaneous or interosseous route) [10], the tension of the transferred tendon, and
the need to use more than one tendon during transference. The subcutaneous (SC)
route is easier and faster to be performed and consists of redirecting the PTT around
the distal tibia, potentially giving more lever arm, better muscle strength, lower risk
of neurovascular injury, and lower chance of adhesions [11]. However, there is a
higher risk of inversion in relation to the interosseous route. The interosseous route
(IO) is the most frequently used and uses a window in the interosseous membrane
to allow the passage of the PTT from the deep posterior compartment to the anterior
compartment of the leg, thus providing a more direct line of traction and better
capacity of dorsiflexion, but has less lever arm (less potential force) and higher risk
of adhesions [12]. Wagner E et al. compared the circumtibial (subcutaneous), above-
retinaculum interosseous, and under-retinaculum interosseous tibialis posterior
transfer routes in cadaveric specimens. They observed that the circumtibial route
showed the highest gliding resistance and produced a supination moment on the
forefoot, while the interosseous route under retinaculum performed better than the
interosseous route above retinaculum with regard to ankle dorsiflexion, with no dif-
ference in gliding resistance, suggesting the retinaculum may work as a fulcrum. In
addition, using magnetic resonance images of lower extremities and a mathematical
model, one study defined that the most adequate window size for interosseous trans-
fer, in order to avoid entrapment, is a minimum of 5 cm or 2.5 times the size of the
tendon diameter [13, 14].
Bridle’s procedure [15] combines the peroneus longus (PL) and tibialis anterior
(TA) tendons for balance and reinforcement of the posterior tibial for its new dorsi-
flexor function. This triple transfer is of great use in cases of multiple tendon dys-
functions, because it can balance the foot in inversion or eversion, given its tripod
configuration. The author does not routinely recommend this technique in cases of
isolated dropfoot, since the tenodesis effect produced causes an intense restriction
of the plantar flexion making it difficult to detach the calcaneus from the floor and
thus damaging the propulsion of the body during walking.
Depending on the pathology, the PT tendon can be transferred single (whole) or
divided into two slings to the dorsum of the foot. When transferred as a whole, it is
transferred to the middle cuneiform or lateral cuneiform. The latter is chosen if there
is an inversion predominance given by healthy flexor hallucis longus (FHL) or FDL
tendons and/or diseased evertors (peroneus longus and brevis tendons, EDL, pero-
neus tertius). When the PTT is transferred as two slings, it could reproduce dorsi-
flexion in a more balanced and physiological way. Nevertheless, it is a demanding
procedure, without evidence of its superiority to whole PTT transfer for dropfoot
cases caused after common peroneal nerve lesion. The author has extensive experi-
ence in the correction of dropfoot in patients with leprosy [16] and in these cases he
uses the technique described by Srinivasan [17] with tendon-tendon fixation and a
split PTT (medial PTT sling to the EHL and lateral sling to the EDL) which will be
described below.
In Charcot-Marie-Tooth disease, PTT transposition is often performed associ-
ated with other surgical procedures for the correction of cavo-varus foot. The
removal of the deforming force of the PTT (without the opposition of the paralyzed
Peroneus brevis-PB tendon) causing the varus deformity of the hindfoot is cor-
rected, while the dorsiflexion is reestablished, thus replacing the anterior tibial ten-
don which is paralyzed (Figs. 5, 6, 7, 8, 9, 10, and 11). We must remember that even
a weak posterior tibial tendon must be transferred since the deforming force is
removed and at least a tenodesis effect will be obtained to assist the dorsiflexion
[18]. In CMT disease, as well as in post-traumatic paralysis of the common fibular
nerve, the author uses the interosseous route and tendon-tendon fixation with the
medial tape sutured to the anterior tibialis and the lateral tape sutured to the PB or
peroneus tertius. It is perfectly acceptable to perform a whole PTT transfer to the
middle or lateral cuneiform as well. The chosen technique will depend on the sur-
geon’s experience.
908 J. C. Cohen
Figs. 5, 6, and 7 Preop clinical image and weight-bearing X-rays of a bilateral cavo-varus feet
with CMT (same patient as in Fig. 1)
6.1 Posterior Tibial Tendon Transfer Using the Interosseous

Membrane Route
Initially, percutaneous triple hemi-section of the Achilles described by Hoke is per-

formed if at least 20 degrees of passive ankle dorsiflexion is not possible. An inci-
sion of 3 to 4 cm is made over the insertion of the posterior tibial tendon (TTP) near
the navicular, sectioning it as distally as possible. After its distal release, a second
incision is made in the posteromedial region of the leg, approximately 8 to 12 cm
Figs. 8, 9, 10, and 11 Postop clinical pictures and X-rays after bilateral correction with plantar
fasciotomy, split PTT transfer to TA and PB through the interosseous membrane, dorsiflexion
osteotomy of the first metatarsal, Chopart fusion, and tendo Achilles Z-lengthening
910 J. C. Cohen
above the medial malleolus (Fig. 12). The fascia is incised and the FDL muscle
belly is identified, moving it away and then the PTT muscle belly is visualized.
Then, the PTT is pulled in the cephalic direction through the proximal incision. The
PTT is then longitudinally divided into two tapes from proximal to distal with a
number 11 scalpel blade (Fig. 13). The tapes are repaired with 2.0 mm Vicryl
sutures. The tendon is passed through the interosseous membrane using wires
passed from anterior to posterior with the aid of the Andersen forceps (Figs. 14 and
15). The incision in the medial region is extended distally for the visualization of the
anterior tibial tendon and a tunnel is created through its sheath, below the retinacu-
lum of the extensors with the Andersen’s colander, and the medial sling of the PTT
is brought distally. A lateral incision is made to identify the fibular tendons and
another tunnel is created through the sheath of the peroneus tertius and EDL ten-
dons under the retinaculum. The lateral tape is then brought distally. Finally, the
medial sling of the PTT is sutured to the anterior tibial tendon and the lateral tape to
the peroneus brevis tendon with the foot in dorsiflexion from 20 to 30 degrees
(Figs. 16 and 17) maintaining maximum distal tension on the tendons to be
transferred.
Figs. 12 and 13 Distal section of the PTT on its navicular insertion and identification of its proxi-
mal muscular belly/TTP split into two strips
Figs. 14 and 15 Passing the splitted PTT through a window created in the interosseous membrane
Figs. 16 and 17 Medial and lateral PTT tapes sutured to the anterior tibial tendon and peroneus
brevis, respectively
If the surgeon assumes PTT is overly thin to be splitted or prefers to use it as a

single tendon, the steps are the same as above, with the exception that the PTT is
anchored to the intermediate cuneiform bone through a bone tunnel using a bioteno-
desis screw (most common) or suture anchor. A longitudinal dorsal incision is car-
ried out in the midfoot, and after retracting the extensor tendons, the intermediate
cuneiform is identified (a fluoroscopic image is helpful) and prepared to receive the
tendon transfer. The foot should be kept in slight dorsiflexion (5–10 degrees) during
the tendon fixation.
7 Whole Transfer of the Posterior Tibial Tendon through

the Subcutaneous Route (Circumtibial Route as Described
by Srinivasan [17])
The steps are identical to the previous procedure, but the PTT is passed directly
through the subcutaneous route with Andersen’s forceps (Fig. 18), inserting the
medial tape in the EHL and the lateral tape to the EDL through a transverse approach
over the dorsum of the foot (Fig. 19). Maximum traction is performed in opposite
directions of the donor and recipient tendons for subsequent fixation with the
Pulvertaft technique (Figs. 20 and 21).
The postoperative period consists of a plaster cast immobilization with 20
degrees dorsiflexion during the first two weeks, followed by another four weeks of
cast boot in neutral without weight bearing. After this period, rehabilitation begins
with the use of a removable boot with partial weight-bearing for an additional
six weeks.
The following figures (Figs. 22, 23, 24, 25, 26, 27, 28, and 29) illustrate a case of
cavo-varus foot of neurological origin with muscular imbalance and shortening of
the Achilles tendon corrected with triple arthrodesis, PTT transfer through the inter-
osseous membrane, and Z-elongation of the Achilles.
912 J. C. Cohen
Fig. 18 Subcutaneous
tendon passage
Fig. 19 Medial and lateral

PTT tapes brought distally
over the dorsum of the foot
Figs. 20 and 21 Pulvertaft fixation of the medial PTT sling to the EHL and from the lateral sling
to the EDL, performing maximum traction of the tendons in opposite directions
Figs. 22 and 23 Pes cavovarus with dorsiflexion deficit due to Duchenne’s muscular dystrophy
914 J. C. Cohen
Figs. 24 and 25 AP/Lateral preoperative weight-bearing radiographs
Fig. 26 Preparation of
joint surfaces of the
subtalar and calcaneo-
cuboid through a sinus
tarsi approach
8 Tendon Transfer with Flexor Hallucis Longus

Tendon (FHL)
The use of FHL for Achilles pathologies was initially described by Mann and
Hansen [19], being used as a reinforcement or as the only substitute for the Achilles
tendon. Currently, it is used in chronic ruptures and in degenerative insertional and
noninsertional Achilles tendinopathies. Its proximity, motor strength, axis of
Fig. 27 Transfer of TTP

through the interosseous
membrane (an extended
posteromedial approach
was also carried out,
including the preparation
of talonavicular joint)
contraction similar to the Achilles tendon and due to its activation during walking
occurring simultaneously with the Achilles, make this tendon preferred by most
surgeons.
The evaluation of soft tissues is particularly important in the use of tendon trans-
fers around the Achilles tendon, since complications of the surgical wound are fre-
quent in this region. We should observe previous scars and/or infection history to
plan the best tendon option to be used, site of the incision, and the need for two step
surgical procedures [20].
Chronic Achilles ruptures cause weakness and significant decrease in the detach-
ment of the calcaneus during gait, while pain often is not present at the time of
diagnosis. Conservative treatment is poorly tolerated by patients and is reserved
only for sedentary patients or those with contraindication to surgical reconstruction.
In chronic Achilles ruptures, FHL transfer is indicated when there is extensive
degeneration of the proximal and distal stump, and reconstruction is not possible
(Fig. 30). The MRI of the whole leg may demonstrate the presence of gastrocne-
mius fat atrophy and thus assist in surgical planning. The presence of a gap larger
than 5–6 cm after debridement is also considered by some authors as an indication
for the use of FHL.
916 J. C. Cohen
Figs. 28 and 29 Postoperative weight-bearing AP/lateral radiographs
Fig. 30 Achilles rupture

with important
degeneration of proximal
and distal stumps in a
previously operated patient
When considering the tendons available for replacement or reinforcement of the

Achilles tendon, the flexor hallucis longus and the flexor digitorum longus present
the most advantageous traction line due to its location in the posterior compartment.
When comparing the relative working capacity of the tendons around the ankle, it is
known that the difference in force between the Achilles (gastrosoleus) and the other
tendons is very pronounced, so that the peak force generated by the Achilles is much
greater than both FHL and FDL tendons. Nevertheless, the FHL tendon is capable
of generating enough power to balance the orthostatic position, and going up and
down stairs [21]. Vega et al. [22] used endoscopic FHL transfer for chronic Achilles
rupture in patients with low demand (mean age of 67 years), obtaining good results
in all patients returning to their daily activities. In those patients where it is neces-
sary to reestablish greater motor power, the use of FHL in isolation is controversial,
being the author’s preference, to use it only as reinforcement or to use surgical
techniques that restore the continuity of the gastrosoleus complex (e.g., v-y elonga-
tion, tendon autograft, and fascia turn-down flap), preserving its functionality and
thus providing greater strength capacity.
The use of peroneus tendons, especially the PB tendon, although much used in
the past as recommended by Turco and Spinella in cases of chronic Achilles rupture
[23], is not recommended by the author, since its removal will sacrifice the main
lateral dynamic stabilizer of the ankle.
Hansen described the FHL use in noninsertional tendinopathies, harvesting it in
the posterior region of the ankle and its insertion in the posterosuperior tuberosity
of the calcaneus (after resection of Haglund’s prominence, if present) through a
bone tunnel. With this, theoretically there is an increase of vascularization brought
by the FHL muscle belly to the Achilles tendon which commonly presents degen-
eration, calcification or cysts, although it has no support in the literature. Den Hartog
[24] recommends that reinforcement with FHL be used when more than 50% of the
Achilles is resected after debridement. In Achilles insertional tendinopathy, after the
failure of conservative treatment, the established surgical treatment involves the
excision of the degenerated tendon, removal of the Haglund deformity, and if neces-
sary, a reinforcement or reconstruction of the Achilles. Although several studies
show good results with the excision of the degenerated tendon, limited resection of
the posterosuperior tuberosity to “decompress” the Achilles associated with the
reinsertion of the tendon with the use of anchors, the use of FHL as reinforcement
is recommended when there is a degeneration (tendinosis) of the Achilles greater
than 50 to 75% of its diameter seen in the axial sections of the MRI [25, 26].
Although some surgeons recommend its use in patients over 50 years of age associ-
ated with Achilles debridement, Hunt et al. [27] demonstrated in a randomized
study that there was no difference in the final result in patients undergoing Achilles
debridement in isolation compared to the group with FHL reinforcement in patients
with insertional tendinopathy.
Wapner et al. [28] reported his technique of FHL transfer, using two incisions,
with the removal of the FHL through an access in the midfoot to obtain a longer
tendon in order to allow it to be passed through two perpendicular orifices in the
calcaneus (Fig. 31) and still with enough tendon to anchor it in the remaining proxi-
mal stump of the Achilles (Fig. 32). Recently, the use of a single posterior incision
with the removal of the FHL tendon in the medial retromalleolar region became
possible with the advent of appropriate implants (interference screws), allowing the
fixation of the tendon to the calcaneus to be performed directly on the posterior
tuberosity of the calcaneus.
918 J. C. Cohen
Fig. 31 Removal of the

FHL at the midfoot with its
exteriorization through
posterior Achilles
approach. Preparation of
perpendicular bone tunnels
in the calcaneus with a
4.5-mm drill
Fig. 32 Passage of FHL

through the calcaneus and
suturing to the remaining
proximal stump
With the advent of posterior endoscopic ankle compartment techniques popular-

ized by Van Dijk, [29] it became possible to endoscopically transfer the FHL to the
calcaneus. The advantages of a minimally invasive procedure with faster functional
recovery, lower morbidity, and lower risk of skin complications have made this
procedure very popular. The disadvantages are the learning curve and the need for
specific equipment, making the procedure more expensive.
9 Surgical Technique of FHL Transfer (Open Method)

for a Chronic Achilles Rupture
The patient is placed in prone position with a cushion placed on the opposite hip to
rotate internally the side to be operated. The foot is placed slightly outside the surgi-
cal table to allow dorsiflexion during the procedure when necessary and ischemia is
installed in the thigh. A medial para-Achilles approach is performed. After opening
the paratenon, we identify the scar tissue interposed between the stumps, which can
present fat degeneration (Fig. 33). After debridement of all scar tissue, the gap
between the stumps is measured and the need for FHL transfer is confirmed. With
Metzenbaum scissors, the deep fascia of the leg is opened medially to the remaining
Achilles. The FHL muscle belly is easily identified after extending the incision over
the proximal and distal fascia. The FHL tendon is pulled and sectioned in the medial
retromalleolar region taking care to direct the scalpel blade from medial to lateral in
order to protect the neurovascular bundle. The ankle should be kept in maximum
flexion with the flexed hallux to obtain the greatest possible length of the tendon.
Next, the tendon is repaired with 3.0- mm Vicryl sutures. The bone tunnel is pre-
pared in the posterosuperior tuberosity of the calcaneus through the passage of the
guide wire and specific drills (the use of fluoroscopy is useful to confirm the posi-
tion of the guide wire) (Fig. 34). The tendon is passed inside the tunnel through the
calcaneus and then pulled by the Vicryl sutures from the sole of the foot until the
muscular belly is almost at the upper limit of the bone tunnel (Fig. 35). An interfer-
ence screw is used to fix the tendon inside the bone canal, keeping the ankle in
plantar flexion from 20 to 30 degrees and the tendon pulled distally (Fig. 36).
Fig. 33 Achilles tendon

presenting fatty
degeneration in its
insertion
920 J. C. Cohen
Fig. 34 Passage of the

drill over the guide wire in
the posterosuperior
tuberosity of the calcaneus

FHL through the bone
tunnel
Fig. 36 Fixing the FHL

with interference screw
10 Surgical Technique of FHL Transfer for Peroneal

Tendon Injury
Irreparable lesions of peroneal tendons or severely compromised tendons after

attempted surgical repair are infrequent. In the literature, there are few articles that
guide the management of these complex lesions. When both tendons are involved,
so that neither can be salvageable, the use of tendon transfer or allograft may be
used, depending on the functionality of the muscle bellies and quality of the local
tendon bed.
The alignment of the ankle and hindfoot is an important factor that predisposes
the patient to fibular tendinopathy. A cavo-varus foot can overload the peroneal
tendons during physical activities, causing tendinosis and ruptures, particularly of
the long peroneal tendon [30]. The calcaneal varus puts both peroneal at a mechani-
cal disadvantage due to reduced lever arm and increased frictional forces at the level
of the lateral malleolus, calcaneal tubercle, and cuboid groove. Peroneal tendon
ruptures are often associated with other changes, such as chronic tenosynovitis,
ankle sprain and fracture, and chronic ankle instability.
Redfern and Myerson [31] classified the lesions of both peroneals tendons into
three types according to intraoperative evaluation. Type 1: Both tendons are mostly
intact, Type 2: One tendon is ruptured but the remaining tendon is functioning, and
Type 3: Both tendons are ruptured and not functioning. In type 3, these authors recom-
mend the use of tendon transfer when the proximal muscles of the peroneals tendons
do not present an adequate excursion (caused by atrophy or muscular fibrosis - type
3a) or when the tendon bed is fibrosed, even in the presence of an excursion of the
proximal muscles (type 3b). These authors use the FDL as recommended by Borton
et al. [32]. However, the FHL can also be used [33] being transferred to the lateral
compartment of the leg, anchored at the base of the fifth metatarsal or at the remaining
distal stump of the PB. Jockel and Brodsky [34] reported good results using both ten-
dons (FHL and FDL), but showed better eversion force, higher AOFAS score, and
better subjective functional evaluation of those patients in whom FHL was used.
11 Technique for FHL Transfer to Peroneals (Author’s

Preference)
A medial approach over the midfoot is used to harvest the FHL. After the subcuta-
neous dissection, the abductor hallucis and the flexor digitorum brevis muscles are
retracted inferiorly. The cauterization of small vessels is performed as the dissection
deepens in the midfoot because they usually bleed and retract in case of injury.
Henry’s knot is identified and the FHL is sectioned as distal as possible. The FHL is
repaired with a 2.0-mm Vicryl suture using the Krakow technique. Next, the lateral
distal leg incision is extended over the fibular muscle-tendon compartment. After
the identification of the peroneal tendons, once retracted it is possible to visualize
922 J. C. Cohen
the deep crural fascia of the leg over the posterior compartment. After incising the
deep fascia, it is possible to directly identify the FHL muscle belly. (An alternative
is to perform a separate posteromedial access at the ankle level to identify the FHL
and then proximally pull it from the posterior compartment to the lateral compart-
ment with a tunneling forceps) (Fig. 37). The muscular belly is proximally pulled,
bringing the FHL tendon directly from the deep posterior compartment to the lateral
side of the leg (Fig. 38). The FHL is sutured to the distal stump of the PB or directly
over the base of the fifth metatarsal with a metallic anchor or through a bone tunnel
(Fig. 39).
The following images (Figs. 40, 41, 42, 43, 44, 45, and 46) show a patient with
progressive unilateral cavus of the right foot with severe dysfunction of the perone-
als with chronically damaged and irreparable lesion.
12 Transfer of the FDL to the Navicular
The loss of arch in flatfoot can end up in a loss of posterior tibial tendon function in
the adult. The main function of PTT is the inversion of the subtalar joint, which
helps stabilize the Chopart joint so that the Achilles tendon can lift the heel from the
Fig. 37 Posteromedial
access for identification of
the FHL in the medial
retromalleolar region

FHL to the lateral
compartment
ground. The combination of soft tissue procedures and osteotomies of the calcaneus
or arthrodesis of the hindfoot is often used in the surgical treatment of this pathol-
ogy. Among soft tissue procedures, the transfer of the FDL to the navicular is com-
monly used in flexible deformities to replace the degenerated PTT. Its proximity and
contraction in phase to the PTT make the FDL a suitable transfer. Besides, there is
no need to cross the neurovascular bundle and it has a similar tendon excursion in
relation to PTT. Although the posterior tibial insertion is mostly over the navicular
plantar region, it is known that distally to its insertion to the navicular, the PTT
branches in several points under the longitudinal arch of the foot, totalling nine
insertions in the midfoot, which assist in the dynamic support of the plantar arch
together with the spring ligament and the calcaneonavicular plantar ligament.
Willeneger et al. [35] in a cadaver study analyzed these ramifications of PTT inser-
tion, observing the following frequency: medial cuneiform (80.5%), intermediate
cuneiform (19.5%), lateral cuneiform (92.7%), cuboid (46.3%), calcaneus (12.2%),
and metatarsal bases (80.5%).
The FDL transfer is usually done through a bone tunnel in the navicular tuberos-
ity after resection of the degenerated PTT tendon. However, due to the peculiar
anatomy of PTT insertion mentioned above, the author’s preference in cases where
924 J. C. Cohen
Fig. 39 Fixing the FHL to

the base of the fifth
metatarsal with a metal
anchor. Lateral approach
over the calcaneus for
Dwyer osteotomy for
simultaneous correction of
varus of the hindfoot
the PTT still presents viable tissue after debridement is to perform a simple redirec-
tion of the FDL to the navicular with the use of an anchor together with the suture
to the PTT distal stump (in situ transference) in order to obtain a more physiological
reproduction of the PTT function. By not sectioning the FDL distally, it is possible
to maintain its tension allowing a stronger and more powerful and functional trans-
ference [36, 37]. In cases where the PTT is totally degenerated, the FDL is trans-
ferred to the navicular through the bone tunnel, as described below.
A longitudinal medial access over the PTT is performed extending immediately

proximally to the medial malleolus to a point slightly distal to the navicular tuberos-
ity. After the identification of its sheath, it is incised exposing the PTT, taking care
to preserve the flexor retinaculum. After debridement, the FDL tendon is identified
immediately below the PTT. It is frequent the presence of small perforating vessels
in this region, being necessary its coagulation before dissecting more deeply.
Figs. 40, 41, and 42 Clinical picture and preop X-rays of a patient with an asymmetric cavus foot
on the right side. He progressively developed hindfoot varus with pain and dysfuncion of the pero-
neal tendons. X-rays show plantarflexed first ray, increased calcaneal pitch on the lateral view. On
AP, there is medial subluxation of the navicular with slight adduction of the forefoot
Henry’s knot is identified, and a FDL to FHL tenodesis is performed. Some authors
consider this tenodesis unnecessary due to the presence of links between these ten-
dons at the knot of Henry [38, 39]. The FLD tendon is then repaired with 2.0-mm
Vicryl suture, a hole is made in the tuberosity of the navicular with a 4.5-mm drill
(or a specific drill when a biotenodesis screw is used) and the FDL tendon is passed
from medial-plantar to dorsal-lateral in an attempt to reproduce the PTT traction
axis. The FDL transfer tensioning is performed in such a way that the forefoot is in
slight adduction before securing the transfer with a biotenodesis screw (Figs. 47 and
48) or the FDL is sutured into himself after passing through the bone tunnel.
The following pictures (Figs. 49, 50, 51, 52, and 53) illustrate a typical case of
PTT dysfunction with a progressive hindfoot valgus, pain, and edema in the pos-
teromedial region of the ankle. The patient was unable to stand on her tiptoes on the
right foot. (The surgical procedure and postoperative clinical images and X-rays are
shown in Figs. 54, 55, 56, 57, 58, 59, 60, and 61).
926 J. C. Cohen
image with severe
degeneration and scarring
of both peroneals tendons
Alternatively, in cases where it is possible to keep the PTT after its debridement,
the FDL tendon is identified and after its repair with Vicryl 2–0 (Fig. 54), it is pulled
and fixed to the navicular plantar surface through an anchor (Fig. 55) together with
the laterolateral tenodesis to the remaining distal stump of the PTT, without the need
to section the FLD distally (Fig. 56). Thus, the dissection is less extensive, minimiz-
ing the risk of neurovascular injury and allowing a more physiological function of
the transfer.
14 Transfer of EHL to the First Metatarsal (Modified

Jones Procedure)
The claw deformity of the hallux is the result of an imbalance of its extrinsic mus-
culature. The hyperactivity of the peroneus longus (PL) and the contracture of both
EHL and FHL participate in the genesis of the claw hallux (hyperextension of the
first metatarsophalangeal joint and flexion of the interphalangeal joint) (Fig. 62). In
neuropathic patients, the increased pressure exerted on the head of the first metatar-
sal and on the tip of the hallux may lead to the appearance of plantar ulcers. Keratosis
on the hallux interphalangeal joint dorsum causes difficulty in wearing shoes. It is
usually associated with some neuromuscular disease, such as Charcot-Marie-Tooth,
Figs. 44, 45, and 46 Postop clinical picture and X-rays after transfer of the FHL to the lateral
compartment, a closing lateral wedge osteotomy of the calcaneus (Malerba z-type) associated with
elevation of the first ray using a closing dorsally wedge of the medial cuneiform
Fig. 47 FDL fixation

through a bone tunnel in
the navicular using an
interference screw
928 J. C. Cohen
Fig. 48 Final clinical view
Figs. 49 and 50 Clinical

images of a flexible flatfoot
with PTTD (stage 2).
There is an increased
valgus of the hindfoot on
the right with bulging in
the medial
retromalleolar area
Figs. 51, 52, and 53 Preop X-rays images showing increased hindfoot valgus on the axial view
on the right, talar uncoverage, and plantarflexion on AP and lateral views, respectively
diabetes mellitus, and rheumatoid arthritis. In cases where the metatarsophalangeal

(MTP) joint is flexible, the procedure described by Jones [40] with the transference
of the EHL to the neck of the first metatarsal and later modified through the inclu-
sion of the arthrodesis of the interphalangeal (IP) joint is indicated.
Breusch et al. [41] reported their results in 51 patients (81 feet) after the correc-
tion of the claw hallux with Jones’ modified procedure, observing 86% satisfaction
of the patients with the correction of the deformity in 80 feet. However, they noticed
frequent complications such as lack of elevation of the hallux when walking bare-
foot, transfer lesions and metatarsalgia, hallux flexus, hallux limitus, and asymp-
tomatic IP nonunion.
930 J. C. Cohen
Fig. 54 Identification of
the FDL and repair with
Vicryl 2–0
A dorsomedial incision over the first metatarsal making a curve over the interpha-
langeal joint is performed. Retract the skin to expose the EHL and section it in its
insertion at the level of the distal phalanx. Open the interphalangeal joint and
remove the cartilage with gouge or delicate saw so that the joint surfaces are con-
gruent. Pass two 2.0-mm Kirschner wires retrogradely through the hallux tip and
return them toward the proximal phalanx. If you prefer, the surgeon may use a 4.0-
mm cannulated screw. Expose the medial first metatarsal diaphysis and divide the
periosteum. Drill a 3.2-mm tunnel through the middle of the metatarsal diaphysis.
Pass the tendon of the EHL through the bone tunnel and suture it into itself with
light tension keeping the ankle in dorsiflexion and passive elevation of the first ray
(Fig. 63). Alternatively, the EHL can be sutured to the extensor hallucis bre-
vis tendon.
If after the tendon transfer, the first metatarsal remains plantarly flexed, a dorsal
metatarsal closing wedge osteotomy is added to help with the extension of the first
metatarsal. Extend the incision proximally to the proximal region of the first meta-
tarsal. Using an oscillating saw, remove a dorsal wedge, taking care not to violate
Fig. 55 Anchor fixation in

the plantar - medial
navicular region
the plantar cortex that will work as a hinge. Close the wedge and fix it with one
3.5-mm screw or Kirschner wires (Fig. 64).
Alternatively, an FHL transfer can be used for claw hallux. It has the potential to
avoid the postoperative complications associated with the modified Jones procedure
mentioned above with comparable results or even better than for the Jones proce-
dure [42, 43].
Surgical technique as described by Kadel NJ et al. [42]: A medial incision is
made from the hallux MTP joint to the IP joint. The plantar hallucal nerve is identi-
fied and retracted plantarly, and the IP capsule released when necessary to correct
deformity. The FHL tendon is identified, then the sheath opened and divided distally
to the distal phalanx. The tendon is clamped and divided from its insertion into the
distal phalanx; it is then split into one-third and two-thirds, with the one-third sec-
tion sutured to create a loop and the two- thirds lateral section kept intact and
threaded with 2–0 resorbable suture. A midline 3.5-mm drill hole was made through
the proximal phalanx from plantar to dorsal approximately 1.0 cm distal to the joint;
a curette was used to slightly widen the hole when necessary. Next, the two-thirds
portion of the FHL tendon was passed through the proximal phalanx using a Keith
932 J. C. Cohen
Fig. 56 Redirection of the

FDL to the navicular and
to the remaining PTT
stump
needle until the toe was in a neutral position with the foot in neutral at the ankle. The
suture weave on the two-thirds portion was sutured into the one-third loop of the
FHL on the medial side of the toe. Both loops of the tendon were then secured into
the surrounding soft tissue.
16 Tendon Transfer for Flexible Claw Toe Correction:

Girdlestone-Taylor
The surgery proposed by Girdlestone [44] in 1947 and popularized by Taylor [45]
in 1951 using FDL transfer is useful in cases where the deformity is still flexible.
The logical basis for its use is the idea that the FDL, when transferred to the dorsum
of the proximal phalanx, can replace the action of the intrinsic musculature. FDL
are divided and attached to the extensor hood. Passive plantar flexion in the MTP
through the plantar fascia is maintained.
Figs. 57 and 58 Postop

clinical pictures with
symmetrical hindfoot
valgus
Girdlestone-Taylor surgical technique (TAYLOR, 1951): The original approach

is performed with a straight plantar incision at the level of the MTP joint, extending
distally to the level of the proximal interphalangeal joint. With careful dissection,
protecting the neurovascular bundle, the FDL tendon is identified after opening its
sheath. The author’s preferred approach is using a dorsolateral incision. With a deli-
cate instrument, the tendon is pulled and its section is made as distal as possible,
close to its insertion in the distal phalanx (Fig. 65). The FDL tendon is then brought
proximally and laterally over the extension hood of the MTP joint and proximal
phalanx, keeping the tendon with adequate traction and with an assistant auxiliary
flexing the MTP around 20 to 30 degrees (Fig. 66). The FDL tendon is then sutured
to the extensor hood (Fig. 67). The elongation of the extensor tendons will be per-
formed only in cases where hyperextension of the proximal phalanx persists after
FDL transfer.
934 J. C. Cohen
Figs. 59, 60, and 61 Postop X-rays showing good alignment. FDL transfer was done using a
suture anchor on the plantar-medial surface of the navicular associated with a medial calcaneal
slide osteotomy
Fig. 62 Forces acting on a

clawed hallux resulting in
hyperextension deformity of
the MTP joint and flexion of
the IP joint
Alternatively, in order to avoid extensive dissection, Parrish [46] described a

modification of Taylor’s original technique cutting the FDL in the distal plantar fold
at the level of its insertion in the distal phalanx. Next, a new plantar incision is made
at the MTP joint, the FDL tendon sheath is identified and opened. After blunt dis-
section, the FDL tendon is extracted proximally and divided into two strips along its
central equator with a scalpel blade 11. The tapes are brought to the dorsum of the
Fig. 63 Transfer of the

EHL to the first metatarsal
diaphysis and arthrodesis
of the interphalangeal
hallux joint
Fig. 64 EHL tendon

already detached and
tagged with 3.0 Vicryl
suture. A dorsally based
wedge was removed and
closed with manual
pressure under the first
metatarsal
936 J. C. Cohen
Fig. 65 Identification of
the FDL after opening its
tendon sheath, then its
distal section is performed
Fig. 66 The FDL tendon

is transferred dorsolaterally
and sutured at the extensor
sheath, maintaining
maximum traction on the
tendon and
metatarsophalangeal joint
at 30 degrees of flexion
Fig. 67 Final aspect after

FDL transfer with
correction of toes
deformities
proximal phalanx and suturing them over the extensor hood with adequate tension
maintaining an MTP flexion of 20 degrees. Currently, it is also widely used in the
treatment of hammer toes and in instability with subluxation of the MTP (plantar
plate rupture). After the tendon transfer, rehabilitation through early mobilization is
fundamental. However, the risk of joint stiffness must be balanced with the risk of
recurrence of the deformity.
References
1. Schweitzer KM Jr, Jones CP. Tendon transfers for the drop foot. Foot Ankle Clin.
2014;19(1):65–71. https://doi.org/10.1016/j.fcl.2013.12.002. PMID: 24548510.
2. Genêt F, Denormandie P, Keenan MA. Orthopaedic surgery for patients with central nervous
system lesions: concepts and techniques. Ann Phys Rehabil Med. 2019;62(4):225–33. https://
doi.org/10.1016/j.rehab.2018.09.004. Epub 2018 Oct 2. PMID: 30290282.
3. Dreher T, Wenz W. Tendon transfers for the balancing of hind and mid-foot deformities in
adults and children. Tech Foot Ankle Surg. 2009;8:178–89.
938 J. C. Cohen
4. Walton L, Villani MF. Principles and biomechanical considerations of tendon transfers. Clin
Podiatr Med Surg. 2016;33(1):1–13. https://doi.org/10.1016/j.cpm.2015.06.001. Epub 2015
Aug 7. PMID: 26590719.
5. Núñez-Pereira S, Pacha-Vicente D, Llusá-Pérez M, Nardi-Vilardaga J. Tendon transfer fix-
ation in the foot and ankle: a biomechanical study. Foot Ankle Int. 2009;30(12):1207–11.
https://doi.org/10.3113/FAI.2009.1207. PMID: 20003881.
6. Rodeo SA, Arnoczky SP, Torzilli PA, Hidaka C, Warren RF. Tendon-healing in a bone tunnel. A
biomechanical and histological study in the dog. J Bone Joint Surg Am. 1993;75(12):1795–803.
https://doi.org/10.2106/00004623-199312000-00009. PMID: 8258550.
7. Wagner E, Ortiz C, Wagner P, Guzman R, Ahumada X, Maffulli N. Biomechanical evalu-
ation of various suture configurations in side-to-side tenorrhaphy. J Bone Joint Surg Am.
2014;96(3):232–6. https://doi.org/10.2106/JBJS.L.01552. PMID: 24500585.
8. Watkins MB, Jones JB, Ryder CT Jr, Brown TH Jr. Transplantation of the posterior tibial ten-
don. J Bone Joint Surg Am. 1954;36-A(6):1181–9. PMID: 13211711.
9. Turner JW, Cooper RR. Anterior transfer of the tibialis posterior through the interosseus membrane.
Clin Orthop Relat Res. 1972;83:241–4. https://doi.org/10.1097/00003086-197203000-00043.
PMID: 4552381.
10. Richard BM. Interosseous transfer of tibialis posterior for common peroneal nerve palsy. J
Bone Joint Surg Br. 1989;71(5):834–7. https://doi.org/10.1302/0301-620X.71B5.2555372.
PMID: 2555372.
11. Bari MM, Islam AK, Haque AK. Surgical reconstruction of leprotic foot-drop. Lepr Rev.
1996;67(3):200–2. https://doi.org/10.5935/0305-7518.19960020. PMID: 8885613.
12. Shah RK. Tibialis posterior transfer by interosseous route for the correction of foot drop in
leprosy. Int Orthop. 2009;33(6):1637–40. https://doi.org/10.1007/s00264-008-0704-y. Epub
2009 Jan 10. PMID: 19137296; PMCID: PMC2899182.
13. Wagner P, Ortiz C, Vela O, Arias P, Zanolli D, Wagner E. Interosseous membrane window
size for tibialis posterior tendon transfer-geometrical and MRI analysis. Foot Ankle Surg.
2016;22(3):196–9.
14. Wagner E, Wagner P, Zanolli D, Radkievich R, Redenz G, Guzman R. Biomechanical evalu-
ation of Circumtibial and Transmembranous routes for posterior Tibial tendon transfer for
Dropfoot. Foot Ankle Int. 2018;39(7):843–9.
15. Rodriguez RP. The bridle procedure in the treatment of paralysis of the foot. Foot Ankle.
1992;13(2):63–9. https://doi.org/10.1177/107110079201300203. PMID: 1572589.
16. Cohen JC, de Miranda ST. Orthopedic surgical foot Management in Hansen Disease. Orthop
Clin North Am. 2020;51(2):279–91. https://doi.org/10.1016/j.ocl.2019.11.012. PMID:
32138865.
17. Srinivasan H, Mukherjee SM, Subramaniam RA. Two-tailed transfer of tibialis posterior for
correction of drop-foot in leprosy. J Bone Joint Surg Br. 1968;50(3):623–8. PMID: 5726913.
18. Ryssman DB, Myerson MS. Tendon transfers for the adult flexible cavovarus foot. Foot Ankle
Clin. 2011;16(3):435–50. https://doi.org/10.1016/j.fcl.2011.08.001. PMID: 21925360.
19. Mann RA, Holmes GB Jr, Seale KS, Collins DN. Chronic rupture of the Achilles tendon: a
new technique of repair. J Bone Joint Surg Am. 1991;73(2):214–9. PMID: 1993716.
20. Neufeld SK, Farber DC. Tendon transfers in the treatment of Achilles' tendon disorders. Foot
Ankle Clin. 2014;19(1):73–86. https://doi.org/10.1016/j.fcl.2013.10.005. Epub 2013 Dec 7.
PMID: 24548511.
21. Andriacchi TP, Andersson GB, Fermier RW, Stern D, Galante JO. A study of lower-limb
mechanics during stair-climbing. J Bone Joint Surg Am. 1980;62(5):749–57. PMID: 7391098.
22. Vega J, Vilá J, Batista J, Malagelada F, Dalmau-Pastor M. Endoscopic flexor Hallucis
longus transfer for chronic noninsertional Achilles tendon rupture. Foot Ankle Int.
2018;39(12):1464–72. https://doi.org/10.1177/1071100718793172. Epub 2018 Aug 19.
PMID: 30124070.
23. Turco VJ, Spinella AJ. Achilles tendon ruptures--peroneus brevis transfer. Foot Ankle.
1987;7(4):253–9. https://doi.org/10.1177/107110078700700407. PMID: 3817670.
24. Den Hartog BD. Flexor hallucis longus transfer for chronic Achilles tendonosis. Foot Ankle
Int. 2003;24(3):233–7. https://doi.org/10.1177/107110070302400306. PMID: 12793486.
25. DeOrio MJ, Easley ME. Surgical strategies: insertional achilles tendinopathy. Foot Ankle Int.
2008;29(5):542–50. https://doi.org/10.3113/FAI-2008-0542. PMID: 18510913.
26. Den Hartog BD. Insertional Achilles tendinosis: pathogenesis and treatment. Foot Ankle Clin.
2009;14(4):639–50. https://doi.org/10.1016/j.fcl.2009.08.005. PMID: 19857838.
27. Hunt KJ, Cohen BE, Davis WH, Anderson RB, Jones CP. Surgical treatment of inser-
tional Achilles tendinopathy with or without flexor Hallucis longus tendon transfer:
a prospective. Randomized Study Foot Ankle Int. 2015;36(9):998–1005. https://doi.
org/10.1177/1071100715586182. Epub 2015 May 19. PMID: 25990545.
28. Wapner KL, Pavlock GS, Hecht PJ, Naselli F, Walther R. Repair of chronic Achilles tendon
rupture with flexor hallucis longus tendon transfer. Foot Ankle. 1993;14(8):443–9. https://doi.
org/10.1177/107110079301400803. PMID: 8253436.
29. van Dijk CN, Scholten PE, Krips R. A 2-portal endoscopic approach for diagnosis and treat-
ment of posterior ankle pathology. Arthroscopy. 2000;16(8):871–6. https://doi.org/10.1053/
jars.2000.19430. PMID: 11078550.
30. Heckman DS, Reddy S, Pedowitz D, Wapner KL, Parekh SG. Operative treatment for pero-
neal tendon disorders. J Bone Joint Surg Am. 2008;90(2):404–18. https://doi.org/10.2106/
JBJS.G.00965. PMID: 18245603.
31. Redfern D, Myerson M. The management of concomitant tears of the peroneus longus and brevis
tendons. Foot Ankle Int. 2004;25(10):695–707. https://doi.org/10.1177/107110070402501002.
PMID: 15566700.
32. Borton DC, Lucas P, Jomha NM, Cross MJ, Slater K. Operative reconstruction after transverse
rupture of the tendons of both peroneus longus and brevis. Surgical reconstruction by transfer
of the flexor digitorum longus tendon. J Bone Joint Surg Br. 1998;80(5):781–4. https://doi.
org/10.1302/0301-620x.80b5.9042. PMID: 9768886.
33. Wapner KL, Taras JS, Lin SS, Chao W. Staged reconstruction for chronic rupture of both pero-
neal tendons using hunter rod and flexor hallucis longus tendon transfer: a long-term followup
study. Foot Ankle Int. 2006;27(8):591–7. https://doi.org/10.1177/107110070602700805.
PMID: 16919211.
34. Jockel JR, Brodsky JW. Single-stage flexor tendon transfer for the treatment of severe con-
comitant peroneus longus and brevis tendon tears. Foot Ankle Int. 2013;34(5):666–72. https://
doi.org/10.1177/1071100712470939. Epub 2013 Jan 14. PMID: 23637234.
35. Willegger M, Seyidova N, Schuh R, Windhager R, Hirtler L. The tibialis posterior tendon
footprint: an anatomical dissection study. J Foot Ankle Res. 2020;13(1):25. https://doi.
org/10.1186/s13047-020-00392-1. PMID: 32430082; PMCID: PMC7236122.
36. Jahss MH. Spontaneous rupture of the tibialis posterior tendon: clinical findings, teno-
graphic studies, and a new technique of repair. Foot Ankle 1982;3(3):158–66. https://doi.
org/10.1177/107110078200300308. PMID: 7152401.
37. Feldman NJ, Oloff LM, Schulhofer SD. In situ tibialis posterior to flexor digitorum lon-
gus tendon transfer for tibialis posterior tendon dysfunction: a simplified surgical approach
with outcome of 11 patients. J Foot Ankle Surg 2001;40(1):2–7. https://doi.org/10.1016/
s1067-2516(01)80034-x. PMID: 11202763.
38. LaRue BG, Anctil EP. Distal anatomical relationship of the flexor hallucis longus
and flexor digitorum longus tendons. Foot Ankle Int. 2006;27(7):528–32. https://doi.
org/10.1177/107110070602700708. PMID: 16842720.
39. O'Sullivan E, Carare-Nnadi R, Greenslade J, Bowyer G. Clinical significance of variations in
the interconnections between flexor digitorum longus and flexor hallucis longus in the region
of the knot of Henry. Clin Anat. 2005;18(2):121–5. https://doi.org/10.1002/ca.20029. PMID:
15696523.
40. Jones R III. The soldier's foot and the treatment of common deformities of the foot. Br Med
J. 1916;1(2892):782–3. https://doi.org/10.1136/bmj.1.2892.782. PMID: 20768157; PMCID:
PMC2349087.
940 J. C. Cohen
41. Breusch SJ, Wenz W, Döderlein L. Function after correction of a clawed great toe by a modi-
fied Robert Jones transfer. J Bone Joint Surg Br. 2000;82(2):250–4. PMID: 10755436.
42. Kadel NJ, Donaldson-Fletcher EA, Hansen ST, Sangeorzan BJ. Alternative to the modified
jones procedure: outcomes of the flexor hallucis longus (FHL) tendon transfer procedure for
correction of clawed hallux. Foot Ankle Int. 2005;26(12):1021–6.
43. Elias FN, Yuen TJ, Olson SL, Sangeorzan BJ, Ledoux WR. Correction of clawed hallux defor-
mity: comparison of the Jones procedure and FHL transfer in a cadaver model. Foot Ankle Int.
2007;28(3):369–76.
44. Girdlestone GR. Physiotherapy for hand and foot. Physiotherapy. 1947;32(11):167–9. PMID:
20251157.
45. Taylor RG. The treatment of claw toes by multiple transfers of flexor into extensor tendons.
J Bone Joint Surg Br. 1951;33-B(4):539–42. https://doi.org/10.1302/0301-620X.33B4.539.
PMID: 14880572.
46. Parrish TF. Dynamic correction of clawtoes. Orthop Clin North Am. 1973;4(1):97–102. PMID:
4682377.
Diabetic Foot
Alexandre Leme Godoy-Santos and Rafael Barban Sposeto
1 Introduction
Diabetes mellitus (DM) is one of the first diseases described—Egyptian papyrus

1550 BC, referred to rapid weight loss and frequent urination. Indians classified the
disease as “madhumeha” or “honey urine” noting that urine attracts ants. Diabetes
comes from the ancient Greek meaning siphon, verb diabanein pass through or pass
the legs separated (as in urination). The first complete clinical description was per-
formed by the Greek Aretaeus of Cappadocia in 100 AD. Sushruta and Charaka in
400 AD describe the types: type 1—associated with childhood and youth and type
2—with obesity in adults. Sir Thomas Willis in 1675 adds the term “mellitus”—
sweet, to differentiate the condition of diabetes insipidus.
By definition, diabetes mellitus is the group of metabolic diseases related to high
levels of glucose in the blood over a prolonged period. When not properly treated, it
results in acute complications such as diabetic ketoacidosis, hyperosmolar coma,
and death and also in chronic complications such as heart disease, stroke, chronic
renal failure, diabetic foot syndrome, and retinopathy. Great watershed in the treat-
ment of DM came by the hands of Frederick Banting and Charles Best (1921), who
purified the insulin hormone from bovine pancreases at the University of Toronto—
Canada; these two scientists won the Nobel Prize in Physiology or Medicine in
1923 [1].
In the middle of the nineteenth century, the first description of diabetic foot
ulcers was done by Calvi Marchal (1852) and Thomas Hodgkin (1854), whom real-
ized that there was an association between diabetes and foot lesions. This situation
A. L. Godoy-Santos
University of São Paulo/Hospital Israelita Albert Einstein, São Paulo, Brazil
R. B. Sposeto (*)
University of São Paulo, São Paulo, Brazil

Switzerland AG 2022
942 A. L. Godoy-Santos and R. B. Sposeto
was treated with prolonged rest, which recurred when the patient walked again.
Frederick Treves (1863), a surgeon who performed the first appendectomy, sug-
gested a different approach, using callus debridement after the application of com-
presses [2–4]. The term “Diabetic foot syndrome” is a situation of ulceration,
infection, or destruction of foot tissues associated with peripheral neuropathy,
peripheral vascular disease, and osteoarticular deformities of the lower limbs [5].
The rates of diabetes-related complications have decreased substantially in the
last two decades, but with a continuous increase in the prevalence of diabetes, the
rates for the general population, where a change in prevalence also affects compli-
cation rates, have increased amputation rates [6]. In South and Central America, the
number of people with diabetes will increase by 55% by 2045 [7].
2 Etiology—Pathophysiology
The spectrum and prevalence of diabetic foot syndrome vary in different regions of
the world, but factors related to its pathophysiology are similar [8, 9].
2.1 Diabetic Neuropathy
It includes a sensitive, motor, and autonomic neuropathy.

Sensitive neuropathy—affects fine fibers resulting in progressive ascending dis-
tal axonopathy with typical boot distribution, leads to loss of protective, vibratory,
and proprioceptive sensitivity.
Motor Neuropathy—affects fine and thick fibers resulting in axonopathy and
demyelination, leads to motor loss in muscle trophism and balance between agonist
and antagonist groups.
Autonomic Neuropathy—results of alteration of blood flow to the nerve, leads to
loss of control of sympathetic tonus of blood vessels, arterio-venous shunts defi-
ciencies, decreased sudomotor function, vasodilatation, and dimming of the secre-
tion of lubricating glands.
2.2 Peripheral Arterial Disease
Higher incidence of atherosclerosis in diabetics, hardening of the arterial walls and

endothelial proliferation, thickening of the basal membrane of the capillaries, results
in microangiopathy and macroangiopathy.
Macroangiopathy considers atherosclerotic blocks in femoro-popliteal and aor-
toiliac vessels. It can be seen in 50% of diabetics after 10 years of the disease.
Microangiopathy refers to disorders in the diffusion of metabolites through the
basal membrane, which can be seen in 45% of patients with pre-diabetes.
Diabetic Foot 943
2.3 Osteoarticular Deformities
Flexible or reducible deformities are secondary to muscle imbalances. Structured or

rigid deformities are secondary to tissue alteration of anatomical structures. Rigid
deformities will be more prone to suffer damage and/or ulcerations specially with
the use of footwear, and care has to be taken to identify these areas.
2.4 Cellular Imbalance
Biological environment with hyperglycemia, dyslipidemia, protein alterations, and

insulin signaling disorders leads to failures in the mechanisms of immunological
factors, loss of bone mineral quality, and joint function loss.
In the diabetic foot syndrome, ulcers mainly affect patients with diabetes who
present two or more risk factors simultaneously. Peripheral neuropathy and periph-
eral arterial disease play a central role [8, 9]. Loss of protective sensitivity, osteoar-
ticular deformities, and limitation of joint mobility may result in mechanical stress
in specific topographies of the foot and ankle [8, 9].
2.4.1 Classification Systems for Diabetic Foot Syndrome
Meggitt-Wagner System [10, 11]
0—corresponds to a pre or post ulcerative site.

1—superficial ulcer, reaching only skin, and subcutaneous tissue.
2—penetrating ulcer in tendon or joint capsule.
3—deeper ulcer with osteomyelitis or abscess.
4—forefoot gangrene.
5—gangrene involving more than two-third of the foot.
Texas University System [12]
Grade 0 Grade 1 Grade 2 Grade 3

Epithelized Superficial Penetrates Penetrates bone/
lesion lesion capsule-tendon joint
A 0A 1A 2A 3A
No infection/ischemia
B 0B 1B 2B 3B
Infected
C 0C 1C 2C 3C
Ischemic
D 0D 1D 2D 3D
Infected and ischemic
S(AD) SAD System [13]
Grade Area Depth Infection Vasculopathy Sensation

0 Intact skin Superficial (subcutaneous) No Palpable pulse Intact
1 <1 cm2 Penetrates tendon/capsule No Reduced pulses Reduced
2 1-3 cm2 Penetrates tendon/capsule Cellulitis Pulse Abscense Abscent
3 >3 cm2 Penetrates bone/joint Osteomyelitis Gangrene Charcot
PEDIS—IWGDF System [14]
Grade Lesion Characteristics

1 No Wound with no Inflammation or Infection Signs
infection
2 Mild Lesion Involving Skin and Subcutaneous Tissue with 2 or More of the Following
infection Increased local temperature, erythema >0,4–2 cm around ulcer, local pain, local
edema, pus
3 Moderate Erythema ≥2 Cm with One of the Above Findings or Infection Involving
Infection Structures Deeper than Skin or Subcutaneous: Fasciitis, Deep Abscess,
Osteomyelitis, Arthritis
4 Severe Any Standing Infection with the Presence of SIRS (90 bpm, FR > 20/min,
Infection PaCO2 < 32 mmHg, leukocytes >12,000 or < 4000/mm3, 10% immature forms)
The authors recommend using the PEDIS system. We consider it is easy and
reproducible use, representing a simple tool for the evaluation of diabetic ulcers.
It was developed specifically to assess ulcer infection. It is already validated as a
prognostic factor for amputation. It establishes a link between microbiology and
antibiotic treatment. And it allows the rational use of antimicrobials for prevention
of bacterial resistance.
3 Diagnosis
The diagnosis starts with prevention and early detection protocol. Regular and stan-
dardized feet inspection in patients diagnosed with DM is the most effective, easy,
least expensive measure to prevent complications from diabetic foot syndrome.
In this sense, the recognition of the most common risk factors for limb loss is
fundamental. Many of these risk factors can be identified based on history data and
a simple foot physical examination [8, 15]:
1. Absence of protective sensation due to peripheral neuropathy.
2. Arterial insufficiency.
3. Foot deformity and callus formation (areas of high pressure).
4. Autonomic neuropathy causing decreased perspiration and dry and cracked skin.
5. Limited joint mobility.
Diabetic Foot 945
6. Obesity.
7. Impaired vision.
8. Irregular metabolic control of glucose.
9. Footwear without skin protection characteristics, allowing high-pressure points
and shear forces.
10. Previous history of ulcer or amputation of lower limbs.
Evaluation of peripheral neuropathy should be done with Semmes-Weinstein
monofilament for checking protective sensitivity, with 128 Hz diapason for check-
ing vibration sensitivity and Ipswich touch test for checking loss of foot sensation.
Evaluation of advanced peripheral arterial disease should be checked by distal
pulses especially posterior tibial artery and pedis artery; absence or gross decrease
of the pulses, the evaluation by vascular surgeon is mandatory.
Orthopedic evaluation should be done through inspection, palpation, and joint
mobility assessment as ankle and foot deformities, reactive hyperemia, poor foot
hygiene, calluses, presence of minor amputations, inadequate footwear, palpation of
bone prominences, and joint mobility test.
3.1 Complementary Investigation of Diabetic Foot Syndrome

with Ulcer
The diagnosis of infection requires standardized research methodology that includes

clinical evaluation, complementary imaging, microbiology, and histopathology. The
most accepted diagnostic criterion for the diagnosis of infection associated with
diabetic foot is the presence of characteristic findings in the histopathological exam-
ination and growth in culture of aseptically obtained sample of bone and soft tissue.
Bone biopsy is, however, an invasive procedure that requires minimal hospital struc-
ture; histology and culture are relatively expensive and time-consuming. The probe-
to-bone test (PTB), laboratory inflammatory markers (hemosedimentation rate,
C-reactive protein, and CBC), and simple X-rays are usually the first steps in further
investigation.
The PTB test, when used in a population of diabetic patients with a foot wound
among whom the prevalence of osteomyelitis was 12%, had a relatively low positive
predictive value, but a negative test may exclude the diagnosis [5].
Simple radiographs of feet with anteroposterior (AP), lateral (P), and oblique (O)
views with load (Fig. 1) play a role in the identification of osteoarticular deformities
and advanced bone infection. We must remember that radiographic alterations are
not specific and may delay the diagnosis of bone infection for some weeks [16].
In diagnostic suspicion, complementary imaging investigation is a less-invasive
method for diagnosis and includes magnetic resonance imaging (MRI), 99mTc-
hexamethylpropylenamineoxime scintigraphy or 111In-oxine labeled leukocytes
with single photon emission computed tomography (SPECT / computed tomogra-
phy, 18F-fluorodeoxyglucose positron emission tomography), or 99mTc-
antigranulocyte antibody scintigraphy (13–18 [16]).
Fig. 1 Weight-bearing bilateral feet X-rays. 1. Lateral left foot X-ray with normal bone relations,
2. right foot lateral view with loss of bone alignment between hindfoot and forefoot, 3. bilateral
anteroposterior foot view with right foot loss of alignment of 2, 3, and 4 tarsometatarsal joint. 4.
Bilateral oblique views with right middle and lateral cuneiform-metatarsal bone alteration
Despite the high cost for most of these modalities, early diagnosis allows fast
treatment start, precise surgical planning, fewer surgical procedures, shorter hospi-
tal stay, and lower volume of high-cost medications.
MRI presents high sensitivity, adequate specificity, and excellent correlation
with biopsy for microbiology and histopathology. The most specific finding is the
low signal in T1-weighted image acquisitions (Fig. 2). In addition, the method pres-
ents greater availability around the world in relation to SPECT/CT and scintigraphy
associated with manipulated human material [16, 17].
4 Management of Non-Infected Plantar Neuropathic Ulcers
Patients with diabetes and non-infected plantar neuropathic ulcer have great benefit
from pressure relief in the ulcer region, which should be part of the treatment strat-
egy [18]. The greatest evidence indicates that non-weightbearing accelerates the
healing of non-infected neuropathic ulcers [19]. Chronic non-infected neuropathic
ulcers usually heal in about 6 weeks with the use of total contact cast and serial
ambulatory debridement (Fig. 3). Therefore, non-removable devices for reducing
body weight load are the first choice to promote skin lesion healing [8, 18, 19].
After ulcer preparation, our preference is using TCC-EZ® Total Contact Cast
System; it is a very easy roll-on cast for installation, one layer only, lightweight
Diabetic Foot 947
a b c
d e f
Fig. 2 Magnetic resonance imaging in sagittal sections: (a, b, and c) bone marrow signal with
hyperintense signal on T2-weighted images of the plantar aspect of the calcaneal tuberosity,
cuboid, medial, middle, and lateral cuneiform and base of the second, third, fourth, and fifth meta-
tarsals; (d, e, and f) bone marrow signal with hypointense signal on T1-weighted images of the
plantar aspect of the calcaneus tuberosity, cuboid, medial, middle, and lateral cuneiforms, and base
of the second, third, fourth, and fifth metatarsals configuring phantom signal
a b c d
Fig. 3 Serial clinical evaluation of a patient with hallux plantar ulcer submitted to treatment with
a full-contact cast for plantar pressure decrease: (a) first evaluation, (b) clinical appearance after
ambulatory debridement and casting, (c) reevaluation after 3 weeks after debridement and use of
the serial casting, (d) reevaluation with 6 weeks after debridement and use of the serial casting
structure associated with an outer boot. The first cast change is recommended after
2–3 days; frequency of changes is every 7 days when new ambulatorial debridement
is performed, and do not use a window for dressing changes.
The expected result is a reduction of the ulcer in depth and diameter and estimat-
ing time to complete healing is around 6 to 8 weeks [20].
5 Management of Infected Plantar Neuropathic Ulcers
For proper surgical planning, take into consideration, in addition to systemic issues,
age, time of illness, and vascular status, the following:
Patient’s Origin:
–– Community infection.
–– Infection related to health service—outpatient or inpatient.
Tissue(s) affected by infection:
–– Non-noble soft tissues.
–– Noble soft tissues (vessels, nerves, tendons, and cartilage).
–– Bone tissue.
Conditions of the Remaining Skin Covering:
–– Biologically responsive to granulation and/or primary closure.
–– Biologically non-responsive to granulation and/or primary closure.
Osteoarticular Deformities:
–– Flexible.
–– Rigid.
–– Bone prominences.
–– Stable.
–– Unstable.
The principles of orthopedic surgical treatment for infected neuropathic ulcers in
diabetic patients are as follows [19–23]:
1. Multi-professional care.
2. Systemic metabolic control.
3. Early diagnostic accuracy.
4. Exclusion of peripheral arterial disease that requires revascularization.
5. Eradication of infection.
6. Debriding / resecting the devitalized tissues.
7. Tissues preserved with good vascularization.
8. Preserve lower limb function.
9. Surgical correction of deformities is staged in second time.
10. Protect surgical wound in the postoperative period.
Diabetic Foot 949
5.1 Infection Eradication
Empirical antibiotic therapy must be based on the patient’s origin and classification
by PEDIS system [8]. The identification of the etiological agent is of fundamental
importance. Patients, in use of previous antibiotic and clinically stable, plan preop-
erative interruption of medication for 10 to 14 days, in order to increase recovery of
etiologic agents [21].
In the intraoperative, materials of interest (minimum 5–6 samples) of differ-
ent deep tissues with identification of the location of the samples have to be sent
in separate flasks. It is necessary to protect the materials for transport to main-
tain viability of bacteria in appropriate media such as thioglycolate or ster-
ile saline.
Specimens must be submitted to Gram staining, cultures for aerobic, anaerobic,
fungi, and mycobacteria bacteria, as well as anatomopathological examina-
tion [22].
Regarding local antibiotic therapy, there is evidence of action through diffusion
vehicles such as polymethyl methacrylate impregnated with antibiotics, calcium
sulfate impregnated with antibiotics, and, more recently, active bioglass. The action
is temporary, ranging from 3 to 14 days; although the mechanism of action is well
documented, there is still no strong scientific evidence [21–23].
5.2 Surgical Procedures
The surgical treatment is usually staged. Soft tissue resection limits and espe-
cially bone limits are guided by imaging findings and intraoperative evaluation
[21–25].
Recent advances in orthopedics and microsurgery associated with a multidisci-
plinary approach have improved the treatment of patients with severely infected
diabetic foot. The long-term functional results for limb preservation procedures
demonstrated in the literature are similar or even better than those reported for
amputated patients (Fig. 4) [26–31].
The decision between amputation or reconstruction depends on the clinical
safety of the patient, the team training, and the degree of bone and soft tissue
involvement. The use of negative pressure therapy, tissue bank, specialized dress-
ings, and hyperbaric oxygen therapy represents important adjuvants in this scenario
[26–31].
The amputations with the best predictability are as follows: trans-tibial, Chopart,
and metatarsal base level (Figs. 5 and 6). The smaller amputations of the toes or of
1 of the central rays also present satisfactory and permanent results (Fig. 7) [26–31].
Please refer to the amputations chapter for more details.
a b c
d e f
Fig. 4 Procedures for hindfoot reconstruction: (a) Initial clinical appearance, (b) clinical appear-
ance after insufficient surgical debridement, (c) intraoperative clinical appearance after cleaning of
all devitalized tissues, (d) intraoperative clinical appearance after bone reconstruction of the calca-
neus with homologous tissue bank graft and large dorsal microsurgical flap, (e) clinical appearance
after complete integration of the flap and partial skin graft, (f) patient in orthostatic position with
full weightbearing
Diabetic Foot 951
a b c d
Fig. 5 Anteroposterior radiographs of different levels of major amputations: (a) trans-tibial, (b)
Syme, (c) Pirogoff, (d) Chopart with tibiotalocalcaneal arthrodesis
Fig. 6 Anteroposterior and oblique radiographs of metatarsal base-level amputation, illustrating

the insertions of the anterior tibial, posterior tibial, short and long fibular, and Achilles tendons
a b c d
e f g h i
Fig. 7 Amputation procedures of the second radius due to second toe and head of the second
metatarsal osteomyelitis: (a and b) Initial clinical appearance. (c) MRI sagittal section with hyper-
intense signal of the bone marrow on T2-weighted images of second toe and head of the second
metatarsal; (d) MRI axial section with hypointense signal of the bone marrow on T1-weighted
images of second toe and head of the second metatarsal (phantom signal), (e and f) Intraoperative
clinical appearance after cleaning of the devitalized tissues and amputation of the second ray, (g).
Intraoperative clinical appearance after closure, (h). clinical appearance at 2 weeks postopera-
tively, (f). patient fully weightbearing
References
1. McKeown KC. The history of the diabetic foot. Diabet Med. 1995;12(1):19–23.
2. Marchal de Calvi A. Des rapports de la gangrène et de la glycosurie [Reports of gangrene and
glycosuria]. Gaz Hôp Civ Mil. 1852;25:178.
3. Hodgkin T. On diabetes. Assoc Med J. 1854;2:916.
4. Treves F. Treatment of perforating ulcer of the foot. Lancet. 1884;2:949.
5. Armstrong DG, Boulton AJM, Bus SA. Diabetic foot ulcers and their recurrence. N Engl J
Med. 2017;376(24):2367–75.
6. Gregg EW, Li Y, Wang J, Burrows NR, Ali MK, Rolka D, Williams DE, Geiss L. Changes
in diabetes-related complications in the United States, 1990-2010. N Engl J Med.
2014;370(16):1514–23.
7. Patterson CC, Karuranga S, Salpea P, Saeedi P, Dahlquist G, Soltesz G, et al. Worldwide esti-
mates of incidence, prevalence and mortality of type 1 diabetes in children and adolescents:
results from the international diabetes federation diabetes atlas, 9th edition. Diabetes Res Clin
Pract. 2019;157:107842.
8. Schaper NC, van Netten JJ, Apelqvist J, Bus SA, Hinchliffe RJ, Lipsky BA, IWGDF Editorial
Board. Practical Guidelines on the prevention and management of diabetic foot disease
(IWGDF 2019 update). Diabetes Metab Res Rev. 2020;36(Suppl 1):e3266.
9. Jalilian M, Ahmadi Sarbarzeh P, Oubari S. Factors related to severity of diabetic foot ulcer: a
systematic review. Diabetes Metab Syndr Obes. 2020;13:1835–42.
10. Meggitt B. Surgical management of the diabetic foot. Br J Hosp Med. 1976;16:227–32.
Diabetic Foot 953
11. Wagner FW. The dysvascular foot: a system for diagnosis and treatment. Foot Ankle.
1981;2:64–122.
12. Lavery LA, et al. Classification of diabetic foot wounds: the University of Texas san Antonio
diabetic wound classification system. Ostomy Wound Manag. 1977;43(2):44–53.
13. Treece KA, Macfarlane RM, Pound N, Game FL, Jeffcoate WJ. Validation of a system of foot
ulcer classification in diabetes mellitus. Diabet Med. 2004;21(9):987–91.
14. Schaper NC. Diabetic foot ulcer classification system for research purposes: a progress report
on criteria for including patients in research studies. Diabetes Metab Res Rev. 2004;20(Suppl
1):S90–5.
15. Armstrong DG, Lavery LA. Diabetic foot ulcers: prevention, diagnosis and classification. Am
Fam Physician. 1998;57(6):1325–32. 1337-8.
16. Lauri C, Tamminga M, Glaudemans AWJM, Juárez Orozco LE, Erba PA, Jutte PC, Lipsky
BA, IJzerman MJ, Signore A, Slart RHJA. Detection of osteomyelitis in the diabetic foot by
imaging techniques: a systematic review and meta-analysis comparing MRI, white blood cell
scintigraphy, and FDG-PET. Diabetes Care. 2017;40(8):1111–20.
17. Ertugrul BM, Lipsky BA, Savk O. Osteomyelitis or Charcot neuro-osteoarthropathy?
Differentiating these disorders in diabetic patients with a foot problem. Diabet Foot Ankle.
2013;5:4. https://doi.org/10.3402/dfa.v4i0.21855.
18. Elraiyah T, Prutsky G, Domecq JP, Tsapas A, Nabhan M, Frykberg RG, Firwana B, Hasan R,
Prokop LJ, Murad MH. A systematic review and meta-analysis of off-loading methods for
diabetic foot ulcers. J Vasc Surg. 2016;63(2 Suppl):59S–68S.e1–2.
19. Cavanagh PR, Lipsky BA, Bradbury AW, Botek G. Treatment for diabetic foot ulcers. Lancet.
2005;366(9498):1725–35.
20. Arnold JF, Marmolejo V. Outcomes achieved with use of a prefabricated roll-on total contact
cast. Foot Ankle Int. 2017;38(10):1126–31.
21. Aragón-Sánchez J, Lipsky BA. Modern management of diabetic foot osteomyelitis. The when,
how and why of conservative approaches. Expert Rev Anti-Infect Ther. 2018;16(1):35–50.
22. Jeffcoate WJ, Vileikyte L, Boyko EJ, Armstrong DG, Boulton AJM. Current challenges and
opportunities in the prevention and Management of Diabetic Foot Ulcers. Diabetes Care.
2018;41(4):645–52.
23. Lipsky BA. Diabetic foot infections: current treatment and delaying the 'post-antibiotic era'.
Diabetes Metab Res Rev. 2016;32(Suppl 1):246–53.
24. Sen P, Demirdal T, Emir B. Meta-analysis of risk factors for amputation in diabetic foot infec-
tions. Diabetes Metab Res Rev. 2019;35(7):e3165.
25. Wukich DK, Hobizal KB, Sambenedetto TL, Kirby K, Rosario BL. Outcomes of osteomyelitis
in patients hospitalized with diabetic foot infections. Foot Ankle Int. 2016;37(12):1285–91.
26. Akhtar S, Ahmad I, Khan AH, et al. Modalities of soft tissue coverage in diabetic foot ulcers.
Adv Skin Wound Care. 2015;28:157–62.
27. Kallio M, Vikatmaa P, Kantonen I, et al. Strategies for free flap transfer and revascularisation
with long-term outcome in the treatment of large diabetic foot lesions. Eur J Vasc Endovasc
Surg. 2015;50(2):223–30.
28. Fiorito J, Trinidad-Hernadez M, Leykum B, et al. A tale of two soles: sociomechanical and
biomechanical considerations in diabetic limb salvage and amputation decision-making in the
worst of times. Diabet Foot Ankle. 2012;3:1–6.
29. Short DJ, Zgonis T. Management of osteomyelitis and bone loss in the diabetic Charcot foot
and ankle. Clin Podiatr Med Surg. 2017;34(3):381–7.
30. Godoy-Santos AL, Amodio DT, Pires A, Lima AL, Wei TH, de Cesar-Netto C, Armstrong
DG. Diabetic limb salvage procedure with bone allograft and free flap transfer: a case report.
Diabet Foot Ankle. 2017;8(1):1270076. https://doi.org/10.1080/2000625X.2016.1270076.
31. Godoy-Santos AL, Rosemberg LA, de Cesar-Netto C, Armstrong DG. The use of bioac-
tive glass S53P4 in the treatment of an infected Charcot foot: a case report. J Wound Care.
2019;28(Sup1):S14–7. https://doi.org/10.12968/jowc.2019.28.Sup1.S14.
Rheumatoid Foot
Sergio Fernandez C. and Hugo Henriquez
1 Introduction
Rheumatological diseases present a population prevalence of 7.7 per 1000 [1] and
commonly affect the foot and ankle during its evolution [2], depending on factors
such as the type of pathology (Rheumatoid Arthritis or RA, Lupus, etc.), the age of
initiation of the disease, the medical/rheumatological treatment and its compliance.
The involvement of the ankle and foot reaches 90% of rheumatological patients in
general, with compromise of the forefoot in 90% of cases, 66% of the subtalar joint,
and 17% of the ankle [3, 4]. The presence of symptoms is variable and can affect the
ankle in 36%, the forefoot in 35%, the rearfoot in 34%, and the midfoot in 32%.
This number can increase as the time of RA evolution increases (5.6). Ankle-foot
involvement is the first reported cause of disability in RA patients [3], particularly
forefoot involvement, with up to a quarter of patients requiring surgery of this seg-
ment [6]. In the first 13 years of the disease, up to 42% of patients suffer worsening
of their ankle symptoms [7].
The clinical presentation of rheumatoid diseases is as varied as one might
think, from mono-arthritis to severe destruction of all the foot and ankle joints.
This pathology can be extremely disabling, both because of the pain inherent to
the rheumatological disease, and because of the deformities, joint instabilities,
and joint and tendon damage that it can cause. It is particularly important to point
S. Fernandez C. (*)
Clínica Santa María, Servicio de Ortopedia y Traumatología, Equipo de Pie y Tobillo,
Santiago, Chile
H. Henriquez
Clínica Santa María, Servicio de Ortopedia y Traumatología, Equipo de Pie y Tobillo,
Santiago, Chile
Instituto Traumatológico de Santiago, Equipo de Pie y Tobillo, Santiago, Chile

Switzerland AG 2022
956 S. Fernandez C. and H. Henriquez
out the role of rheumatologists in terms of the time of diagnosis of the segment’s
compromise. An early diagnosis allows for reconstruction procedures, preserving
joints. If, on the contrary, the diagnosis is late, the therapeutic options will be
limited to radical and aggressive procedures, with fusion and resection of the
damaged joints.
The initial management of the alterations of the hindfoot and ankle is almost
always conservative. An adequate pharmacological treatment of the systemic dis-
ease by the rheumatologist leads to an adequate control of the inflammatory process
in a global way, decreasing the symptoms in the ankle and foot. The use of different
types of custom-made insoles, footwear modifications or orthopedic shoes helps
support, unload, and decrease the symptoms. Local steroid infiltrations serve for
local management of pain and inflammation. Patients with persistent symptoms and
deformities that cannot be improved with orthotics, significant joint deterioration,
or with severe joint instability are candidates for surgery.
It is important to consider the systemic, chronic, and progressive nature of the
disease when making the surgical decision [8]. The treatment alternatives must nec-
essarily consider the current and future state of the disease, the joints involved, and
the patient’s expectations.
The constant evolution of disease-modifying antirheumatic drugs (DMARDs)
and the emergence of biological therapies have significantly improved the control of
this disease; however, despite these advances, ankle-foot involvement remains sig-
nificant and causes functional restrictions in a large number of RA patients.
Within the joint and bone disease manifestations, we can find synovitis, arthritis,
Charcot’s arthropathy, exostosis, and stress fractures, between others. These altera-
tions can lead to dislocations or subluxations determining different degrees of
deformity [8, 9]. As extra-articular manifestations, tenosynovitis, intermetatarsal
bursitis, neuropathic ulcers, vasculitis, tendinitis, rheumatoid nodules, plantar fasci-
itis, and neuritis (tarsal tunnel syndrome) can be found [9, 10].
With respect to tenosynovitis, these can occur in any tendon; however, the most
studied has been the Posterior Tibial Tendon (PTT) and its role in hindfoot defor-
mity. In a comparative study, Gutiérrez [11] found ultrasound involvement in 87%
of 216 ankles of asymptomatic people with RA, compared to 28% in the control
group of 200 ankles in patients without the disease. The most frequent finding was
PTT tenosynovitis (32%), followed by Peroneus longus Tendon inflamma-
tion (27%).
Avoiding surgery, when indicated, leads to a progressively disabled individual,
both because of the progression of the deformity and because of pain. Early sur-
gery allows better functional results by preserving the joint and with them the
normal function of the ankle-foot, although it increases the risk of recurrence of
the deformity or instability treated. In turn, joint fusion is stable in time, but it
could be avoided due to the constant evolution of disease-modifying antirheumatic
drugs (DMARDs) and the emergence of biological therapies which have signifi-
cantly improved the control of this disease; however, despite these advances,
ankle-foot involvement remains significant and causes functional restrictions in a
large number of RA patients.
Rheumatoid Foot 957
2 Normal Anatomy
2.1 Forefoot
The motor control of the toes and the lesser metatarsophalangeal joints (MTP)
depends on the balance between the intrinsic and extrinsic muscles of the toes. This
balance is also a fundamental element in the stability and position of the MTP,
proximal interphalangeal (PIPJ), and distal interphalangeal (DIPJ) joints.
The stability of the MTP joints depends passively on both the ligaments and the
plantar plate; it actively responds to the balance of flexor and extensor forces of the
intrinsic and extrinsic muscles of the toes. The position of the intrinsic muscle ten-
dons in relation to the center of rotation of the MTP joint is key to this delicate bal-
ance. Under normal conditions, the tendons of the interosseous muscles are located
slightly plantar from this center of rotation, acting as stabilizers in flexion of the
proximal phalanx (P1) and extensors of the PIPJ and DIPJ. The shift toward the
dorsum of the MTP center of rotation given an increased laxity or degeneration of
the plantar plate causes the intrinsic muscles to now act as extensors of the MTP,
destabilizing it, while the non elongated Flexor Digitorum Brevis (FDB) and Longus
(FDL) tendons pull the PIPJ and DIPJ in flexion. This generates a claw toe, initially
flexible that progresses to rigidity.
The hallux must be considered separately since it has its own characteristics. The
stability of the first MTP joint (MTP1) is fundamental for its function, the same as
the alignment of the flexor apparatus: flexor hallucis brevis (FHB), flexor hallucis
longus (FHL), and sesamoids. The FHB inserts into the base of the P1, forming with
the sesamoids, the “plantar plate” of the hallux, a critical element in sagittal stabil-
ity. The medial and lateral collateral ligaments keep the hallux in axis; their attenu-
ation or lengthening facilitates and causes the varus and valgus displacements.
The intermetatarsal ligaments are the structures that maintain the width of the
forefoot and allow a harmonic function in its pronosupination. The presence of
intermetatarsal synovitis is another risk factor for compression-attenuation of these
ligaments allowing the splay of the forefoot.
2.2 Midfoot, Rearfoot, and Ankle
It is difficult to separate the functions and action of these three segments since they
are interrelated during the gait phases. The control of the joints present in these seg-
ments depends on both the static (bone and ligament stabilizers) and dynamic (ten-
dons) stabilizers and the forces that these exert according to the axis of rotation in
which they perform their action. Flexion and extension of the ankle are conse-
quences of tendons actions depending if they cross it anterior (Tibial Anterior (TA),
Extensor Hallucis Longus (EHL), Extensor Digitorum Longus (EDL)) or posterior
to its axis of rotation (TP-FDL-FHL, Peroneus Longus (PL), Peroneus Brevis (PB),
Achilles tendon (AT)). In the hindfoot, the axes of the talus and the calcaneus are
not parallel, existing a variable angulation between them, that in average is 42°
(29°–47°) in the sagittal plane and 16° (8°–24°) with respect to the central axis of
the foot [12]. The varus and valgus of the hindfoot combined with the adduction,
abduction, pronation, and supination of the midfoot, generate the movements of
inversion and eversion. From the dynamic point of view, the TP is the most powerful
supinator of the midfoot and the PL, the most powerful pronator. If the lower limb
is analyzed as a closed chain (foot fixed to the ground), the TP is a tibial external
rotator and the PL is a tibial internal rotator.
The action of the joints-tendons previously described allows for all different gait
stages to take place. A healthy gait is based on the ability to block the subtalar joint
in varus together with an adduction of the talonavicular joint. This blockade stiffens
the Chopart joint, allowing the Achilles tendon to generate an efficient ankle flec-
tion, vital for a functional gait.
3 Etiology and Physiopathology
3.1 Forefoot
The maintained presence of synovitis at the MTP joints causes the distension of the
joint capsule and stabilizing elements, which, associated with the load, destabilizes
the MTP causing subluxation and then dorsal dislocation of the P1 on the meta-
tarsal [5].
With the dorsal dislocation of the MTP, the toe intrinsics move toward the dorsum
acting as extenders of the MTP, but conserving the flexor action in PIPJ and DIPJ,
causing the appearance of claw and hammer toe deformities [5], a fundamental
deformity that limits patient’s activities [13]. The degenerative destruction of the
plantar plate (PP) is present in up to 80% of patients [14] and is part of this process,
allowing dorsal displacement of the P1 base. The P1 on the dorsum of the metatarsal
increases the flexor moment on the metatarsal head, increasing the load and damage
of the plantar bearing surface and aggravating the symptoms by plantar prominence
of the metatarsal heads. The “windlass” mechanism is also lost due to the breakage
of the plantar plate, producing a greater loss of lesser toe flexion strength. This fur-
ther decreases the lesser MTP stability [15], which overloads the medial foot ray [16].
The erosion of the joint surfaces adds another factor of chronic inflammation,
perpetuating the cycle of synovitis – instability – joint destruction.
3.2 Midfoot and Rearfoot
In the midfoot, given the limited mobility of each particular joint, with the exception
of the talonavicular (TN), the damage appears to be initially capsular, due to syno-
vitic distension, allowing the development of instability that progresses to severe
deformities. The presence of intercuneiform osteophytes would be a sign of this
Rheumatoid Foot 959
instability. The midfoot is fundamental in the load transmission from the rearfoot to
the forefoot. The compromise of this segment causes important restrictions in
Activities of Daily Living (ADL) and in walking [17, 18].
The involvement of the hindfoot joints is late in this disease. One of the explana-
tions is that the maintained pronation of the forefoot generates an overload in the
rearfoot joints, which, associated to the RA synovitis, leads to rearfoot compromise,
described for the talonavicular (39%), subtalar (29%), and calcaneal-cuboid (25%)
joints [19]. Subtalar instability drives calcaneus into valgus. The TN compromise
generates plantar and medial displacement of the talar head, which leads into mid-
foot and forefoot abduction [20]. This deformity generates an arch collapse, present
in 80% of patients with RA and hindfoot compromise [21]. With increasing hind-
foot valgus, the calcaneus can impact the fibula, producing a lateral impingement
that can end up into a fibular stress fracture. The role of the PTT in the generation
of the valgus plane in these patients is a matter of discussion. Michelson [22] reports
an 11% dysfunction of the posterior tibial tendon in 99 rheumatic patients with
valgus of the hindfoot. It has been reported that initially there is hyperactivation of
the PTT to compensate the existing valgus deformity. However, although the PTT is
intact, its function as a stabilizer is insufficient [22]. There is controversy as to
whether the origin of the valgus deformity presented by these patients is secondary
to the joint, ligamentous or capsular alteration, or secondary to the PTT dysfunc-
tion. The PTT does not present a greater frequency of rupture, but it is frequently
weak and thin [8, 11].
3.3 Ankle
Ankle involvement in patients with RA develops mainly as a consequence of hind-

foot instability, which would explain the later involvement of this joint. These alter-
ations lead to different degrees of osteoarthritis, deformity, and instability.
4 Diagnosis
There are different diagnoses related to autoimmune pathologies (Table 1), not only
rheumatoid arthritis. The involvement of the ankle-foot segment has great variabil-
ity in the presentation of these diseases and there is no clinical feature that is unique
for each diagnosis.
Although the diagnosis is the rheumatologist responsibility, we must know that
foot and ankle compromise is frequently seen in Rheumatoid Arthritis, Systemic
Lupus Erythematosus, and Psoriatic Arthropathy. The clinical picture is varied,
existing diagnostic criteria, both clinical and serological (see Table 2).
The magnitude of erosive joint damage, the existence of synovitis, tenosynovitis,
and typical deformities are elements that guide us toward rheumatoid pathology.
The laboratory studies lead to define the specific diagnosis, which are usually
already made at the time of consultation with the orthopedic surgeon.
Table 1 Connective tissue diseases – mesenchymopathies

Rheumatoid arthritis. Lupus erythematosus. Drug-induced lupus. Polymyositis. Mixed
connective tissue disease. Sjôgren’s syndrome. Progressive systemic sclerosis. Rheumatic
polymyalgia. Seronegative Spondyloarthropathies: Ankylosing Spondyloarthritis,
Spondyloarthritis associated with inflammatory bowel diseases, Reiter and reactive arthritis,
Psoriatic arthritis
Systemic autoimmune diseases: Antiphospholipid syndrome
Vasculitis: Giant Cell Arteritis, Takayasu, Wegener’s Granulomatosis, ANCA-associated
Vasculitis, Polyarteritis Nodosa, Churg-Straus Granulomatosis, Schoenlein-Henoch Purpura,
Urticarial Vasculitis, Cryoglobulinemias, Bechet, Recurrent Polychondritis
Table 2 ACR/EULAR 2010: classification criteria for RA

Articular compromise (0–5)
1 Major joint 0
2–10 Major joints 1
1–3 Minor joints (major joints are not 2
considered)
4–10 Minor joints (major joint not 3
considered)
>10 Joints (at least one minor joint) 5
Serology (0–3)
Rheumatoid factor and anticitrulline peptide 0
negative
Mild positive rheumatoid factor and anticitrulline 2
peptide
Rheumatoid factor and anticitrulline peptide 3
intense positive
Duration of symptoms
<6 weeks 0
>6 weeks 1
Acute phase reagents (0–1)
PCR & VHS normal 0
Abnormal PCR and VHS 1
Sum equal to or greater than 6 points: definitely AR
Translation by the authors from: Arthritis & Rheumatism Vol. 62, No. 9, September 2010,
pp. 2569–2581 https://doi.org/10.1002/art.27584 © 2010, American College of Rheumatology.
Aletaha, et al. [23]
Generally, the reasons for orthopedic evaluation are gait difficulty, inflammation,
foot deformity, and pain. These patients present a greater risk of falling [24]. On
rare occasions, the initial RA diagnosis is made with the physical examination find-
ings [25].
In the physical examination, we must look for calluses, ulcers, rheumatoid nodules,
and check the neurovascular state of both extremities. The neurological examination
(sensory and motor), should include the protective sensitivity using the Semmes
Weinstein’s 5.07 monofilament. Wilson [26] reports a 59% alteration in plantar
Rheumatoid Foot 961
sensitivity in 51 RA patients studied. Signs of Charcot neuroarthropathy such as edema,

redness, and local temperature could be identified as well. Nerve entrapment should
also be ruled out by using the Tinnel test along the tibial nerve (Tarsal Tunnel Syndrome).
Joint mobility should be evaluated for stiffness, increased volume or pain in the
joint excursion. Likewise, the integrity of the tendons, their function, and their tra-
jectory should be examined, looking for inflammation or pain upon mobilization.
The shortening or contracture of the Achilles or Gastrosoleus tendon should be
evaluated with the Silfverskjöld test.
In the osseous evaluation, the presence of exostosis or inflammation must be
determined. The foot analysis should be performed in a standing position, evaluat-
ing the arch, the relative varo-valgus hindfoot position, and any other deformities
present. The most frequent presentation is a valgus flat foot, with Hallux valgus,
valgus deviation of the lesser toes, metatarsal overload, and claw toes (see Fig. 1).
Fig. 1 Clinical presentation in advanced and moderate stages. In the advanced stage, (left image) severe
hallux valgus deviation can be observed, prominence of the first metatarsal head, signs of skin irritation
over the bunion and valgus and claw deformities of the lesser toes. In the moderate stage, (right image)
hallux valgus deformity can be observed, with prominent bunion and valgus deviation of the toes
Patients present with varying degrees of functional limitation, foot pain, and joint
stiffness. Although the presence of pes cavus associated with RA has been described,
it is reported in juvenile RA [6].
Gait analysis should not be overlooked. Deformities at other limb segments must
be ruled out.
6 Images
The use of images is key in defining the state of progress of the disease. The study
should be started routinely with anteroposterior (AP), lateral (L) and oblique (O)
weight-bearing foot and ankle X-rays. The radiological findings in these projections
vary from no or minimal alterations in early disease stages, to joint erosions, arch
loss, joint collapse, and dislocations. It is frequent, in advanced stages of the dis-
ease, to observe 1–5 MTP dislocation since, as previously mentioned, the greatest
compromise of the disease affects the forefoot.
Radiological destruction is progressive and usually more severe and early in
MTP1, MTP5, and TN but as the evolution progresses, the compromise of the whole
foot becomes evident [17] (see Fig. 2). Larsen [27] generated a radiological classi-
fication based on radiographs that defines the progression of skeletal damage, being
this, the most used in the literature because it is adequately validated. It is presented
in Table 3 [28–30].
Ultrasound (US), in experienced hands, is reliable for early soft tissues changes,
detecting synovitis and tenosynovitis with greater precision than specialized clinical
evaluation. Early diagnosis is key to the prognosis, particularly since the appearance
of biological therapies. The US has shown to be effective and more sensitive than
the guidelines for evaluation of RA activity, allowing an accurate diagnosis of RA
activity and, therefore, a better objective control of active/inactive patients. This
Fig. 2 Grade V radiological appearance according to Larsen’s classification. Severe deformity

and joint destruction can be seen with subtalar and talonavicular collapse and dislocation
Rheumatoid Foot 963
Table 3 Larsen’s radiological classification

Grade 0. NORMAL radiology
Grade I. Mild abnormality. Periarticular edema. Scarce narrowing of the joint space,
periarticular osteopenia
Grade II. Mild abnormality. Joint space narrowing. Erosion (not mandatory in load-bearing joints)
Grade III. Medium destructive abnormality. Obvious narrowing of the joint space. Periarticular
erosion (mandatory in all joints)
Grade IV. Severe destructive abnormality. Marked narrowing of the joint space. Obvious
periarticular erosion. Skeletal deformity in load-bearing joints
Grade V. Mutilating abnormality. Disappearance of the joints. Severe deformity of the load
bearing joints
Subluxation and dislocation are not considered parts of this deformity graduation, because it is late
and secondary to skeletal deformity
Translation by authors from: Larsen et al. [27]
avoids the under-treatment of active RA patients with mild symptoms [31].

Particularly in midfoot, the US is significantly more sensitive to the presence of
osteophytes and joint erosions when compared to plain radiography [32].
Magnetic resonance imaging (MRI) is more sensitive in detecting early skeletal
erosions. Special attention should be paid to MTP5, because of the high frequency
and precocity of its soft tissues and osseous compromise [32].
Most patients do not present significant limitations or deformities at the time of the
initial consultation. Nonsurgical management of the disease is useful as an initial
approach. In asymptomatic patients, preventive education regarding adequate medi-
cal control, regular physical activity, knowledge of red flags, and recommended
footwear are the first recommendations.
The use of insoles is initiated when symptoms such as metatarsalgia, medial arch or
midfoot pain appear. This moment is key to reinforce the need for regular medical con-
trol, as well as to initiate the delivery of information regarding possible future surgeries.
Initially, an over-the-counter insole is enough to achieve satisfactory clinical
results, but, given that RA is progressive, the use of custom molded UCBL-type
inserts should be considered. In patients who are not candidates for surgery or do
not wish to undergo surgery, the hindfoot stabilizing orthoses associated with
UCBL-type inserts achieve adequate symptoms relieve and partial function recovery.
The absence of medical, orthopedic or surgical treatment condemns the patient to

the progression of deformities and joint damage, causing a progressive deterioration
of joint function and foot deformity. When faced with the indication for surgery,
there is classically a tendency not to stop DMARDs treatment, but to do stop bio-
logical therapies [33], although this is under review [34, 35].
The indication for surgery is based on the patient’s general and functional condi-
tions. The objectives are pain relief and functional recovery. While targeting these
objectives, cosmetics are also improved [36]. The decision to perform joint
reconstruction-preservation procedures versus joint resection- arthrodesis tech-
niques depends, among other factors, on the extent of skeletal damage as a conse-
quence of RA. Larsen’s classification [27] helps with this decision, considering the
stages II and III are generally susceptible to reconstruction-articular conservation
techniques and stages IV and V to resection-arthrodesis procedures. Every patient
should be considered as a whole, his age, general health status, expectations,
involvement of other systems (liver, kidney) and joints, social dependence, etc.,
keeping in mind the possible benefits and risks of surgery [36]. The advanced stages
also appear in patients with worse control of the disease and with a longer time of
evolution, so a “radical” arthrodesis-type surgery seems to be the best option in this
group. The reconstruction – joint conservation generates, without a doubt, better
functional results by preserving the mobility of the segment, but the risk of reap-
pearance of the deformity in time must be taken into account, with the possibility of
requiring new surgeries.
8.1 Forefoot
In the forefoot, we must differentiate the first ray and the lesser metatarsals and toes
treatment. The magnitude of joint damage and the stability of the MTP are funda-
mental elements in surgery selection. The hallux valgus deformity is present
between 10% and 30% of RA feet [36]. The greater the destruction/instability, the
greater the need to perform arthrodesis MTP of the hallux, both to obtain a satisfac-
tory solution and to generate stability to the rest of the toes.
8.2 First Metatarsophalangeal Joint
8.2.1 Articular Preservation
If MTP1 joint destruction is mild – moderate, joint preservation surgery is possible.

Distal shortening and lateral displacement osteotomy of the first metatarsal allow
for valgus correction and adequate weight-bearing capabilities. The shortening
should not exceed 4 mm. A chevron-type osteotomy is recommended, which allows
shortening and a plantar displacement of the metatarsal head.
When significant shortening and lateral displacement are required, diaphyseal
scarf osteotomy allows for proper planning of major axial corrections and shorten-
ing. During surgery, a wide synovectomy of the MTP1 joint should be performed,
Rheumatoid Foot 965
as well as the resection of bursas and/or rheumatic pannus within reach of the
approach. Joint preservation surgery for MTP1 has the advantage of producing
fewer biomechanical alterations, compensating for proximal stiffness and allowing
for eventual future revision; the disadvantages involve persistent pain and possible
recurrence of the deformity in both the hallux and the lesser toes [37].
8.2.2 Arthrodesis
Arthrodesis of the MTP1 is indicated for patients who present with severe joint
damage with dislocation or subluxation of this joint. The objective of arthrodesis is
to alleviate pain and achieve bone healing in an adequate Hallux alignment,
described as 5° of valgus, no rotation, with 5° of dorsal extension.
The surgical approach selection (medial or dorsal), depends on the surgeon’s
experience and on the type of synthesis selected for fixation. Fusion should be car-
ried out in an anatomical way, by resecting the metatarsal head and proximal pha-
lanx cartilage by means of drills specially designed for this purpose (cup and cone
reamers). It can be performed in a nonanatomical way as well, with straight cuts.
With the latter is more difficult to perfectly achieve alignment without losing a sig-
nificant amount of first ray length, but bone contact is excellent achieving great
compression with standard osteosynthesis.
Our choice for performing MTP1 arthrodesis is through a medial approach, per-
forming a straight capsulotomy and resection of the existing synovial and/or pan-
nus. The preparation of the surfaces is done with straight cuts with a saw, trying to
avoid the varus, the rotation, the flexo, and or extension of the first toe. For this
purpose, once the cuts have been made, we fix them temporarily with Kirschner
wires (KW) (1.5–2.0 mm) and then rest the foot on a flat surface. With this we check
the clinical axis of the arthrodesis. After checking the appropriate clinical axis, we
drill holes in the surfaces and fix it again transiently with KW. Considering the
diminished bone quality of these patients, when in the surgical plan a Hoffman pro-
cedure is performed, we maintain a transient fixation at MTP1, perform the Hoffman,
and then stabilize the arthrodesis definitively.
The arthrodesis can be stabilized only with interfragmentary compression
screws, with compression screws in addition to a locking or nonlocking plate. The
best results of these techniques are achieved with the combination of interfragmen-
tary screw and a dorsal neutralization plate [38]. Locking plates have shown results
that are still uncertain with respect to their potential improvement in healing rates in
comparison to nonlocking plates [39]. Our choice is to perform the stabilization
with one 3.5-mm compressive screw from the neck of the first metatarsal to the
proximal phalanx plus a dorsal metatarsal anatomical locking plate.
Independently of the approach and type of stabilization to use, in our experience
the preparation of the surfaces making multiple perforations of the subchondral
bone is fundamental to obtain bone fusion.
Good results and complete pain relief at medium- and long-term show that
arthrodesis is a valuable tool in the forefoot AR treatment.
8.2.3 Arthroplasty
Another option for MTP1 treatment is arthroplasty. The technique of interposition

arthroplasty uses soft tissues (capsule or synthetic materials) as a spacer-resurfac-
ing of the MTP1. It is described and recognized as an alternative, and presents
results comparable to MTP1 fusion [40, 41]. The MTP 1 joint replacement tech-
niques are both hemiarthroplasties of the proximal phalanx base or the metatarsal
head as well as total arthroplasties (both joint surfaces). The published results are
mostly short- and medium-term, showing better results in terms of pain and mobil-
ity (nonsignificant) for hemiarthroplasties [42]. These implants, whether partial or
total, do not have a long- or medium-term follow-up, and show a significant failure
rate. Therefore, this type of implant is not currently recommended in patients with
RA, since the destruction of the stabilizing elements, as well as the frequent
malalignment and diminished bone quality, makes the rate of complications par-
ticularly high [41]. Synthetic cartilage replacement is not yet proven in RA patients,
basically because of the poor bone quality of this group [43, 44]. Silicone arthro-
plasty (Swanson) implants have a long history. It has been described as lasting up
to 10 years in 93% of patients [16, 44], but are not the current recommended
treatment.
8.3 Tarsometatarsal Joint
In the event of medial metatarso-cuneiform joint compromise, with severe metatarsal

varus, instability or joint destruction, an arthrodesis of this joint should be performed.
The stabilization can be done with screws alone or in addition to neutralization
plates. Always bear in mind the diminished bone quality in RA patients. MTP1 com-
promise is managed according to the severity of the damage. Although proximal and
distal arthrodesis of the first metatarsal are not usually recommended, we must con-
sider the condition of the rheumatic patient, as well as the possible evolution of unad-
dressed joints to painful deterioration and instability. Thus, double arthrodesis should
be considered as a valid option in these patients (Fig. 3). The shortening amount of
the first metatarsal is decided according to the surgical plan for the lesser metatarsals;
the shortening of first metatarsal should be greater when a resection of the lesser
metatarsal heads is planned (Hoffmann procedure).
As it is an arthrodesis, it is important to consider the adequate preparation of the
articular surfaces, as well as the coaptation of these. Stabilization options for cuneo-
metatarsal arthrodesis range from two screws in compression, which require a pro-
longed unloading period that is difficult for patients to comply with; to the use of
locking compression/neutralization plates that facilitate postoperative weight-
bearing, with better reported fusion rates.
Rheumatoid Foot 967
8.4 Lesser Metatarsals
8.4.1 Resection
In lesser metatarsals, resection or shortening techniques achieve adequate results in

terms of pain and function in 70–90% of patients [36]. The classic technique is the
Hoffmann procedure (Figs. 3 and 4), which consists of the resection of the lesser
metatarsal heads. The associated synovectomy of these joints augurs a good local
prognosis with good control of the disease [15, 37]. We indicate a resection arthro-
plasty of the minor metatarsals in all “older” patients (over 50–60 years), with rigid
dislocation of the lesser MTP joints, who want greater certainty of duration, avoid-
ing the risk of reoperation, and whose functional requirements are moderate.
The surgery can be performed by a double dorsal approach or by a plantar arch
approach (Fig. 5), with or without resection of the plantar skin in relation to the
prominent lesser metatarsal heads. The advantage of the plantar approach lies in the
ease of access to the heads of the metatarsals that are prominent, with minimal
injury risk to the vascular or tendinous structures.
Our choice is a plantar approach with resection of the plantar skin; once the cap-
sulotomy is performed, we extensively resect the joint capsule with its synovium to
then perform an oblique osteotomy, parallel to the sole of the foot, at the neck of all
the lesser metatarsals. We start the osteotomies with the second metatarsal. We
a b c
Fig. 3 Woman, 57-years-old, longstanding RA with previous reconstructive surgery. (a) Current
consultation is for deformity and pain recurrence. (b) Arthrodesis MTP1 plus Hoffmann procedure
is performed. Stabilization of arthrodesis with 3.5-mm compressive screw plus anatomical locking
plate. Kirschner wire stabilization for the second to fifth toes. (c) X-ray 4-years postsurgery shows
maintenance of the alignment correction
a b
c d
Fig. 4 Hoffmann procedure and Hallux arthrodesis. (a) Preoperative X-ray. It shows the deformity
and severe destruction of all the MTP joints. (b) Preoperative clinical aspect. (c) X-ray at 12-weeks
postop. It shows good alignment of the lesser toes and MTP1 arthrodesis technique with
compression screws. (d) Clinical appearance at 12 weeks shows postoperative normal swelling and
satisfactory toes correction
Rheumatoid Foot 969
Fig. 5 Plantar arciform

approach for metatarsal
head resection, second to
fifth. The evident plantar
protrusion of the metatarsal
heads, almost at skin level,
as well as the absence of
“noble” elements (tendons,
nerves) in the operating
field, stands out. These are
dislocated to the
intermetatarsal spaces
perform a “closed” reduction of the toes and pin them in a retrograde fashion with a
1.6-mm Kirschner wire, which is then placed in the medullary cavity of the respec-
tive metatarsal. The toes are aligned with the respective metatarsal, and a “dermode-
sis” effect is achieved with the resection of the plantar skin lozenge which helps to
avoid toes dorsiflexion. Kirschner wires are maintained for at least 6 weeks.
A variant of this “resection arthroplasty” of the lesser metatarsals, is adding the
resection of the first metatarsal head (Tillmann’s procedure), which considers a har-
monic cadence of the metatarsals length. It requires stabilization with Kirschner wires
(KW) for all toes to their respective metatarsal. This technique describes similar results
to the arthrodesis variant of MTP1 [45] in terms of duration and pain relieve [46].
8.4.2 Joint Reconstruction
Joint reconstruction, without lesser metatarsal heads resection, is a procedure with

satisfactory results comparable to Hoffmann procedure [47]. One of these proce-
dures corresponds to a shortening metatarsal osteotomy performed in the middle
third [48] and its respective osteosynthesis; in the distal third, with an oblique oste-
otomy from the distal dorsal to the proximal plantar [47] or a distal neck resection
osteotomy with dorsal and medial displacements of the respective metatarsal heads
[49]. This generates an elevation and shortening of the metatarsal head, with the
possibility of reducing the joint. The authors prefer the triple distal resection-
elevation osteotomy according to Weil and Maceira, stabilized with an appropriate
screw. The magnitude of the shortening is appropriate if a smooth reduction of the
toe is achieved. To keep P1 from dislocating, the Girdlestone-Taylor technique

(transferring the FDL to the base of the proximal phalanx) is a good complement.
The toes are transfixed with Kirschner wires for 6 weeks.
The indication for joint reconstruction considers a “young” patient (under
60 years of age), with mild-moderate joint destruction, subluxation or reducible
dislocation, who is willing to risk further surgery in the future and with increased
functional requirements.
Both techniques, head resection and metatarsal shortening, do not recover the
windlass mechanism of the plantar fascia. Deformity relapse and metatarsalgia can
occur in all RA forefoot surgeries, usually in connection with an inadequate length
of the lesser metatarsals and also by load transfer from an insufficient first metatar-
sal due to shortening or proximal instability. Complication ranges from 3% to 20%
depending on the series. When performing arthrodesis on hallux, nonunion ranges
from 4% to 25%, being lower in those surgeries where stability is increased with
specific plates. The hallux valgus deformity relapse is related to the technique;
fusion avoids it while arthroplasties have relapses up to 30% [5, 15, 35, 36, 44].
8.5 Lesser Toes
The treatment of the claw toes will depend on the technique used in the respec-
tive metatarsal and the rigidity present at the proximal interphalangeal joint
(PIPJ) and distal interphalangeal joint (DIPJ). When performing reconstructions
while preserving the MTP, a DIPJ arthrodesis with resection of the proximal
phalanx condyle’s is indicated, adding a Girdlestone -Taylor technique (transfer
of FDL to EDL). Stabilization is carried out both with a retrograde Kirschner
wire or with specific implants for the PIPJ arthrodesis. If the correction of the
forefoot is performed with a Hoffmann procedure, no further shortening is
required. For those cases, a closed osteoclasia of the PIPJ and DIPJ is per-
formed, stabilizing the whole ray with a Kirschner wire. Kirschner wires remain
for 6 weeks.
8.6 Midfoot
The midfoot is the segment where better results are obtained with conservative
treatments (orthosis, footwear modifications, etc.) [49]. Midfoot symptoms have a
peak between 5 and 10 years of disease evolution, diminishing afterwards its symp-
tomatology [17]. This decrease would occur due to the stabilization effect of degen-
eration osteophytes and the fact that there is a limit to the flattening of the foot,
recovering the articular stability and diminishing the symptomatology. If the
Rheumatoid Foot 971
symptoms persist or become intense, arthrodesis of the symptomatic joints is indi-

cated. In our opinion, in the eventuality of being indicated, the surgical stabilization
should be done in all the cuneometatarsal and intercuneiform joints to achieve the
expected stability; the Naviculo-cuneiform joint (NC) should also be addressed
when it presents signs of damage or synovitis. Metatarso-cuneiform fusions present
minimal rates of nonunion. The infection rates are not higher than in other non-RA
patients, and the use of DMARDs or biological treatments do not implying an
increased risk [50]. The authors perform midfoot arthrodesis with a single approach
in line with the second metatarsal. There are multiple ways to stabilize this joints,
being our choice interfragmentary compression with screws associated to specific
neutralization plates of the operated segments.
8.7 Hindfoot
Surgical management of the hindfoot and ankle can be divided into the treatment of
soft tissue and joints.
8.7.1 Hindfoot: Soft Tissues
Rheumatoid Nodules Histologically they correspond to an accumulation of

inflammatory cells with central necrosis. The main reason for consultation is the
pain or discomfort they cause when wearing shoes. In the initial handling, a modi-
fication of footwear is indicated or the use of orthosis in the form of a donut around
the nodule to diminish the pressure. In the case of symptoms persistence, nodule
resection is indicated, having the precaution that when these are in the plantar region
of the heel, the plantar fat is not completely resected, to avoid pain due to loss of
cushioning.
Retrocalcaneal Bursitis The modifications of the footwear and the corticoids

infiltration achieve a good symptom relief. The failure of these modifications
implies the indication of surgical resection of this bursa.
Plantar Fasciitis It should be handled in a similar way to a fasciitis in a non-RA

patient, with elongation exercises and modification of the footwear. In a second stage,
eventually the use of local steroids, shock wave therapy, and percutaneous electrolysis
have shown fare results. If pain persists, a fasciotomy and/or proximal Achilles length-
ening should be considered. Our preference is to perform a proximal gastrosoleus
lengthening of the medial gastrocnemius fascia (see corresponding chapter).
Ulcers These should be treated with advanced wound care and antibiotic treatment
as needed. In case of conservative management failure, deep ulcer or deep infection,
surgical cleaning, culture primary closure or the use of flaps should be considered.
We suggest a plastic surgery consultation in these cases.
Neuritis: Tarsal Tunnel Syndrome The presence of tarsal tunnel syndrome in

these patients may be due to synovitis of the FHL or traction neuropathy in patients
with hindfoot valgus. Immobilization, local NSAIDs, and physical therapy are usu-
ally enough to relieve symptoms.
Posterior Tibial Tendon (PTT) Dysfunction (PTTD) Although RA is described

as a cause of PTT tenosynovitis [51, 52], which may be part of the patient’s clinical
picture of pain, partial or total ruptures of the posterior tibial tendon are not present
in all patients, with 0–11% reported [21, 53]. An increase in electromyographic
activity has even been described in patients with flat feet, PTT tenosynovitis, and
RA [54], which would explain the initial compensation of PTT against the hindfoot
valgus caused by progressive medial ankle-foot ligament damage (flatfoot). Whether
it is the PTTD or the hind-midfoot joint instability-ligaments insufficiency that
leads primarily to the flatfoot seen in these patients has been a subject of contro-
versy. However, in these patients it should be considered that even with an intact
PTT, the tendon can become insufficient as a medial foot stabilizer, since the biome-
chanics are altered [20] (see Fig. 6). Regardless of the cause, PTTD-flatfoot treat-
ment in a RA patient should be confronted in a similar way to the treatment of the
acquired flatfoot of the non-RA adult, taking special care in the control of the dis-
ease and the articular changes in the forefoot, midfoot, and rearfoot that these
patients may present.
Fig. 6 Patient, 65-years-

old, presents with Hallux
valgus, claw toes, and
midfoot and hindfoot
planovalgus
Rheumatoid Foot 973
8.7.2 Hindfoot: Joints
The indication for a triple arthrodesis is reserved for patients in whom the disease
involves two or more joints of the hindfoot (subtalar (SBT), talonavicular (TN),
calcaneocuboid (CC)) or there is a rigid deformity of the forefoot, midfoot or hind-
foot. It is important, when considering a hindfoot correction, to estimate the defor-
mities present in the forefoot, as well as whether they are flexible or rigid.
In our experience, we prefer to perform the triple “modified” arthrodesis [57, 58]
or double fusion (TN and SBT). Good results have been described in terms of fusion
rates and satisfaction with this technique [19, 58]. We prefer to use a single medial
approach, which allows good access to the SBT and TN joints. During the resection
of the remaining cartilage, we take care not to impact the talus head or the subtalar
joint. After the preparation of the surfaces, the articular reduction is made, having as
a precaution to correct the hindfoot valgus and forefoot supination at the TN joint.
We fix the joints temporarily with Kirschner wires (KW), after which stabilization
is performed at the SBT joint with 6.5-mm screws in divergent configuration, which
has proven to be biomechanically more stable [12, 55]. At the TN joint, fixation is
performed with three 4.5-mm cannulated screws paying special attention to correct
the forefoot supination (see Figs. 7 and 8). The use of graft in this arthrodesis is a
Fig. 7 AP-L weight-bearing foot and ankle X-rays of a 60-year-old patient with media foot pain
and flatfoot deformity
Fig. 8 Two years postop of previous case (Fig. 7), bone healing is observed in good axis both at
subtalar and talonavicular level. A double arthrodesis was performed by medial approach.
Stabilization of subtalar arthrodesis with two cannulated headless screws of 6.5 mm plus talona-
vicular stabilization with three 4.5-mm cannulated headless screws
topic of discussion. Although there are reports of good results when not using graft
in patients not RA, the majority recommends the use of bone graft in RA patients
[52, 60, 62] to compensate the poor bone quality. In our case, we use autologous
iliac bone graft when required.
The patient is immobilized in a cast and kept nonweight-bearing for 6 weeks.
After bone healing is achieved, partial protected weight-bearing is allowed with a
removable walking boot and a rehabilitation protocol begins, which focuses on the
ankle range of motion and gait training.
Although there is controversy regarding the progression of joint degeneration in
the neighboring joints (ankle, midfoot) when performing a triple or double arthrod-
esis, there is no clear clinical consequence [60, 61, 63]. Knupp [60] reports a radio-
logical progression of joint damage at 5.2 years of 17 (71%) of 24 rheumatic patients
who had triple arthrodesis. The greatest changes were found in the midfoot (15/17);
however, these findings did not affect patient satisfaction. Performing a triple “mod-
ified” arthrodesis would allow to decrease the stress (overload) on the neighboring
joints by keeping the lateral column mobile, because the calcaneocuboid joint is not
fused [59, 60].
The bone healing rate is key in the results; there are reports of arthrodesis non-
union that go from 0% to 20% [58, 60, 61, 63]. In this respect, a good joint prepara-
tion, achieving a good bone surface coaptation associated to the use of bone graft,
is key point to achieve a satisfactory bone healing rate. Surgical wound
Rheumatoid Foot 975
complications can be superficial or deep. The use of immunosuppressive drugs, the

skin condition, and the chosen surgical approach must be taken into account. A
greater incidence of complications has been described when the wound is left in
tension after arthrodesis [58], when correcting the valgus of the hindfoot and per-
forming a lateral approach for SBT arthrodesis, for example. In our experience, the
use of a single medial approach to perform SBT and TN arthrodesis allows us to
close the medial soft tissues without tension.
It is very important to achieve a good bone alignment. A mal-aligned hindfoot
arthrodesis will lead to compensations at the level of the ankle, midfoot, and/or
forefoot, which will generate greater overload, pain, and inability to walk. In sum-
mary, a healed arthrodesis of the hindfoot, in good axis, will diminish significantly
the patients symptoms [58, 60, 61].
8.8 Ankle
With respect to the surgical management of the ankle, it is necessary to consider that
the main deformity of the ankle in rheumatic patients is in valgus, being this defor-
mity three times more frequent than varus [64]. It should be remembered that the
alterations in the ankle are mainly secondary to the displacements that are produced
in the hindfoot, although a causal effect is also attributed to the joint and synovial
damage characteristic of the disease [65].
Once conservative treatment has failed, there are different surgical alternatives to
be considered, depending on the joint involvement and associated deformities: tib-
iotalar fusion, joint replacement, tibio-talo-calcaneal fusion (TTC), and pan-
arthrodesis (ankle and hindfoot).
8.8.1 Arthrodesis
Ankle arthrodesis continues to be the gold-standard in rheumatic patients in

advanced stages of arthrosis [65, 66], with good results described in terms of pain
reduction, deformity correction, function, and union rates [56, 65–67]. The union
rates in general reported with internal fixation, open or arthroscopic, range from
70% to 100% [68, 69]; however, in patients with RA, the union rates are lower,
varying from 65% to 96%, averaging 85% [65]. In this regard, Miehlke [56] reports
a 92% union rate in ankle-foot arthrodesis with compressive technique in 43 patients
with RA, with a healing time of 8–16 weeks. Kennedy [66] reports a 90% union rate
in ankle arthrodesis in 20 RA patients in 3.8 months on average (range 2–10 months).
The ideal indication for an arthrodesis is a RA patient with intractable joint pain
and diffuse joint compromise, with no response to conservative management. In
addition, it is necessary to consider that many of these patients already present com-
promise of the rearfoot, forefoot, knee, etc., reason why all the existing joints com-
promise and deformities in the foot, knee, and hip, must be evaluated before
proceeding with an ankle arthrodesis. It is essential to have a clear discussion with

the patient about the objectives of this surgery, as well as his or her expectations.
Special attention must be paid to the state of the subtalar joint (degeneration, dislo-
cation, and subluxation). Subtalar arthrodesis must be considered together with the
ankle arthrodesis. In this case, the TTC arthrodesis should be evaluated.
8.8.2 Mild to Moderate Deformities: Anterior Approach
Although there are many techniques described for performing ankle arthrodesis,
either with respect to the approach routes (anterior, lateral transfibular, posterior,
and arthroscopic) or with the forms of fixation (internal fixation with screws, plates,
and external fixation) [56, 65, 66], in our experience, in cases with mild to moder-
ate deformity (<10° ankle deformity), we use an anterior ankle approach. For fixa-
tion, we use three 6.5-mm compressive screws, one from posterior tibia – anterior
talus (home-run) and two from anterior tibia to posterior talus (see Fig. 9). It is
important to achieve compression, regardless of the fixation method used. If the
surfaces are well matched, we do not use grafting, although due to osteoporosis and
poor bone stock frequently present in these patients, many times the use of auto-
graft (or allograft) is the rule. We reserve the use of plate to increase stability in
Fig. 9 Ankle arthrodesis,

fixed with three 7.0-mm
screws
Rheumatoid Foot 977
cases with severe osteoporosis, nonstable fixation with screws, and in revisions of
cases with nonunion of arthrodesis. Although there are different types of plates
described, we prefer the anatomical ones for ankle arthrodesis, which allow com-
pression and can be locked.
8.8.3 Arthroscopic Arthrodesis
With respect to arthroscopic arthrodesis, the main advantage over the open one is
the lesser exposure of soft tissues, with a lower risk of infection, shorter hospitaliza-
tion time, and lower rate of reported complications [70]. However, the experience of
the surgeon [68] and the presence of malalignment must be considered, since it is
not possible to perform angular corrections with this technique [65].
8.8.4 Severe Ankle Deformities: Lateral Approach
In cases of severe angular deformities in both valgus and varus, we recommend

first approaching the apex of the deformity to perform the angular correction and
then the arthrodesis, so as not to generate tension at the time of closure. Soft tissue
tension increases the risk of dehiscence, necrosis, and infection. The use of a
transfibular approach, performing an osteotomy 8–10 cm proximal to the fibular
tip, preserving the irrigation by keeping the posterior soft tissues attached to the
fibula, allows an adequate visualization of the tibiotalar joint. Later, the fibula is
added as a graft to the fusion site. The fixation of the arthrodesis is done by plac-
ing screws as previously described adding two screws from the fibula to tibia and
fibula to talus. Although varus and valgus deformities can be addressed with this
technique, special care must be taken when correcting valgus, since, probably a
medial tibial wedge resection will be needed to achieve alignment (this osteotomy
is performed through a separate medial approach). Independent of the technique
used, the anterior osteophytes should be resected to avoid an equinus
malposition.
Although the use of external fixation for arthrodesis in RA patients has been
described with variable reported results of union [65, 71], this is reserved mainly for
those patients in which infection exists and for those with a nonunion of a previous
arthrodesis with poor soft tissues.
9 Complications
Among complications, nonunion occurs in approximately 12% of cases, with RA

being one of the reported risk factors. There are others that should be considered
and evaluated in conjunction with the presence of RA: obesity, smoking, infection,
and the surgeon’s experience [69]. The presence of malalignment after bone healing
is generally due to subsidence by osteoporosis or to poor surgical technique. Soft

tissue complications are a special concern in these patients. These can include
delayed healing, edge necrosis, dehiscence, and superficial and deep infections.
10 Total Arthroplasty
The absolute loss of mobility, the possibility of nonunion, and the overloading of
neighboring joints, which would lead to an increase in inflammatory symptoms in
these patients, have been arguments against arthrodesis. Thus, total ankle arthro-
plasty (TAA) has emerged as a treatment alternative to arthrodesis, based on the
potential benefits of regaining movement, improving gait, reducing pain, and pro-
tecting the neighboring joints. Some authors have even proposed that, in patients
with inflammatory diseases such as RA, the results would be the same, even better,
than in those with post-traumatic osteoarthritis [72]. However, despite the fact that
there is more experience in the technique and design of implants (not cemented,
less constrained), TAA is not exempt from complications. This is especially notori-
ous in rheumatic patients, in which there is poor bone quality and an alteration of
soft tissues, facts that can lead to a greater risk of re-operations [72, 73]. Raikin
[72], in a study of 106 TAA, found that inflammatory arthritis was a significant
independent predictor of major soft tissue complications. Yano [73] reports in the
analysis of 39 ankle joint replacements in RA patients, with a minimum follow-up
of 2 years, good functional results, pain improvement, and better functional scores,
as well as footwear use, with an 88.4% implant survival at 10 years. However, it
also reports a high rate of radiological complications at 9 years, such as radiolucent
lines of the tibial component (73.7%), subsidence of the talar component (28.9%),
and migration of the tibial component (21%), as well as other complications such
as surgical wound dehiscence (25.6%), need for implant removal (10.3%), medial
malleolus intraop fractures (7.7%), and deep infections (2.6%).
The ideal RA patient for arthroplasty is one who has a mild-moderately active
disease, controlled with antirheumatic medications, without a current flare-up, with-
out ankle malalignments (up to 10° of deformity), and a mobile hindfoot [67]. Other
local conditions to consider against the indication of TAA are the presence of exten-
sive subchondral cysts, bone destruction, and osteoporosis, since the tibial and/or
talar component could fail if these are present.
11 Tibio-Talo-Calcaneal Arthrodesis (TTC)
The TTC fusion is reserved for patients with severe deformities that involve the
subtalar and ankle joints. It is necessary to keep in mind that it is not always feasible
to correct the whole hindfoot malalignment. It should be considered as a salvage
procedure, since both tibiotalar and subtalar mobility are completely lost. Currently,
Rheumatoid Foot 979
fixation with specifically designed endomedullary compressive nails is the standard

technique for this fixation. It provides stability and allows early weight-bearing
which is especially important for patients who present osteopenia/osteoporosis and
who are usually unable to walk with two crutches to unload the operated foot.
12 Pan-Arthrodesis
Pan-arthrodesis, or arthrodesis of the TN, CC, subtalar, and ankle joints, is indicated
in rheumatic patients with severe deformities of both the foot and ankle, which are
all symptomatic. Although there is controversy about the loss of mobility after this
surgery, it must be considered that the degree of severe deformity these patients
present, as well as the alteration in gait and quality of life they have, makes pan-
arthrodesis a well-tolerated technique. Mckinley [72] in a study of 17 patients with
RA, all with severe flat feet associated with ankle joint involvement, who underwent
pan-arthrodesis, reports good results in terms of pain reduction and physical and
mental improvement at 1 year of follow-up. There is concern in these patients
regarding the midfoot joints overload after a pan-arthrodesis. However, as already
mentioned, the described degeneration is mainly radiological, not having a clear
clinical correlation.
References
1. Stolt M, Suhonen R, Leino-Kilpi H. Foot health in patients with rheumatoid arthritis-a scoping
review. Rheumatol Int. 2017;37(9):1413–22. https://doi.org/10.1007/s00296-017-3699-0.
2. Șerban O, Bădărînză M, Fodor D. The relevance of ultrasound examination of the foot
and ankle in patients with rheumatoid arthritis - a review of the literature. Med Ultrason.
2019;21(2):175–82. https://doi.org/10.11152/mu-1967.
3. Grondal L, Tengstrand B, Nordmark B, Wretenberg P, Stark A. The foot: still the most important
reason for walking incapacity in rheumatoid arthritis: distribution of symptomatic joints in 1,000
RA patients. Acta Orthop. 2008;79(2):257–61. https://doi.org/10.1080/17453670710015067.
4. Fleming A, Crown JM, Corbett M. Early rheumatoid disease. I. Onset. Ann Rheum Dis.
1976;35(4):357–60. https://doi.org/10.1136/ard.35.4.357.
5. Burra G, Katchis S. Rheumatoid arthritis of the forefoot. Rheum Dis Clin N Am.
1998;24(1):173–80. https://doi.org/10.1016/s0889-857x(05)70384-7.
6. Brooks F, Hariharan K. The rheumatoid forefoot. Curr Rev Musculoskelet Med.
7. Michelson J, Easley M, Wigley FM, Hellmann D. Foot and ankle problems in rheumatoid
arthritis. Foot Ankle Int. 1994;15(11):608–13. https://doi.org/10.1177/107110079401501106.
8. Loveday DT, Jackson GE, Geary NP. The rheumatoid foot and ankle: current evidence. Foot
Ankle Surg. 2012;18(2):94–102. https://doi.org/10.1016/j.fas.2011.06.001.
9. Aronow MS, Hakim-Zargar M. Management of hindfoot disease in rheumatoid arthritis. Foot
Ankle Clin. 2007;12(3):455–vi. https://doi.org/10.1016/j.fcl.2007.05.003.
10. O’Brien TS, Hart TS, Gould JS. Extraosseous manifestations of rheumatoid arthri-
tis in the foot and ankle. Clin Orthop Relat Res. 1997;340:26–33. https://doi.
org/10.1097/00003086-199707000-00005.
11. Gutierrez M, Pineda C, Salaffi F, et al. Is ankle involvement underestimated in rheumatoid

arthritis? Results of a multicenter ultrasound study. Clin Rheumatol. 2016;35(11):2669–78.
12. Piazza SJ. Mechanics of the subtalar joint and its function during walking. Foot Ankle Clin.
2005;10(3):425–v. https://doi.org/10.1016/j.fcl.2005.04.001.
13. Nixon DC, McKean R, et al. Rheumatoid forefoot reconstruction in nonrheumatoid patient.
14. Siddle H, Hodgson R, et al. Plantar plate pathology is associated with erosive disease in
the painful forefoot of patients with rheumatoid arthritis. BMC Musculoskelet Disord.
2017;18(1):308. https://doi.org/10.1186/s12891-017-1668-0.
15. Guzman JZ, Vulcano E. Resection arthroplasty: current indications and tips. Foot Ankle Clin.
16. Hanyu T, Yamazaki H, Ishikawa H, et al. Flexible hinge toe implant arthroplasty for rheu-
matoid arthritis of the first metatarsophalangeal joint: long-term results. J Orthop Sci.
2001;6(2):141–7. https://doi.org/10.1007/s007760100062.
17. Matsumoto T, Nakamura I, Miura A, Momoyama G, Ito K. Radiologic patterning of joint
damage to the foot in rheumatoid arthritis. Arthritis Care Res (Hoboken). 2014;66(4):499–507.
https://doi.org/10.1002/acr.22174.
18. Jeong HJ, Sohn IW, Kim D, et al. Impact of midfoot and Hindfoot involvement on func-
tional disability in Korean patients with rheumatoid arthritis. BMC Musculoskelet Disord.
2017;18(1):365. Published 2017 Aug 24. https://doi.org/10.1186/s12891-017-1726-7.
19. Seltzer SE, Weissman BN, Braunstein EM, Adams DF, Thomas WH. Computed tomography
of the hindfoot with rheumatoid arthritis. Arthritis Rheum. 1985;28(11):1234–42. https://doi.
org/10.1002/art.1780281107.
20. Cracchiolo A 3rd. Rheumatoid arthritis. Hindfoot disease. Clin Orthop Relat Res.
1997;(340):58–68. https://doi.org/10.1097/00003086-199707000-00009.
21. Jaakkola JI, Mann RA. A review of rheumatoid arthritis affecting the foot and ankle. Foot
22. Michelson J, Easley M, Wigley FM, Hellmann D. Posterior tibial tendon dys-
function in rheumatoid arthritis. Foot Ankle Int. 1995;16(3):156–61. https://doi.
org/10.1177/107110079501600309.
23. Aletaha D, Neogi T, Silman AJ, et al. 2010 rheumatoid arthritis classification criteria: an
American College of Rheumatology/European League Against Rheumatism collaborative ini-
tiative [published correction appears in Ann Rheum Dis. 2010 Oct;69(10):1892]. Ann Rheum
Dis. 2010;69(9):1580–8. https://doi.org/10.1136/ard.2010.138461.
24. Brenton-Rule A, Dalbeth N, Menz HB, Bassett S, Rome K. Foot and ankle characteristics
associated with falls in adults with established rheumatoid arthritis: a cross-sectional study.
BMC Musculoskelet Disord. 2016;17:22. Published 2016 Jan 13. https://doi.org/10.1186/
s12891-016-0888-z.
25. Enache L, Popescu CC, Micu M, et al. Ankle involvement in rheumatoid arthritis - a compari-
son of inflammatory signs on musculoskeletal ultrasound and magnetic resonance imaging.
Med Ultrason. 2019;21(3):265–72. https://doi.org/10.11152/mu-2038.
26. Wilson O, Kirwan JR. Measuring sensation in the feet of patients with rheumatoid arthritis.
Musculoskeletal Care. 2006;4(1):12–23.
27. Larsen A, Dale K, Eek M. Radiographic evaluation of rheumatoid arthritis and related condi-
tions by standard reference films. Acta Radiol Diagn (Stockh). 1977;18(4):481–91. https://doi.
org/10.1177/028418517701800415.
28. Larsen A. How to apply Larsen score in evaluating radiographs of rheumatoid arthritis in long-
term studies. J Rheumatol. 1995;22(10):1974–5.
29. Eliasziw M, Young SL, Woodbury MG, Fryday-Field K. Statistical methodology for the con-
current assessment of interrater and intrarater reliability: using goniometric measurements as
an example. Phys Ther. 1994;74(8):777–88. https://doi.org/10.1093/ptj/74.8.777.
30. Larsen A, Edgren J, Harju E, Laasonen L, Reitamo T. Interobserver variation in the evaluation
of radiologic changes of rheumatoid arthritis. Scand J Rheumatol. 1979;8(2):109–12. https://
doi.org/10.3109/03009747909105347.
Rheumatoid Foot 981
31. Ciurtin C, Jones A, Brown G, et al. Real benefits of ultrasound evaluation of hand and foot
synovitis for better characterisation of the disease activity in rheumatoid arthritis. Eur Radiol.
32. Camerer M, Ehrenstein B, Hoffstetter P, Fleck M, Hartung W. High-resolution ultrasound of
the midfoot: sonography is more sensitive than conventional radiography in detection of osteo-
phytes and erosions in inflammatory and non-inflammatory joint disease. Clin Rheumatol.
2017;36(9):2145–9. https://doi.org/10.1007/s10067-017-3658-x.
33. Kushioka J, Hirao M, Tsuboi H, et al. Modified scarf osteotomy with medial capsule interpo-
sition for hallux valgus in rheumatoid arthritis: a study of cases including severe first meta-
tarsophalangeal joint destruction. J Bone Joint Surg Am. 2018;100(9):765–76. https://doi.
org/10.2106/JBJS.17.00436.
34. Ortega-Avila AB, Moreno-Velasco A, Cervera-Garvi P, Martinez-Rico M, Chicharro-Luna
E, Gijon-Noqueron G. Surgical treatment for the ankle and foot in patients with rheumatoid
arthritis: a systematic review. J Clin Med. 2019;9(1):42. Published 2019 Dec 24. https://doi.
org/10.3390/jcm9010042.
35. Dougherty CD, Hung YY, Weintraub MLR, Patel S, King CM. Osseous and soft tissue com-
plications associated with foot and ankle surgery in patients with rheumatoid arthritis taking
a variety of antirheumatic medications. J Foot Ankle Surg. 2019;58(3):508–13. https://doi.
org/10.1053/j.jfas.2018.09.030.
36. Louwerens JW, Schrier JC. Rheumatoid forefoot deformity: pathophysiology, evaluation
and operative treatment options. Int Orthop. 2013;37(9):1719–29. https://doi.org/10.1007/
s00264-013-2014-2.
37. Whitt KJ, Rincker SA, Hyer CF. Sustainability of forefoot reconstruction for the rheumatoid
foot. J Foot Ankle Surg. 2016;55(3):583–5. https://doi.org/10.1053/j.jfas.2016.02.003.
38. Doty J, Coughlin M, Hirose C, Kemp T. Hallux metatarsophalangeal joint arthrodesis with a
hybrid locking plate and a plantar neutralization screw: a prospective study. Foot Ankle Int.
39. Hunt KJ, Ellington JK, Anderson RB, Cohen BE, Davis WH, Jones CP. Locked versus non-
locked plate fixation for hallux MTP arthrodesis. Foot Ankle Int. 2011;32(7):704–9. https://
doi.org/10.3113/FAI.2011.0704.
40. Kumar CS, Holt G. Hallux metatarsophalangeal arthroplasty in the rheumatoid forefoot. Foot
Ankle Clin. 2007;12(3):405–vi. https://doi.org/10.1016/j.fcl.2007.04.001.
41. Esway JE, Conti SF. Joint replacement in the hallux metatarsophalangeal joint. Foot Ankle
Clin. 2005;10(1):97–115. https://doi.org/10.1016/j.fcl.2004.09.002.
42. Stibolt RD, Patel HA, Lehtonen EJ, et al. Hemiarthroplasty versus total joint arthroplasty for
hallux rigidus: a systematic review and meta-analysis. Foot Ankle Spec. 2019;12(2):181–93.
43. Baumhauer JF, Daniels T, Glazebrook M. New technology in the treatment of hallux rigidus
with a synthetic cartilage implant hemiarthroplasty. Orthop Clin North Am. 2019;50(1):109–18.
https://doi.org/10.1016/j.ocl.2018.08.007.
44. Lee H, Ishikawa H, Shibuya T, et al. Changes in radiographic findings and plantar pressure
distribution following forefoot reconstructive surgery for patients with rheumatoid arthritis
[published online ahead of print, 2019 Oct 24]. Mod Rheumatol. 2019:1–8. https://doi.org/1
0.1080/14397595.2019.1680094.
45. Simon MJK, Strahl A, Mussawy H, et al. Forefoot reconstruction following metatarsal
head resection arthroplasty with a plantar approach-a 20-year follow-up. Foot Ankle Int.
46. Thomas S, Kinninmonth AW, Kumar CS. Long-term results of the modified Hoffman proce-
dure in the rheumatoid forefoot. Surgical technique. J Bone Joint Surg Am. 2006;88 Suppl 1
Pt 1:149–57. https://doi.org/10.2106/JBJS.E.00900.
47. Horita M, Nishida K, Hashizume K, et al. Outcomes of resection and joint-preserving arthro-
plasty for forefoot deformities for rheumatoid arthritis. Foot Ankle Int. 2018;39(3):292–9.
48. Hansen ST Jr. Functional reconstruction of the foot and ankle. Primera Edicion. Chapter 15,
Rheumatoid Artrhitis and other inflammatory arthritides, pp 236 y 342. Editorial Lippincot
Williams & Wilkins.
49. Hirao M, Ebina K, Tsuboi H, et al. Outcomes of modified metatarsal shortening offset osteot-
omy for forefoot deformity in patients with rheumatoid arthritis: short to mid-term follow-up.
Mod Rheumatol. 2017;27(6):981–9. https://doi.org/10.1080/14397595.2016.1276512.
50. Bibbo C, Goldberg JW. Infectious and healing complications after elective orthopaedic foot
and ankle surgery during tumor necrosis factor-alpha inhibition therapy. Foot Ankle Int.
51. Bare AA, Haddad SL. Tenosynovitis of the posterior tibial tendon. Foot Ankle Clin.
2001;6(1):37–66. https://doi.org/10.1016/s1083-7515(03)00078-0.
52. Tokunaga D, Hojo T, Takatori R, et al. Posterior tibial tendon tenosynovectomy for rheu-
matoid arthritis: a report of three cases. Foot Ankle Int. 2006;27(6):465–8. https://doi.
org/10.1177/107110070602700613.
53. Masterson E, Mulcahy D, McElwain J, McInerney D. The planovalgus rheumatoid foot –
is tibialis posterior tendon rupture a factor? Br J Rheumatol. 1995;34(7):645–6. https://doi.
org/10.1093/rheumatology/34.7.645.
54. Barn R, Turner DE, Rafferty D, Sturrock RD, Woodburn J. Tibialis posterior tenosynovitis
and associated pes plano valgus in rheumatoid arthritis: electromyography, multisegment
foot kinematics, and ultrasound features. Arthritis Care Res (Hoboken). 2013;65(4):495–502.
https://doi.org/10.1002/acr.21859.
55. Astion DJ, Deland JT, Otis JC, Kenneally S. Motion of the hindfoot after simulated arthrodesis. J
Bone Joint Surg Am. 1997;79(2):241–6. https://doi.org/10.2106/00004623-199702000-00012.
56. Miehlke W, Gschwend N, Rippstein P, Simmen BR. Compression arthrodesis of the
rheumatoid ankle and hindfoot. Clin Orthop Relat Res. 1997;(340):75–86. https://doi.
org/10.1097/00003086-199707000-00011.
57. Mann RA, Beaman DN. Double arthrodesis in the adult. Clin Orthop Relat Res.
1999;(365):74–80. https://doi.org/10.1097/00003086-199908000-00010.
58. Bagwe MR. Arthrodesis of the subtalar and talonavicular joints for correction of
symptomatic hindfoot malalignment. Foot Ankle Int. 2006;27(9):661–6. https://doi.
org/10.1177/107110070602700901.
59. Jastifer JR, Alrafeek S, Howard P, Gustafson PA, Coughlin MJ. Biomechanical evalua-
tion of strength and stiffness of subtalar joint arthrodesis screw constructs. Foot Ankle Int.
60. Knupp M, Skoog A, Törnkvist H, Ponzer S. Triple arthrodesis in rheumatoid arthritis. Foot
Ankle Int. 2008;29(3):293–7. https://doi.org/10.3113/FAI.2008.0293.
61. Pell RF 4th, Myerson MS, Schon LC. Clinical outcome after primary triple arthrodesis. J Bone
Joint Surg Am. 2000;82(1):47–57. https://doi.org/10.2106/00004623-200001000-00006.
62. McKinley JC, Shortt N, Arthur C, Gunner C, MacDonald D, Breusch SJ. Outcomes fol-
lowing pantalar arthrodesis in rheumatoid arthritis [published correction appears in Foot
Ankle Int. 2011 Oct;32(10):vi]. Foot Ankle Int. 2011;32(7):681–5. https://doi.org/10.3113/
FAI.2011.0681.
63. Smith RW, Shen W, Dewitt S, Reischl SF. Triple arthrodesis in adults with non-paralytic dis-
ease. A minimum ten-year follow-up study. J Bone Joint Surg Am. 2004;86(12):2707–13.
https://doi.org/10.2106/00004623-200412000-00018.
64. Kirkup J. Rheumatoid arthritis and ankle surgery. Ann Rheum Dis. 1990;49 Suppl 2(Suppl
2):837–44. https://doi.org/10.1136/ard.49.suppl_2.837.
65. Sammarco VJ. Ankle arthrodesis in rheumatoid arthritis: techniques, results, and complica-
tions. Foot Ankle Clin. 2007;12(3):475–vii. https://doi.org/10.1016/j.fcl.2007.04.002.
66. Kennedy JG, Harty JA, Casey K, Jan W, Quinlan WB. Outcome after single technique ankle
arthrodesis in patients with rheumatoid arthritis. Clin Orthop Relat Res. 2003;412:131–8.
https://doi.org/10.1097/01.blo.0000071755.41516.a0.
Rheumatoid Foot 983
67. Ng SY, Crevoisier X, Assal M. Total ankle replacement for rheumatoid arthritis of the ankle
[published correction appears in Foot Ankle Clin. 2013 Mar;18(1):xiii. Sean, Ng Y C [cor-
rected to Ng, Sean Y C]; Xavier, Crevoisier [corrected to Crevoisier, Xavier]]. Foot Ankle Clin.
68. Park JH, Kim HJ, Suh DH, et al. Arthroscopic versus open ankle arthrodesis: a systematic
review. Arthroscopy. 2018;34(3):988–97. https://doi.org/10.1016/j.arthro.2017.08.284.
69. Thevendran G, Younger A, Pinney S. Current concepts review: risk factors for nonunions in
foot and ankle arthrodeses. Foot Ankle Int. 2012;33(11):1031–40. https://doi.org/10.3113/
FAI.2012.1031.
70. Turan I, Wredmark T, Felländer-Tsai L. Arthroscopic ankle arthrodesis in rheumatoid arthritis.
Clin Orthop Relat Res. 1995;320:110–4.
71. Felix NA, Kitaoka HB. Ankle arthrodesis in patients with rheumatoid arthritis. Clin Orthop
Relat Res. 1998;349:58–64. https://doi.org/10.1097/00003086-199804000-00008.
72. Raikin SM, Kane J, Ciminiello ME. Risk factors for incision-healing complications following
total ankle arthroplasty. J Bone Joint Surg Am. 2010;92(12):2150–5. https://doi.org/10.2106/
JBJS.I.00870.
73. Yano K, Ikari K, Okazaki K. Radiographic outcomes of mobile-bearing total ankle arthro-
plasty for patients with rheumatoid arthritis. Foot Ankle Int. 2019;40(9):1037–42. https://doi.
org/10.1177/1071100719851469.
Charcot Neuroarthropathy
Rafael Barban Sposeto and Alexandre Leme Godoy-Santos
1 Introduction
Charcot’s Neuroarthropathy (CN), or Charcot’s osteoneuroarthropathy [1], is an

osteoarticular pathology with descriptions of the involvement of various body seg-
ments, such as the knee, spine, shoulder, hip, and wrist, but the foot and ankle are
the most frequently affected segments [2].
CN is a chronic disease, with an immense negative impact on quality of life [3],
especially when it affects the foot and ankle, destroying bone and joint structures in
patients with neuropathy [2], evolving with decreased mobility, amputations, and
increased mortality [4].
The CN presents descriptions in the literature associating it with tertiary syphilis,
Charcot-Marie-Tooth, congenital neuropathies, Hansen’s disease, polio, multiple
sclerosis, rheumatoid arthritis, and diabetes mellitus (DM) [1, 5, 6], mostly with
some component of sensory neuropathy.
Jean Martin Charcot in 1868 described osteoarticular alterations in patients with
tabes dorsalis neuropathy [6], becoming notorious in the identification of this
pathology. Although controversial, other authors had already observed similar
osteoarticular alterations. In 1703, Sir William Musgrave described a neuropathic
arthritis associated with venereal disease [1, 6], and JK Mitchel, in 1831, identified
the relationship between tuberculosis infection in the spine and articular phlogistic
alterations, creating the term “lower limb rheumatism” [1, 6].
In 1936, Jordan WR [7], made a publication associating diabetes mellitus to
CN. Due to the high prevalence of diabetes mellitus worldwide, this is the most
related pathology to CN today [4, 8].
R. B. Sposeto (*)
University of São Paulo, São Paulo, Brazil
A. L. Godoy-Santos
University of São Paulo/Hospital Israelita Albert Einstein, São Paulo, Brazil

Switzerland AG 2022
986 R. B. Sposeto and A. L. Godoy-Santos
Even so, the CN is underdiagnosed, with prevalence values questioned in the

literature [1, 4]. Single limb involvement is more common, with annual incidence
ranging from 0.1% to 29% and prevalence from 0.08% to 13% [9, 10]. It is more
prevalent in men [4], between the fifth and sixth decades of life, with DM duration
of at least 10 years [11].
Patients with DM and CN have higher rates of amputation, ranging from 35% to
67%, so that CN is the highest risk factor for lower limb amputation among diabet-
ics [9], which increases to 28% with the presence of ulcer [12]. Forty to 50% of
patients with DM and CN undergo at least 1 foot surgery. Chaudhary S et al. [4]
show a threefold chance of mortality in patients with DM and CN.
Thus, it is understood that in patients with DM, CN is a complication of their
evolution, and we should research other organs and systems potentially affected
by diabetes, for the full treatment of the patient [3, 11]. Therefore, the approach
with a multidisciplinary team, with orthopedist, endocrinologist, vascular sur-
geon, and depending on the comorbidities infectious disease specialist, ophthal-
mologist, nephrologists, and nurses, is essential for the best possible treatment
outcome [3].
2 Physiopathology
The pathophysiology of CN is not yet completely clear [13]. Physiopathological

theories have been postulated, some more than a century old. They probably com-
plement each other in explaining the disease [2].
2.1 Neurovascular Theory
This theory is supported by Charcot and Mitchell [2, 6, 14], who consider that the
osteoarticular alteration of the CN is triggered by a hypervascularization of the seg-
ment due to an autonomic neuropathy. This alteration in the sympathetic system
would increase blood flow, due to alterations in vascular reflexes, which increases
the arteriovenous shunts [14].
In this theory, osteopenia of the affected segment would be caused by increased
blood flow, leading to bone fragility and multiple fracture-dislocations [9].
2.2 Inflammatory Theory
It has been demonstrated that bone mineral density in the acute phase of foot
involvement by the CN is decreased, and this fragility may predispose to fracture-
dislocations [14–16].
Charcot Neuroarthropathy 987
Some authors [17–19] believe that an environment of inflammation exacerbated

in patients with acute CN, increases osteoclastic activity, generating absorption,
osteopenia, and bone fragility.
Jeffcoat and collaborators [17] consider that in the acute phase of CN there is an
inflammatory response to exaggerated trauma, increasing the expression of pro-
inflammatory cytokines such as TNF-α, IL-6, and IL-1β, increasing the number and
local function of osteoclasts [14].
In this intensely inflamed environment, monocytes differentiate into osteo-
clasts, generating a disproportion in the osteoclast-osteoblasts ratio. In addition
to the increase in their number, these cells present an increased expression of
TNF-α, IL-6, and IL-1β, potentiating local inflammation and bone destruction
[17, 20].
Studies of the last decade show an imbalance between the relationship of RANKL
(ligand for receptor activator of nuclear factor B) and its antagonist OPG (osteopro-
tegerin), favoring osteoclastic activity [2, 8, 14, 17].
The RANK is a receptor, located on the surface of the osteoclast progenitor cells,
that regulates its differentiation. It is activated by RANKL promoting osteoclasto-
genesis and bone absorption. In turn, OPG is a cytokine produced by activated
osteoblasts that antagonizes the RANKL bond in the osteoclast membrane. Thus,
the regulation of the RANKL/OPG ratio is one of the mechanisms of bone metabo-
lism control, with impact on its density [13].
Patients with acute CN present this increased ratio [20, 21], favoring osteoclastic
activity, with bone resorption and fragility. Jansen and collaborators [22] show this
increase in the acute phase of CN, but not in the chronic phase, and may even be a
potential marker of Charcot’s activity [14].
2.3 Neurotraumatic Theory
This theory considers the loss of protective sensitivity caused by neuropathy.

Patients suffer repeated microtrauma or acute trauma without noticing, due to lack
of sensitivity. This generates cumulative bone mechanical lesions and inflammation,
fracturing the bone and making the joints incongruous [2, 9, 14].
These theories are not exclusive, neuropathy (sensitive and autonomic) and
inflammation are prerequisites for the development of CN [9, 17]. It is possible that
patients accumulate consecutive lesions from minimal traumas, increasing the
inflammation in the foot and ankle, triggering an exacerbated inflammatory response
through inflammatory mediators and the RANKL/OPG cascade, further weakening
the bone structures of the foot and ankle.
The nonenzymatic glycosylation of tendons and ligaments, typical of a DM
hyperglycemic environment, adds more instability to this panorama. A circle of
injury is created that perpetuates through the tripod trauma–injury–inflammation,
fracturing the bones and destabilizing the joints, with deformities and more distur-
bances in the load distribution [9].
3 Classification
The most commonly used classifications are clinical and anatomical. The best
known is from Eichenholtz, published in 1966 [1, 23, 24]. He describes three stages
of evolution of the pathology, in a progressive way, from acute to chronic phase. It
uses as parameters the clinical and radiographic characteristics: Table 1.
3.1 Stage 1: Acute Development
Patient presents with inflammation of the foot, with hyperemia, edema, increased
temperature associated with radiographic signs of bone fragmentation, fracture, dis-
locations, and subluxations.
3.2 Stage 2: Coalescence
It is the phase of clinical and radiographic intermediate evolution, with signs and
symptoms of intermediate resolution with acute characteristics. Clinically, the pres-
ence of inflammation is also observed, but diminished in relation to stage 1.
Radiographically, bone sclerosis is noted, denoting the beginning of the bone heal-
ing process.
Table 1 Eichenholtz classification modified by Shibata et al. and Yu GV et al. [23]

Stage Image Physical examination
0 – Inflammatory Xr: No change Edema and hyperemia. Alteration >2°
MRI: Alteration of signal in bone to the contralateral limb
marrow and subchondral bone 1 – Acute phase
1 – Acute phase Xr: Bone fragmentation (acute Edema, hyperemia, and local increased
aspect). temperature
Joint incongruity
2 – Coalescence Xr: Bone formation in fracture Decrease of inflammatory signs
phase sites.
Resorption of bone fragments.
Beginning of the healing process of
the affected joints
3 – Remodeling Xr: Bone healed. Ankylosis Absence of inflammatory signs.
phase Possible foot misalignment and
deformities
Modified by Botek G et al. [14]
PE physical examination, Xr radiograph, MRI magnetic resonance imaging
3.3 Stage 3: Remodeling
The inflammatory phase is finished, with reduction of edema, increased tempera-

ture, and hyperemia. Radiographically, the fracture healing is observed, with the
establishment of the deformities acquired by the bone and joint deviations of phases
1 and 2 (Figs. 1 and 2).
Fig. 1 Clinical example of residual ankle deformity of a patient with CN at stage 3

Fig. 2 Radiographic images of the right ankle residual deformity of the patient exemplified in
stage 3, Fig. 1
3.4 Stage 0: Inflammatory
In 1990, Shibata and collaborators [23] added stage 0 to the classification, which
consists of the initial clinical presentation with edema, heat, and hyperemia, but
without visible changes to the radiograph. Yu GV and Hudson JR [24] consider that
acute foot and ankle trauma in patients with sensory neuropathy should be consid-
ered stage 0.
Establishing a correlation between pathophysiology and Eichenholtz classifica-
tion, it is understood that in stages 0 and 1 the patient is intensely expressing pro-
inflammatory cytokines with increased osteoclastic activity, associated with
repetitive, nonsense traumas resulting from basic daily activities, fracturing and
stabilizing the foot bones. In stages 2 and 3, the osteoclastic and inflammatory activ-
ity decreases and ceases, resulting in bone healing with the residual deformities.
These residual bone deformities will impact the load distribution during the
patient’s gait, causing tissue injury and ulceration. Depending on the anatomical
region of the foot, the tissue lesion may be greater [11]. Therefore, some authors
classify the CN on the foot and ankle according to the anatomical location of the
involvement. In 1993, Brodsky and Rouse [1] described one of the classifications,
as well as the prevalence of each type.
Table 2 shows anatomic classification.
4 Diagnosis
The diagnosis begins with anamnesis and physical examination. The patient clini-
cally presents with edema, increased local temperature, and hyperemia in the foot
or ankle [9]. The difference in temperature compared to the contralateral side is
Table 2 Anatomical classification of Charcot’s arthropathy of Brodsky
Type Anatomic location Prevalence %

1 Midfoot 60
2 Hindfoot 25
3A Ankle 10
3B Calcaneal tuberosity 5
Modified from Crim BE, et al. [1]
usually greater than 2 °C [2, 25, 26]. Three quarters of patients, despite the neuropa-
thy, complain of some degree of pain. Deformities in the segment may be present,
as well as ulcerations [2]. Determining the time of onset of signs and symptoms is
important, since the inflammatory phase can last up to 18 weeks [27].
The initial clinical presentation may simulate or even coexist with some differ-
ential diagnoses, especially inflammatory diseases such as gout and infections such
as cellulitis and osteomyelitis [2, 9]. Aspects of the physical examination such as
ulceration, secretion, and wounds may be useful.
Laboratory tests such as CBC, CRP, VHS help in the diagnostic evaluation, but
we must take into consideration that these tests can be negative in patients with DM,
even in the presence of infection. The association between CN and infection exists
and should be considered [9].
The presence of neuropathy contributes to the diagnosis, and its evaluation is
imperative with the Semmes-Weinstein monofilament of 10 g and diapason of
128 Hz [28]. Likewise, vascular conditions must be evaluated (Fig. 3).
The imaging evaluation begins with frontal, lateral, and oblique ankle and feet
X-rays, preferably under load. The segment alignment is evaluated in the exam, but
we look for signs of fractures, dislocations, consolidations, and eventually radiolu-
cency compatible with osteomyelitis, despite the low specificity (50%) for bone
infection of the method. The expected findings follow what was described in the
modified Eichenholtz classification, emphasizing that in stage 0 we should not find
any changes [11, 26].
In Magnetic Resonance Imaging (MRI), at stage 0, it is possible to observe sub-
tle articular incongruities in the tarsal regions and Lisfranc, associated with edema
and bone fractures [24], being considered the imaging exam of choice at this stage,
due to its high diagnostic accuracy [14].
In the diagnostic doubt between CN and chronic osteomyelitis (COM), or even
in its association, we will have the option of nuclear imaging studies and
MRI. Scintigraphy with marked leukocytes presents high sensitivity and specificity
for osteomyelitis [29], but has limited availability and does not have the anatomical
definition of sectional imaging studies.
PET-CT with fluorodeoxyglucose may be useful in evaluating the presence of
osteomyelitis, with a sensitivity of 100% and specificity of 87.5% for bone infection
[30]. Additionally, PET-CT is less susceptible to imaging artifacts caused by metal-
lic material [14], but it is not widely available.
MRI presents high sensitivity, with a slightly lower specificity than PET-CT in
the differentiation of CN with COM [31]. In spite of this, it will provide important
a b c
Fig. 3 Physical examination of a patient at stage 3 of Eichenholtz. (a) Inspection of feet, anterior
view, evidencing the deformity in foot abduction. (b) Standing inspection, medial view, showing
the deformity on the foot plane. Green arrow positioned on the bone eminence sequel the fracture-
dislocations. (c) Plantar view of the foot, blue circles show the points that should be examined with
the 10 g Semmes-Weinstein monofilament test
information regarding the extent and anatomy of the infectious involvement in bone
and soft tissues, assisting in an eventual surgical planning [32].
5 Treatment
The treatment of CN must be defined by the stage of the disease in which the patient
presents. The objective is that the patient’s feet are plantigrade, with adequate align-
ment and stable, for a good load distribution, avoiding ulcerations and reactivation
of arthropathy [14, 26].
In stages 0, 1, and 2, the goal is to prevent the fractures from deviating and the
joints from dislocating [26].
In stage 3, in an aligned and stable foot, we must protect them with appropriate
footwear during walking. Pinzur in 2004 [33] followed 198 patients with midfoot
CN for a period of 6 years and showed that 60% remained adapted to footwear or
orthoses, with acceptable function, without the need for surgical treatment. However,
feet with deformities and/or instabilities that are noncompatible with the use of
orthoses or shoes should be preferably reconstructed [9, 14, 33].
During the inflammatory stages (0, 1, and 2), the approach consists in protecting the
foot, avoiding the progression of the deformity, while the inflammation ceases.
There are three main strategies to achieve this goal: unloading, protected weight-
bearing with a total contact cast, or protected weight-bearing with removable ortho-
ses [9, 14, 26, 34, 35]. Regardless of the approach chosen, it should be maintained
until there are signs of the end of the inflammatory process and complete bone
healing [9].
Radiography will show bone consolidation, but the best way to evaluate the end
of inflammation still generates controversy, and clinical criteria are used as param-
eters, including temperature difference decrease to less than 2 °C [25, 26].
Generally, the time needed for this phase of treatment varies from 8 to
12 weeks [26] but can reach 1 year [36] This long period of time decreases the
adherence of patients to the unloading treatment proposal. For this reason, many
authors propose forms of limb protection that allow the load but avoid the defor-
mity [34, 35].
The use of a removable walker orthoses has proven to be safe, with results com-
parable to the use of full contact plaster or fully unloading, favoring comfort, treat-
ment adherence, and mobility [9, 34], but it is important that the patient understands
the need for use and remains adherent. The fact that it is removable enables skin
care, especially in the case of wounds and associated infections.
Feet and ankles with severe deformities sometimes do not adapt to the volume of
the prefabricated orthosis. In these cases, molding a total contact cast is a safe
option, which allows protected load, without compressing bone prominences caused
by the deformity [9, 35].
The total contact cast has some peculiarities. It must be changed every 14 days
to allow the inspection of the skin coverage and because along its use, the edema of
the limb decreases and the plaster needs to be remodeled. Patients with vascular
pathologies and infections of the limb present contraindication of the use of a total
contact cast [26].
Pharmacological treatment seeking to increase bone mineral density, decrease
healing time, and inflammation time is being investigated [2, 14, 26].
Bisphosphonates, calcitonin, and parathormone have shown effect in modifying
bone metabolism and decreasing temperature of the limb affected by CN, but with-
out presenting better clinical results or faster evolution compared to other nondrug
approaches [2].
Immunomodulatory drugs that interact with the RANKL/OPG system are being
tested, but there is still no clear evidence indicating their use [2].
Although some authors indicate early surgical approach in stages 1 and 2 [37, 38],
surgical treatment is traditionally indicated in the chronic phase, stage 3, in which
the inflammation has subsided and there is less potential for complications, espe-
cially in relation to soft tissue coverage [14].
Surgical treatment will be indicated in patients with deformities that cannot be

adapted to footwear or orthoses, instabilities, or ulcers associated to osteomyelitis.
The objective is to realign the foot in order to make it plantigrade and stabilize it.
When there is infection, most of the time the treatment is performed in a staged
manner [1, 2, 9, 14].
Proper patient selection is of paramount importance, since most are DM patients
with multiple comorbidities. Rettendal D and collaborators [39] retrospectively
evaluated 46 patients with DM and CN who underwent foot reconstruction, in
search of prognostic factors for their postoperative evolution. The authors created a
preoperative prognostic score (Table 3), concluding that patients with score < 4 have
an 85% chance of evolution without ulceration or major amputations and better
surgical prognosis.
The surgical treatment options are varied, depending on the characteristics of
each deformity and patient.
5.2.1 Achilles Lengthening
Deformities resulting from CN in the midfoot and hindfoot often lead to equinus in
these regions. In addition, with tendon imbalance, secondary to motor neuropathy
and calcaneal tendon glycosylation, the deformity increases [40].
Table 3 Preoperative Charcot reconstruction prognostic score
Factor Score
Age (years) <50 0
>50 1
IMC (KG/M2) <30 0
30–35 1
35–40 2
>40 3
Ulcer No 0
Yes 1
Oosteomyelitis No 0
Yes 1
Location Excluding ankle 0
Including ankle 1
Clinically active Arthropathy No 0
Yes 1
Glycated hemoglobin (%) <8 0
8–10 1
>10 2
Total possible 10
Modified Rettedal D, et al. [39]
Procedures for gastrosoleus myotendinous lengthening are used, usually associ-

ated with bone procedures, to correct any associated deformity [14, 40]. Among
them are lengthening of the Achilles tendon, gastrocnemius recession, and the
Baumann procedure.
5.2.2 Exostectomy: Bony Prominence Resection
This procedure consists in resecting the bone prominence caused by fracture-

dislocations and misalignment of the initial CN phases, removing the pressure
point on the soft tissue, therefore decreasing the overload and chance of ulcer-
ation [14].
Exostectomy is indicated when the foot is stable and the volume of bone resec-
tion will not result in instability [41]. When exostosis is associated with an ulcer, the
surgical approach can be done through the ulcer or by an accessory route. The dis-
advantage of the ulcer approach is the potential spread of infectious agents; on the
other hand, it has the advantage of treating the ulcer and deformity with a single
incision (Fig. 4).
In the postoperative period, we should keep the patient without load until there is
complete skin healing.
5.2.3 Arthrodesis: Joint Fusion
Arthrodesis is indicated in patients with rigid deformities of the foot or ankle not
adaptable to footwear or orthoses [33]. Ulcers appear due to poor load distribution
or in cases with gross joint instability [26]. Due to the poor bone quality typical of
CN, conventional bone fixation techniques are more prone to failure in these cases
[1]. For this reason, Sammarco described the concept of superconstructs [42], based
on four principles:
• Fusions should be extended to joints and bones not affected by the CN in order
to promote better quality bone fixation.
• Bone resection in the preparation of the fusion should be performed in order to
correct the deformity together with a bone shortening, to decrease the tension in
the soft tissue envelope and its possible complications.
• Choose the most robust synthesis material possible, as long as it is tolerated by
the skin coverage.
• Position the fixation material in order to obtain the greatest possible mechanical
advantage of the construct.
Following these principles of a superconstruct, we will have the following fixa-
tion options.
Fig. 4 Example of plantar exostectomy. (a) Aspect of the plantar region, with ulcer in the midfoot.
(b) Radiography in profile of the foot, showing stable dislocation fractures in the midfoot, with
plantar exostosis compatible with the ulcer. (c) Final aspect of plantar exostectomy, with complete
resection of the plantar bone volume
5.2.4 Plantar Plate
The fixation of the arthrodesis with the aid of a plantar plate adds the mechanical
benefit of the plate positioned at the tension region, which transforms the plantar
tension forces into dorsal compression [1, 14]. Mainly used for the medial arch
stabilization, the plates can be fixed in the metatarsals, which have normally good
bone quality.
The principle of this construct is absolute stability, so it is necessary to position
the plantar plate with a high number of screws, with some form of compression
through the plate. Adding compressive axial screws through the fused joints
increases the construct stability. The disadvantage of this method is the amount of
dissection and desperiostization required for the plantar approach [1, 42, 43].
The locking plates have a mechanical advantage related to the fact that the screw
heads lock to the plate itself, providing greater stability to the constructs, even posi-
tioned outside the plantar region [9, 42]. These plates are low profile (causing less
impact on the soft tissue envelope) and moldable, having a better adaptation to the
foot anatomy. Even so, the association of some axial compression mechanism is
desired (Figs. 5 and 6).
Fig. 5 Medial column fusion with locking plate and joint screws. Images above: preoperative with
the deformity. Images below: 1 month post-op
5.2.5 Beaming Screws
Axial screw is an intramedullary fixation obtained with long wide screws

(5.0/6.0/7.0/8.0 mm) [40], cannulated or solid, usually crossing the medullary cav-
ity of the metatarsals up to the hindfoot [1].
As their purpose is to fix joints arthrodesis, joint preparation is necessary. This
approach can be done with smaller accessory pathways, damaging less soft tissue
envelope.
Its fixation can be done in a less invasive way, decreasing the aggression of
extensive dissection when plates are used. The point of entry of the axial screw is
most commonly located at the head of the metatarsals [40]. Small accessory path-
ways are made on the joints that will be fused to remove their cartilage, limiting the
surgical lesion to the soft tissue envelope [1, 40]. Some authors fix in the posterior
to anterior direction, without damaging the metatarsophalangeal joint (Fig. 7).
Although it is not a screw, the intramedullary retrograde tibio-talo-calcaneous
nail works with the same mechanical concept, especially if it has a compression
mechanism (Fig. 8).
There is still controversy over which form of fixation is mechanically more rigid,
the plantar plate or the axial screw. Simonik M and collaborators [44] in 2018 car-
ried out a biomechanical study with five pairs of body feet, evaluating the properties
Fig. 6 Tibiotalocalcaneal arthrodesis with medial and lateral blocked plate associated with trac-
tion screws. Images above: preoperative with the deformity. Images below: postoperative 6 weeks
Fig. 7 Arthrodesis of the midfoot and hindfoot, fixed with axial beaming screws
of the axial screw construction (cannulated 7.0) compared to the plantar plate
(3.5 mm non-locking plate). No statistical differences were observed regarding
stiffness and strain on the dorsal and plantar surfaces, but the screw tolerated a
greater load before failure and proved to be more robust.
On the other hand, Pope EJ and collaborators [45] in 2013 performed a biome-
chanical study on seven pairs of cadaver feet, compared the stability of the con-
struction with 5.0 intramedullary screw and third tube non-locking plate applied on
the plantar face. They showed no biomechanical differences between the two
methods.
The conventional postoperative protocol for both fixation techniques is to keep
the patient non-weight-bearing for 10 to 12 weeks postoperatively, protected with a
cast or a removable orthosis [40]. The advantage of the orthosis is the possibility to
initiate early mobility of the remaining joints and muscle strengthening. Considering
that the fixations are stable enough, some authors propose to start the load ear-
lier [14].
5.2.6 External Fixator
The External Fixator (EF) is an option in the correction of foot and ankle deformi-
ties of the CN. In cases of osteomyelitis, where bone resection is necessary, the EF
can be positioned to begin the correction of the deformity until the end of infection
treatment [46].
In situations without infection, it is also possible to perform the correction with
EF, including increasing the construct stability by associating axial beaming
screws [40].
Fig. 8 Panarthrodesis. Example of tibiotalocalcaneal fixation with an intramedullary retrograde

nail in addition to talonavicular and calcaneocuboid stabilization. Images above: preoperative.
Images below: 1 week post-op
The surgery can be performed in two stages. In the first stage, the circular exter-
nal fixator is positioned; it allows a gradual correction of the ankle and foot position.
Often Achilles lengthening is necessary to correct hindfoot equinus. In cases of
severe deformities, it is possible to perform osteotomies at the apex of the deformity
to provide a more accurate correction. In this aspect, the use of hexapod presents
advantages for its precision (accuracy of 0.7° and 2 mm of correction) [40]. The
second stage consists in preparing the joints to be arthrodesed and fixing them with
intramedullary screws with the external fixator in place. One of the advantages of
this sequence is that the foot has been previously aligned with the EF, and then fixed
with axial screws percutaneously [40]. These two stages can be done in an inverse
order in cases of small deformities and good soft tissue condition. The advantage is
that the external fixator wires do not hinder the previously positioned screws path,
something that frequently happens when the external fixator is positioned before
the screws.
5.2.7 Amputation
The primary objective of the treatment of the foot’s CN is to preserve a functional

limb, allowing for walking, free of ulcers and infection.
Limb preservation may not be possible in extreme cases with great bone loss,
intense instability and deformity, extensive infection, failure of previous surgical
treatment or even patients with multiple comorbidities [26]. In these situations,
amputation should be considered and planned in a way that preserves the highest
possible degree of function.
6 Complications
CN is a pathology that limits mobility, increases morbidity, and worsens the quality
of life of patients. Proper treatment minimizes this but presents complications.
Exostectomies present a recurrence rate of ulceration in 25% of cases, improving to
10% when associated with Achilles tendon lengthening [47]. Lowery NJ and col-
laborators [47] published a systematic review in 2012 of 96 articles, with 1143
patients with CN associated with DM who underwent surgical procedures for treat-
ment. The authors show a nonunion rate of 22.4% and a postoperative amputation
rate of 1.2%. However, Safavi OS and collaborators [48] show a rate of postopera-
tive amputation of 6%. Grant WP and collaborators [49] in a retrospective series of
50 CN cases treated surgically obtained 26% of infection in the EF wire path, 18%
of dehiscence, and 16% of osteomyelitis.
References
1. Crim BE, Lowery NJ, Wukich DK. Internal fixation techniques for midfoot Charcot neu-
roarthropathy in patients with diabetes. Clin Podiatr Med Surg [Internet]. 2011;28:673–85.
Available from: https://doi.org/10.1016/j.cpm.2011.08.003.
2. Dardari D. An overview of Charcot’s neuroarthropathy. J Clin Transl Endocrinol. 2020;22
3. Labovitz JM, Shofler DW, Ragothaman KK. The impact of comorbidities on inpatient Charcot
neuroarthropathy cost and utilization. J Diabetes Complications [Internet]. 2016;30:710–715.
Available from: https://doi.org/10.1016/j.jdiacomp.2016.01.004.
4. Chaudhary S, Bhansali A, Rastogi A. Mortality in Asian Indians with Charcot’s neuroarthropa-
thy: a nested cohort prospective study. Acta Diabetol [Internet]. 2019;56:1259–64. Available
from: https://doi.org/10.1007/s00592-019-01376-9.
5. Singh D, Gray J, Laura M, Reilly MM. Charcot neuroarthropathy in patients with Charcot Marie
Tooth Disease. Foot Ankle Surg [Internet]. 2020. Available from: https://doi.org/10.1016/j.
fas.2020.11.005.
6. Gupta R. A short history of neuropathic arthropathy. Clin Orthop Relat Res [Internet]. 1993
[cited 2020 Dec 17];43–9. Available from: https://pubmed.ncbi.nlm.nih.gov/8222448/.
7. Jordan WR. Neuritic manifestations in diabetes mellitus. Arch Int Med. 1936;57:307–66.
8. Johnson-Lynn SE, McCaskie AW, Coll AP, Robinson AHN. Neuroarthropathy in diabetes:
pathogenesis of charcot arthropathy. Bone Joint Res. 2018;7:373–8.
9. Dodd A, Daniels TR. Charcot neuroarthropathy of the foot and ankle. J Bone Joint Surg Am.
2018;100:696–711.
10. Frykberg RG, Belczyk R. Epidemiology of the Charcot foot [Internet]. Vol. 25, Clinics in
podiatric medicine and surgery. Clin Podiatr Med Surg; 2008 [cited 2020 Dec 17]. p. 17–28.
Available from: https://pubmed.ncbi.nlm.nih.gov/18165108/.
11. O’Loughlin A, Kellegher E, McCusker C, Canavan R. Diabetic charcot neuroarthropathy: prev-
alence, demographics and outcome in a regional referral centre. Ir J Med Sci. 2017;186:151–6.
12. Schneekloth BJ, Lowery NJ, Wukich DK. Charcot neuroarthropathy in patients with dia-
betes: an updated systematic review of surgical management. J Foot Ankle Surg [Internet].
2016;55:586–90. Available from: https://doi.org/10.1053/j.jfas.2015.12.001
13. Yates TH, Cooperman SR, Shofler D, Agrawal DK. Current concepts underlying the
pathophysiology of acute Charcot neuroarthropathy in the diabetic foot and ankle. Expert
Rev Clin Immunol [Internet]. 2020;16:839–45. Available from: https://doi.org/10.108
0/1744666X.2020.1804869.
14. Botek G, Figas S, Narra S. Charcot neuroarthropathy advances: understanding pathogenesis
and medical and surgical management. Clin Podiatr Med Surg [Internet]. 2019;36:663–84.
Available from: https://doi.org/10.1016/j.cpm.2019.07.002.
15. Petrova NL, Foster AVM, Edmonds ME. Calcaneal bone mineral density in patients with
Charcot neuropathic osteoarthropathy: differences between type 1 and type 2 diabetes. Diabet
Med [Internet]. 2005 [cited 2020 Dec 18];22:756–61. Available from: https://pubmed.ncbi.
nlm.nih.gov/15910628/.
16. Barwick AL, de Jonge XAKJ, Tessier JW, Ho A, Chuter VH. The effect of diabetic neuropathy
on foot bones: a systematic review and meta-analysis. Diabet Med [Internet]. 2014 [cited 2020
Dec 18];31:136–47. Available from: https://pubmed.ncbi.nlm.nih.gov/24151985/.
17. Jeffcoate WJ, Game F, Cavanagh PR. The role of proinflammatory cytokines in the cause of
neuropathic osteoarthropathy (acute Charcot foot) in diabetes. Lancet [Internet]. 2005 [cited
2013 Nov 3];366:2058–61. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16338454
18. Pasquier J, Spurgeon M, Bradic M, Thomas B, Robay A, Chidiac O, et al. Whole-methylome
analysis of circulating monocytes in acute diabetic Charcot foot reveals differentially methyl-
ated genes involved in the formation of osteoclasts. Epigenomics [Internet] 2019 [cited 2020
Dec 18];11:281–96. Available from: https://pubmed.ncbi.nlm.nih.gov/30753117/.
19. Pasquier J, Thomas B, Hoarau-Véchot J, Odeh T, Robay A, Chidiac O, et al. Circulating mic-
roparticles in acute diabetic Charcot foot exhibit a high content of inflammatory cytokines,
and support monocyte-to-osteoclast cell induction. Sci Rep [Internet]. 2017 [cited 2020 Dec
18];7. Available from: https://pubmed.ncbi.nlm.nih.gov/29180664/.
20. Jansen RB, Svendsen OL. A review of bone metabolism and developments in medical treatment
of the diabetic Charcot foot [Internet]. Vol. 32, J Diabetes Complications. Elsevier Inc.; 2018
[cited 2020 Dec 18]. p. 708–12. Available from: https://pubmed.ncbi.nlm.nih.gov/29857955/.
21. Ndip A, Williams A, Jude EB, Serracino-Inglott F, Richardson S, Smyth J V., et al. The
RANKL/RANK/OPG signaling pathway mediates medial arterial calcification in dia-
betic charcot neuroarthropathy. Diabetes [Internet]. 2011 [cited 2020 Dec 18];60:2187–96.
22. Jansen RB, Christensen TM, Bülow J, Rørdam L, Holstein PE, Jørgensen NR, et al. Bone
mineral density and markers of bone turnover and inflammation in diabetes patients with or
without a Charcot foot: an 8.5-year prospective case-control study. J Diabetes Complications
[Internet] 2018 [cited 2020 Dec 18];32:164–70. Available from: https://pubmed.ncbi.nlm.nih.
gov/29196119/.
23. Shibata T, Tada K, Hashizume C. The results of athrodesis of the ankle for leprotic neuroar-
thropathy. J Bone Joint Surg Ser A. 1990;72:749–56.
24. Yu GV, Hudson JR. Evaluation and treatment of stage 0 Charcot’s neuroarthropathy of the foot
and ankle. J Am Podiatr Med Assoc. 2002;92:210–20.
25. Moura-Neto A, Fernandes TD, Zantut-Wittmann DE, Trevisan RO, Sakaki MH, Santos ALG,
et al. Charcot foot: skin temperature as a good clinical parameter for predicting disease out-
come. Diabetes Res Clin Pract. 2012;96:4–7.
26. Pitocco D, Scavone G, Di Leo M, Vitiello R, Rizzi A, Tartaglione L, et al. Charcot
Neuroarthropathy: from the laboratory to the bedside. Curr Diabetes Rev. 2019;16:62–72.
27. Idusuyi OB. Surgical management of Charcot neuroarthropathy. Prosthetics Orthot Int.
2015;39:61–72.
28. The International Working Group on the Diabetic Foot. Diretrizes do IWGDF sobre a pre-
venção e o tratamento de pé diabético [Internet]. 2019. Available from: www.iwgdfguide-
lines.org.
29. Palestro CJ, Mehta HH, Patel M, Freeman SJ, Harrington WN, Tomas MB, et al. Marrow
versus infection in the Charcot joint: Indium-111 leukocyte and technetium-99m sulfur colloid
scintigraphy. J Nucl Med [Internet]. 1998 [cited 2020 Dec 19];39:346–50. Available from:
https://pubmed.ncbi.nlm.nih.gov/9476948/.
30. Zhuang H, Duarte PS, Pourdehand M, Shnier D, Alavi A. Exclusion of chronic osteomyeli-
tis with F-18 fluorodeoxyglucose positron emission tomographic imaging. Clin Nucl Med
[Internet]. 2000 [cited 2020 Dec 19];25:281–4. Available from: https://pubmed.ncbi.nlm.nih.
gov/10750968/.
31. Hastings MK, Johnson JE, Strube MJ, Hildebolt CF, Bohnert KL, Prior FW, et al. Progression
of foot deformity in Charcot neuropathic osteoarthropathy. J Bone Jt Surg - Ser A [Internet].
2013; [cited 2020 Dec 19];95:1206–13. Available from: https://pubmed.ncbi.nlm.nih.
gov/23824389/
32. Höpfner S, Krolak C, Kessler S, Tiling R, Brinkbäumer K, Hahn K, et al. Preoperative imag-
ing of charcot neuroarthropathy in diabetic patients: comparison of ring PET, hybrid PET, and
magnetic resonance imaging. Foot Ankle Int [Internet]. 2004 [cited 2020 Dec 19];25:890–5.
33. Pinzur M. Surgical versus accommodative treatment for charcot arthropathy of the midfoot
[Internet]. Vol. 25, Foot and ankle international. AOFAS – American Orthopaedic Foot and
Ankle Society; 2004 [cited 2020 Dec 19]. p. 545–9. Available from: https://pubmed.ncbi.nlm.
nih.gov/15363375/.
34. Parisi MCR, Godoy-Santos AL, Ortiz RT, Sposeto RB, Sakaki MH, Nery M, et al. Radiographic
and functional results in the treatment of early stages of Charcot neuroarthropathy with a
walker boot and immediate weight bearing. Diabet Foot Ankle [Internet] 2013 [cited 2014 Jun
20];4. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3813827&t
ool=pmcentrez&rendertype=abstract.
35. Pinzur MS, Lio T, Posner M. Treatment of Eichenholtz stage I Charcot foot arthropathy with a
weight-bearing total contact cast. Foot Ankle Int. 2006;27:324–9.
36. Christensen TM, Gade-Rasmussen B, Pedersen LW, Hommel E, Holstein PE, Svendsen
OL. Duration of off-loading and recurrence rate in Charcot osteo-arthropathy treated with less
restrictive regimen with removable walker. J Diabetes Complications [Internet]. 2012 [cited
2020 Dec 19];26:430–4. Available from: https://pubmed.ncbi.nlm.nih.gov/22699112/.
37. Sella EJ, Barrette C. Staging of Charcot neuroarthropathy along the medial column of the foot
in the diabetic patient. J Foot Ankle Surg [Internet]. [cited 2013 Mar 31];38:34–40. Available
from: http://www.ncbi.nlm.nih.gov/pubmed/10028468.
38. Simon SR, Tejwani SG, Wilson DL, Santner TJ, Denniston NL. Arthrodesis as an early alter-
native to nonoperative management of Charcot arthropathy of the diabetic foot. J Bone Jointt
Surg Ser A [Internet] 2000 [cited 2020 Dec 19];82:939–50. Available from: https://pubmed.
ncbi.nlm.nih.gov/10901308/
39. Rettedal D, Parker A, Popchak A, Burns PR. Prognostic scoring system for patients undergoing
reconstructive foot and ankle surgery for Charcot neuroarthropathy: the Charcot reconstruc-
tion preoperative prognostic score. J Foot Ankle Surg [Internet]. 2018;57:451–5. Available
from: https://doi.org/10.1053/j.jfas.2017.10.021.
40. LaPorta GA, D’Andelet A. Lengthen, alignment, and beam technique for midfoot Charcot
neuroarthropathy. Clin Podiatr Med Surg [Internet]. 2018;35:497–507. Available from: https://
doi.org/10.1016/j.cpm.2018.05.008.
41. Laurinaviciene R, Kirketerp-Moeller K, Holstein PE. Exostectomy for chronic midfoot plantar
ulcer in Charcot deformity. J Wound Care [Internet]. 2008 [cited 2013 Oct 28];17:53–5, 57–8.
Available from: http://www.ncbi.nlm.nih.gov/pubmed/18389829.
42. Sammarco VJ. Superconstructs in the treatment of charcot foot deformity: plantar plating,
locked plating, and axial screw fixation. Foot Ankle Clin [Internet]. 2009 [cited 2013 Apr
8];14:393–407. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19712882.
43. Connors JC, Hardy MA, Kishman LL, Botek GG, Verdin CJ, Rao NM, et al. Charcot patho-
genesis: a study of in vivo gene expression. J Foot Ankle Surg [Internet] 2018 [cited 2020 Dec
18];57:1067–72. Available from: https://pubmed.ncbi.nlm.nih.gov/30368423/.
44. Simonik MM, Wilczek J, LaPorta G, Willing R. Biomechanical comparison of intramedullary
beaming and plantar plating methods for stabilizing the medial column of the foot: an in vitro
study. J Foot Ankle Surg [Internet]. 2018;57:1073–9. Available from: https://doi.org/10.1053/j.
jfas.2018.03.043.
45. Pope EJ, Takemoto RC, Kummer FJ, Mroczek KJ. Midfoot fusion: a biomechanical compari-
son of plantar planting vs intramedullary screws. Foot Ankle Int. 2013;34:409–13.
46. Conway JD. Charcot salvage of the foot and ankle using external fixation [Internet]. Vol. 13,
Foot and ankle clinics. Foot Ankle Clin; 2008 [cited 2020 Dec 19]. p. 157–73. Available from:
https://pubmed.ncbi.nlm.nih.gov/18328419/.
47. Lowery NJ, Woods JB, Armstrong DG, Wukich DK. Surgical management of Charcot neuro-
arthropathy of the foot and ankle: a systematic review. Foot Ankle Int [Internet]. 2012 [cited
2013 Oct 28];33:113–21. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22381342.
48. Shazadeh Safavi P, Jupiter DC, Panchbhavi V. A systematic review of current surgical
interventions for Charcot neuroarthropathy of the midfoot. J Foot Ankle Surg [Internet].
2017;56:1249–1252. Available from: https://doi.org/10.1053/j.jfas.2017.06.011
49. Grant WP, Garcia-Lavin SE, Sabo RT, Tam HS, Jerlin E. A retrospective analysis of 50 con-
secutive Charcot diabetic salvage reconstructions. J Foot Ankle Surg [Internet]. 2009 [cited
2020 Dec 19];48:30–8. Available from: https://pubmed.ncbi.nlm.nih.gov/19110157/
Nerve Entrapment Syndromes
of the Lower Limbs
Marcelo Pires Prado and Guilherme Honda Saito
1 Introduction
Compressive pathologies of peripheral nerves are important causes of lower limb

pain in the general population. Specifically, in athletes, the incidence is up to 15%.
This syndrome should always be on the list of differential diagnoses, since the delay
in diagnosis can cause worsening on pain, difficulties to maintain activities, and
irreversible lesions [18].
The clinical complaint is usually nonspecific, and deep burning pain may occur,
eventually associated with paresthesia, dysesthesias, shocks, numbness, and muscle
weakness. The Tinel sign (pain and shock sensation to the digital percussion at the
site of peripheral nerve compression) is individually the most specific sign [18].
Due to this irregularity of clinical presentation and variations in physical examina-
tion, these pathologies have often a delay in the diagnosis [8].
The electromyographic study assists in the diagnosis but may be negative due to
intermittent compression. Imaging tests can help in the location of compression, in
the diagnosis of extrinsic compressions, and through indirect signs such as muscle
atrophies secondary to denervation.
Differential diagnoses affecting peripheral nerves, but not related to peripheral
compressions, should be remembered. Myopathic diseases include inflammatory
myopathies (polymyositis, dermatomyositis), endocrine myopathies (toxic or drug-
induced), muscular dystrophies, myotonic dystrophy, acid maltase deficiency,
M. P. Prado (*)
Department of Orthopaedics, Hospital Israelita Albert Einstein, Sao Paulo, SP, Brazil
Hospital Israelita Albert Einstein, Foot and Ankle Department, Sao Paulo, SP, Brazil
G. H. Saito
Department of Orthopaedics, Hospital Sírio Libanês, Sao Paulo, SP, Brazil

Switzerland AG 2022
1006 M. P. Prado and G. H. Saito
benign congenital myopathies (myotubular, nemaline), neuromuscular blockage

pathologies such as myasthenia gravis, Lambert Eaton syndrome, Guillain Barré
syndrome, and chronic demyelinating polyneuropathy. Neurogenic pathologies
include diabetic neuropathy, lumbar root lesions, motor neuron diseases, and spinal
muscle atrophy. Other causes such as muscle atrophies secondary to joint patholo-
gies and upper motor neuron lesions should also be remembered [17].
Other pathologies that often cause pain in the lower limbs, especially in athletes,
should also be searched and ruled out. Such pathologies include medial tibial stress,
stress bone injuries, popliteal functional artery compression syndrome, and exercise-
related compartment syndromes [15].
2 Compressive Pathologies of the Lower Limbs
2.1 Common Peroneal Nerve
The common peroneal nerve is a sensory and motor nerve with contributions from
L4 to S2 roots. It is a branch of the sciatic nerve, just above the knee, supplying the
short head of the biceps femoral muscle. It curves laterally and distally, passing
through an osteofibrous tunnel at the fibular neck, deep to the origin of the peroneus
longus muscle (fibular tunnel), where it is divided into superficial and deep peroneal
nerve and lateral sural skin branch.
The most common site of irritation of this nerve is in the neck of the fibula, in its
subcutaneous trajectory. It may be affected by internal compressions (intra and
extra-neural masses), external compressions (pneumatic cuffs), traction (associated
to ankle inversion traumas), and local direct trauma, the most common cause of this
neuropathy.
The prognosis, in the great majority of the cases, is satisfactory, showing no
signs of severity in most patients [19]. The clinical presentation includes alteration
of sensitivity in the lateral aspect of the leg and dorsum of the foot, in addition to
weakness of the extensor and evertor musculature of the foot. It may evolve to the
classic drop foot, and consequent alteration of the gait pattern. Tinel at the neck of
the fibula may be present in up to 97% of patients [6].
When compressive pathologies of the common peroneal nerve are suspected, the
imaging evaluation includes radiographs to assess the presence of bone alterations
that may cause compression, ultrasonography, and magnetic resonance imaging to
assess local soft tissue masses. Electroneuromyography can be also helpful in iden-
tifying the lesion, its severity and location [16]. About 38% of cases are considered
idiopathic, that is, without known cause [24].
Clinical treatment includes mainly removal of extrinsic irritant factors (position
of crossing the legs or stockings with high elastic at the level of the fibula neck). Full
or partial recovery is expected depending on the nerve injury extent. The prognosis
in the case of neuropraxia is excellent with nonsurgical treatment [31].
Nerve Entrapment Syndromes of the Lower Limbs 1007
In the case of severe motor and sensory deterioration (>50% conduction delay)
or when there is no recovery within 4–6 months from the injury, surgical treatment
should be indicated.
In open lesions, wound should be clean and nerve repaired within 72 hours, to
improve chances of recovery.
Masses that cause extrinsic compression should be removed in the usual way,
and intra-nervous masses (schwannomas and neurofibromas) should be approached
by specialists so as not to aggravate the nerve lesion. In cases of idiopathic compres-
sive neuropathy, early decompression shows, in a series of cases, superior results
with better motor recovery [29]. On the other hand, open lesions should be surgi-
cally addressed and corrected in the acute phase of the lesion [22].
Decompression is performed through a curvilinear incision that follows common
peroneal nerve route, starting at the fibular neck with an anteromedial extension.
Release of the common peroneal nerve starts at the fibular neck (easily identified
through palpation), following the nerve into the fibular tunnel (peroneal longus fas-
cia or posterior intermuscular septum). Then release should also include the anterior
intermuscular septum (septum between anterior and lateral compartments). This
septum is exposed through retraction of the peroneus muscle belly [22].
2.2 Solear Arch Syndrome
It refers to the compression of the tibial nerve in the proximal portion of the leg,
when it passes under a fibrous arch at the origin of the soleus muscle [32]. Patients
complain of pain and discomfort in the calf. In cases of failure of surgical treatment
of a patient diagnosed with tarsal tunnel syndrome, this compressive pathology
should be remembered as a differential diagnosis.
Clinically, pain is noted on palpation of the proximal portion of the leg, 9 cm
from the popliteal fold. There may be alteration of sensitivity in the sensory inner-
vation territory of tibial nerve and weakness of the flexor hallucis longus.
Electroneuromyography is frequently not useful. High-resolution magnetic reso-
nance imaging may show suggestive changes at the site of compression.
Conservative treatment modalities include removal of extrinsic causes of com-
pression, changes in exercise pattern, anti-inflammatory drugs, and infiltrations.
Surgical treatment with release of compression tissue and adhesions shows satisfac-
tory results without major associated complications.
2.3 Deep Peroneal Nerve
After the common peroneal nerve division, the deep peroneal nerve turns around the
fibular neck and passes to the anterior leg compartment through a septum between the
lateral and anterior compartments, located 3–4 cm distally to the fibular neck (place
of possible compression). It innervates the anterior tibial muscle (AT), extensor digi-
torum longus (ELD), extensor hallucis longus (ELH), and peroneus tertius. The EHL
crosses this nerve approximately 3 cm above the anterior ankle joint line. The deep
peroneal nerve runs its course between the EHL and the EDL, under the upper exten-
sor retinaculum, until it is divided into medial and lateral branches. The medial
branch follows the dorsal pedis artery and is responsible for the sensitivity of the first
interdigital web space. The lateral branch innervates the extensor digitorum brevis
muscle. This branch passes under the two bands of the lower extensor retinaculum.
The most common site of deep peroneal nerve compressions is under the upper
extensor retinaculum, known as anterior tarsal tunnel syndrome. This space con-
tains the dorsal pedis artery and vein, the deep peroneal nerve, besides the peroneus
tertius, anterior tibialis, EDL, and EHL. Among the causes of compression are
space-occupying lesions in the anterior ankle (osteophytes, ganglions, synovitis, or
low myotendinous insertion), local trauma, and the use of compressive shoes.
Clinically, the patient presents with uncharacteristic pain in the anterior ankle
and foot dorsum, and there may be a sensitivity change on the first interdigital space
or weakness of toes extension. The discomfort may be aggravated by forced plantar
flexion of the ankle, which stretches the deep peroneal nerve. Tinel’s sign may be
present on the nerve pathway. The most common differential diagnosis is the chronic
compartment syndrome of the anterior leg compartment.
Imaging investigation and anesthetic blocks may help in identifying the cause
and location of compression. Electroneuromyography should be performed to eval-
uate the location of the compression. Ultrasonography and magnetic resonance
imaging can also be useful in diagnosis and location of extrinsic compression fac-
tors (Figs. 1 and 2).
Conservative treatment is initiated with ankle repositioning, use of footwear that
reduces extrinsic compression, topical or systemic anti-inflammatory drugs and
analgesics, and infiltration with lidocaine or corticoids [10].
If conservative treatment fails, surgical release should be indicated, with care
being taken to remove all possible causes of compression, including retinaculum
release. The prognosis of this procedure is very good, with good and excellent
results in up to 80% of patients, once the proper diagnosis has been made [2].
2.4 Superficial Peroneal Nerve
After the division of the common peroneal nerve, the superficial peroneal nerve
enters the lateral compartment, and crosses the crural fascia on the anterolateral side
of the leg 9–14 cm above the lateral malleolus, the crural tunnel. It innervates the
peroneal (brevis and longus) muscles. As it approaches the anterior ankle, it divides
into the medial and intermediate dorsal cutaneous branch, sensory branches of the
foot dorsum.
The most common cause of neuropathy of this nerve are repetitive traumas and
ankle sprains [21], related to the practice of physical activities (hockey, tennis,
Fig. 1 Axial T2-weighted

magnetic resonance
imaging section showing a
large synovial cyst in the
path of the deep peroneal
nerve just after the
common peroneal nerve
division, causing
neuropathic pain and
weakness of the ankle and
toe extensors
Fig. 2 T2-weighted MRI

axial view, from the
proximal portion of the leg,
showing the same synovial
cyst shown in Fig. 1
soccer). Compression at the crural tunnel by muscle hernias, local tumors, or just
local changes of the fascia can cause irritation of this nerve. The chronic lateral
compartment syndrome may simulate the symptoms of superficial peroneal nerve
compression, as well as compressive pathologies of L5. Iatrogenic lesions should be
remembered by frequency (lateral portal of anterior ankle arthroscopy or surgical
incisions for ankle fractures).
The most common complaint is related to pain, burning, and tingling on the lat-
eral distal leg and foot dorsum. The typical pain pattern is located in the distal lateral
leg portion, with or without a burning sensation. It is usually aggravated by activity.
Diagnostic investigation includes imaging examinations such as ultrasonography
and magnetic resonance imaging. The dynamic character of ultrasonography can be
useful, since the muscle hernias can disappear at rest. The electroneuromyography
can also be useful in identifying the cause and location of neuropathy.
The treatment of superficial peroneal nerve neuropathy will depend on its cause.
Conservative treatment consists of shoe adjustment, physiotherapy to strengthen the
peroneal muscles and insoles. Infiltrations can bring symptoms relief. If conserva-
tive treatment fails, surgical treatment should be employed. Decompression through
localized fasciotomy and neurolysis present success rates of up to 80% [28]. If
chronic ankle instability and chronic lateral compartmental syndrome are associ-
ated, these should be treated as well.
2.5 Saphenous Nerve
The saphenous nerve is a cutaneous branch of the femoral nerve, with fibers of L3
and L4, following distally through the inner face of the thigh through the adductor
canal together with the artery and femoral vein. In the lower portion of the canal, it
crosses the sartorius muscle fascia, dividing at this level into an infrapatellar branch
and a descending sartorius branch. The infrapatellar branch innervates the skin on
the anteromedial side of the knee. The sartorius branch follows up to the foot as the
saphenous nerve, following the great saphenous vein, up to the anteromedial surface
of the ankle, innervating the skin of the medial surface of the leg, region over the
medial malleolus and the medial surface of the foot.
The saphenous nerve is most commonly affected in the region of the adductor
canal, due to direct trauma (dislocation of the patella), extrinsic compressions,
scars, irritation related to cycling or rowing, and iatrogenically when the saphenous
vein is dissected for revascularization procedures.
The most common symptom is vague pain on the medial surface of the knee and/
or the medial surface of the foot and leg. Diagnostic imaging investigation can help
in situations related to trauma or extrinsic compression, but the electrophysiological
study in most cases is negative.
Conservative treatment with local protection, and infiltrations can be performed.
In the failure of conservative treatment, decompression, neurolysis, or even neurec-
tomies may be indicated. The resection of neuromas can cause changes of sensitiv-
ity in the territory of this nerve.
2.6 Sural Nerve
The sural nerve receives contribution from the tibial nerve (medial sural cutaneous
branch) and common peroneal nerve (lateral sural cutaneous branch) in 80% of the
population [23]. The nerve begins in the distal portion of the popliteal fossa, passes
between the gastrocnemius heads and through the deep fascia in the middle portion
of the leg, to its subcutaneous trajectory. At the ankle, its path is posterior to the
lateral malleolus (between the Achilles tendon and fibula), where it innervates the
skin of the lateral aspect of the calcaneus and foot. Distal to the lateral malleolus, it
emits calcaneal branches, responsible for the sensation on the lateral side of the heel.
The compression of the sural nerve is more common in athletes, related to extrinsic
compression (shoes), due to trauma such as ankle sprains, and iatrogenic lesions after
foot and ankle surgery. Iatrogenic causes are relatively common, especially when inci-
sions are made on the lateral side of the hindfoot. Symptoms include diffuse burning
or pain and changes in sensitivity in this nerve territory. Tinel’s sign may be present.
Investigation with electroneuromyography can assist in site diagnosis and cause
of compression. Conservative treatment should be instituted initially, and in its fail-
ure neurolysis or neurectomy can be performed.
2.7 Tibial Nerve
It is the terminal branch of the sciatic nerve, with roots from L4 to S3. It begins in
the popliteal fossa and passes deeply into the gastrocnemius and soleus, entering the
deep posterior compartment of the leg. It traverses in the posterior and medial ankle,
through the tarsal tunnel, giving then origin to the calcaneal branch. It divides then
into medial and lateral plantar nerve, which are responsible for the plantar cutane-
ous innervation of the foot. It innervates the muscles of the posterior compartments
of the leg (superficial and deep compartments) and the intrinsic plantar musculature
of the foot.
The most common site of compression of this nerve is the tarsal tunnel, a space
limited medially by the tibia, talus, and calcaneus, and laterally by the flexor reti-
naculum (lancinate ligament) as its roof. The tarsal tunnel contains the tibial nerve,
the posterior tibial tendon, flexor digitorum longus (FDL) tendon, flexor hallucis
longus (FHL), and the posterior tibial artery and vein. Compressions occur mainly
in athletes, and between the causes are valgus alignment of the hindfoot, direct
compression by space-occupying lesions inside the tarsal tunnel (tumors, cysts,
varicose veins), extrinsic compressions (shoes), plantar fasciitis, and direct trauma.
However, in more than 50% of cases the compression cause in not identified, being
classified as idiopathic [14, 32].
The patients present plantar and medial pain in the foot and ankle, with burning
sensation, shocks, and alteration on sole of the foot sensibility (Fig. 3). The symp-
toms worsen with the activity and when the patient remains in orthostatic position
for a prolonged period of time. Tinel’s sign may be present, as well as motor altera-
tions of the foot intrinsic musculature.
The evaluation of the hindfoot alignment should be performed. Ultrasonography
can be very useful in the diagnosis and identification for most lower limb compres-
sive pathologies [3]. Magnetic resonance imaging is another option, and is capable
of demonstrating a compressive cause in up to 80% of patients with this syndrome
(Fig. 4) [9]. On the other hand, the electromyographic study has a high rate of false
positive results, and it should be interpreted using caution [20].
Fig. 3 Illustration
showing the tarsal tunnel
area in red, the most
common location of tibial
nerve compression
Fig. 4 Posterior tibial

nerve cyst in the tarsal
tunnel causing a tarsal
tunnel syndrome
photo demonstrating the
tibial nerve and its
branches (calcaneal, lateral
plantar, and medial plantar
nerves)
Conservative treatment includes immobilization, use of analgesics and anti-

inflammatory drugs, insoles to partially correct a hindfoot valgus, and muscle rebal-
ancing exercises. Corticoid infiltrations guided by ultrasonography can help as well.
Surgical treatment with tarsal tunnel decompression is reserved for cases of fail-
ure of conservative treatment.
The decompression is performed through a posteromedial incision, following the
nerve trajectory, and includes release of the retinaculum (lancinate ligament – prox-
imal tunnel) and the tibial nerve and its branches (distal tunnel), taking care to
release even the nerve to the abductor digiti minimi, which can be compressed at the
medial edge of the plantar fascia (Fig. 5). The results are good, especially when a
cause is identified and treated (extrinsic compression). In so-called idiopathic cases,
the prognosis is less favorable [7].
2.8 First Branch of the Lateral Plantar Nerve: Baxter Nerve
It is the motor nerve for the abductor digiti minimi muscle or calcaneal inferior
nerve. It originates in most cases from the lateral plantar nerve, but it can be a direct
branch of the tibial nerve as well, in the lower portion of the tarsal tunnel. It tra-
verses into the space between the quadratus plantae muscle and the abductor hallu-
cis muscle. It innervates the quadratus plantae, flexor digitorum brevis (FDB), and
the abductor digiti minimi muscles.
It can be a source of pain in athletes, especially runners, dancers, and gymnasts.
It should be considered in the differential diagnosis of sub-calcaneal pain in ath-
letes, along with plantar fasciitis, calcaneal fat pad atrophy, apophysitis, and calca-
neal stress fractures [4]. The nerve is most commonly compressed between the
abductor hallucis fascia and the quadratus plantae muscle, but compression may
also occur between the FDB and the calcaneus.
Clinically, the patient typically presents with medial plantar pain in proximal
portion of the plantar fascia. Tinel’s sign may be present, along with burning pain
irradiated to the lateral and central portion of the hindfoot. Characteristically, the
patient complains of tenderness at a point located 5 cm distal from the posterior
edge of the calcaneus at the transition of the dorsal and plantar skin on the medial,
central, and/or lateral surface of the heel. Causes of compression include hypermo-
bile foot, abductor hallucis, and quadratus plantae hypertrophy, presence of acces-
sory muscles, and thickening of the proximal portion of the plantar fascia (Fig. 6)
[12]. Electroneuromyography is often able to detect focal neurologic abnormalities,
but the exact sensitivity of the examination is uncertain [27]. Magnetic resonance
imaging may show signs of atrophy of the abductor digiti minimi.
Conservative treatment with orthoses, arch-supported insoles, and strengthening
of the plantar musculature has satisfactory results in up to 90% of patients, and
Fig. 6 T1-weighted
sagittal resonance imaging,
showing thickening of the
proximal portion of the
plantar fascia, causing
symptoms related to Baxter
nerve compression
the release of Baxter’s
nerve
should be attempted for a period of 12–20 months [30]. In case of failure of conser-
vative treatment, the release of the nerve associated with plantar fasciotomy has a
satisfaction rate higher than 85% [11]. The procedure can be performed openly
(Fig. 7) or arthroscopically.
2.9 Medial Plantar Nerve
After passing through a single osteofibrous tunnel in the tarsal canal, the medial
plantar nerve follows distally along the medial surface of the foot, between the
abductor hallux muscle and the FDL. At the height of Henri’s knot, it is divided into
digital branches for the three medial toes. It is responsible for the motor innervation
of the abductor hallucis (AbH), flexor hallucis brevis (FHB), FDB, and first lumbri-
cal. It is responsible for the sensation in the medial plantar portion of the forefoot,
the two medial toes, and the medial aspect of the third toe.
The compressive pathology that affects this nerve is known as the runner foot. It
occurs most commonly at the level of Henri’s knot. It may occur by extrinsic com-
pression (raised arch insole), or intrinsic (between the AbH fascia and its origin in
the calcaneus, by AbH hypertrophy, running, hyperpronation, or hindfoot valgus)
[25]. Iatrogenic lesions of this nerve related to previous surgical procedures in the
medial plantar region of the foot should be remembered as well.
Compression causes neuropathic pain in the arch, usually related to exercises,
with irradiation to the medial toes and changes in sensitivity in its territory. The
symptom worsens with the forefoot support, which tensions or compresses the
AbH. Investigation with magnetic resonance imaging is mandatory and can identify
atrophy of the AbH.
Conservative treatment should be attempted initially, with use of anti-
inflammatory drugs, infiltrations, physiotherapy, changes in training pattern, and
Fig. 8 Image of surgical

dissection of large
neuroma of the medial
plantar nerve caused by
iatrogenic lesion in
previous surgery to obtain
the flexor hallucis longus
tendon, which was used to
reconstruct a calcaneal
tendon lesion
correction of the hindfoot alignment with shoes or insoles. If conservative treatment

fails, surgical decompression is indicated through a medial incision in the foot, with
release of the medial plantar nerve up to Henri’s knot (Fig. 8). The literature is
scarce in the description of the results of this treatment.
2.10 Medial Digital Nerve of the Hallux
The so-called Joplin neuritis occurs by irritation of the medial digital branch of the
hallux at the level of the medial sesamoid or hallux metatarsophalangeal joint,
where it exits the fascia of the AbH. On physical examination, local compression
causes pain. Often this pathology can be confused with medial sesamoiditis.
Conservative treatment is usually indicated, with the use of silicone cushioning in
footwear to relieve the overload. When it fails, surgical release by medial approach
is recommended [13]. This neuritis can occur in hallux valgus patients as well given
the medial prominence.
2.11 Interdigital Nerves
Interdigital nerves are branches of the lateral and medial plantar nerves and are
located below the transverse intermetatarsal ligament. The nerve that occupies the
third interdigital space is formed by the union of terminal branches of the medial and
lateral plantar nerves, this being the most common site of involvement of these nerves.
Compressive neuritis causes the formation of a nervous thickening, known as
Morton’s neuroma, which corresponds to a neuralgia caused by perineural
fibrosis [5].
Clinically, it manifests as pain related to the use of narrow shoes, associated with
a burning sensation or paresthesia in the toes. Pain on palpation of the affected space
is present, and the compression of the metatarsal heads causes worsening of the pain
and clicking sensation in the space occupied by the neuroma (Mulder positive test).
The conservative treatment is based on the correction of footwear, lidocaine infil-
trations, corticoids, or sclerosing agents with or without ultrasonography guidance.
The results are satisfactory in the early stages of the pathology. Surgical treatment
with neuroma resection is indicated in cases refractory to conservative treatment.
The procedure is usually performed through the dorsal route (Fig. 9). The plantar
route is recommended for revision cases. The nerve section should be performed as
proximal as possible to prevent recurrence of symptoms, typically caused by plantar
branches that were not resected (a minimum of 4 cm nerve resection is recom-
mended). The resection prognosis is very good, with up to 85% satisfactory results
(for more information, go to Morton’s neuroma chapter).
2.12 Diabetic Neuropathy
Neuropathy caused by diabetes causes symptoms of neuropathic pain, which must

be differentiated from peripheral compressive pathologies. In the literature, there
are indications that early decompression of nerves affected by diabetic neuropathy
diminishes the consequences in the medium and long term, decreasing the inci-
dence of plantar ulcerations, a situation of difficult control that can lead patients to
chronic infection and amputations [1].
There is evidence in the literature that young patients, with positive Tinel sign,
adequate metabolic control, and no major sensitivity changes, are those who respond
best to surgical decompression [26].
the presence of interdigital
neuroma in the third
intermetatarsal space
(Morton’s neuroma)
3 Summary
Compressive neuropathies are common and can have varied clinical presentations,
which make clinical diagnosis difficult.
Small incidence of these compressive peripheral nerve pathologies must be
related to lack of diagnosis, or late diagnosis, and it may affect negatively treatment
prognosis.
The knowledge of these pathologies, its symptoms and presentations, the impor-
tance of the adequate evaluation through physical examination, imaging, and elec-
trodiagnosis facilitate its identification, and as a consequence, its adequate treatment.
The patient should be well oriented regarding the pathology and prognosis of the
various forms of treatment, since the results are not homogeneous, and sequelae
can remain.
References
1. Albers JW, Jacobson R. Decompression nerve surgery for diabetic neuropathy: a structured
review of published clinical trials. Diabetes Metab Syndr Obes Targets Ther. 2018;11:493–514.
https://doi.org/10.2147/DMSO.S146121.
2. Allan Maples R, Thom AT et al. Entrapment of deep peroneal nerve in dorsal midfoot pain.
Mississippi Orthop Soc Annu Meet Greenwood. 2005.
3. Chari B, McNally E. Nerve entrapment in ankle and foot: ultrasound imaging. Semin
Musculoskelet Radiol. 2018;22(3):354–63. https://doi.org/10.1055/s-0038-1648252.
4. Davis PF, Severud E, Baxter DE. Painful heel syndrome: results of nonoperative treatment.
5. Espinosa N. Peripheral nerve entrapment around the foot and ankle. In: Miller MD, Thompson
SR, Delee J, et al., editors. DeLee & Drez’s orthopaedic sports medicine: principles and prac-
tice. 4th ed. Philadelphia: Elsivier/Saunders; 2014. p. 1351–68.
6. Fabre T, Piton C, Andre D, Lasseur E, Durandeau A. Peroneal nerve entrapment. J Bone Joint
Surg Am. 1998;80(1):47–53. https://doi.org/10.2106/00004623-199801000-00009.
7. Ferkel E, Davis WH, Ellington JK. Entrapment neuropathies of the foot and ankle. Clin Sports
Med. 2015;34(4):791–801. https://doi.org/10.1016/j.csm.2015.06.002.
8. Flanigan RM, Digiovanni BF. Peripheral nerve entrapments of the lower leg, ankle, and foot.
Foot Ankle Clin. 2011;16(2):255–74. https://doi.org/10.1016/j.fcl.2011.01.006.
9. Frey C, Kerr R. Magnetic resonance imaging and the evaluation of tarsal tunnel syndrome.
Foot Ankle. 1993;14(3):159–64. https://doi.org/10.1177/107110079301400309.
10. Gessini L, Jandolo B, Pietrangeli A. The anterior tarsal syndrome. Report of four cases. J Bone
Joint Surg Am. 1984;66(5):786–7.
11. Goecker RM, Banks AS. Analysis of release of the first branch of the lateral plantar nerve. J
Am Podiatr Med Assoc. 2000;90(6):281–6. https://doi.org/10.7547/87507315-90-6-281.
12. Jaring MRF, Khan AZ, Livingstone JA, Tr F, Chakraverty J, Dip PG. The journal of foot &
ankle surgery a case of bilateral Baxter ’ s neuropathy secondary to plantar fasciitis. J Foot
Ankle Surg. 2019;58(4):771–4. https://doi.org/10.1053/j.jfas.2018.11.010.
13. Kennedy JG, Baxter DE. Nerve disorders in dancers. Clin Sports Med. 2008;27(2):329–34.
https://doi.org/10.1016/j.csm.2008.01.001.
14. Lau TC, Daniels TR. Tarsal tunnel syndrome: a review of the literature. Foot Ankle Int.
1999:201–9.
15. Lohrer H, Malliaropoulos N, Korakakis V, Padhiar N. Exercise-induced leg pain in athletes:

diagnostic, assessment, and management strategies. Phys Sportsmed. 2019;47(1):47–59.
https://doi.org/10.1080/00913847.2018.1537861.
16. Marciniak C. Fibular (peroneal) neuropathy electrodiagnostic features and clinical correlates.
Phys Med Rehabil Clin N Am. 2013;24(1):121–37. https://doi.org/10.1016/j.pmr.2012.08.016.
17. McCrory P, Bell S, Bradshaw C. Nerve entrapments of the lower leg, ankle and foot in sport.
Sport Med. 2002;32(6):371–91. https://doi.org/10.2165/00007256-200232060-00003.
18. Meadows JR, Finnoff JT. Lower extremity nerve entrapments in athletes. Curr Sports Med
Rep. 2014;13(5):299–306. https://doi.org/10.1249/JSR.0000000000000083.
19. Mitsiokapa E, Mavrogenis AF, Drakopoulos D. Peroneal nerve palsy after ankle sprain
: an update. Eur J Orthop Surg Traumatol. 2017;27(1):53–60. https://doi.org/10.1007/
s00590-016-1845-0.
20. Mullick T, Dellon AL. Results of decompression of four medial ankle tunnels in the treat-
ment of tarsal tunnels syndrome. J Reconstr Microsurg. 2008;24(2):119–26. https://doi.
org/10.1055/s-2008-1076089.
21. O’Neill PJ, Parks BG, Walsh R, Simmons LM, Miller SD. Excursion and strain of the superfi-
cial peroneal nerve during inversion ankle sprain. J Bone Joint Surg Am. 2007;89(5):979–86.
https://doi.org/10.2106/JBJS.F.00440.
22. Poage C, Roth C, Scott B. Peroneal nerve palsy: evaluation and management. J Am Acad
Orthop Surg. 2016;24(1):1–10.
23. Ortigiiela ME, Wood MB, Cahill DR. Anatomy of the sural nerve complex. J Hand Surg Am.
1987;12(6):1119–23. https://doi.org/10.1016/S0363-5023(87)80129-6.
24. Piton C, Fabre T, Lasseur E, André D, Geneste M, Durandeau A. Common fibular nerve
lesions. Etiology and treatment. Apropos of 146 cases with surgical treatment. Rev Chir
Orthop Reparatrice Appar Mot. 1997;83(6):515–21.
25. Pomeroy G, Wilton J, Anthony S. Entrapment neuropathy about the foot and ankle. J Am Acad
Orthop Surg. 2015;23(1):58–66. https://doi.org/10.5435/JAAOS-23-01-58.
26. Rinkel WD, De Kleijn JL, Macaré VanMaurik JFM, Henk CJ. Optimization of surgical outcome
in lower extremity nerve decompression surgery. Plast Reconstr Surg. 2018;141(2):482–96.
https://doi.org/10.1097/PRS.0000000000004042.
27. Schon LC, Glennon TP, Baxter DE. Heel pain syndrome: electrodiagnostic support for nerve
entrapment. Foot Ankle. 2000;14(3):129–35. https://doi.org/10.1177/107110079301400304.
28. Styf J, Morberg P. The superficial peroneal tunnel syndrome. J Bone Joint Surg Br.
1997;79(5):801–3. https://doi.org/10.1302/0301-620X.79B5.7799.
29. Tarabay B, Abdallah Y, Kobaiter-maarrawi S, Yammine P, Maarrawi J. Outcome and
prognosis of microsurgical decompression in idiopathic severe common fibular nerve
entrapment: prospective clinical study. World Neurosurg. 2019:1–7. https://doi.org/10.1016/j.
wneu.2019.02.042.
30. Watson TS, Anderson RB, Davis WH, Kiebzak GM. Distal tarsal tunnel release with partial plan-
tar fasciotomy for chronic heel pain: an outcome analysis. Foot Ankle Int. 2002;23(6):530–7.
31. Weber R, Boyd KMS. Repair and grafting of peripheral nerves. In: Neligan P, editor. Plastic
surgery. 3rd ed. Philadelphia: Elsevier; 2013. p. 464–78.
32. Williams EH, Williams CG, Rosson GD, Dellon LA. Anatomic site for proximal tibial nerve
compression: a cadaver study. Ann Plast Surg. 2009;62(3):322–5. https://doi.org/10.1097/
SAP.0b013e31817e9d81.
Part VII
Adult Sports Lesions and Traumatology
Peroneal Tendon Tears: Evaluation
and Treatment
James W. Brodsky and Daniel D. Bohl
1 Introduction
Patients with peroneal tendon tears present with lateral ankle pain, which has a
broad differential diagnosis that includes ankle sprain, chronic lateral ligament lax-
ity, fractures of the anterior calcaneal process and lateral talar process, subfibular
impingement, ankle, subtalar and calcaneocuboid joint osteochondral lesions, pero-
neal tendonitis, and peroneal anatomic anomalies, subluxation or dislocation.
Notably, because many of these pathologies are the result of inversion injuries,
which can affect the ankle or the hindfoot, or both, they are often multiple, concur-
rent, and/or difficult to distinguish. Preceding trauma may range from multiple inci-
dents of remote mild injury, to cases of progressive and insidious onset, or to an
acute episode of severe injury. Overall, peroneal tendon tears are thought to account
for about a third of patients with lateral ankle pain [1]. The variable history and wide
range of potential pathologies often lead to a delay in diagnosis.
Conservative treatment for peroneal tendon tears may include immobilization
with a cast or walking boot, bracing, physical therapy, nonsteroidal anti-inflammatory
medications, and activity modification, and is variably successful, depending on the
patient’s goals and activities, the chronicity and severity of pain and dysfunction,
and the stage in the natural history at which the patient presents to the surgeon.
Many, if not most, cases ultimately require surgical reconstruction. As the under-
standing of the pathophysiology, imaging, and operative outcomes has advanced, so
too have the specific indications and surgical techniques.
J. W. Brodsky (*) · D. D. Bohl

Baylor University Medical Center, Dallas, TX, USA

Switzerland AG 2022
1024 J. W. Brodsky and D. D. Bohl
2 Anatomy, Etiology, and Pathophysiology
Most patients with peroneal tendon tears present for evaluation of chronic lateral
ankle symptoms, with only a minority presenting with an acute injury [2]. As many
as half of patients may recall an initial event marking the onset of their ankle pain;
however, that event is usually remote with subsequent resolution followed by gradu-
ally progressive chronic symptoms [2, 3].
There are two main theories regarding the pathophysiology of peroneal tendon
tears. The first, most important, and best documented is that mechanical stress is the
primary cause of peroneal tendon tears. This is strongly supported by the typical
patterns of tear location, which have few exceptions, and by the characteristic dif-
ference in those patterns between the peroneus brevis and the peroneus longus ten-
dons. A mechanical etiology is supported by the fact that tears occur at the bony
prominences that serve as fulcrums, or pulleys for the tendons as they change direc-
tion [2–5]. These act as pulleys to convert tendon motion in one plane to a vector in
a different plane. For the peroneus brevis, that fulcrum is the posterolateral bony
edge at the tip of the fibula. For the peroneus longus, it is most commonly the cuboid
groove, and less often, the peroneal tubercle of the calcaneus. The second theory is
that tears occur at regions of hypovascularity [6, 7], postulating that an attenuated
blood supply deprives the tendons of oxygenation and nutrition, predisposing to
injury and diminished healing potential. Of note, these regions are similar to the
above-noted areas of mechanical stress. The pathophysiologic and pathoanatomic
patterns of tears of each of the two peroneal tendons will be discussed in turn, begin-
ning with the tendon that is most commonly injured.
2.1 Peroneus Brevis
The most common pattern by far is longitudinal split tearing of the peroneus brevis
centered at the inferior-lateral tip of the fibula, comprising 73% of all tears (Fig. 1)
[8]. When the tendon subluxes or dislocates over the posterolateral edge of the ret-
romalleolar groove, the fibular fulcrum becomes the source of friction, gradually
fraying and then splitting the tendon with repetitive motion of each step [3, 9]. The
peroneus longus, which is posterior to the brevis at the malleolus, compresses it
against the bone, contributing to the subluxation and compounding the mechanism
of damage [3].
At least two studies support the vascular theory of injury to the peroneus brevis
tendon, finding a “watershed” area at the retromalleolar groove [6, 7], while two
other studies refuted this concept, finding that the tendon is well vascularized
throughout [10, 11].
When considering the pathophysiology of peroneus brevis tears, the superior
peroneal retinaculum deserves specific mention [2, 12]. Inversion injury of the ankle
can lead to attenuation of the tissue of the superior peroneal retinaculum, allowing
Peroneal Tendon Tears: Evaluation and Treatment 1025
a b
Fig. 1 Intraoperative photos of a longitudinal split tear of the peroneus brevis. (a) The typical
appearance of a longitudinal split tear of the peroneus brevis is a flattened tendon with a longitudi-
nal window of several centimeters within its mid-substance. (b) The typical location of a longitu-
dinal split tear of the peroneus brevis is at the tip of the fibula, within and just distal to the
retromalleolar groove. Intra-sheath subluxation of part of the tendon likely contributes to tearing
of the tendon as the tip of the fibula pieces through. (Used with permission from James W. Brodsky,
M.D. Baylor University Medical Center, Dallas, USA)
photo of an insertional tear
of the peroneus brevis. In
this location, tears tend to
be more degenerative than
mechanical in nature.
Insertional tears are
generally multiple,
incomplete, and
longitudinal in nature.
(Copyright 2020, James
W. Brodsky, M.D. Baylor
University Medical Center,
Dallas, USA)
brevis subluxation. Moreover, the origin of the retinaculum on the lateral surface of
the fibula can become widely elevated [12, 13], allowing intra-sheath or frank sub-
luxation/dislocation of the peroneus brevis, which in turn may further attenuate the
retinaculum. A similar pattern may result from chronic retromalleolar overstuffing
due to tendinopathic enlargement, accessory peroneal musculature (i.e., peroneus
quartus), or a low-lying muscle belly of the peroneus brevis [14–16].
A distinct form of tendon tear occurs at the insertion of the peroneus brevis into
the base of the fifth metatarsal (Fig. 2), although little has been written on this sub-
ject [17]. In our experience, this can be seen on MRI, but most often presents as
multiple, incomplete, longitudinal splits in the fibers of the tendon just proximal to
the insertion. In this location, it appears to be more degenerative than mechanical,

and is less consistently symptomatic.
2.2 Peroneus Longus
Isolated peroneus longus tears are the least common, representing 8% of all tears
[8]. They occur most often at the cuboid tunnel, much less often at the peroneal
tubercle, and in the region in between, where the peroneus longus is redirected from
moving in line with the long axis of the leg to an acutely angled distal-medial trajec-
tory across the plantar foot (Fig. 3) [3, 18]. While the mechanical theory is clearly
supported by tears occurring along this prolonged fulcrum, the vascular theory has
been less well supported for the peroneus longus [6, 7, 10, 11]. Above the peroneal
tubercle, the peroneus longus and brevis share a tendon sheath; below the peroneal
tubercle, they are divided into two separate sheaths. Enlargement or irregularity of
the peroneal tubercle can cause increased wear on the peroneus longus at that level
[4, 19, 20].
In about 4–30% of the general population, there is a sesamoid bone, the os pero-
neum, within the peroneus longus just proximal to the cuboid groove and serving to
increase tendon power, just as other sesamoid bones do at the hallux, or the knee
(the patella) [5]. The os peroneum can become fractured, osteophytic, or enlarged,
causing the so-called painful os peroneum syndrome [21], but more importantly,
those changes cannot occur without accompanying tearing and degeneration of the
peroneus longus tendon in which it is embedded.
photo of a peroneus longus
tear just proximal to the os
peroneum. The peroneus
longus has been transected
just distal to the os
peroneum in preparation
for peroneus longus to
brevis transfer. (Copyright
2020, James W. Brodsky,
M.D. Baylor University
Medical Center,
Dallas, USA)
3 Diagnosis
3.1 Physical Examination
The peroneus brevis inserts on the base of the fifth metatarsal, rendering it the pri-
mary abductor of the forefoot [22]. The peroneus longus inserts on the base of the
first metatarsal, rendering it the primary plantarflexor of the first ray. Both tendons
pass lateral to the axis of the subtalar joint and slightly posterior to the axis of the
tibiotalar joint, rendering them primary evertors of the hindfoot. They are consid-
ered weak plantarflexors of the tibiotalar joint, although a recent study showed sig-
nificant loss of ankle plantarflexion power and moment when neither is functioning
[23]. In order to isolate their effects, the tendons are best examined with the tibiota-
lar joint in plantarflexion.
The most consistent examination findings are tenderness to palpation, swelling,
and enlargement along the tendons. This is especially true for peroneus brevis tears.
In one review, tenderness was present in 100% of patients with surgically confirmed
tears of the peroneus brevis [2]. Swelling was present in 90%. Tenderness and
swelling at and proximal to the lateral malleolus is more consistent with a peroneus
brevis tear, whereas tenderness and swelling from the peroneal tubercle to the
cuboid groove is more consistent with a peroneus longus tear [2, 18]. The examiner
should also be able to distinguish distal tenderness and swelling at the peroneus
brevis insertion from that at the peroneus longus in the cuboid groove due to the
peroneus brevis’s more dorsal location.
Pain with resisted eversion is another commonly noted physical exam finding;
however, like tenderness to palpation and swelling, it may frequently also occur
with tendinitis, and so cannot be used in isolation to confirm a tear. Pain may also
be provoked with passive inversion of the hindfoot, which tensions both peroneal
tendons over their bony fulcrums. The tendons should also be evaluated in the clinic
for intra-sheath subluxation, although in the absence of frank dislocation, peroneal
instability may be difficult to detect.
Finally, it is critical that the examiner conduct a thorough examination of the
lower extremities, with a focus on identifying confounding or contributing diagno-
ses. The examiner should note hindfoot and forefoot position and range of motion,
because cavovarus deformity predisposes to peroneal tendon tears [8] and may
require treatment in some cases. While peroneal tendon tears can be seen in pla-
novalgus deformities, especially when associated with lateral ligament instability,
the diagnosis can be confounded by subtalar or subfibular impingement. Lateral
ligament instability commonly co-occurs with peroneal tendon pathology and may
need to be simultaneously addressed. Sural neuritis, Achilles pathology, and hind-
foot arthritis can occasionally confound the picture as well.
3.2 Radiography
The imaging assessment starts with plain film radiography, including anterior-
posterior, oblique, and lateral views of both the foot and the ankle. It provides infor-
mation on alignment of the hindfoot and forefoot and helps to rule out potentially
confounding conditions such as hindfoot arthritis. For example, when present, an os
peroneum will be visible in its normal location. The os lies within the peroneus
longus tendon at the level of the calcaneucobid joint and proximal cuboid groove.
Migration of the os peroneum proximal to the calcaneocuboid joint indicates a pero-
neus longus tear distal to the os [5], as seen on the 45-degree internal rotation and
lateral views of the foot (Fig. 4) [24]. Fracture of the os peroneum often represents
a peroneus longus tear through the os. Hypertrophy of the os peroneum seen radio-
graphically can support painful os peroneum syndrome in the absence of a definitive
peroneus longus tear [21].
3.3 Magnetic Resonance Imaging (MRI)
MRI is the definitive imaging modality for peroneal tendon tears, but requires cer-
tain refinements and an experienced reader for best results. MRI was initially
reported to have poor diagnostic ability with respect to peroneal pathology. However,
improvements in MRI technology and better evidence regarding clinical-
radiographic correlation has now positioned MRI as the leading imaging modality
a b
Fig. 4 Plain film radiographs of a proximally migrated os peroneum (arrow). (a) Lateral view. (b)
45-degree internal rotation oblique view. (Used with permission from James W. Brodsky,
M.D. Baylor University Medical Center, Dallas, USA)
for peroneal evaluation [2, 25–28]. Peroneal tendon tears are diagnosed both by
changes in the shape of the tendon, including splits into distinct strands, and by
increased signal (edema) within the tendon. The single most important and essential
innovation is a para-axial oblique reconstruction because it is oriented at 90 degrees
to the tendons at and just below the lateral malleolus (Fig. 5a–c). This gives the most
accurate depiction of the morphology, and signal within the peroneal tendons, which
is much more difficult on the routine exam along the axial and coronal planes of the
ankle joint. T2 fat-suppressed images are essential to judge signal within the
tendons.
A critical concept regarding MRI of the peroneal tendons surrounds the “magic
angle effect.” [28, 29] This is a phenomenon of MRI technology in which a tendon
intersecting the magnetic vector at 55 degrees appears with factitiously heteroge-
neous signal on both T1 and T2 sequences. Unfortunately, this is approximately the
natural position of the peroneal tendons at the tip of the lateral malleolus, the most
common area of peroneus brevis injury. Acquisition of MRI images in the para-
axial oblique plane perpendicular to the tendons at this location mitigates the magic
angle artefact. Authors have also provided evidence for imaging in alternate posi-
tions [30] and with specific sequences [31] to mitigate this effect. We image in 20
degrees of plantarflexion which separates the two peroneal tendons within the
sheath by reducing tension and mitigates the magic angle effect on the most critical
portion of the peroneus brevis.
Tears of the peroneus brevis appear as c-shaped or split tendons; abnormal intra-
tendinous signal can vary based on the age of the tear (Fig. 5a, b) [25]. The oblique
views can aid evaluation for subluxation and dislocation out of the retromalleolar
groove, injury to the fibrocartilaginous ridge, and attenuation and detachment of the
retinaculum from the fibula (false pouch) [32].
Tears of the peroneus longus appear as a linear or round area of increased intra-
tendinous signal between the peroneal tubercle and cuboid groove (Fig. 5c, d) [33,
34]. These are well visualized on the peroneal oblique views more proximally, as
well as coronal images of the ankle more distally. Oblique coronal images of the
ankle perpendicular to the metatarsals can be added for a true cross section of the
peroneus longus as it courses along the lateral hindfoot. Complete disruption with a
defect is more common in longus than brevis tears.
Despite the power of MRI, the importance of a careful history and physical
examination cannot be overstated, as demonstrated in a study showing a high rate of
peroneal tendon pathology on MRI in asymptomatic patients [35].
3.4 Ultrasound
Ultrasound can be a useful modality for diagnosis of peroneal tendon pathology

[36]. A study of patients who underwent both ultrasonic evaluation and operative
intervention found that ultrasound’s sensitivity for detecting tears is 100%, specific-
ity 85%, and overall accuracy 90% [37]. The disadvantage of ultrasound is that it is
a b
c d
Fig. 5 Peroneal tendon tears on MRI. (a) Sagittal reconstruction showing orientation of para-axial
reconstructions. (b) Para-axial reconstruction showing peroneus brevis tear at the level of the ret-
romalleolar groove. (c) Peroneal oblique reconstruction showing peroneus longus split tear near
the level of the peroneal tubercle. (d) Coronal reconstruction showing peroneus longus tear within
the cuboid groove. (Used with permission from James W. Brodsky, M.D. Baylor University
Medical Center, Dallas, USA)
much more highly dependent on experience and expertise than MRI. Trained ultra-
sonographers are much less readily available in the USA, although more common
in other countries.
4 Treatment
Conservative treatment for peroneal tendon tears consists of immobilization in cast

or walking boot, physical therapy, nonsteroidal anti-inflammatory medications,
activity modification, and bracing. If the symptoms are chronic and/or severe, or if
the patient has failed conservative management, it is reasonable to proceed with
advanced imaging and consideration of surgical reconstruction.
4.2 Tendonoscopy
Groups of authors have advocated tendoscopy for cases of patients with persistent
symptoms but negative imaging, as well as more advanced cases. They describe
experience including debridement, synovectomy, and even tendon and retinacular
repair and reconstruction [13, 16, 38–40].
4.3 Classifications to Guide Surgical Treatment
Two major classification systems have pushed forward our understanding of treat-
ment for peroneal tendon tears. The first was proposed by Krause and Brodsky in
1998 and concerned the most common pattern, tears of the peroneus brevis tendon
[2]. These authors proposed that peroneus brevis tears be divided into grades 1 and
2, based on intraoperative observation. By this system, grade 1 tears have <50%
total cross-sectional area injured and should be repaired by debridement and tubu-
larization, as there is enough remaining healthy tendon to bear the functional load
once repaired. In contrast, grade 2 tears have >50% total cross-sectional area injured
and should be reconstructed with resection of the injured segment and tenodesis to
the peroneus longus. The 50% threshold was analyzed in a cadaveric study [41].
Wagner et al. recently tested cyclic loading and load to failure in cadaver specimens
with partial longitudinal resection of the peroneal tendons, up to 66%. There were
no tendon failures after 100 cycles, and the study raised interesting questions, but no
conclusions can be drawn for three reasons. The number of cycles were extremely
few, and so cannot be interpreted as clinically relevant; it is not possible extrapolate
the biomechanical function of an undiseased cadaver tendon to a pathologic one;

and there are other issues which determine the outcomes of partially resected ten-
dons more than mechanical strength, that is, that the primary mode of failure is
scarring, adhesion, and degeneration of the residual repaired tendon. The authors’
rationale for excision and tenodesis in severe cases has been further reinforced by
their subsequent observation that the peroneus brevis, when repaired, commonly
scars to the deep tissue and to the peroneus longus, causing pain and restricted motion.
The second classification was proposed by Redfern and Myerson in 2004 [42].
These authors expanded on the prior classification to include both peroneus longus
tears and concomitant tears of both the peroneus brevis and peroneus longus. In
their algorithm, for tendons that are grossly intact, the authors recommend debride-
ment and tubularization (analogous to Krause and Brodsky grade 1, but without a
specified threshold). When one tendon is severely torn, and its muscle belly has
good excursion, the authors recommend tenodesis to the adjacent tendon. Finally, if
one tendon is severely torn and its muscle belly lacks excursion, or if both tendons
are severely torn, the authors recommend reconstruction with a tendon transfer or
tendon graft.
4.4 Tendon Repair
In general, for tendons with small reconstructable tears, the recommended proce-
dure consists of tenolysis, synovectomy, excision of the degenerated unhealthy
appearing tendon, and tubularization of the remaining healthy appearing tendon.
Techniques for tubularization vary, including recommendations for absorbable
suture to minimize soft tissue irritation2 and nonabsorbable suture to maximize
strength and durability [42]. In one clinical study comparing suture types, there was
no difference between absorbable and nonabsorbable suture in patient outcomes
[43]. Once the tendon has been repaired, the superior peroneal retinaculum is recon-
structed, as described below. Postoperatively, patients are splinted for 2 weeks,
placed into a non-weight-bearing cast for 2 weeks, and then progressed to a con-
trolled ankle motion boot for an additional 4–6 weeks. Physical therapy begins at
8 weeks postoperatively.
Reported outcomes have been generally positive following debridement and
repair. Krause and Brodsky reported that 91% of 11 patients who underwent
debridement and repair of the peroneus brevis were satisfied with their outcome [2].
Those authors also reported an AOFAS score of 85 postoperatively. Demetracopoulos
et al. reported improvement in VAS pain scores and 94% return to full sporting
activity among 34 patients undergoing debridement and repair (24 brevis only, 3
longus only, 7 both tendons) [44]. Among 71 patients undergoing debridement and
repair of the peroneus brevis, Steginsky et al. reported that 76% of patients returned
to pre-injury activities, but only 62% performed at preinjury levels [45]. Nevertheless,
85% of patients reported satisfaction and 91% indicated they would undergo the
procedure again. Finally, Steel and DeOrio reported less promising results in a study
of 29 patients undergoing debridement and repair that was focused on return to

sport [43]. These authors reported that 46% of patients returned to at least some
sport, whereas 42% returned only to activities of daily living (the remaining 12%
did not play sports prior to injury). Moreover, 54% continued to experience swelling
and 31% pain at rest.
4.5 Tenodesis
For tendon tears above or approaching 50% of the cross-sectional area, or for tears
that are very long or complex, debridement and repair is unlikely to be successful
[2]. Such repairs tend to result in scarring and adhesion to the deep surface, the
peroneal sheath, and the adjacent tendon causing persistent pain which is usually
unrelieved by conservative measures. Moreover, scarring of the previously debrided
tendon and loss of excursion render it mechanically ineffective.
In most cases of a severe tear of one tendon, most often the peroneus brevis, but
with a relatively well-preserved adjacent tendon, the best solution is tenodesis (or
transfer) to the adjacent tendon above and below the zone of the tear, and excision
of the damaged segment (Fig. 6). This has the advantages of simplicity, the use of
autogenous tissue, the mechanical similarities of the two peroneals, and the preser-
vation of the function of the corresponding muscle. In addition to a straightforward
surgical technique, there is a low risk of complications.
For a severely torn peroneus brevis tendon, the operative technique of peroneus
brevis to longus tenodesis proceeds as follows. First, the site of proximal tenodesis
is identified. The site should be sufficiently proximal both to be well above the zone
of the damaged and torn tendon, and also proximal to the superior peroneal reti-
naculum such that the bulk of the tenodesis does not pass through the retromalleolar
groove or retinaculum. The appropriate level is corroborated by the change to
a b
Fig. 6 Intraoperative photo of a peroneus brevis to longus tenodesis. (a) Prior to reconstruction of
the superior peroneal retinaculum. (b) With the superior peroneal retinaculum in the forceps in
preparation for retinacular reconstruction. (Copyright 2020, James W. Brodsky, M.D. Baylor
University Medical Center, Dallas, USA)
normal color and texture of the tendon, compared to the zone of injury. At the site
of the tenodesis, the adjacent tendon surfaces are debrided of synovium and rough-
ened. It is important to tension the tendons appropriately. To do so, the surgeon
should position the ankle in neutral and the hindfoot in eversion. The surgeon may
gently pull the proximal end of the torn tendon distally to stretch the proximal mus-
culotendinous unit. The tenodesis is done with nonabsorbable suture, usually 0 or
2–0 in size, in a pattern such as a complex running stitch, which has been shown to
be strongest for early motion [46]. To minimize symptomatic prominence of the
knots and to avoid strangling the tendons, mattress sutures are used so that the
suture never loops around the tendons. Ideally, the knots are placed internally
between the tendons, but never on the surface, because the knots can be painful, or
erode the skin in this area that lacks a subcutaneous fat layer.
Second, a decision must be made whether to reconstruct the retinaculum before
or after the distal portion of the reconstruction. When in doubt, the safest and most
reliable result is obtained by performing it at this point with, of course, the tendon
located behind the lateral malleolus. The reason is that the most accurate measure
of final alignment and length (and therefore, the tension) of the reconstruction
occurs when the tendon is located in its functional position behind the fibula. Third,
the site of distal tenodesis or tendon transfer is identified. A tenodesis is performed
just proximal to the peroneus brevis insertion, so that the force of the two muscles
act through the native insertion on the fifth metatarsal base. If the distal peroneus
brevis insertion is degenerative or otherwise unsuitable, the longus is transferred
directly to base of the fifth metatarsal using suture anchors, a biointerference screw,
suturing to itself through a drill hole, or a combination thereof. Fourth, the diseased
portion of the peroneus brevis tendon is excised. Finally, if the superior peroneal
retinaculum is not yet reconstructed, it is done, which is described in the next
section.
For a severely torn peroneus longus tendon, the technique is almost the same
as for the brevis, with the exception of the distal tenodesis or transfer. After the
proximal tenodesis of the longus to the brevis above the superior peroneal reti-
naculum, the diseased portion of the peroneus longus is excised down to the level
of the cuboid groove. Distal to the cuboid groove, the longus is inaccessible as it
courses along the plantar aspect of the foot, and so the longus is simply tenoto-
mized at the level of the cuboid groove. The peroneus brevis and longus muscle
bellies both contract through the peroneus brevis tendon which runs through the
retromalleolar groove and acts through its native insertion on the base of the fifth
metatarsal.
Postoperatively, patients are splinted for 2 weeks, placed in a weight-bearing cast
for 4 weeks, and then allowed to weight bear as tolerated in a boot for an additional
4–6 weeks. The patient is instructed to begin gentle home range of motion exercises
when casting is discontinued, and physical therapy begins at 12 weeks.
Krause and Brodsky reported that 100% of nine patients who underwent tenode-
sis of the peroneus brevis to the peroneus longus were satisfied with their outcome
[2]. Those authors also reported an AOFAS score of 86 postoperatively. Among 14
patients undergoing peroneus longus to peroneus brevis tenodesis, Burkhard et al.
reported postoperative AOFAS score of 86 and no difference in isokinetic eversion

compared to the contralateral foot [47]. Finally, among 12 patients with peroneus
longus tears associated with pathology of the os peroneum who underwent peroneus
longus to peroneus brevis tenodesis, Stockton and Brodsky reported AOFAS score
increased from 61 to 92, SF-36 score increased from 36 to 52, and VAS scores
decreased from 6.3 to 1.0 [5].
4.6 Superior Peroneal Retinaculum Reconstruction
Reconstruction of the superior peroneal retinaculum is essential in all cases, to pre-

vent development of recurrent subluxation or dislocation. The surgeon’s task
includes a judgment regarding the volume and tightness of the retinaculum, ensur-
ing that the tendons are neither too tightly compressed nor is the retinaculum so
loose that the tendon may subluxate around the fibula again. A pants-over-vest type
suture is recommended because it is self-adjusting, depending on the tension
applied. This allows control over the volume and tightness of the retinacular recon-
struction. Placing the knot posteriorly makes it less likely to be symptomatic. The
authors use 2–0 nonabsorbable suture. If the retinaculum was stripped from the
lateral surface of the fibula (intra-sheath dislocation), it must be reattached to the
bone at the same time. This can be done by roughening the fibular cortex, and pass-
ing the retinacular sutures through a series of small drill holes along the posterolat-
eral fibular margin. The sequence of retinacular reconstruction is critical in many
peroneal reconstructions, and is especially critical in allograft reconstructions for
loss of both peroneal tendons (see below), because the main risk is loss of power
through stretching of the allograft over time.
For any peroneal reconstruction, if the entire tendon construct is excessively
short, it will not fit behind the lateral malleolus, or if it is made to do so by force, the
ankle is pushed into plantarflexion. The retinacular repair will be under stress, and
will be more likely to fail.
In some cases, the superior peroneal retinaculum is attenuated, and reconstruc-
tion of the inferior peroneal retinaculum is a valuable adjunct. It is wise to keep this
in mind during the initial distal dissection, and to maximally preserve the flaps of
the inferior peroneal retinaculum.
4.7 Reconstruction for Concomitant Tears of Peroneus Brevis

and Longus
Patients in whom both tendons have severe and unreconstructable tears present the
greatest surgical challenge to restoration of peroneal function (Figs. 7 and 8). The
primary choices include autologous tendon transfer or allograft substitution, which
are described below.
a b
Fig. 7 Intraoperative photo of a patient with both peroneus brevis (a) and peroneus longs (b) tears.
(Used with permission from James W. Brodsky, M.D. Baylor University Medical Center,
Dallas, USA)
photo of a patient with
both peroneus brevis and
peroneus longus complete
ruptures resulting from
prolonged and severe
interstitial degeneration
and nonviable tendon.
(Copyright 2020, James
W. Brodsky, M.D. Baylor
University Medical Center,
Dallas, USA)
4.8 Flexor Hallicus Longus (FHL) and Flexor Digitorum

Longus (FDL) Transfers
For these techniques, the tendon is harvested at the knot of Henry, passed proxi-
mally and laterally around the tibia and fibula, and then attached to the lateral border
of the foot, either through tenodesis to the insertion of the peroneus brevis or by
direct transfer to the base of the fifth metatarsal, as described in the section on pero-
neus brevis reconstruction.
In a series of FDL or FHL transfers for eight patients with unreconstructable
concomitant tears, Jockel and Brodsky reported that AOFAS score increased from
64 to 86, with seven of eight patients reporting good-to-excellent results and return-
ing to preoperative activity levels [48]. In a study of nine patients with FHL (five
patients) or FDL transfers (4 patients), Seybold et al. found that all patients were
satisfied with their results at mean 35.7 months [49]. Two patients developed tibial
neuritis, and patients had about 75% of eversion strength compared to their contra-
lateral side. Sherman et al. studied 15 patients who underwent FDL transfer, finding
that all were satisfied with the surgery and reported a reduction in VAS of 5.6 points
[50]. Patients had on average 42% of eversion strength compared to the contralateral
side. Wapner et al. proposed a staged FHL transfer to reduce the risk of tendon adhe-
sions and scarring, wherein stage one consists of peroneal excision and placement
of a Hunter rod into the residual peroneal sheath, and stage two, 3 months later,
consists of removal of the Hunter rod and transfer of the FHL into the improved
peroneal sheath. Among seven patients, six had complete relief of symptoms and
returned to full pre-injury activity levels. They reported five excellent, one good,
and one fair result. However, other authors have noted high levels of scarring even
with this staged protocol. Without evidence of superiority, staged procedures are not
currently performed.
There are several reasons to suspect that the FHL transfer may be superior to the
FDL transfer for peroneal tendon reconstruction: (1) anatomic studies have demon-
strated that FHL harvest results in a longer usable tendon length [51], (2) the muscle
belly is larger [52], (3) the strength is greater with comparable excursion [53], and
(4) there may be a lower risk of tibial nerve injury [49].
The major advantage of using FHL/FDL tendon transfer is the use of autologous
tissue. The disadvantages are, first, that the muscles are weak functional substitutes
for the peroneal muscles. Specifically, based on a study using MRI to estimate mus-
cle strength [52], (1) the strength of the FHL was about half the combined strength
of the two peroneals, (2) the strength of the FDL was about half the strength of
either peroneal alone, and (3) muscles are further weakened beyond these numbers
in a transfer because of changes in line of pull and tensioning. Analogous to FDL
“transfer” for posterior tibial tendon dysfunction, tendon transfer for peroneal dys-
function might be best thought of, and utilized as, an intercalary autograft tendon
bridge, rather than a true tendon transfer. In other words, the goal of reconstruction
should be to restore best possible function of the native peroneal musculotendinous
units, by reestablishing their insertion on the lateral border of the foot. Second, the
FHL and the FDL transfers are anatomically limited options because the musculo-
tendinous junctions are very distal. This is exacerbated in the course of using either
one for a transfer because as the transferred flexor tendon is tightened, the musculo-
tendinous junction is drawn even further distally. This is a problem when the pero-
neal tendon tears are severe, multiple, and especially, when the proximal extent of
the tears is at or above the superior peroneal retinaculum.
4.9 Allograft Transfers
In cases of severe, irreparable tears of both the peroneus brevis and longus, allograft
reconstruction is an important, and possibly the best option (Fig. 9). Allograft ten-
dons can be used to span the intercalary defect after excision of one or both peroneal
tendons. This concept was originally advocated for by Redfern and Myerson as
a b
Fig. 9 Intraoperative photo of a patient with both peroneus brevis and peroneus longus tears
treated with peroneal tendon allograft. (a) Tears of both the peroneus brevis and peroneus longus
tendons prior to debridement. (b) In the final construct, the allograft serves as an intercalary seg-
ment between the native peroneal tendons proximally and the peroneus brevis insertion distally.
The allograft reconstruction is seen deep to a reconstructed peroneal retinaculum. (Copyright
2020, James W. Brodsky, M.D. Baylor University Medical Center, Dallas, USA)
ideal in cases where the muscle belly or bellies have intact excursion [42]. The tech-
nique is indicated because these are the most severe of all peroneal tears, or any
peroneal pathology. In many cases, the unreconstructable condition of the tendons
is insufficiently described as concomitant “tears.” Rather, many of these cases have
had previous surgery, and some have not, but they are often scarred into an adherent
mass which has no motion and may have entirely lost the morphology of actual
tendons. The zone of tendon damage extends very proximally into the lateral com-
partment, often far above the superior peroneal retinaculum. Surprisingly, most of
these cases still have viable proximal muscles.
The goal of reconstruction is to bridge the very large gap between the proximal
peroneal musculotendinous units and the brevis insertion on the lateral border of the
foot. Only a free tendon graft can bridge these defects, which can extend from the base
of the fifth metatarsal to just distal to the peroneal muscles, anywhere from 18 to 25 cm,
or more. While an autologous hamstring could be harvested, use of cadaver allograft
has fewer surgical complications and lower morbidity. These cases are technically
demanding and require long follow-up, but most patients obtain a functional result with
pain relief, demonstrable tendon excursion, and excellent improvement in gait.
A clinical study by Mook et al. reported on allograft peroneal tendon reconstruc-
tion, but interpretation of its results is complicated by the heterogeneity of the pro-
cedures included in the study. Eleven of 14 procedures involved reconstruction of
the peroneus brevis alone, two of the peroneus longus alone, and only one for both
tendons [54]. Hence, this study is not representative of the allograft reconstruction
of irreparable and concomitant tears of both tendons advocated for in the previous
two paragraphs, and is better seen as a studied alternative to tenodesis in cases of
severe single-tendon tears. In any case, at mean 17 months follow-up, there were
improvements in VAS pain score and patient-reported outcomes of a similar magni-
tude as those seen for peroneal tenodesis [2, 5, 47].
4.10 Hindfoot Arthrodesis
In some cases of reconstruction for tears of both peroneal tendons, no form of tendon
reconstruction alone is sufficient to restore function. For example, in patients with
very chronic tears, in whom there is extensive fatty infiltration and scarring of the
peroneal muscles, or in elderly patients with weak muscular function, the reconstruc-
tion is best done by or in combination with hindfoot arthrodesis. This can be triple
arthrodesis, to hold the hindfoot and midfoot sufficiently everted to assure a planti-
grade position for standing and walking. Another option is the use of subtalar arthrod-
esis in eversion, with concomitant peroneal reconstruction. The arthrodesis reduces
the load on the tendon reconstruction, while preserving more hindfoot/midfoot motion.
4.11 Concomitant Procedures for Associated Pathologies
Taniguchi et al. have recently proven the association of cavovarus deformity with
peroneal tendon tears, and the subtypes thereof, and elucidated which radiographic
measurements of cavovarus are significant [8]. Numerous authors have recommended
correction of these deformities simultaneous to peroneal tendon reconstruction [42,
43, 44], although there are neither established criteria for its indications nor for the
surgical techniques. The authors choose reconstructive procedures based on whether
the hindfoot varus is driven by the forefoot (in most cases, plantarflexion of the first
ray) or the hindfoot (usually stiff and/or arthritic subtalar joint in varus). In addition
to correction of cavovarus deformities themselves, the association of cavovarus
deformities with other pathologies, such as lateral ankle ligament instability, ankle
varus, and lateral talar dome osteochondral lesions, should be recognized, as these are
often surgically treated at the same time as the peroneal tendons [5, 8, 42–44, 46].
4.12 Complications
Sural nerve branches invariably cross the skin incision to approach the peroneal
tendons. As a result, by far the most common complication is skin numbness ante-
rior to the distal portion of the incision, distal to the peroneal tubercle, followed by
injury to the main portion of the sural nerve more proximally. The latter can result
in retrograde dysesthesias and pain in the lower leg. Wound healing complications
are the next most common complication due to the subcutaneous position of the
peroneal tendon retinaculum and the lack of subcutaneous tissue over the ankle and
hindfoot. Peroneal complications including recurrent tears, scarring, or complete
tendon degeneration require revision reconstruction of higher complexity. For
example, a failed brevis repair might merit a tenodesis; a failed tenodesis might
merit a tendon transfer or allograft.
4.13 Postoperative Rehabilitation
Postoperative rehabilitation for peroneal tendon reconstruction varies from author

to author and from procedure to procedure, but in our experience is most commonly
6–8 weeks. Timing of initiation of therapy is highly variable. In general, we immo-
bilize patients for 2 weeks in a splint, followed by 4 to 10 weeks in a progression
from casts to boots, from non-weight-bearing to weight-bearing, and from immobi-
lization to controlled active motion. These are modified depending upon the extent
of the reconstruction. Repairs require the least postoperative protection, and allograft
reconstruction for tears of both peroneals require the most. Physical therapy is very
helpful to most patients once healing and immobilization are complete.
5 Summary
Peroneal tendon tears present most commonly as chronic lateral ankle and/or hind-
foot pain and swelling, with variable levels of diminished ability and endurance,
from participation in sport, to walking in activities of everyday life. There may or
may not be a history of an inciting inversion event. Physical examination is key for
differentiating peroneal pathology from other causes of lateral ankle pain, and MRI
is the most definitive confirmatory diagnostic test. Published surgical classifica-
tions, based on intraoperative findings, guide operative management, but in general,
small, reconstructable tears can be debrided and repaired, although a substantial
number will fail through scarring or recurrent tears. For larger, unreconstructable
tears, reconstruction options include tenodesis to the adjacent tendon, FHL or FDL
tendon transfer, or allograft substitution. Retinacular reconstruction is critical, and
in some patients the surgical treatment of associated cavovarus deformity must be
done. While further study will advance our understanding of surgical techniques
and outcomes, most patients obtain meaningful and lasting pain relief and improve-
ment in function.
References
1. Sammarco GJ, DiRaimondo CV. Chronic peroneus brevis tendon lesions. Foot Ankle.
1989;9(4):163–70.
2. Krause JO, Brodsky JW. Peroneus brevis tendon tears: pathophysiology, surgical reconstruc-
tion, and clinical results. Foot Ankle Int. 1998;19(5):271–9.
3. Brandes CB, Smith RW. Characterization of patients with primary peroneus longus tendinopa-
thy: a review of twenty-two cases. Foot Ankle Int. 2000;21(6):462–8.
4. Celikyay F, Yuksekkaya R, Almus F, Bilgic E. Tenosynovitis of the peroneal tendons associ-
ated with a hypertrophic peroneal tubercle: radiography and MRI findings. BMJ Case Rep.
2014;2014:bcr2013200204.
5. Stockton KG, Brodsky JW. Peroneus longus tears associated with pathology of the os pero-
neum. Foot Ankle Int. 2014;35(4):346–52.
6. Mota Gomes T, Guerra-Pinto F, Soares S, et al. The vascularization of the peroneal tendons: an
anatomic study. Foot Ankle Surg. 2020;27:450.
7. Petersen W, Bobka T, Stein V, Tillmann B. Blood supply of the peroneal tendons: injection and
immunohistochemical studies of cadaver tendons. Acta Orthop Scand. 2000;71(2):168–74.
8. Taniguchi A, Alejandro SF, Kane JM, Daoud Y, Tanaka Y, Ford SE, Brodsky JW. Association
of cavovarus foot alignment with peroneal tendon tears. Foot Ankle Int. 2021;42(6):750–6.
PubMed ID: 33847151.
9. Munk RL, Davis PH. Longitudinal rupture of the peroneus brevis tendon. J Trauma.
1976;16(10):803–6.
10. Sobel M, Geppert MJ, Hannafin JA, Bohne WH, Arnoczky SP. Microvascular anatomy of the
peroneal tendons. Foot Ankle. 1992;13(8):469–72.
11. van Dijk PA, Madirolas FX, Carrera A, Kerkhoffs GM, Reina F. Peroneal tendons well vascular-
ized: results from a cadaveric study. Knee Surg Sports Traumatol Arthrosc. 2016;24(4):1140–7.
12. Raikin SM, Elias I, Nazarian LN. Intrasheath subluxation of the peroneal tendons. J Bone Joint
Surg Am. 2008;90(5):992–9.
13. Vega J, Golanó P, Dalmau A, Viladot R. Tendoscopic treatment of intrasheath subluxation of
the peroneal tendons. Foot Ankle Int. 2011;32(12):1147–51.
14. Trono M, Tueche S, Quintart C, Libotte M, Baillon J. Peroneus quartus muscle: a case report
and review of the literature. Foot Ankle Int. 1999;20(10):659–62.
15. Miller CP, Smith SE, Goodman EM, et al. Peroneal sheath volumes are greater in patients
with peroneal pathology compared with controls. Foot Ankle Spec. 2020; https://doi.
org/10.1177/1938640020950897.
16. Bojanić I, Knežević I, Dimnjaković D. Importance of space-occupying anatomi-
cal variations in peroneal tendoscopy. Foot Ankle Int. 2020;42:448. https://doi.
org/10.1177/1071100720966325.
17. Squires N, Myerson MS, Gamba C. Surgical treatment of peroneal tendon tears. Foot Ankle
Clin. 2007;12(4):675–95, vii
18. Sammarco GJ. Peroneus longus tendon tears: acute and chronic. Foot Ankle Int.
1995;16(5):245–53.
19. Bruce WD, Christofersen MR, Phillips DL. Stenosing tenosynovitis and impingement of
the peroneal tendons associated with hypertrophy of the peroneal tubercle. Foot Ankle Int.
1999;20(7):464–7.
20. Taki K, Yamazaki S, Majima T, Ohura H, Minami A. Bilateral stenosing tenosynovitis of the
peroneus longus tendon associated with hypertrophied peroneal tubercle in a junior soccer
player: a case report. Foot Ankle Int. 2007;28(1):129–32.
21. Sobel M, Pavlov H, Geppert MJ, Thompson FM, DiCarlo EF, Davis WH. Painful os peroneum
syndrome: a spectrum of conditions responsible for plantar lateral foot pain. Foot Ankle Int.
1994;15(3):112–24.
22. Gomes MDR, Pinto AP, Fabián AA, Gomes TJM, Navarro A, Oliva XM. Insertional anatomy
of peroneal brevis and longus tendon – a cadaveric study. Foot Ankle Surg. 2019;25(5):636–9.
23. Chinitz N, Bohl DD, Reddy M, Tenenbaum S, Coleman S, Brodsky JW. Preoperative gait
analysis of peroneal tendon tears. Foot Ankle Int. 2022;43(2):233–43. Pubmed ID: 34596438.
24. Bianchi S, Bortolotto C, Draghi F. Os peroneum imaging: normal appearance and pathological
findings. Insights Imaging. 2017;8(1):59–68.
25. Major NM, Helms CA, Fritz RC, Speer KP. The MR imaging appearance of longitudinal split
tears of the peroneus brevis tendon. Foot Ankle Int. 2000;21(6):514–9.
26. Wang XT, Rosenberg ZS, Mechlin MB, Schweitzer ME. Normal variants and diseases of the
peroneal tendons and superior peroneal retinaculum: MR imaging features. Radiographics.
2005;25(3):587–602.
27. Taljanovic MS, Alcala JN, Gimber LH, Rieke JD, Chilvers MM, Latt LD. High-resolution US
and MR imaging of peroneal tendon injuries. Radiographics. 2015;35(1):179–99.
28. Gyftopoulos S, Bencardino JT. Normal variants and pitfalls in MR imaging of the ankle and
foot. Magn Reson Imaging Clin N Am. 2010;18(4):691–705.
29. Erickson SJ, Cox IH, Hyde JS, Carrera GF, Strandt JA, Estkowski LD. Effect of tendon ori-
entation on MR imaging signal intensity: a manifestation of the "magic angle" phenomenon.
Radiology. 1991;181(2):389–92.
30. Mengiardi B, Pfirrmann CW, Schöttle PB, et al. Magic angle effect in MR imaging of ankle
tendons: influence of foot positioning on prevalence and site in asymptomatic subjects and
cadaveric tendons. Eur Radiol. 2006;16(10):2197–206.
31. Ieong E, Rafferty M, Khanna M, Walker M, Rosenfeld P. Use of fat-suppressed T2-weighted
MRI images to reduce the magic angle effect in peroneal tendons. Foot Ankle Spec.
2019;12(6):513–7.
32. Adachi N, Fukuhara K, Kobayashi T, Nakasa T, Ochi M. Morphologic variations of the
fibular malleolar groove with recurrent dislocation of the peroneal tendons. Foot Ankle Int.
2009;30(6):540–4.
33. Rademaker J, Rosenberg ZS, Delfaut EM, Cheung YY, Schweitzer ME. Tear of the peroneus
longus tendon: MR imaging features in nine patients. Radiology. 2000;214(3):700–4.
34. Khoury NJ, el-Khoury GY, Saltzman CL, Kathol MH. Peroneus longus and brevis tendon
tears: MR imaging evaluation. Radiology. 1996;200(3):833–41.
35. O'Neil JT, Pedowitz DI, Kerbel YE, Codding JL, Zoga AC, Raikin SM. Peroneal tendon
abnormalities on routine magnetic resonance imaging of the foot and ankle. Foot Ankle Int.
2016;37(7):743–7.
36. Lee SJ, Jacobson JA, Kim SM, et al. Ultrasound and MRI of the peroneal tendons and associ-
ated pathology. Skelet Radiol. 2013;42(9):1191–200.
37. Grant TH, Kelikian AS, Jereb SE, McCarthy RJ. Ultrasound diagnosis of peroneal tendon
tears. A surgical correlation. J Bone Joint Surg Am. 2005;87(8):1788–94.
38. Urguden M, Gulten IA, Civan O, Bilbasar H, Kaptan C, Cavit A. Results of peroneal tendos-
copy with a technical modification. Foot Ankle Int. 2019;40(3):356–63.
39. Guelfi M, Vega J, Malagelada F, Baduell A, Dalmau-Pastor M. Tendoscopic treatment of pero-
neal intrasheath subluxation: a new subgroup with superior peroneal retinaculum injury. Foot
Ankle Int. 2018;39(5):542–50.
40. Vega J, Batista JP, Golanó P, Dalmau A, Viladot R. Tendoscopic groove deepening for chronic
subluxation of the peroneal tendons. Foot Ankle Int. 2013;34(6):832–40.
41. Wagner E, Wagner P, Ortiz C, Radkievich R, Palma F, Guzmán-Venegas R. Biomechanical
cadaveric evaluation of partial acute peroneal tendon tears. Foot Ankle Int. 2018;39(6):741–5.
42. Redfern D, Myerson M. The management of concomitant tears of the peroneus longus and
brevis tendons. Foot Ankle Int. 2004;25(10):695–707.
43. Steel MW, DeOrio JK. Peroneal tendon tears: return to sports after operative treatment. Foot
Ankle Int. 2007;28(1):49–54.
44. Demetracopoulos CA, Vineyard JC, Kiesau CD, Nunley JA 2nd. Long-term results of debride-
ment and primary repair of peroneal tendon tears. Foot Ankle Int. 2014;35(3):252–7.
45. Steginsky B, Riley A, Lucas DE, Philbin TM, Berlet GC. Patient-reported outcomes and return
to activity after peroneus brevis repair. Foot Ankle Int. 2016;37(2):178–85.
46. Wagner E, Ortiz C, Wagner P, Guzman R, Ahumada X, Maffulli N. Biomechanical evalu-
ation of various suture configurations in side-to-side tenorrhaphy. J Bone Joint Surg Am.
2014;96(3):232–6.
47. Burkhard MD, Wirth SH, Andronic O, Viehöfer AF, Imhoff FB, Fröhlich S. Clinical and func-
tional outcomes of peroneus longus to brevis tendon transfer. Foot Ankle Int. 2021;42:699.
48. Jockel JR, Brodsky JW. Single-stage flexor tendon transfer for the treatment of severe con-
comitant peroneus longus and brevis tendon tears. Foot Ankle Int. 2013;34(5):666–72.
49. Seybold JD, Campbell JT, Jeng CL, Short KW, Myerson MS. Outcome of lateral transfer of the
FHL or FDL for concomitant peroneal tendon tears. Foot Ankle Int. 2016;37(6):576–81.
50. Sherman TI, Koury K, Orapin J, Schon LC. Lateral transfer of the flexor digitorum longus for
peroneal tendinopathy. Foot Ankle Int. 2019;40(9):1012–7.
51. Seybold JD, Campbell JT, Jeng CL, Myerson MS. Anatomic comparison of lateral transfer of
the long flexors for concomitant peroneal tears. Foot Ankle Int. 2013;34(12):1718–23.
52. Jeng CL, Thawait GK, Kwon JY, et al. Relative strengths of the calf muscles based on MRI
volume measurements. Foot Ankle Int. 2012;33(5):394–9.
53. Silver RL, de la Garza J, Rang M. The myth of muscle balance. A study of relative
strengths and excursions of normal muscles about the foot and ankle. J Bone Joint Surg Br.
1985;67(3):432–7.
54. Mook WR, Parekh SG, Nunley JA. Allograft reconstruction of peroneal tendons: operative
technique and clinical outcomes. Foot Ankle Int. 2013;34(9):1212–20.
Anterior Ankle Impingement and Ankle
Instability
Jordi Vega and Miki Dalmau-Pastor
1 Anterior Impingement Syndromes
Ankle impingement syndrome is defined as mechanical pain secondary to friction

or impingement between pathological bone or soft tissue structures. Both bone and
soft tissue impingement share a clinical presentation of mechanical pain along the
anterior joint line of the ankle [1].
J. Vega (*)
Laboratory of Arthroscopic and Surgical Anatomy, Department of Pathology and
Experimental Therapeutics (Human Anatomy Unit), University of Barcelona,
Barcelona, Spain
Foot and Ankle Unit, iMove Traumatology-Clinica Tres Torres, and Hospital Quirón
Foot and Ankle Consultant, Clinique Montchoisi, Lausanne, Switzerland
M. Dalmau-Pastor
Laboratory of Arthroscopic and Surgical Anatomy, Department of Pathology and
Experimental Therapeutics (Human Anatomy Unit), University of Barcelona,
Barcelona, Spain

Switzerland AG 2022
1046 J. Vega and M. Dalmau-Pastor
1.1 Bone Impingement
Bone impingement syndrome is created by the presence of osteophytes at the ante-

rior edge of the distal tibia and/or at the neck of the talus. The formation of osteo-
phytes in the ankle can have multiple causes. In the past, repeated capsulo-ligamentous
traction of the anterior region of the ankle was believed to be the cause of osteo-
phyte formation [2]. Subsequently, a second hypothesis stated that direct contact of
the anterior articular rim of the tibia against the neck of the talus during forced
dorsiflexion of the ankle could lead to the formation of osteophytes [3]. However,
today we know that these two hypotheses are not true.
It is currently known that osteophytes develop as a result of repetitive micro-
trauma in the anterior region of the ankle joint [4, 5], or in the presence of chronic
ankle instability [6] or a combination of both.
The patient’s symptomatology should make us suspect the presence of an ante-
rior impingement. However, asymptomatic osteophytes have been found in ankle of
soccer players and dancers in 45% and 59% of cases, respectively [7]. When symp-
tomatic, clinical features include chronic pain with mechanical characteristics in the
anterior part of the ankle and variable degrees of limitation of the range of mobility
of the ankle, either in dorsiflexion, the most common scenario, or in plantar
flexion [1].
A simple radiological study can demonstrate the presence of osteophytes. On
some occasions, osteophytes located in the neck of the talus are not observed in the
frontal or lateral projections of the ankle, and if they are suspected, a lateral projec-
tion in external rotation of 15° is recommended [8].
Depending on the etiology of the osteophytes, they have different morphological
characteristics [6, 9, 10]. The osteophytes along the entire length of the anterior
tibial edge are usually related to chronic ankle instability (Fig. 1) [11, 12]. In addi-
tion, this osteophyte has a “parrot beak” shape. This particular formation is intended
to stop the anterior translation of the talus that occurs as a result of ankle instability
[10]. The osteophyte resulting from repetitive microtraumatisms is located in the
bony area most protruding from the ankle and corresponding to the anterior and
central region of the distal tibial border and/or in the medial region of the talus neck.
Repetitive microtrauma osteophytes are usually “mountainous” in shape and occupy
space in the anterior compartment of the ankle [4, 5, 10] (Fig. 2).
Other imaging studies such as computerized tomography (CT) or magnetic reso-
nance imaging (MRI) may be helpful in better defining the size and characteristics
of the osteophyte, as well as diagnosing other causes of ankle pain or the presence
of concomitant intra-articular injuries.
In the early stages of bone impingement, conservative treatment options are rec-
ommended. These include nonsteroidal anti-inflammatory drugs (NSAIDs), corti-
costeroid injections, and physical therapy, among others. However, when the patient
has a long history of symptoms, conservative treatment options are not successful,
and therefore are not recommended [13].
Anterior Ankle Impingement and Ankle Instability 1047
Fig. 1 Radiological and arthroscopic view of an anterior tibial osteophyte secondary to chronic
ankle instability
The surgical approach to this pathology consists of preferably arthroscopic

resection of osteophytes and any pathological hypertrophic soft tissue [14]. This
results in 64–88% good or excellent outcomes [13, 15–18]. The size and location of
the osteophyte, history of ankle fracture, concomitant intra-articular pathology, and
the presence of degenerative joint changes will affect overall outcomes [14,
15, 19–21].
In our experience, patients who undergo surgical treatment of osteophytes sec-
ondary to ankle instability obtain better results if they undergo a stabilization proce-
dure during the same surgical act and after the excision of the osteophyte. If it is
decided not to treat the ankle instability, partial resection of the osteophyte is recom-
mended to maintain retention of the anterior tibial translation and thus avoid the
appearance of symptoms due to instability. The amount of resected osteophyte
should be sufficient so that it does not produce the pinch.
The resection of osteophytes related to repetitive microtraumatisms has excellent
results [13, 14]. Although it has been demonstrated that the rates of recurrence and
formation of new osteophytes are 66–100%, especially if the activity that had
caused them is maintained, the recurrence of osteophytes does not imply the reap-
pearance of symptoms [1, 22, 23]. In general, in the presence of degenerative joint
changes, the clinical results obtained from the resection of osteophytes are inferior
compared to joints without chondral damage [1].
Fig. 2 Radiological and arthroscopic vision of a tibia and talus neck osteophyte secondary to
repetitive trauma
1.2 Soft Tissue Impingement
Soft tissue impingement syndrome was described by Ferkel [24, 25]. The most
common origin occurs after an ankle sprain (ankle inversion) and presents as pain
in the anterolateral region of the ankle. Different types of soft tissue impingement
have been described: that produced by the inferior fascicle of the anterior tibiofibu-
lar ligament (ATiFL) or Bassett’s ligament, that caused by the generation of patho-
logical soft tissue at the level of the lateral recess of the ankle, and finally that
caused after an ankle fracture or prolonged immobilization after trauma.
The presence of chronic anterolateral mechanical pain after an ankle inversion
should make the surgeon suspect the presence of soft tissue impingement. Similarly,
chronic pain following a properly treated ankle fracture should also make the sur-
geon suspect the presence of pathological soft tissue impingement as the cause of
this pain.
1.2.1 Impingement by the Lower Fascicle of the ATiFL (Fig. 3)
Etiology
In the past, increased contact between the inferior fasciculus of ATiFL and the talus
was considered to be a cause of ankle pain at the anterolateral level [26]. However,
contact between the inferior fasciculus of ATiFL and the anterolateral portion of the
talus is a constant finding [27]. Anterior laxity or chronic ankle instability may
cause increased contact between the lower fascicle of the ATiFL and the talus dome
due to abnormal anterior translation of the talus [10, 28–30]. For this reason, in the
case of pain located in the region of the lower fascicle of the LFTF, the ankle should
always be inspected for mechanical instability due to ligament injury of the lateral
collateral complex [30].
Diagnosis
The presence of chronic pain in the anterior region of the syndesmosis, after an ankle
sprain and in the absence of instability of the tibiofibular joint, should make the sur-
geon suspect the presence of impingement by the inferior fascicle of the ATiFL.
Imaging studies in this type of impingement are not very useful and will only
inform us of concomitant intra-articular pathology. On the other hand, instability of
the syndesmal joint must be ruled out. In the case of suspicion of possible instability
of the syndemosis as a cause of pain in the area, it is recommended that an arthros-
copy be carried out and the joint explored directly [31].
Treatment
Initial treatment in this type of impingement should always be conservative in the
form of oral NSAIDs, corticosteroid injections, and physical therapy. When
a b
Fig. 3 Impingement of ankle soft tissue by anterior tibiofibular ligament (ATiFL) pathology. (a)
The hook probe explores a pathological fibrous band of the ATiFL that causes a chondral imprint
on the anterolateral edge of the talus (indicated with arrows). (b) The hook probe explores the
chondral lesion caused by a pathological ATiFL (1)
conservative treatment fails, surgical treatment should be considered, which will

consist of debriding the pathological soft tissue located in the area, and if necessary,
resection of the lower fascicle of the ATiFL [26, 28]. The decision to resect or not
the lower fascicle of the ATiFL will be based on the presence of anatomical variants
or thickening of this fascicle. However, it should be considered that in the presence
of lateral instability of the ankle and with a normal appearance of the lower fascicle
of ATiFL, it is recommended only to stabilize the ankle when repairing or recon-
structing the lateral ligament complex [10]. Stabilization of the ankle will slow the
anterior translation of the talus, and consequently the excess friction between the
lower fascicle of ATiFL and the talus will be diminished making it unnecessary to
resect the fascicle.
1.2.2 Impingement Due to the Presence of Pathological Soft Tissue After

Ankle Sprain (Fig. 4)
Etiology
In the classic description of soft tissue impingement [24, 25], patients usually pres-
ent a history of ankle inversion and injury of the anterolateral capsule and lateral
ligament structures. It is considered that inadequate treatment of ankle sprains
could lead to an inflammatory process in the area of the injury, followed by the
creation of synovitis and sometimes the formation of prominent scar tissue.
However, we now know that the isolated soft tissue impingement described by
Ferkel is rare, and that the vast majority of these patients have a ligament injury,
usually an isolated lesion of the upper anterior talofibular ligament (ATFL). Injury
a b
Fig. 4 Impingement of ankle soft tissues secondary to ankle sprain due to the presence of
inflammatory-scar tissue in the lateral ankle recess (a) and in the anterolateral region of the ante-
rior compartment (b). 1. Peroneal malleolus. 2. Anterior region of the tibia. 3. Talus
to this upper fascicle of the ATFL is related to a lesser degree of ankle instability or
microinstability [10, 30].
Diagnosis
Patients who suffer from anterolateral impingement due to the presence of patho-
logical soft tissue often present with chronic anterolateral pain, feelings of instabil-
ity, recurrent episodes of ankle sprain, or a combination of these symptoms.
Simple radiology and CT are not very useful for performing the image diagnosis
of soft tissue impingement. However, they can allow the diagnosis of other con-
comitant pathologies in addition to ruling out other causes of ankle pain.
MRI is the most widely used test for the study of soft tissue impingement. The
most frequent finding is the presence of a soft tissue mass in the lateral recess,
which is hypointense in T1 and hypo-isointense in T2. However, it should be con-
sidered that the diagnostic capacity of soft tissue impingement by MRI is very vari-
able, finding sensitivities from 39% to 100% and specificities from 50% to
100% [32].
MRI with intra-articular injected contrast can improve diagnostic accuracy by
obtaining a sensitivity of 96%, a specificity of 97% and a negative predictive value
of 100% [33, 34].
Treatment
Conservative treatment is the first line of treatment in the form of oral NSAIDs,
corticosteroid injections, and physical therapy. Preferably, arthroscopic debride-
ment of pathological soft tissues should be considered when conservative treatment
fails. Since most patients have an underlying microinstability of the ankle due to an
upper fascicle ATFL injury, treatment of this ligament injury by repair or recon-
struction will prevent recurrence of symptoms.
Several studies report the results of arthroscopic debridement isolated from
pathologic soft tissue. Although there is great heterogeneity in study design, one
systematic review showed good to excellent results ranging from 74% to 100% of
cases [25, 34–43]. None of the studies addressed the component of instability dur-
ing arthroscopic ankle joint debridement. These results should be interpreted with
caution due to the difficulty of comparing studies. In our experience, no recurrence
of symptoms has been observed in patients treated with a combination of arthroscopic
soft tissue debridement and ligament repair. This contrasts with the reported recur-
rence of 26% of symptoms when isolated debridement of pathologic soft tissue is
performed without ligament repair [42].
1.2.3 Soft Tissue Impingement as a Consequence of an Ankle Fracture
Etiology
After ankle fractures or after prolonged immobilization, patients may experience
residual discomfort that is often caused by synovitis and arthrofibrosis, and occa-
sionally by the presence of intra-articular free bodies [44].
Arthrofibrosis is the main cause of joint discomfort after an ankle fracture, being
found in 73% of patients. For ankles with symptoms after a fracture, arthrofibrosis
is present in 100% of cases [45].
Diagnosis
Arthrofibrosis, or the presence of pathological scar tissue within the joint, often
causes the “feeling of joint occupation” in the ankle or stiffness. Although a
decrease in the ankle’s range of motion may be observed, the most common patient
complaint is discomfort created by the joint’s occupation of the pathological
scar tissue.
Treatment
When conservative treatment consisting of rehabilitation and intra-articular steroid
injections fails, arthroscopic debridement has been shown to be effective in improv-
ing joint function [46–48]. Resection of the fibrous bands in the anterior compart-
ment, as well as debridement of the leaks, offers excellent results [46, 49]. In our
experience, preoperative clinical symptoms will improve after resection of the
fibrous bands, but the range of motion of the ankle joint will not necessarily improve
in cases where it is impaired.
2 Ankle Instability
Instability is a common problem in the ankle area. Classically, two types of ankle
instability have been described: functional instability and mechanical instability.
Mechanical instability occurs as a consequence of an injury to the lateral ligament
complex, while functional instability involves neuromuscular alteration without
ligament injury.
In general, mechanical instability of the ankle occurs as a consequence of an
ankle sprain in inversion. It is estimated that between 10% and 15% of ankle sprains
will suffer from mechanical instability [50].
The origin of any lateral ankle instability is a sprain in inversion. Ankle sprains
are one of the most common incidents in both sports and everyday activities. Despite
this high incidence, even today, ankle sprains are considered to be a minor incident
with little impact. In general, ankle sprains are usually reversed and of a lower or
moderate energy level. The anterior talofibular ligament (ATFL) is the first ligament
to be injured after an ankle inversion injury, and on many occasions, it is the only
one that is injured. The susceptibility to injury of this ligament, particularly its
upper fascia, is due to the fact that ATFL is the weakest component of the lateral
collateral ligament of the ankle, and that it is the first ligament to be stretched during
ankle inversion. In more severe cases, the reversal trauma continues, and the injury
can spread to injure the lower fascia of the ATFL, and then the calcaneal-fibular
ligament (CFL). Eventually, the posterior talofibular ligament may be injured,
resulting in dislocation of the ankle.
2.1 Anatomy in Ankle Instability
A thorough understanding of the anatomy and biomechanics of the ankle ligaments

is necessary to understand and treat ankle instability, and new concepts such as
microinstability and rotational instability that affect the ankle.
Classically, ATFL has been described as a ligament consisting of 1, 2, or 3 fas-
cicles [51]. However, in a recent study, it was confirmed that ATFL is a ligament
constantly formed by two fascicles, one upper and one lower [52]. The upper fas-
cicle has been shown to be a different ligament than the lower fascicle. The upper
fascia of ATFL is an intra-articular structure that relaxes in dorsal flexion and tight-
ens in plantar flexion of the ankle. Due to its intra-articular location, when it is
injured and as a consequence of the synovial environment of the joint [53], the
upper fascicle of ATFL has no healing capacity and always remains deficient. From
a clinical point of view, injury to the upper fascicle of ATFL will result in a lesser
degree of instability or microinstability [30].
On the other hand, the lower fascicle of ATFL is observed to be related to
CFL. Both ligaments have a common fibular origin and are connected to each other
by the presence of arch-shaped fibers. The connection fibers observed between both
ligaments are crucial for their functioning. The arch-shaped fibers are strong enough
to transmit the tensions between the lower bundle of the ATFL and the CFL, which
causes both ligaments to work simultaneously as a single functional unit. This func-
tional and anatomical unit has been referred to as the lateral fibulocalcaneal liga-
ment complex (LFTCL) [52]. The LFTCL is an extra-articular ligament structure,
and therefore when injured has some capacity for repair if treated properly. Its defi-
cit would result in ankle instability as classically described.
2.2 Treatment of Ankle Instability
The initial form of treatment for ankle instability is conservative. When the instabil-
ity and its symptoms fail and are maintained, surgery should be considered.
Neuromuscular training is the basis for conservative treatment of ankle instabil-
ity. However, neuromuscular training only appears effective in the short term, and
its effect disappears over time [54–56].
Ankle instability has been shown to be a predisposing factor in the generation
of arthrosis and other intra-articular disorders. For this reason, the restoration of
stability of the tibiotalar joint is critical to curb such joint alterations. Although
the conservative treatment can reduce the symptomatology in the patients with
chronic instability of the ankle, it usually does not stop the instability that in
many cases is going to need a surgical treatment to obtain a correct articular
stabilization.
More than 80 surgical procedures have been described for the treatment of ankle
instability [57]. In general, we can group them into three major groups: anatomical
ligament repair, anatomical ligamentoplasty or reconstruction, and nonanatomical

ligamentoplasty or reconstruction.
Anatomical ligament repair aims to restore joint stabilization by repairing the
remaining ligament. Some type of augmentation can be added to the repair to pro-
tect that repair. The use of the lower extensor retinaculum is the anatomical struc-
ture most frequently used to augment ligament repair.
The reconstruction or ligamentoplasty is the technique that replaces the liga-
ments usually by tendons. This substitution can be done in an anatomical or nonana-
tomical way.
Anatomical techniques are preferred to nonanatomical techniques, and repair to
reconstruction.
Anatomic ligament repair restores the anatomy of the ligaments while maintain-
ing joint kinematics [58]. In this sense, anatomic repair is above all other surgical
techniques and is currently considered the gold standard technique [59–63].
In the anatomical repair of the ligaments by means of open surgery or the
Broström technique, the patient is placed in a supine position with the limb in inter-
nal rotation, or in a lateral position. The most common incision is made along the
anterior edge of the distal fibula, curving into a posterior J shape, and stopping at the
level of the peroneal tendons. Alternative incisions can be used if concomitant
pathology is to be treated. The lateral branch of the superficial peroneal nerve should
be avoided before, and the sural nerve afterwards. Next, a dissection is performed
down to the ankle joint capsule and its ligaments. The injured ligament may be
avulsed or elongated. In the case of elongation, the ligament and capsule must be
sectioned at the fibular level and then repaired with greater tension. For the repair,
one or more anchors inserted into the fibula are usually used. The anchorage sutures
are passed through the injured ligament and the capsule to subsequently provide
tension when the sutures are tied. The ligaments are repaired in a neutral position
and with discreet eversion of the ankle.
Multiple studies have shown excellent results with anatomical repair [62, 64, 65].
In addition, these results have been shown to be sustained over time [65].
However, patients with instability and poor-quality ligament tissue, history of previ-
ous repair, widespread ligament laxity, or cavus-varus deformity of the foot have
had poor results with anatomical repair. In these patients, another type of stabilizing
technique should be considered, with the modifications of the technique described
by Broström obtaining better results [59]. The main modification described is that
which performs a biological augmentation using the distal extensor retinaculum as
a reinforcement, or Gould’s modification. Recently, nonbiological augmentation
using high-strength suture has been described with excellent results and has become
popular as an internal brace®.
When the ligamentary remnant is of poor quality or is absent, and its repair is not
possible, reconstruction or ligamentoplasty is recommended.
The nonanatomical reconstruction techniques are based on procedures that
achieve stabilization of the ankle by restricting the mobility of the ankle without
repairing the ligaments. Usually, a tendon is used that is arranged without following
the anatomical orientation of the ligaments. The most frequently used tendon is the
peroneus brevis, which is totally or partially removed and is oriented with different
configurations. In long-term studies, high rates of complications have been found,
especially joint stiffness, in addition to arthrosis in the ankle and subtalar joints.
This is attributed to an alteration of the joint mechanics after this type of procedure
[61, 66]. Anatomical reconstruction techniques aim to replace the ligaments with a
tendon graft and following the anatomy of the original ligaments. The techniques of
reconstruction or ligamentoplasty can cause morbidity of the donor site especially
when using the peroneus brevis, so it is recommended that other tendons such as
gracilis, or the use of allograft, are used and thus avoid sacrificing the peroneal ten-
dons [67, 68].
2.3 Arthroscopic Treatment of Ankle Instability
Arthroscopic treatment of ankle instability has generated great interest among foot
and ankle surgeons. In chronic ankle instability, the presence of secondary intra-
articular pathology with the potential to generate pain and dysfunction is frequent.
Treatment of the pathology associated with ankle instability is essential to obtain a
better outcome [69–73]. For this reason, when treating ankle instability, arthroscopy
should be considered prior to treatment of the ligaments.
In recent years, a greater role for arthroscopy in the definitive treatment of ankle
instability has been proposed following the development of arthroscopic techniques
that make it possible to repair or replace injured ligaments.
After the appearance of thermal contraction or thermoretraction for shoulder lax-
ity, similar methods were contemplated in the ankle [74, 75]. However, thermal
contraction of the capsuloligamentous structures of the ankle has shown worse
results than in the shoulder when it comes to mechanical instability, and at present
this technique is not in use [76].
Although some attempts at arthroscopic repair of the lateral ligament complex
have been reported in the past [77, 78], no successful results were obtained mainly
due to the lack of adequate instrumentation. Advances in ankle instrumentation and
arthroscopic techniques contributed to successful results in the treatment of mechan-
ical ankle instability.
More recently, a mixed, percutaneous, and arthroscopically assisted technique,
popularized as ArthroBroström, expanded rapidly because it was a simple technique
with excellent results [79–82]. Although originally described as a safe procedure
[83], a high rate of complications has been reported (5.3–29%) [79–81]. The most
common complications include damage to the superficial peroneal nerve or the
sural nerve, probably related to the percutaneous steps of the procedure. Other com-
mon complications of this procedure include pain or discomfort from a prominent
anchor or suture knot.
To avoid the inherent risks of percutaneous steps, an arthroscopic technique was
developed that repairs the lateral collateral ligament using a completely arthroscopic
procedure with knotless suture anchors [84]. With this technique popularized as an
all-inside repair, the lateral collateral ligament is repaired under direct arthroscopic
vision. This technique has been shown to be a safe and reproducible procedure [85].
Excellent results have been reported, with low rates of complications, most of which
are minor (Fig. 5).
The arthroscopic technique that repairs “all-inside” the ankle ligaments uses the
usual anterolateral and anteromedial portals. By means of an arthroscopic technique
without joint distraction and after treating the possible concomitant pathology, the
ligamentary remnant is evaluated and the insertional footprint of the injured liga-
ment is debrided with an arthroscopic shaver (Fig. 6). An accessory anterolateral
portal is then created just anterior to the fibula, and approximately 1–1.5 cm proxi-
mal to the tip of the lateral malleolus. With a suture pin inserted through the antero-
lateral portal, and under direct arthroscopic visualization, the injured ligament is
penetrated from lateral to medial. The nitinol in the suture pin is pushed and retrieved
through the accessory portal with the aid of an arthroscopic forceps (Fig. 7). The
nitinol is exchanged for a high-strength suture bent in half. With the help of an
arthroscopic forceps introduced through the anterolateral portal, the suture is recov-
ered. Then, one or both ends of the suture are inserted into the loop, and by pulling
on the ends of the suture, the loop descends and ends up grasping the ligament.
Finally, the correct location for the placement of the bone anchor is identified, and
the tunnel for the anchorage is made. A knotless anchor is loaded with the suture
and inserted into the tunnel with the ankle in dorsiflexion and valgus (Fig. 8).
In a recent comparative study between ArthroBroström and all-inside repair, it
has been observed that although the clinical results may be similar, allowing both to
stabilize correctly, ArthroBroström has a greater number of complications, most of
which are related to entrapment of the superficial peroneal nerve and painful restric-
tion of plantar flexion [86].
a b
Fig. 5 Arthroscopic vision of an anterior talofibular ligament (ATFL) rupture (a), and after its
completely arthroscopic repair (b)
a b
Fig. 6 The fibular footprint of the ATFL must be debrided with the help of an arthroscopic shaver
before ligament repair (a). View of the footprint and ATFL prepared for repair (b)
Fig. 7 Steps of fully arthroscopic ATFL repair. The ATFL is penetrated by a suture pin whose
nitinol is removed by an accessory portal and subsequently replaced by a suture
Fig. 8 Steps of the arthroscopic ATFL repair. Once the suture has grasped the ligament, the ATFL
is reinserted into its fibular footprint with a knotless anchorage
Repair techniques have as a limitation the repair of a poor quality ligamentary

remnant. In these cases, the use of augmentations added to the repair is recom-
mended. Augmentations are intended to protect the ligament repair for at least the
period in which the ligament is biologically repaired. Two types of arthroscopic
augmentation have been described: biological and nonbiological. Biological aug-
mentation uses the lower extensor retinaculum (arthroscopic Gould) [87], or the
distal portion of the tibiofibular ligament (arthroscopic Bassett’s ligament transfer)
[88]. Recently, nonbiological augmentation using a high-strength suture has become
popular, and the arthroscopic version has also been described [89].
In the absence of a ligamentary remnant, repair is not possible and a ligamento-
plasty must be indicated. The arthroscopic ligamentoplasty procedure has been
described [90–92]. Using a gracilis autograft, both the ATFL and the CFL are recon-
structed at the same time. However, ligamentoplasty has limited indications [92]. In
addition, arthroscopic ligamentoplasty is a demanding technique, even for an expe-
rienced foot and ankle arthroscopist. Some structures are at risk of injury during the
procedure (superficial and sural peroneal nerve, peroneal tendons, distal portion of
the fibula, and talus neck). Although this technique opens up a new treatment pos-
sibility, more studies are needed to confirm the accuracy and reproducibility of
arthroscopic ligamentoplasty reconstructions.
2.4 New Concepts in Ankle Instability
Recently, two new concepts have been described in the mechanical instability of the
ankle: the microinstability and the rotational instability of the ankle.
2.4.1 Microinstability of the Ankle
Microinstability is not a new concept in orthopedics. However, it is a young concept

in the ankle [10, 30, 93].
Ankle microinstability is a potential cause of ankle pain and disability. The path-
ological mechanism of ankle microinstability is an injury to the upper fasciculus of
the ATFL as a result of an ankle sprain [30]. The ligament deficit caused by the
injury would cause an abnormal increase in movement of the talus with respect to
the tibia. Eventually, this alteration may damage the articular cartilage of the ankle
joint, or injure the medial ligament complex, or cause impingement syndromes, or
a combination of all [94].
Although injury to the upper fascia of the ATFL can be seen in most patients after
an ankle sprain, ankle microinstability is usually asymptomatic. When patients
become symptomatic, they describe a subjective feeling of ankle instability, or
recurrent symptomatic ankle sprains, or anterolateral pain, or a combination of
these symptoms. Many of the patients diagnosed with the diagnosis of anterolateral
soft tissue impingement syndrome have an upper ATFL fascicle injury, and as a
consequence, may have ankle microinstability as a source of pain [30].
The diagnosis of ankle microinstability is based primarily on the patient’s medi-
cal history and a physical examination to rule out the presence of chronic ankle
instability as classically described or other ankle disorders [93]. Stress radiographic
evaluation will not show any signs of instability. Conventional MRIs are generally
not useful in reaching a diagnosis, since they are not capable of showing the upper
ATFL fascicle injury. The evaluating radiologist or surgeon needs to have a high
level of suspicion to detect the upper ATFL fascicle lesion, which is often a smaller
lesion. The use of other imaging techniques can be helpful in reaching a diagnosis
of ankle microinstability, especially ultrasound or MRI with intra-articular contrast,
but studies are required to know the value of these studies.
As with other joints, ankle microinstability should be treated initially conserva-
tively with rehabilitation. Surgical treatment of ankle microinstability should focus
on addressing the underlying etiology and associated intra-articular pathology. The
recommended surgical treatment will consist of arthroscopic repair of the ligamen-
tous injury [93].
2.4.2 Rotational Instability of the Ankle
Patients with chronic ankle instability may have both medial and lateral symptoms
[70]. Deltoid ligament abnormalities have been described in patients with chronic
ankle instability [70, 95–97]. Under loading conditions, ankle with ATFL deficiency
show a significant increase in anterior, superior, and internal rotation of the talus
[98]. These biomechanical changes may lead to partial injury of the deltoid liga-
ment in its most anterior part and control the external rotation of the talus. Injury to
this area of the deltoid ligament, together with injury to the lateral ligament com-
plex, will lead to a release of the rotation of the talus within the tibiofibular shroud.
Injury of the anterior region of the deltoid ligament, together with injury of the
lateral ligament complex suggests rotational instability. The lesion observed at the
deltoid level has been described as an “open book lesion,” as the most anterior com-
ponent of the deltoid ligament is observed to be separated from the medial malleo-
lus. Because the deltoid ligament provides stability in external rotation [99, 100],
patients with lateral collateral ligament deficiency and secondary deltoid ligament
injury may express complaints in both the medial and lateral ankle areas. In those
cases, the ankle presents no limitations for internal and external rotation.
Rotational instability is difficult to evaluate clinically, and it is not uncommon
for patients to not report any medial complaints [101]. MRI or MRI with intra-
articular contrast may be useful when this type of instability is suspected. Although
a lack of medial discomfort may be observed in patients with rotational instability,
some patients may experience medial discomfort after lateral ligament repair or
reconstruction if a deltoid ligament is injured. Therefore, it is always recommended
to evaluate the medial ligament complex when performing a lateral ligament repair
or reconstruction. The presence of an open book injury to the deltoid ligament in
patients with chronic ankle instability suggests rotational instability. In addition to

repair or reconstruction of the lateral collateral ligament, the deltoid ligament should
also be repaired [101].
References
1. Tol JL, van Dijk CN. Anterior ankle impingement. Foot Ankle Clin. 2006;11(2):297–310, vi.
2. McMurray TP. Footballer’s ankle. J Bone Joint Surg. 1950;32-B(1):68–9.
3. O'Donoghue DH. Impingement exostoses of the talus and the tibia. J Bone Joint Surg.
1957;39-A(4):835–52.
4. Tol JL, Slim E, van Soest AJ, van Dijk CN. The relationship of the kicking action in soccer
and anterior ankle impingement syndrome. A biomechanical analysis. Am J Sports Med.
2002;30(1):45–50.
5. Tol JL, van Dijk CN. Etiology of the anterior ankle impingement syndrome: a descriptive
anatomical study. Foot Ankle Int. 2004;25(6):382–6.
6. van Dijk CN, Bossuyt PM, Marti RK. Medial ankle pain after lateral ligament rupture. J Bone
Joint Surg Br. 1996;78(4):562–7.
7. Cheng JC, Ferkel RD. The role of arthroscopy in ankle and subtalar degenerative joint dis-
ease. Clin Orthop Relat Res. 1998;349:65–72.
8. Van Dijk CN, Wessel RN, Tol JL, Mass M. Oblique radiograph for the detection of bone spurs
in anterior ankle impingement. Skelet Radiol. 2002;31:214–21.
9. Vaseenon T, Amendola A. Update on anterior ankle impingement. Curr Rev Musculoskelet
Med. 2012;5(2):145–50.
10. Vega J, Dalmau M, Malagelada F, Fargues-Polo B, Peña F. Ankle arthroscopy: An update. J
Bone Joint Surg Am. 2017;99:1395–407.
11. Scranton PE Jr, McDermott JE, Rogers JV. The relationship between chronic ankle instability
and variations in mortise anatomy and impingement spurs. Foot Ankle Int. 2000;21(8):657–64.
12. Hayeri MR, Trudell DJ, Resnick D. Anterior ankle impingement and talar bony outgrowths:
osteophyte or enthesophyte? Paleopathologic and cadaveric study with imaging correlation.
AJR Am J Roentgenol. 2009;193(4):334–8.
13. van Dijk CN, Tol JL, Verheyen CP. A prospective study of prognostic factors concerning
the outcome of arthroscopic surgery for anterior ankle impingement. Am J Sports Med.
1997;25(6):737–45.
14. Tol JL, Verheyen CP, van Dijk CN. Arthroscopic treatment of anterior impingement in the
ankle. J Bone Joint Surg Br. 2001;83(1):9–13.
15. Scranton PE Jr, McDermott JE. Anterior tibiotalar spurs: a comparison of open versus
arthroscopic debridement. Foot Ankle. 1992;13(3):125–9.
16. Ogilvie-Harris DJ, Mahomed N, Demazière A. Anterior impingement of the ankle treated by
arthroscopic removal of bony spurs. J Bone Joint Surg Br. 1993;75(3):437–40.
17. Branca A, Di Palma L, Bucca C, Visconti CS, Di Mille M. Arthroscopic treatment of anterior
ankle impingement. Foot Ankle Int. 1997;18(7):418–23.
18. Rasmussen S, Hjorth JC. Arthroscopic treatment of impingement of the ankle reduces pain
and enhances function. Scand J Med Sci Sports. 2002;12(2):69–72.
19. Cavallo M, Natali S, Ruffilli A, Buda R, Vannini F, Castagnini F, Ferranti E, Giannini
S. Ankle surgery: focus on arthroscopy. Musculoskelet Surg. 2013;97(3):237–45.
20. Parma A, Buda R, Vannini F, Ruffilli A, Cavallo M, Ferruzzi A, Giannini S. Arthroscopic
treatment of ankle anterior bony impingement: the long-term clinical outcome. Foot Ankle
Int. 2014;35(2):148–55.
21. Zwiers R, Wiegerinck JI, Murawski CD, Fraser EJ, Kennedy JG, van Dijk CN. Arthroscopic
treatment for anterior ankle impingement: a systematic review of the current literature.
Arthroscopy. 2015;31(8):1585–96.
22. Coull R, Raffiq T, James LE, Stephens MM. Open treatment of anterior impingement of the
ankle. J Bone Joint Surg Br. 2003;85(4):550–3.
23. Walsh SJ, Twaddle BC, Rosenfeldt MP, Boyle MJ. Arthroscopic treatment of anterior ankle
impingement: a prospective study of 46 patients with 5-year follow-up. Am J Sports Med.
2014;42(11):2722–6.
24. Ferkel RD, Fisher SP. Progress in ankle arthroscopy. Clin Orthop. 1989;240:210–20.
25. Ferkel RD, Karzel RP, Del Pizzo W, Friedman MJ, Fischer SP. Arthroscopic treatment of
anterolateral impingement of the ankle. Am J Sports Med. 1991;19(5):440–6.
26. Bassett FH 3rd, Gates HS 3rd, Billys JB, Morris HB, Nikolaou PK. Talar impingement by
the anteroinferior tibiofibular ligament. A cause of chronic pain in the ankle after inversion
sprain. J Bone Joint Surg Am. 1990;72(1):55–9.
27. Dalmau M, Malagelada F, Kerkhoffs GMMJ, Karlsson J, Manzanares MC, Vega J. The ante-
rior tibiofibular ligament has a constant distal fascicle that contacts the antererolateral part of
the talus. Knee Surg Sports Traumatol Arthrosc. 2020;28(1):48–54. https://doi.org/10.1007/
s00167-018-5123-z.
28. Akseki D, Pinar H, Yaldiz K, Akseki NG, Arman C. The anterior tibiofibular ligament and talar
impingement: a cadaveric study. Knee Surg Sports Traumatol Arthrosc. 2002;10(5):321–6.
29. Am C, Lee JY, Spritzer CE, Easley ME, Deorio JK, Nunley JA 2nd, Defrate LE. In
vivo kinematics of the tibiotalar joint after lateral ankle instability. Am J Sports Med.
2009;37(11):2241–8.
30. Vega J, Peña F, Golanó P. Minor or occult ankle instability as a cause of anterolateral pain
after ankle sprain. Knee Surg Sports Traumatol Arthrosc. 2016;24(4):1116–23.
31. Takao M, Ochi M, Naito K, Iwata A, Kawasaki K, Tobita M, Miyamoto W, Oae K. Arthroscopic
diagnosis of tibiofibular syndesmosis disruption. Arthroscopy. 2001;17(8):836–43.
32. Spiga S, Vinci V, Tack S, Macarini L, Rossi M, Coppolino F, et al. Diagnostic imaging of
ankle impingement syndromes in athletes. Musculoskelet Surg. 2013;97(Suppl 2):S145–53.
33. Robinson P, White LM, Salonen DC, Daniels TR, Ogilvie-Harris D. Anterolateral impinge-
ment of the ankle: MR arthrographic assessment of the anterolateral recess. Radiology.
2001;221:186–90.
34. Datir A, Connell D. Imaging of impingement lesions in the ankle. Top Magn Reson Imaging.
2010;21:15–23.
35. Meislin RJ, Rose DJ, Parisien JS, Springer S. Arthroscopic treatment of synovial impinge-
ment of the ankle. Am J Sports Med. 1993;21(2):186–9.
36. Liu SH, Raskin A, Osti L, Baker C, Jacobson K, Finerman G, Barber C. Arthroscopic treat-
ment of anterolateral ankle impingement. Arthroscopy. 1994;10(2):215–8.
37. Gulish HA, Sullivan RJ, Aronow M. Arthroscopic treatment of soft-tissue impingement
lesions of the ankle in adolescents. Foot Ankle Int. 2005;26(3):204–7.
38. Urgüden M, Söyüncü Y, Ozdemir H, Sekban H, Akyildiz FF, Aydin AT. Arthroscopic treat-
ment of anterolateral soft tissue impingement of the ankle: evaluation of factors affecting
outcome. Arthroscopy. 2005;21(3):317–22.
39. Hassan AH. Treatment of anterolateral impingements of the ankle joint by arthroscopy. Knee
40. Villarreal JM, Cerecedo RB, Cal y Mayor FF, González IL. Arthroscopic treatment for
anterolateral ankle impingement of athletes. Acta Ortop Mex. 2008;22(2):103–6.
41. Moustafa El-Sayed AM. Arthroscopic treatment of anterolateral impingement of the ankle. J
Foot Ankle Surg. 2010;49(3):219–23.
42. Franco R, Vega J, Pérez M, Redó D, Ramazzini JR, Dalmau A. Results in the arthroscopic
treatment of soft-tissue impingement of the ankle. Rev Pie Tobillo. 2010;24(2):24–9.
43. Mardani-Kivi M, Mirbolook A, Khajeh-Jahromi S, Hassanzadeh R, Hashemi-Motlagh K,

Saheb-Ekhtiari K. Arthroscopic treatment of patients with anterolateral impingement of the
ankle with and without chondral lesions. J Foot Ankle Surg. 2013;52(2):188–91.
44. van Dijk CN, Verhagen RA, Tol JL. Arthroscopy for problems after ankle fracture. J Bone
Joint Surg Br. 1997;79(2):280–4.
45. Thomas B, Yeo JM, Slater GL. Chronic pain after ankle fracture: an arthroscopic assessment
case series. Foot Ankle Int. 2005;26(12):1012–6.
46. Utsugi K, Sakai H, Hiraoka H, Yashiki M, Mogi H. Intra-articular fibrous tissue formation
following ankle fracture: the significance of arthroscopic debridement of fibrous tissue.
Arthroscopy. 2007;23(1):89–93.
47. Kim HN, Park YJ, Kim GL, Park YW. Arthroscopy combined with hardware removal for
chronic pain after ankle fracture. Knee Surg Sports Traumatol Arthrosc. 2013;21(6):1427–33.
48. Dawe EJ, Jukes CP, Ganesan K, Wee A, Gougoulias N. Ankle arthroscopy to manage sequelae
after ankle fractures. Knee Surg Sports Traumatol Arthrosc. 2015;23(11):3393–7.
49. Valkering KP, Golanó P, van Dijk CN, Kerkhoffs GM. “Web impingement” of the ankle: a
case report. Knee Surg Sports Traumatol Arthrosc. 2013;21(6):1289–92.
50. Ferran NA, Maffulli N. Epidemiology of sprains of the lateral ankle ligament complex. Foot
Ankle Clin N Am. 2006;11:659–62.
51. Milner CE, Soames RW. Anatomy of the collateral ligaments of the human ankle joint. Foot
Ankle Int. 1998;19:757–60.
52. Vega J, Malagelada F, Manzanares MC, Dalmau M. The lateral fibulotalocalcaneal ligament
complex: an ankle stabilizing isometric structure. Knee Surg Sports Traumatol Arthrosc.
2020;28(1):8–17.
53. Murray MM. Current status and potential for primary ACL repair. Clin Sports Med.
2009;28(1):51–61.
54. Lentell G, Baas B, Lopez D, McGuire L, Sarrels M, Snyder P. The contributions of proprio-
ceptive deficits, muscle function, and anatomic laxity to functional instability of the ankle. J
Orthop Sports Phys Ther. 1995;21:206–15.
55. Gerber JP, Williams GN, Scoville CR, Arciero RA, Taylor DC. Persistent disability associ-
ated with ankle sprains: a prospective examination of an athletic population. Foot Ankle Int.
1998;19:653–60.
56. De Vries JS, Krips R, Sierevelt IN, Blankevoort L, van Dijk CN. Interventions for treating
chronic ankle instability. Cochrane Database Syst Rev. 2011;10(8):CD004124.
57. DiGiovanni CW, Brodsky A. Current concepts: lateral ankle instability. Foot Ankle Int.
2006;27:854–66.
58. Broström L, Sprained ankles V. Treatment and prognosis in recent ligament ruptures. Acta
Chir Scand. 1966;132:537–50.
59. Liu SH, Baker CL. Comparison of lateral ankle ligamentous reconstruction procedures. Am
J Sports Med. 1994;22:313–7.
60. Hollis JM, Blasier RD, Flahiff CM, Hofmann OE. Biomechanical comparison of reconstruc-
tive techniques in simulated lateral ankle ligament injury. Am J Sports Med. 1995;23:678–82.
61. Bahr R, Pena F, Shine J, Lew WD, Tyrdal S, Engebretsen L. Biomechanics of ankle ligament
reconstruction: An in vitro comparison of the Brostrom repair, Watson-Jones reconstruction,
and a new anatomic reconstruction technique. Am J Sports Med. 1997;25:424–32.
62. Krips R, van Dijk CN, Halasi PT, Lehtonen H, Corradini C, Moyen KJ. Long-term outcome
of anatomical reconstruction versus tenodesis for the treatment of chronic anterolateral insta-
bility of the ankle joint: a multicenter study. Foot Ankle Int. 2001;22(5):415–21.
63. Fujii T, Kitaoka HB, Watanabe K, Luo ZP, An KN. Comparison of modified Brostrom and
Evans procedures in simulated lateral ankle injury. Med Sci Sports Exerc. 2006;38:1025–31.
64. Hamilton WG, Thompson FM, Snow SW. The modified Brostrom procedure for lateral ankle
instability. Foot Ankle. 1993;14(1):1–7. 71
65. Bell SJ, Mologne TS, Sitler DF, Cox JS. Twenty-six-year results after Brostrom procedure for
chronic lateral ankle instability. Am J Sports Med. 2006;34(6):975–8.
66. Kennedy JG, Smyth NA, Fansa AM, Murawski D. Anatomical lateral ligament recon-
struction in the ankle. A hybrid technique in the athletic population. Am J Sports Med.
2012;40:2309–17.
67. Colville M, Grondel RJ. Anatomic reconstruction of the lateral ankle ligaments using a split
peroneus brevis tendon graft. Am J Sports Med. 1995;23:210–3.
68. Schenck RC, Coughlin MJ. Lateral ankle instability and revision surgery alternatives in the
athlete. Foot Ankle Clin N Am. 2009;14:205–14.
69. Komenda GA, Ferkel RD. Arthroscopic findings associated with the unstable ankle. Foot
Ankle Int. 1999;20(11):708–13.
70. Hintermann B, Boss A, Schäfer D. Arthroscopic findings in patients with chronic ankle insta-
bility. Am J Sports Med. 2002;30(3):402–9.
71. Cannon LB, Slater HK. The role of ankle arthroscopy and surgical approach in lateral ankle
ligament repair. J Foot Ankle Surg. 2005;11(1):1–4.
72. Ferkel RD, Chams RN. Chronic lateral ankle instability: arthroscopic findings and long-term
results. Foot Ankle Int. 2007;28(1):24–31.
73. Hua Y, Chen S, Li Y, Chen J, Li H. Combination of modified Broström procedure with
ankle arthroscopy for chronic ankle instability accompanied by intra-articular symptoms.
Arthroscopy. 2010;26(4):524–8.
74. Maiotti M, Massoni C, Tarantino U. The use of arthroscopic thermal shrinkage to treat
chronic lateral ankle instability in young athletes. Arthroscopy. 2005;21(6):751–7.
75. Berlet GC, Saar WE, Ryan A, Lee TH. Thermal-assisted capsular modification for functional
ankle instability. Foot Ankle Clin. 2002;7(3):567–76.
76. de Vries JS, Krips R, Blankevoort L, Fievez AW, van Dijk CN. Arthroscopic capsular shrink-
age for chronic ankle instability with thermal radiofrequency: prospective multicenter trial.
Orthopedics. 2008;31(7):655.
77. Hawkins RB. Arthroscopic stapling repair for chronic lateral instability. Clin Podiatr Med
Surg. 1987;4(4):875–83.
78. Kashuk KB, Landsman AS, Werd MB, Hanft JR, Roberts M. Arthroscopic lateral ankle sta-
bilization. Clin Podiatr Med Surg. 1994;11(3):407–23.
79. Corte-Real NM, Moreira RM. Arthroscopic repair of lateral ankle instability. Foot Ankle Int.
2009;30(3):213–7.
80. Kim ES, Lee KT, Park JS, Lee YK. Arthroscopic anterior talofibular ligament repair for
chronic ankle instability with a suture anchor technique. Orthopedics. 2011;34(4):1–5.
81. Acevedo JI, Mangone PG. Arthroscopic lateral ankle ligament reconstruction. Tech Foot
Ankle Surg. 2011;10:111–6.
82. Nery C, Raduan F, Del Buono A, Asaumi ID, Cohen M, Maffulli N. Arthroscopic-assisted
Broström-Gould for chronic ankle instability: a long-term follow-up. Am J Sports Med.
2011;39(11):2381–8.
83. Acevedo JI, Ortiz C, Golanó P, Nery C. ArthroBroström lateral ankle stabilization technique:
an anatomic study. Am J Sports Med. 2015;43(10):2564–71.
84. Vega J, Golanó P, Pellegrino A, Rabat E, Peña F. All-inside arthroscopic lateral collateral
ligament repair for ankle instability with a knotless suture anchor technique. Foot Ankle Int.
2013;34(12):1701–9.
85. Guelfi M, Vega J, Malagelada F, Dalmau M. The arthroscopic all-inside ankle lateral col-
lateral ligament repair is a safe and reproducible technique. Knee Surg Sports Traumatol
Arthroscopy. 2020;28(1):63–9. https://doi.org/10.1007/s00167-019-05427-0.
86. Guelfi M, Nunes GA, Malagelada F, Cordier G, Dalmau M, Vega J. Arthroscopic-assisted vs
all-arthroscopic ankle stabilization technique. A comparative clinical study. Foot Ankle Int.
2020; https://doi.org/10.1177/1071100720938672.
87. Cordier G, Lebecque J, Vega J, Dalmau M. Arthroscopic ankle lateral ligament repair
with biological augmentation gives excellent results in case of chronic ankle instabil-
ity. Knee Surg Sports Traumatol Arthrosc. 2020;28(1):108–15. https://doi.org/10.1007/
s00167-019-05650-9.
88. Vega J, Poggio D, Heyrani N, Malagelada F, Guelfi M, Sarcon A, Dalmau M. Arthroscopic

all-inside ATiFL’s distal fascicle transfer for ATFL’s superior fascicle reconstruction or
biological augmentation of lateral ligament repair. Knee Surg Sports Traumatol Arthrosc.
2020;28(1):70–8. https://doi.org/10.1007/s00167-019-05460-z.
89. Vega J, Montesinos E, Malagelada F, Baduell A, Dalmau M. Arthroscopic all-inside anterior
talo-fibular ligament repair with suture augmentation gives excellent results in case of poor
ligament-tissue remnant quality. Knee Surg Sports Traumatol Arthrosc. 2020;28(1):100–7.
https://doi.org/10.1007/s00167-018-5117-x.
90. Guillo S, Archbold P, Perera A, Bauer T, Sonnery-Cottet B. Arthroscopic anatomic recon-
struction of the lateral ligaments of the ankle with gracilis autograft. Arthrosc Tech.
2014;3(5):e593–8.
91. Michels F, Cordier G, Burssens A, Vereecke E, Guillo S. Endoscopic reconstruction of the
CFL and the ATFL with a gracilis graft: a cadaveric study. Knee Surg Sports Traumatol
Arthrosc. 2016;24(4):1007–14.
92. Takao M, Glazebrook M, Stone J, Guillo S, Ankle Instability Group. Ankle arthroscopic
reconstruction of lateral ligaments (ankle anti-ROLL). Arthrosc Tech. 2015;4(5):e595–600.
93. Vega J, Guelfi M, Heyrani N, Malagelada F, Dalmau M. Ankle microinstability. Tech Foot
Ankle Surg. 2019;18:73–9.
94. Vega J, Malagelada F, Dalmau M. Ankle microinstability: arthroscopic findings reveal four
types of anterior talofibular ligament’s superior fascicle lesion. Knee Surg Sports Traumatol
Arthrosc. 2020. https://doi.org/10.1007/s00167-020-06089-z.
95. Hertel J. Functional instability following lateral ankle sprain. Sports Med. 2000;29(5):361–71.
96. Hintermann B, Knupp M, Pagenstert GI. Deltoid ligament injuries: diagnosis and manage-
ment. Foot Ankle Clin. 2006;11(3):625–37.
97. Alparslan L, Chiodo CP. Lateral ankle instability: MR imaging of associated injuries and
surgical treatment procedures. Semin Musculoskelet Radiol. 2008;12(4):346–58.
98. Am C, Lee JY, Spritzer CE, Easley ME, Deorio JK, Nunley JA 2nd, Defrate LE. In
vivo kinematics of the tibiotalar joint after lateral ankle instability. Am J Sports Med.
2009;37(11):2241–8.
99. Rasmussen O, Kromann-Andersen C, Boe S, Deltoid ligament. Functional analy-
sis of the medial collateral ligamentous apparatus of the ankle joint. Acta Orthop Scand.
1983;54(1):36–44.
100. Hintermann B, Sommer C, Nigg BM. Influence of ligament transection on tibial and calca-
neal rotation with loading and dorsi- plantarflexion. Foot Ankle Int. 1995;16(9):567–71.
101. Vega J, Allmendinger J, Malagelada F, Guelfi M, Dalmau M. Combined arthroscopic all-
inside repair of lateral and medial ankle ligaments is an effective treatment for rotational
ankle instability. Knee Surg Sports Traumatol Arthrosc. 2020;28(1):132–40. https://doi.
org/10.1007/s00167-017-4736-y.
Diagnosis and Treatment of Talus
Osteochondral Lesions: Current Concepts
Caio Nery and Marcelo Pires Prado
1 Introduction
The knowledge about osteochondral lesions has evolved enormously since 1888,
when Konig [1] described the pathology as “osteochondritis dissecans” because he
imagined that it was a necrotic process resulting from changes in local
microcirculation.
The physiopathology, diagnosis, and treatment of these lesions on the talus has
been of great interest from the description by Kappis [2] in 1922. The lesions of
chondral and osteochondral ankle tissues are commonly related to ankle sprain [3],
which affects one in every 10,000 people daily in the USA. In half of severe sprains,
particularly those related to sports activities, it is possible to detect osteochondral
lesions of the tibiotalar joint [4].
Severe trauma can cause small lesions of the articular cartilage, allowing the
formation of fissures where the synovial fluid penetrates, initiating the formation of
osteochondral lesions by detachment of the articular cartilage layer or formation of
subchondral cysts. One of the most probable explanations for the appearance of
osteochondral lesions is attributed to small chondral fractures, resulting from acute
trauma, the important alterations in the vascularization of the subchondral bone that
are complicated by the physical and functional destructuring of local tissues. This is
also the most plausible explanation for the production of pain in osteochondral
ankle injuries [5]. Complementing this idea, the participation of repeated low inten-
sity and chronic traumas in the genesis of these lesions is suggested. According to
this theory, the small fissures of the joint cartilage evolve from the surface layers to
the deep ones and from there to the subchondral bone where they find favorable
conditions for its inexorable progression [6].
C. Nery (*) · M. P. Prado

Hospital Israelita Albert Einstein, São Paulo, Brasil

Switzerland AG 2022
1066 C. Nery and M. P. Prado
Considering as valid the theories of production of osteochondral lesions that we

have just mentioned, it is easy to imagine the enormous importance of ankle insta-
bility – acute or chronic – in the genesis of these lesions. The anomalous movement
of joint surfaces under instability conditions favors mechanical overload and
repeated trauma, ideal conditions for the production of osteochondral talus
lesions [7].
About 40% of patients diagnosed with chronic ankle instability present con-
firmed osteochondral lesions at the time of surgical treatment. In the long run, the
instability becomes the most common cause of degenerative ankle disease and, cer-
tainly, the undiagnosed osteochondral lesions play an important role in this
causal action.
2 Diagnosis
The diagnostic suspicion of osteochondral lesion of the talus starts with the com-
plaint of pain related to physical activities, usually with a history of previous trau-
mas. Joint effusion, false sensation, joint blockage, or painful clamping may occur.
The typical pain is considered deep and related to axial load [8].
Despite the complaints already mentioned, the physical examination is unclear
and limited to diffuse joint pain during maximum flexion and extension and touch-
sensitive areas in the tibiotalar joint line and, eventually, the presence of small joint
effusion.
Testing ankle stability is essential for the diagnosis of ligament injuries, which
are often associated or the main cause of osteochondral ankle injury.
The tibiotalar alignment and the foot posture during the static and dynamic sup-
port should be observed because they can determine overload in specific areas of the
ankle joint, as well as participate in the joint instability.
Despite the great chance of false negative diagnoses, simple ankle radiographs in
AP, lateral and oblique views are the first imaging exams to be obtained in the diag-
nostic process of osteochondral talar lesions [9].
Simple radiographs are extremely limited in the identification, characterization,
typification, and measurement of these lesions. The identification of details such as
fragmentation, presence of subchondral cysts, degree of detachment, and displace-
ment of osteochondral fragments and even the measurement of the dimensions of
the lesions is not safe. The most common finding in simple radiology is the presence
of an ill-defined radiolucency area on the talar dome at the site where the pathologi-
cal process characteristic of osteochondral talar2 lesions was installed (Fig. 1).
Axial computed tomography (CT) presents as main limitation the inability to
provide data on the quality and vitality of joint cartilage, but it is the main resource
in the evaluation of bone changes associated with the lesion, measurement, and
location, in addition to the definition of fragment deviations. Therefore, this imag-
ing modality has the capacity to typify the lesions [10] (Fig. 2). Intra-articular con-
trast injection for computed arthrotomography increases the sensitivity of the
examination and improves information both qualitatively and quantitatively.
Diagnosis and Treatment of Talus Osteochondral Lesions: Current Concepts 1067
Fig. 1 Ankle X-rays E in AP, Lateral and OI incidences of a patient with osteochondral lesion of
the thallus to illustrate the most frequently found appearance that is characterized only by a radio-
lucency zone different from the normal in the affected zone (arrows)
Magnetic resonance imaging (MRI) provides information about areas of bone

contusion in acute trauma, allows the evaluation of joint cartilage and the presence
of subchondral inflammatory changes. MRI images correlate positively in 65% of
cases with the abnormalities observed during arthroscopy [11, 12] and allow the
identification of the depth of the chondral lesion [13] and are, therefore, consid-
ered the gold standard resource in the diagnosis of osteochondral lesions [14, 15]
(Fig. 3).
The most widespread classification used for osteochondral lesions of the talus is
that proposed by Berndt and Harty [16] in 1959, which is based on radiographic and
anatomical parameters through histological analysis of amputated limbs submitted
to preestablished traumatic movements. Berndt and Harty’s classification is based
on the degree of displacement of the osteochondral fragment and has four stages:
Stage I – Small area of focal subchondral trabecular compression; Stage II – Partially
loose fragment (incomplete fracture); Stage III – Loose fragment (complete frac-
ture), but not displaced and Stage IV – Loose fragment (complete fracture) and
displaced from its bed.
In 2001, Scranton and McDermott [17] added Stage V to the Berndt and Harty
classification characterized by the presence of osteochondral cysts of the size cor-
responding to the original lesions, just below the damaged joint surface.
Fig. 2 Computerized axial tomography of the same patient presented in Fig. 1: The CT allows
exact identification, measurement, and typification of the osteochondral lesion of the talus. The
lower images correspond to the three-dimensional reconstruction that aids in the planning of
the surgery
Raikin [18] in 2004 added stage VI to the same classification, defined by the
combination of osteochondral talus lesion and massive subchondral cyst formation,
usually with volumes above 3 cm3.
Loomer et al. [19] in 1993 developed a classification based on Berndt and Harty’s
classification but using images from computed axial tomography. According to this
classification, five stages are possible, described as follows: Stage 1 – Chondral
compression without fragmentation; Stage 2 – Partial fracture, without fragment
deviation; Stage 3 – Complete fracture, with the fragment not deviated; Stage 4 –
Fragment displaced from its bed; Stage 5 – Radiolucent fibrous defect.
In 1995, Cheng et al. [20] classified osteochondral lesions of the talus using as
basis the macroscopic findings of the region obtained through arthroscopy.
According to this classification, six different stages of lesion are possible: Stage
A – Soft and smooth cartilage; Stage B – Rough but integral cartilage; Stage C –
Fibrillation and cartilaginous fissures; Stage D – “Flap” of cartilage or exposed
bone; Stage E – Free fragment devitalized but not deviated; Stage F – Osteochondral
fragment deviated from its bed.
Hepple et al. [21] classified LOT using magnetic resonance imaging (MRI).
According to their system, five different stages are possible with a subdivision in the
Fig. 3 Ankle radiographs and magnetic resonance imaging of the same patient presented in Figs. 1
and 2 at the sixth postoperative month. The patient was submitted to arthroscopic treatment with
debridement and microfractures. In the magnetic resonance images, it is clear the presence of
material with characteristics and cartilage signal filling the bed of the old lesion
second: Stage 1 – Damage restricted to joint cartilage; Stage 2 – Cartilage injury

with bone lesion accompanied by local bone edema; Stage 2b – Cartilage injury
with bone lesion without local bone edema; Stage 3 – Detached but not displaced
fragment; Stage 4 – Detached and displaced fragment; Stage 5 – Subchondral cyst
formation.
Mintz et al [22]. combined arthroscopic observations with magnetic resonance
imaging to design their classification for osteochondral lesions of the talus that fol-
lows the same dynamics as the other classifications. Six different stages are possi-
ble: Stage 0 – Normal cartilage; Stage 1 – Hypersignal of cartilage at MRI, but with
normal arthroscopic appearance; Stage 2 – Fibrillation and fissures that do not reach
the bone; Stage 3 – Presence of cartilaginous flap, with exposure of the subchondral
bone; Stage 4 – Loose fragment, not deviated; Stage 5 – Deviated fragment.
Despite the known possibility of overestimating the lesions, there is a clear and
well-defined tendency in the literature to value LOT images obtained through MRI
[23], especially those of high resolution [24], due to their excellent correlation with
arthroscopic findings, which greatly aids in therapeutic planning and prognostic
prediction.
MRI is the best resource for diagnosis and follow-up of subchondral bone mar-
row involvement due to the pumping of synovial fluid through the area of joint
cartilage fissuration or erosion. The increase of hydrostatic pressure in the bone

marrow, just below the subchondral bone plate, interferes with local perfusion,
which determines the appearance of osteonecrosis and consequent formation of
subchondral cysts [17, 25].
3 Prognostic Factors
3.1 Size
The dimensions, especially the area, of the osteochondral lesions have always been
considered as one of the main prognostic factors. It seemed clear from numerous
clinical observations that the best indication for the treatment of lesions with areas
smaller than 1.5 cm2, even if relapsed, would be debridement of the injured area
followed by bone marrow stimulation through multiperforation or subchondral
bone plate micro-fractures by arthroscopic route [26–30].
Recent studies, however, suggest that lesions with diameters greater than
10.2 mm present worse prognosis with this modality of treatment [31, 32].
This finding can be explained by the failure in the distribution of forces in lesions
with larger surfaces, which creates unsustainable overload to the regions surround-
ing the lesion, extending its limits to previously normal cartilage areas [33].
3.2 Location
The location of the lesions influences the prognosis, more because of the stability of
the repair tissue (contention) than by the area or quadrant in which the lesion is
positioned. It is known that lesions located in the rounded marginal areas of the joint
surface of the talus, also known as talar “shoulders,” offer more precarious condi-
tions for stabilization of the repair tissue – non-contained lesions – and are therefore
of more reserved prognosis [26, 31]. Sometimes, the lesion is not exactly on the
talus “shoulders,” but during debridement of the lesion, the involvement of its walls
and, therefore, its containment capacity is identified – which also represents a risk
for prognosis [26–33].
Without good quality edges, the cartilage that forms becomes more unstable,
increasing the chances of formation of mechanically unfavorable fibrocartilage [34,
35], rich in type I collagen.
In lesions where the main treatment option is osteochondral grafting, the lack of
stability of the grafted cylinders also negatively influences treatment success rates.
Raikin et al. [36] divided the joint surface of the talus into nine regions and
evaluated the frequency of incidence of osteochondral talus lesions in each of these
regions. Unlike the classical concept that mentioned the higher incidence of
osteochondral lesions in the posteromedial and anterolateral quadrants of the talus

surface, it was shown that the lesions most commonly occur in the equatorial zone
of the talus (Raikin’s areas 4, 5 and 6).
In Fig. 4, we present the articular surface areas of the talus and the incidence
frequencies of osteochondral lesions.
3.3 Age
The patient’s age at the time of the lesion is considered an important prognostic fac-
tor [37]. Youth is considered an advantage in the healing of cartilage lesions, a fact
clinically observed with better results in younger patients treated for osteochondral
lesions of the knee [38]. However, there is controversy about this statement, since
some authors have not identified differences in results when only age is taken into
account, denying this correlation [39, 40].
Baxter et al. [41] demonstrated the decreased potential for proliferation of mes-
enchymal cells, complementing Banfi et al. [42] observations that identified the
decreased potential for proliferation and differentiation of these cells at more
advanced ages.
Based on these data, Giannini et al. [43] developed their treatment algorithm
using the limit of 50 years of age as a determinant point of change in behaviors.
Fig. 4 Division of the

dorsal joint surface of the
talus into nine regions
according to Raikin et al.
[36]. The incidences of
osteochondral lesions in
each region are presented
in percentages
Younger patients and those under 50 years of age were submitted to joint repair
techniques while older patients were submitted to salvage procedures such as
arthrodesis or ankle arthroplasties due to their different evolution and repair capacity.
Contradicting these opinions, Choi et al., in 2012 [40], did not observe any cor-
relation between the age of the patients and the results obtained in the treatment of
osteochondral lesions of the talus in a study involving 173 patients.
3.4 Subchondral Cysts and Depth
The occurrence of subchondral cystic lesions indicates a worse prognosis [17, 44]
and unsatisfactory results can be expected in 53% of patients in this group [45].
Although there are authors who maintain the indication for treatment of osteo-
chondral lesions of the talus with small subchondral cysts through the method of
bone marrow stimulation [46], most observations suggest that this is an important
factor of deterioration of tissue response and consequently of the prognosis of
lesions [47].
The presence of multichamber cysts or large volumes that compromise the sub-
chondral bone structure and the quality of local irrigation itself are decisive in
changing operative tactics and are important indicators at the time of decision-
making in the development of a therapeutic program.
Massive cysts are difficult to approach and require large grafts, often bank coun-
terparts, with the consequences and disadvantages inherent in the method [18].
3.5 Other Possible Prognostic Factors
Chondral lesions × Osteochondral lesions – Through observation of 283 patients

over an average time of 52 months, Choi et al. [48] demonstrated that there were no
differences in the prognosis of lesions that compromised only the chondral layers
versus those that went beyond the subchondral bone plate. The explanation for this
finding may lie in the failure of the “integrity” of the intermediate and deep layers
of the articular cartilage responsible for the impermeabilization of the subchondral
and medullary bone to the synovial fluid. Conditions for the installation and pro-
gression of osteochondral lesions of the talus may be present, regardless of the
depth of the original lesion.
Body Weight Support: While some authors believe that early loading does not
interfere with the final result of small and medium osteochondral lesions [49], Gill
et al. [50] demonstrated histologically that maintenance of load suppression in the
postoperative period definitely influences the filling speed and quality of the osteo-
chondral lesions repair tissue. These authors suggest that early loading determines
the predominance of fibrocartilage in the repair tissue while a period of 8–12 weeks
without load may lead to the formation of hyaline cartilage with biological and
physical characteristics very similar to the original cartilage.
Bone Marrow Edema: The clinical picture as well as the prognosis of osteochon-
dral lesions is inversely related to the intensity of bone marrow edema observed on
magnetic resonance imaging. This finding also serves as an indicator for the resolu-
tion of the therapeutic process and may help in the phase of release and return to
normal activities of treated patients [51].
Joint instability and repeated traumas: Joint instability and repeated traumas,
besides the presence of marginal joint osteophytes, are indirect indications of poor
prognosis of osteochondral talus lesions [52].
4 Treatment
The treatment of osteochondral lesions of the talus should be restricted to symptom-

atic lesions. The occasional finding of asymptomatic osteochondral lesions, regard-
less of their location, type, and dimensions, should be reported to the patient or his
relatives and the case should be followed at regular intervals in search of possible
joint deterioration [53]. No modality of treatment or intervention is necessary as
long as the patient remains without complaints about this lesion.
As these are lesions related to joint deterioration in the medium/long term, the
patient and his/her family should be alerted of the dangers of devaluation and rela-
tive disregard for the finding.
The nonsurgical treatment modalities available in the literature include modification

of daily life activities, intra-articular infiltration with steroids, use of orthoses, load
suppression, immobilizing boots and orthoses, and others.
Several authors consider the conservative treatment – characterized by a period
without weight bearing on the affected limb, the use of boots and crutches – as a
valid attempt for each and every patient with osteochondral lesions of the talus [4,
16, 21].
The result of this type of treatment is quite variable and does not exceed the fig-
ure of 45% of excellent results as demonstrated by Tol et al. [54] in a systematic
analysis of the literature of the year 2000.
Shearer et al. [55] in 2002 obtained 54% of good results with the conservative
treatment of severe osteochondral lesions, with a follow-up time of 38 months, and
concluded that this type of treatment is feasible, with very low risks of secondary
arthrosis development.
Intra-articular injections of hyaluronate and platelet-rich plasma (PRP) have
been pointed out as intermediate options between conservative and surgical forms
for the treatment of osteochondral lesions. A prospective study involving 15 patients

showed an improvement in pain intensity and functional evaluation that continued
for 6 months after a weekly intra-articular injection (totaling three) of 20 mg of
sodium hyaluronate [56]. Another study compared the functional outcome and pain
after the injection of hyaluronate or PRP in 32 patients, and the authors consider that
there was improvement in both groups until the sixth month. From this point on, the
group that received PRP presented better results, but these are still not consistent or
predictable [57].
The adepts of this resource consider it as first-line treatment for patients with
primary osteochondral lesions, and second-line treatment for patients who maintain
symptoms after surgical treatment. It can also be indicated in symptomatic patients,
not candidates for surgery due to medical contraindications, or in those patients
where it is intended to postpone the surgical treatment because of the long recovery
period, as is the case of athletes.
Plasma rich in growth factors is a form of PRP considered a biological carrier of
a complex mixture of bioactive proteins essential to the normal healing process,
including anabolic and protective factors for cartilage, as the Transforming Growth
Factor beta 1 (TGF-β1), Platelet-derived Growth Factor (PDGF), and Insulin-like
Growth Factor 1 (IGF-1) [56, 57] and which has potential effects on the repair of
osteochondral and arthrosis lesions. This information and therapeutic applications
still need further studies to consolidate its applicability in daily practice.
Once the osteochondral lesion has been diagnosed and the lesion staging has been
performed, it is necessary to choose the best tactic for the surgical treatment of each
patient.
The surgical treatment of osteochondral ankle injuries can be divided into five
main groups of procedures [35, 58]:
1. Reduction and fixation of osteochondral fragments
2. Bone marrow stimulation
3. Joint cartilage replacement
4. Regenerative cell therapy
5. Metallic implants
The development and dissemination of arthroscopic surgery has collaborated
enormously in the treatment of osteochondral lesions of the talus since the first line
of treatment of the great majority of these lesions can be performed through
this method.
1. Reduction and Fixation of Osteochondral Fragments
Acute osteochondral fractures, mostly produced by ankle inversion trauma, are
usually accompanied by much pain and exuberant joint clinical signs. Radiographic
images may point to the presence of completely detached and detached fragments
of their beds. CT images may be necessary for the exact location and measurement
of lesions as well as for the clarification of suspicious cases.
In these conditions, the patient should be treated urgently and the fragments,
when feasible, should be reduced and fixed in their original bed. The procedure can
be performed arthroscopically and the fragments fixed with darts or screws of
absorbable material which provides excellent functional results.
When the fragments are smaller or devitalized, they are resected and the bottom
of the lesions are treated through bone marrow stimulation.
Despite the good prognosis for fracture healing, deterioration of the cartilage
covering the fragments can be expected in one third of the cases (Fig. 5).
2. Bone Marrow Stimulation
If the joint cartilage presents only areas of softening (chondromalacia) or fibril-
lation, without exposure of the subchondral bone and with good tissue stability,
surface debridement and “sealing” of the chondral surface with the use of radio
frequency can be performed as an alternative to the use of microfractures [59]. In
patients with intact cartilage, retrograde perforation and bone grafting in the sub-
chondral region is the best option [60].
a b c
d e f
Fig. 5 Reinsertion of osteochondral fragment resulting from acute fracture: (a). The fragment is
reduced to its bed with the aid of an arthroscopic spatula; (b). The fragment is kept in its original
location by the pressure of a perforated acrylic stabilization cylinder, which was introduced by the
arthroscopic portal; (c). Through one of the perforations of the stabilization cylinder, a drill with a
“stop” is inserted in order to produce a perforation with the exact dimensions of the dart to be
introduced. (d) The “stop” of the drill appears through the acrylic cylinder; (e). Introduction of
polylactic acid dart (PLLA) into the newly produced hole; (f). Final appearance – the arrows point
to the upper extremities of two of the three darts used in the arthroscopic fixation of the acute
osteochondral fragment
2.A Anterograde Perforations and Microfractures

The rationale behind multi- or micro-perforations for the treatment of osteochon-
dral talar lesions is based on the perforation of the subchondral bone allowing the
contact of the bone marrow with the focus of the lesion (Fig. 6). Besides the migra-
tion of multipotent mesenchymal cells to the lesion bed, there is also induction to
local neovascularization with cell influx to the repair zone. Some basic precepts
must be followed for the success of these procedures: (1) the edges of the lesion
should be healed and the soft tissue removed until a healthy cartilage is reached and
firmly adhered to the subchondral bone; (2) the edges should be as regular and per-
pendicular to the subchondral bone plate as possible; (3) perforations or microfrac-
tures to the subchondral bone should be made perpendicular to the surface and at
intervals of 3–4 mm from each other; (4) its depth should be at least 3 mm to be sure
to cross the subchondral bone; and (5) should be initiated at the periphery of the
lesion, ending at the center [53]. Bleeding at the bottom of the lesion from the sub-
chondral capillaries is essential. The blood deposited at the bottom of the lesion
contains precursor cells and cytokines responsible for the onset of the healing
process, which includes the formation of a fibrin clot and subsequent formation of
fibrocartilaginous tissue [33] (Fig. 7).
a b c
d e f
Fig. 6 Multiple drilling in the talar osteochondral lesion: (a). The bottom of the lesion already
cleaned and prepared; (b). A hypodermic needle (Jelco) is introduced through the most favorable
arthroscopic portal and, with a slight pressure, stabilized at the bottom of the lesion; (c). A thin
Kirschner thread (1 mm) is introduced inside the needle and conducted so as to penetrate at least
3 mm inside the lesion. The goal is to cross the subchondral bone plate so that the bone marrow is
stimulated to help repair the lesion; (d). When the correct depth is reached, we can notice the exte-
riorization of fat droplets from the bone marrow; (e and f). The process is repeated until the entire
surface of the lesion is perforated
a b c
d e f
Fig. 7 Microfractures at the bottom of the osteochondral talar lesion: (a). After cleaning and
preparation, the bottom of the lesion is reached by a curved metallic instrument, especially for
drilling and microfractures (“ice-picking”); (b and c). The tip of the instrument must perforate the
subchondral bone and penetrate the bone marrow; (d). The instrument is repositioned in order to
produce microfractures in all the bottom of the lesion; (e). Fat droplets can be exteriorized through
the holes of the microfractures if the depth reached is correct; (f). At the end of the process, the
lesion will be covered with holes resulting from the microfractures
The tissue formed from the clot at the bottom of the newly treated lesion has
been carefully studied, showing that it is formed mainly by type I collagen, while
the original hyaline cartilage has predominantly type II collagen [61]. The scar tis-
sue thus formed has inferior resistance to compression and shear forces when com-
pared to normal joint cartilaginous tissue [62–64].
In a systematic review, it was demonstrated the consistency of the results obtained
with the treatment of osteochondral lesions through debridement and microfrac-
tures, with an average AOFAS score of 86.8 points, reaching 80.2% of excellent and
good results [65].
The comparison between microfracture procedures and auto osteochondral graft-
ing for the treatment of recurrent osteochondral lesions shows similar results in the
short term, but there is significant deterioration of results after 4.2 years of the pro-
cedure [35]. The justification for this finding may lie in the biomechanical proper-
ties of repair fibrocartilage, which is inferior to normal hyaline cartilage, explaining
its deterioration and worsening of the symptoms over time.
In a more recent meta-analysis, the success rate of the combination of excision
of fragments, curettage of the bottom of the lesion, and stimulation of the bone mar-
row was 85%, while the good results of isolated excision of the fragment reached
32% and the combination of excision and curettage of the bottom of the lesion
reached 77% [66].
The repetition of debridement, curettage, and bone marrow stimulation in

patients who presented unfavorable evolution has a bad reputation among special-
ists, a fact that is not based on concrete data. On the contrary, Savva et al [67].
obtained 92% of good results characterized by a return to previous sports activities,
including professional activity. Only 8% of patients needed reintervention and a
change in therapeutic tactics.
The result of the microfractures can be potentiated through intra-articular injec-
tion of hyaluronate soon after the surgery. In consecutive series, there was improve-
ment in function and pain when compared to patients who did not receive this
treatment [68, 69].
In animal models, the use of platelet-rich plasma in association with bone mar-
row stimulation procedures showed a better capacity to repair joint cartilage, com-
pared to the isolated surgical procedure, although no hyaline cartilage was obtained
in the final result [70]. The same observation is true for the use of medullary aspirate
concentrate [71, 72]. Jung et al. [73] in 2011 advocated debridement and microfrac-
tures for major osteochondral lesions associated with subchondral cysts, based on
the good results observed in 22 patients over an average period of 32 months.
2.A Retrograde Drilling
Retrograde drilling with radiographic control is considered very effective as a
treatment option for osteochondral lesions with intact joint cartilage. This proce-
dure is not indicated when there is joint cartilage erosion with exposed subchondral
bone [74]. After a guide wire is placed inside the lesion with the aid of radioscopy
combined with arthroscopy, a cannulated drill is passed over this guide wire never
going beyond the intact cartilage. Through the tunnel formed, it is possible to place
bone graft to fill the lesion. Currently, several models of articulated and extremely
efficient guiding instruments help the surgeon to position an olive in the joint area
of the lesion and reach it safely without putting at risk the intact joint cartilage.
3. Joint Cartilage Replacement
3.A Osteochondral Autologous Graft
The autologous osteochondral grafting system known as “mosaicplasty” involves
obtaining cylindrical cartilage and bone grafts of varying sizes, most commonly
originating from the anterolateral portions of the lateral femoral condyle, and their
transfer to areas of osteochondral lesion on the load surface of the talar dome. This
procedure presents encouraging results [75]. In fact, the term “mosaicplasty” refers
to the procedure that uses osteochondral cylinders of smaller diameter placed side
by side, remembering the composition of a mosaic. Its use minimizes the adverse
effects in the donor area, favors the incorporation in the receiving area, and facili-
tates the reproduction of the talus outline [76]. Even with the most refined tech-
nique, areas corresponding to 20–40% of the defect remain without cartilaginous
coverage, between the osteochondral plugs [77] (Fig. 8).
Indications for osteochondral grafting include lesions larger than 1.5 cm2, recur-
rent or irresponsive lesions to milder treatment methods [78, 79] and, especially,
lesions associated with subchondral cysts [80].
Fig. 8 Autologous
osteochondral graft for the
treatment of osteochondral
talar lesion. The two
cylinders are covering
most of the lesion, but
there are always some
small areas of “uncovered”
(arrows) that will be filled
with fibrocartilage with
physical and biological
characteristics inferior to
those of normal hyaline
cartilage
The proper positioning of the graft is of great importance in the outcome of the
procedure, as it restores the load distribution between the tibia and talus. While the
sub-leveling of the grafted cylinder produces cartilage overload around the lesion,
its supra-leveling determines important overload of the cylinder itself with immedi-
ate delamination of the cartilage that covers it [81] leading to deterioration of clini-
cal results.
Like microfractures, mosaicplasty has its technical standards to be followed aim-
ing at better results: (1) the donor zone can never be a loading region; (2) the osteo-
chondral cylinders must be inserted perpendicularly to the receiving surface; (3) its
cartilaginous portion must have the shape and curvature as close as possible to the
receiving zone; (4) the cylinder must be at least 15 mm long in chondral lesions and
25 mm when there are subchondral cysts; (5) the plug cartilage must remain per-
fectly leveled with the edges of the receptor region, not being tolerated steps or
unevenness in relation to the neighbor cartilage [53].
Several studies point out satisfactory results for this modality of treatment, high-
lighting the low incidence of symptoms related to the donor area [77, 82–84]. There
are, however, authors that point out the complications related to the donor area as an
impediment and restriction to the use of autologous osteochondral grafting in the
treatment of osteochondral talus lesions, especially in patients over 40 years of age
(36%) [85]. Respecting the indications for each procedure, the results of autologous
osteochondral grafting are superior to those of the combination of debridement and
microfractures [86] (Fig. 9). Autologous osteochondral grafting is a procedure that
has no contraindications and its results are impaired only by the location of the
lesion, especially when the talus “shoulders” are involved. The number of grafts
used, the previous procedures, the need for malleolus osteotomy, and the presence
of mild arthrosis of the affected joint have not influenced the final result of this pro-
cedure [85]. The arthroscopic observation of the region of tibial osteotomy and its
vicinity 1 year after the autologous osteochondral grafting showed that there was
overload and impact around the graft, findings related to the final results. With this
Fig. 9 Magnetic resonance imaging obtained 6 months after the osteochondral autologous graft
for the treatment of osteochondral talar lesion. The cylinders are well integrated and the medullary
reaction (T2) is quite reduced, indicating the complete integration of the graft
in mind, the importance of carefully performing osteotomies increases, as well as

the anatomical fixation of fragments in the osteotomy area [86].
When we focus on the donor area, the most frequent residual symptoms are the
sensation of instability during activities of daily life and pain, present in 12% of
operated patients [85]. The occurrence of these symptoms is related to the very large
para-patellar incisions and exaggerated tensioning during closure. For this reason, it
is recommended to perform low-invasive arthrotomies with incisions limited to the
necessity of the procedure and extreme care with soft tissues during handling and
closing the incisions. For most authors, the symptoms in the donor area are of little
intensity and importance [75, 87, 88]. The functional prognosis of the knee does not
seem to be affected by the number of osteochondral cylinders harvested, the size of
these cylinders, or the age of the patient; however, there is a potential negative effect
of high body mass index [89, 90].
3.B Homologous Osteochondral Graft (Allograft)
When the osteochondral lesions exceed 3 cm2, when they become not contained,
affect the shoulder of the talus or are accompanied by subchondral cysts of large
volume, the autologous osteochondral graft begins to become more difficult to be
performed, with greater chance of poor results. The osteochondral allograft of a
fresh cadaver then becomes an interesting option [91].
The treatment of large osteochondral lesions is quite difficult, and the fresh
cadaver allograft that has viable chondrocytes and normal subchondral bone appears
as an interesting option, especially for not presenting morbidity in the donor area or
areas without coverage between the grafted plugs [91] (Fig. 10).
Cryopreservation determines an important decline in the number of viable chon-
drocytes, with cell survival reaching 20–30% in 2 weeks [92], a period within which
the procedure should be performed according to most authors [93, 94].
Despite the prospect of good results [95–99], the method presents as main obsta-
cles the transmission of diseases, the possibility of adverse immunological reaction,
and the difficulty in incorporating the graft into the bed that hosts it. The availability
of tissue banks and the technology of conservation of the material are also important
barriers for its use.
In a study of 17 patients with large osteochondral lesions treated with fresh
osteochondral allograft, there was failure in five patients (29%), four were
a b
c d
Fig. 10 Homologous osteochondral graft used for the treatment of extensive medial shoulder talar
lesion: (a). Identification and measurement of the lesion; (b). Measurements are transferred to the
talar of a donor; (c). The sections are carefully prepared; (d). The segment to be grafted is removed
from the donor piece and transferred to the recipient area where it is fixed with intrinsic compres-
sion screws; (e). Intraoperative radiographic image demonstrates the perfect adequacy of the
grafted fragment and the restitution of the ankle anatomy. (We thank Dr. Mark S. Myerson for the
cession of these figures)
asymptomatic (24%), and eight with symptoms (47%), two of these requiring
arthroscopy to improve the condition, so the indication of this procedure should still
be performed with criteria, since its results are unfavorable when compared to those
of autograft [100–102].
El-Rashidy et al. [98, 103] evaluated 38 patients with osteochondral talar lesions
treated with fresh allograft, with 10% failure. They also showed that the failure of
the previously performed procedure does not worsen the prognosis for a new attempt
of allograft, arthrodesis, or total ankle arthroplasty.
Both the autograft and the allograft have good results documented in the litera-
ture. The ease of obtaining and the presence of viable chondrocytes in the autograft
makes it the ideal treatment for recurrent, deep (>5 mm), and moderate-sized
(<2 cm2) osteochondral lesions. For larger diameter defects, large cystic component,
and talus shoulder involvement, the allograft becomes the preferred option.
Familiarity with the risks and morbidity in the donor area of the autograft and the
complexity of the subject related to chondrocyte viability, availability, and integra-
tion of the allograft are very important factors and should be taken into consider-
ation when indicating these procedures [102–104].
It is a consensus among the authors to consider the osteochondral allograft as a
salvage treatment for large lesions and for those in which other methods have
repeatedly failed. However, the high incidence of procedure failure (30%) and high
rate of secondary procedures (40%) [103, 104] should be taken into account.
4. Regenerative Cell Therapy
4.A Chondrocyte Autologous Implant (ACI)
The first time in history that chondrocytes were used for the attempt to repair
osteochondral lesions was in 1994 through the studies of Brittberg and col-
leagues [106].
The procedure begins by obtaining viable chondrocytes through the resection of
a small fragment of healthy cartilaginous tissue from the joint to be treated or any
other joint of the same individual. This tissue is digested enzymatically and the
chondrocytes isolated and cultivated to multiply. Using counting techniques and
following the evolution of the culture, the optimal number of cells for implantation
is reached after a period of 3–6 weeks of culture. The second part of the procedure
consists in the preparation of the receiving area and the implantation of the cultured
cells [107]. The curettage and debridement of the bottom and edges of the lesion are
integral parts of this process until the limits of healthy cartilage are established and
firmly adhered to the subchondral bone. The possible subchondral cysts are filled
with cancellous graft, and periosteum slides in the appropriate dimensions are
sutured and glued with fibrin to the lesion edges in order to create an airtight cham-
ber inside which the cultivated cells will be implanted. The suturing and sealing of
the cover is completed with sutures and fibrin glue (Fig. 11).
The indication of this therapy includes recurrent osteochondral lesions of any
size and the primary treatment of lesions larger than 2.5 cm2 with or without sub-
chondral cysts, in patients aged between 15 and 55 years, without degenerative
Fig. 11 Chondrocyte autologous implant: (a). Measurement of the lesion; (b and c). Immediately
after debridement of the lesion and preparation of its bottom, fibrin glue is applied, which will keep
adhered a layer of periosteum removed from the distal tibia; (d). A second periosteum flap is
sutured to the edges of the lesion and also to the leaflet that was adhered to the bottom of the lesion
creating an airtight and resistant pouch, inside which the cultivated autologous chondrocytes will
be deposited (sandwich technique)
arthritis or mirror osteochondral lesions and without instability or changes in joint

alignment [107].
Preliminary studies have indicated satisfactory results and low incidence of com-
plications with the use of chondrocyte autologous implant for the treatment of
extensive osteochondral lesions [108–112]. This low rate of complications made the
chondrocyte autologous implant the procedure of choice in the treatment of large
(>3.0 cm2) and long-lasting (119 months on average) [113] osteochondral lesions,
and this caused complications, especially those related to hypertrophy and delami-
nation of the periosteal membranes used to cover the lesions, to reach higher lev-
els – 18–33% [114, 115].
This procedure was evaluated in a meta-analysis [116] including 213 patients,
from 16 studies that confirmed the improvement in joint function with the method,
but also identified the absence of homogeneity in the choice of patients, size of
lesions, and existence of previous procedures, which prevented the safe establish-
ment of the real indications and results of the ACT.
In order to reduce the morbidity and technical difficulty of autologous chondro-

cyte implantation, several attempts have been made to obtain carriers for the culti-
vated chondral cells.
Lee et al. [117] used a combination of fibrin and thrombin (Chondron, Sewon
Cellontech Co., Seoul, South Korea) to which the cultivated chondrocytes are
added, for their implantation in the talus receptor zone. According to these authors,
the mixture receives approximately 1.2 × 107 cells and becomes a gel that is depos-
ited on the lesion. The gel solidifies in 5 min and the ankle can already be mobilized
without losing the graft. The result of the procedure performed in 10 patients was
quite satisfactory.
The second generation of autologous chondrocyte transplants involves the use of
collagen membranes to carry the cells, eliminating the need to obtain the periosteum
with all the difficulties and complications inherent to this operative time. The chon-
drocyte’s own membrane can be sutured or glued to the bottom of the lesion with
fibrin glue. Until now, however, they present the disadvantage of triggering the pro-
duction of type I collagen instead of the desired type II collagen, although the results
obtained are encouraging [118–120]. Anders et al. [121] in 2012 demonstrated the
result of this procedure after 5 years of observation in 22 patients with lesions of
1.94 cm2 on average with significant improvement in function and pain.
One step forward represented the performance of autologous chondrocyte
implantation through arthroscopic procedure. This was only possible thanks to the
use of a flexible collagen membrane called MACI (matrix-induced autologous
chondrocyte implantation). Besides the advantage of arthroscopy, the morbidity of
the procedure was reduced by not violating another joint, since the talus itself was
used as a source for the chondrocytes sent to the culture. This procedure showed
satisfactory results, with great clinical improvement of the patients [122, 123].
4.B Mesenchymal Stem Cells
Stem cell therapy is based on two mechanisms of action. In the first, the cells
differentiate themselves and mimic the final cells of human tissues and organs; in
the second, the production of substances (cytokines and growth factors) occurs that
favorably influence angiogenesis, the reduction of cell apoptosis, and induce endog-
enous regeneration [124].
The stem cells derived from bone marrow have been studied in depth; however,
the acquisition of these cells is associated with possible complications such as pain
and infection at the puncture site [125, 126]. Giannini and collaborators show in
clinical studies the efficiency of the use of stem cells obtained from bone marrow
aspirate [127, 128].
Good initial results of a single procedure with the use of bone marrow-derived
cells BMDCT (Bone Marrow-Derived Cell Transplantation) in 49 patients with
osteochondral lesions of the talus were observed by Giannini et al. [129] in 2013, in
a two-year follow-up. This study showed worsening of results based on the AOFAS
score for hindfoot and ankle evaluations after 2 years of surgery, showing a possible
tendency to deterioration of results. Apparently the repair occurs through the forma-
tion of hyaline cartilage, with the advantage of being a single procedure and
arthroscopic [130].
Fat-derived stem cells were related to good results in 18 patients treated, with
two failures of the procedure. These cells showed that they maintain their differen-
tiation capacity in the same way as bone marrow derivatives and may have better
potential for chondrogenesis [131, 132]. Koh et al. [133] treated 25 patients with
chondral lesion of the knee using this type of stem cells associated with PRP
(Platelet-Rich Plasma).
Stem cells obtained from synovia apparently have good differentiation in chon-
drocytes, but only with animal studies [132].
Stem cells obtained from bone marrow may still be submitted to culture for num-
ber expansion and subsequent clinical use, as shown in the studies by Haleem [131]
and Nejadnik [135].
Intra-articular injection of mesenchymal stem cells (Mesenchimal Stem Cells)
favorably influenced the treatment results of patients over 50 years of age, lesions
larger than 109 mm2 associated with subchondral cysts, which may have some ben-
efit in slowing the evolution to degenerative disease [136]. However, this type of
therapy has not yet been adequately studied in the literature, and the best source for
these cells, their dosage, the best type of carrier (when necessary), the indications
and against indications are still to be established.
4.C Induction of Chondrogenesis by Autologous Matrix
The association of the use of collagen membranes with mesenchymal stem cells
(MSC), bone marrow concentrate (BMC), and bone marrow-derived stem cells
(BMSC) proved to be more advantageous than chondrocyte implantation [136, 137].
The matrix-induced chondrocyte-induced technique in which autologous chon-
drocytes are used (MACT or MACI – Matrix-associated autologous chondrocyte
transplantation/implantation) was described by Behrens et al. in 2006 [138], for the
treatment of full-thickness chondral lesions in the knee. An acellular collagen
matrix type I and III is placed in the clot that forms after the microfracture to pro-
vide a favorable environment for chondral regeneration. Clinical results with 5 years
of follow-up show encouraging results [139].
Walther et al. [140] reported 42 cases of this procedure with 12-month follow-up,
with good results. In deep bone grafting lesions, it is used in subchondral bone
reconstruction [141], with good clinical results and improved appearance at MRI in
26 patients [142].
4.D Particulate Juvenile Joint Cartilage
Stimulation of osteochondral talus repair can be done from the articular cartilage
of children and adolescents’ cadavers, particulated in 1 mm cubes implanted in the
previously prepared lesion bed (DeNovo Natural Tissue, Zimmer Inc., Warsaw,
USA). After debridement and preparation of the lesion by arthroscopic route, the
saline solution flow is interrupted and the lesion is dried. A thin layer of fibrin glue
is applied to the entire extent of the chondral lesion and the particulate cartilage is
introduced until the osteochondral defect is fully covered. A new layer of fibrin is
applied over the region to increase graft stability. Studies with animal models and
the short-term evolution in patients show good results, with the formation of hyaline
cartilage in the defect [143, 144] (Fig. 12).
Fig. 12 Particulate
juvenile cartilage deposited
on the bottom of an
extensive osteochondral
talar lesion. (We thank Dr.
Rebecca Cerrato, Mercy
Hospital, Baltimore, USA,
for ceding this image)
In a prospective multicenter study, 25 patients were treated by this method and

showed clinical improvement [145, 146]. Other studies indicate that 92% of good
results were obtained in the treatment of lesions smaller than 1.5 cm2 of total area
[144–147].
5. Metallic Implants
The filling of the osteochondral lesion area of the talus with the use of a metallic
implant – surface prosthesis – has the purpose of redoing the contour of the injured
area and improving the load distribution in the ankle joint. It was described by van
Bergen et al. in 2011 [148], who studied 20 consecutive patients in the only series
described in the literature. They obtained substantial improvement of pain and func-
tion in 90% of the patients after an average follow-up of 3 years. The authors con-
sidered the method as valid in the treatment of recurrent osteochondral lesions
resistant to other forms of treatment.
5 Osteochondral Lesions of the Distal Tibia
Osteochondral lesions of the distal tibia are unusual findings and appear in the pro-
portion of 2.6% of all osteochondral lesions of the ankle [149].
This lower incidence may be related to the concave shape of the lower tibial joint
surface and to the higher resistance of the tibial cartilage to compression when com-
pared to the talus cartilage [150, 151].
The treatment of these lesions is much more complex due to the difficulty of
access and the shape of the tibial joint surface. Through the arthroscopic approach,
curettage, excision of fragments, thermal ablation, and stimulation of the bone mar-
row can be performed.
When accompanied by cysts, their filling with bone grafting can be performed
transmalleolarly under arthroscopic assistance (Fig. 13).
As well as the joint surface of the talus, the tibia was subdivided into nine regions
and the incidence of osteochondral lesions was mapped indicating the most affected
areas. Figure 14 shows the dividing grid of the distal tibial joint surface, as well as
the frequency of incidence of the lesions according to Elias et al. [151] (Fig. 14).
It is a consensus among the authors that osteochondral lesions of the tibia present
a worse prognosis than osteochondral lesions of the talus when the same physical
characteristics of the lesions are considered [149–152].
Fig. 13 Magnetic resonance imaging of a patient with osteochondral lesion of the tibia in which
the presence of a large cyst (intraosseous ganglion) in the medial malleolar region is clearly
perceived
Fig. 14 Division of the

lower tibial joint surface
into nine regions according
to Elias et al. [148]. The
incidences of
osteochondral lesions of
each region are presented
in percentages
6 Evaluation of Repaired Cartilage
MRI mapping on T2-weighted images is becoming the most useful and popular
resource for the evaluation of repaired joint cartilage, as an important alternative to
arthroscopy, an invasive and uncomplicated procedure. As an extra advantage, MRI
assessments encompass the repaired region as a whole, whereas arthroscopy has a
restricted and superficial field of view that a local biopsy would provide [153].
The integration of MOCART morphological scale parameters and biochemical
mapping by MRI in T2 weighting are essential for the complete and accurate non-
invasive assessment of repaired cartilage, improving the interpretation of clinical
scales. The mapping is suitable for qualitative assessment of the cartilage, being
able to differentiate hyaline cartilage from fibrocartilage and correlate with clinical
results [153, 155].
6.1 Comments
The systematic reviews of the literature, due to the heterogeneity of the available
works, do not allow the definition of absolute standards of conduct [66, 155].
However, important information on the efficiency of the various treatment methods
and their respective success rates are emerging. With this information we are able to
substantiate, despite the lack of mathematical confirmation, our choices until the
emergence of the expected prospective, comparative, and well-controlled studies.
In the algorithm we present below are covered the most common occurrences as
well as the solutions that find support in literature.
Some of the solutions presented are not available in our environment, which does
not prevent us from getting to know them and continue to seek alternatives for
patients who seek us with the problems pointed out here.
Algorithm 1: OCL Algorithm
Ankle OCL
Clinical signals / Plain RX /

CAT scan / MRI
Observation No Symptomatic? Yes
Reduction + Fixation Detached

debridement + Yes fragment Articular
Bone marrow stimulation surface
Conservative treatment
No
attempt
Intact articular surface ?
Retrograde drilling
Bone graft + Yes
Bone marrow stimulation
No
Lesion < 1,5 cm2 Lesion < 1,5 cm2 Lesion < 2,0 cm2
No subchondral No Subchondral With massive
cysts cysts subchondral
present cysts
Debridement + Bone grafting + Bone grafting +

Microfractures or Osteochondral Autologus
Drilling graft chondrocyte
bone marrow transplantation implantation
stimulation
Autologous Homologus
chondrocyte osteochondral
implantation graft
Cellular therapy transplantation
6.2 Osteochondral Talus Injury in the Immature Skeleton
In children and adolescents, we can observe two types of osteochondral lesions that
affect the ankle, especially the joint surface of the talus.
Due to the plasticity and elasticity of the young tissues, the classical traumatic
lesions are rarer than in adults and it is added to the “osteochondritis dissecans” of
the talus associated by the classical literature to vascular pictures of the medullar
and subchondral region of the talus.
The most convincing theory for the genesis of these lesions suggests the exis-
tence of ischemic areas in the subchondral bone – by hypoplasia or vascular apla-
sia – that favor the emergence of foci of avascular necrosis [156]. The ischemic
areas may evolve to spontaneous resolution or, when in unfavorable conditions,
with the instabilization of hyaline cartilage that coats them generating symptomatic
osteochondral lesions.
The ankle is the third most frequent location of the pathology, which affects the
knee and elbow with higher incidence.
6.3 Clinical Picture
The clinical picture includes (1) joint blocking sensation, (2) deaf pain accompa-
nied or not by joint effusion, which can be related to the practice of more intense
physical activities, (3) instability sensation that can be accompanied by more intense
and acute pain.
In up to 38% of cases, the diagnosis is incidental, due to the lack of symptoms,
or the presence of mild and uncharacteristic symptoms [155].
An important clinical finding that serves to differentiate traumatic osteochondral
lesions from osteochondritis dissecans of the talus is the bilaterality and symmetry
of the lesions. Due to its “vascular” character, it is assumed that the bilaterality and
symmetry of the lesions result from the same embryopathic moment acting on both
ankles creating a mirror image.
Despite the small incidence, the diagnosis must be remembered so that the
appropriate and early treatment can be instituted.
6.4 Diagnosis by Image
The diagnostic investigation includes simple radiology (Fig. 15a–c), which charac-
teristically shows changes in the normal bone pattern and subchondral irregularities
most often located on the talus “shoulders.”
Computed tomography shows with greater clarity and definition the bone
changes, being the best resource for measuring the depth and extent of the area
affected by the lesion.
b c
Fig. 15 (a) Ankle radiography in the lateral incidence of an adolescent patient showing medial
posternal irregularity in the domus talar (black arrows); (b) Infantile ankle radiography in the AP
incidence showing irregularity in the medial shoulder of the talus (white arrows); (c) Infantile
ankle radiography in the lateral incidence – of the same patient shown in b showing irregularity in
the medial posterior portion of the talus (white arrows)
a b c
Fig. 16 Magnetic resonance imaging in sagittal (a and b) and coronal (c) slices showing a large
osteochondral lesion on the medial talus
Magnetic resonance imaging (Figs. 16, 17, 18, 19, and 22) allows the evaluation
of the affected bone, the vitality of the fragments, and assists in the identification of
the instability criteria of the lesion, allowing the adequate staging of the disease.
The classical Berndt-Harty classification is widely used in the evaluation of these
lesions, allowing the decision about the best form of treatment.
6.5 Treatment
The treatment of osteochondral talus lesions in children and adolescents follows

practically the same rules already outlined for the treatment of adult lesions.
However, given the great plastic potential of the immature skeleton, the chances of
success with noninvasive treatment are greater.
It is always advisable to start the treatment through conservative measures such as

load suppression, stabilization, and joint protection besides the improvement of
local circulatory conditions.
The conservative treatment should be extended for 6 months during which the
exams are repeated to follow the evolution of the lesions (Figs. 16 and 17).
Both osteochondritis dissecans of the talus and traumatic osteochondral lesions
respond satisfactorily to conservative treatment by reducing pain and edema in 16%
of patients [157]; however, the contingent of patients who evolve unsatisfactorily is
quite expressive (Figs. 18 and 19).
It is not rare to identify scar alterations in asymptomatic patients who did not
have a clinical picture and were not treated in childhood or adolescence.
a b
c d
Fig. 17 (a–d) Magnetic resonance imaging of the same patient in Fig. 2, after conservative treat-
ment, showing resolution of the lesion on T1 (a) and T2 (b) images, and on T2-weighted images
for more detailed assessment of joint cartilage (c and d)
Fig. 18 T2-weighted sagittal MRI sections showing small cysts under the lesion area, and bone
edema in the surrounding bone
b
a
c d
Fig. 19 MRI images (a – sagittal; b – coronal) including T2-weighted images of the joint cartilage
(c and d) showing worsening of the lesion pattern, with increased subchondral cysts
The only factor indicating poor prognosis for the conservative treatment of
osteochondral talus lesions found in the literature is the presence of grade III lesions
by Berndt-Harty’s classification in preadolescents [158].
Surgical treatment should be indicated when conservative treatment fails, in unsta-

ble lesions or with fragment deviations, in the presence of signs of lesion progres-
sion or in the presence of free bodies [159]..
There are several forms of surgical treatment for osteochondral talus lesions in
the immature skeleton that include osteochondritis dissecans of the talus, and the
indications depend on the characteristics of the lesion, and previous treatments per-
formed. By the very characteristics of the developing skeleton, the use of open
procedures involving malleolar osteotomies, potentially harmful to the growth
phases, is limited. Therefore, arthroscopic procedures are especially useful in this
group of patients.
Among the possible surgical procedures, we list (1) retrograde perforation, (2)
excision of detached fragments, (3) debridement of the bottom of the lesion fol-
lowed by reduction and fixation of viable fragments, (4) bone marrow stimulation,
(5) procedures that use different forms of “scaffolds” associated or not with the use
of orthobiological resources, and (6) replacement procedures [160]..
Retrograde drilling is a procedure indicated for situations in which the subchondral
bone associated with intact articular cartilage is involved. The objective is to perform
multiple perforations in the pathological area of the subchondral bone by trans-talar
approach using the sinus of the tarsus and driving the drill proximally. Under radio-
scopic vision, the penetration of the perforating instrument is interrupted before it
touches the healthy cartilage that covers the injury area (Fig. 20). The microperfora-
tions thus performed stimulate a cellular crisis in the lesion focus and the neovascular-
ization of the bone marrow and subchondral plate, leading to the lesion healing.
Currently, the “retrograde drilling” procedure combines the use of radioscopy
with ankle arthroscopy, minimizing location difficulties and microperforation errors
(Fig. 21). Special guides assist the surgeon in determining the ideal anatomic region
and position the perforating instrument in order to reach the intended areas with
minimum damage to neighboring tissues [161] (Figs. 20, 21, and 22).
Fig. 20 Arthroscopic image

of the ankle joint showing
the position of the blunt end
of the instrument used for
retrograde perforation in a
patient with a subchondral
lesion with intact cartilage
Fig. 21 Radioscopic
image obtained during
retrograde perforation
where the presence of the
blunt end of the perforation
guide is perceived touching
the whole cartilage (a), the
arthroscopic optics (b), and
the metal wire used to
perform the perforation (c)
The conventional bone marrow stimulation, performed through microperforations

at the bottom of the lesions is a simple method, with low morbidity and high efficiency
especially when performed arthroscopically in shallow lesions and with diameters
smaller than 10 mm. Its efficiency falls, however, in larger lesions and in those where
there are more important alterations in the subchondral bone or adjacent bone marrow
(edema, cysts, necrotic areas, etc...) and should be used with criteria in these patients.
More recently, the use of orthobiology has been gaining attention in the litera-
ture, with studies showing that the use of bone marrow stimulation procedures asso-
ciated with the use of collagen membranes can improve the prognosis of larger and
deeper osteochondral lesions.
Specifically, in the case of osteochondritis dissecans, there is work showing good
results in seven patients treated with the use of collagen membrane associated with
bone marrow aspirate [162].
Autologous chondrocyte implantation (ACI) and bone marrow cell transplanta-
tion (BMDCT) are cited in the literature still with small casuistry although they are
considered very promising [163].
The success of surgical treatment of osteochondritis dissecans of the talus is
around 78%, although a large number of patients require revision procedures,
according to a 2012 systematic review [155, 156].
The importance of this subject lies in the fact that the diagnosis of osteochondri-
tis dissecans of the talus should be remembered as a possible differential diagnosis
of ankle pain in children and adolescents. Detailed and careful imagenological
investigation is mandatory and conservative treatment, in early stages of the pathol-
ogy, has resulted very favorable. In cases of failure of conservative treatment and in
the presence of signs of fragment instability or deviation from its bed, surgical treat-
ment allows a better recovery and better prognosis.
a b
c d
Fig. 22 Postoperative MRI images performed, including T2 mapping of the joint cartilage, show-
ing resolution of the subchondral lesion and complete reversal of previously observed changes
References
1. Konig F. Ueber freie Korper in den Gelenken. Dtsch Z Chir. 1888;27:90–109.

2. Kappis M. Weitere beitrage zur traumatisch-mechanischen entstehung der “spontanen” knor-
pela biosungen. Dtsch Z Chir. 1922;171:13–29.
3. Baltzer AW, Arnold JP. Bone-cartilage transplantation from the ipsilateral knee for chondral
lesions of the talus. Arthroscopy. 2005;21(2):159–66.
4. Flick AB, Gould N. Osteochondritis dissecans of the talus (transchondral fractures of the
talus): review of the literature and new surgical approach for medial dome lesions. Foot
Ankle. 1985;5(4):165–85.
5. van Dijk CN, Reilingh MI, Zengerink M, van Bergen CJ. Osteochondral defects of the ankle:
why painful? Knee Surg Sports Traumatol Arthrosc. 2010;18(5):570–80.
6. Frenkel SR, Di Cesare PE. Degradation and repair of articular cartilage. Front Biosci.
1999;4:D671–85.
7. Hintermann B, Boss A, Schafer D. Arthroscopic findings in patients with chronic ankle insta-
bility. Am J Sports Med. 2002;30(3):402–9.
8. Gianakos AL, Yasui Y, Hannon CP, Kennedy JG. Current management of talar osteochondral
lesions. World J Orthop. 2017;8(1):12–20.
9. Dheer S, Khan M, Zoga AC, Morrison WB. Limitations of radiographs in evaluating non-
displaced osteochondral lesions of the talus. Skelet Radiol. 2012;41:415–21.
10. Ferkel RD, Flannigan BD, Elkins BS. Magnetic resonance imaging of the foot and ankle:
correlation of normal anatomy with pathologic conditions. Foot Ankle. 1991;11:289–305.
11. Mintz DN, Tashjian GS, Connell DA, et al. Osteochondral lesions of the talus: a new mag-
netic resonance grading system with arthroscopic correlation. Arthroscopy. 2003;19:353–9.
12. Van Bergen CJA, Baur OL, Murawski CD, Spennacchio P, et al. International Consensus
Group on Cartilage Repar of the Ankle. Diagnosis: history, physical examination, imaging
and arthroscopy. Proceedings of the international consensus meeting on cartilage repair of the
ankle. Foot Ankle Int. 2018;31(1_suppl):3S–8S.
13. Lusse S, Claassen H, Gehrke T, et al. Evaluation of water content by spatially resolved trans-
verse relaxation times of human articular cartilage. Magn Reson Imaging. 2000;18:423–30.
14. Cuttica DJ, Smith WB, Hyer CF, Philbin TM, Berlet GC. Osteochondral lesions of the talus:
predictors of clinical outcome. Foot Ankle Int. 2011;32:1045–51.
15. O’Loughlin PF, Heyworth BE, Kennedy JG. Current concepts in the diagnosis and treatment
of osteochondral lesions of the ankle. Am J Sports Med. 2010;38:392–404.
16. Berndt AL, Harty M. Transchondral fractures (osteochondritis dissecans) of the talus. J Bone
Joint Surg Am. 1959;41:988–1020.
17. Scranton PE, McDermott JE. Treatmento of type V osteochondral lesions of the talus with
ipsilateral knee osteochondral autografts. Foot Ankle Int. 2001;22(5):380–4.
18. Raikin SM. Stage VI: massive osteochondral defects of the talus. Foot Ankle Clin.
2004;9(4):737–44.
19. Loomer R, Fisher C, Lloyd-Smith R, Sisler J, Cooney T. Osteochondral lesions of the talus.
Am J Sports Med. 1993;21(1):13–9.
20. Cheng MS, Ferkel RD, Applegate GR. Osteochondral lesions of the talus: a radiologic and
surgical comparison. AAOS meeting, New Orleans, 1995.
21. Hepple S, Winson IG, Glew D. Osteochondral lesions of the talus: a revised classification.
Foot Ankle Int. 1999;20:789–93.
22. Mintz DN, Tashjian GS, Connell DA, Deland JT, O’Malley M, Potter HG. Osteochondral
lesions of the talus: a new magnetic resonance grading system with arthroscopic correlation.
Arthroscopy. 2003;19:353–9.
23. Bae SH, Lee HK, Lee K, Lim S, Rim NJ, Kim JS, Cho J. Comparison of arthroscopic and
magnetic resonance imaging findings in osteochondral lesions of the talus. Foot Ankle Int.
2012;33:1058–62.
24. Griffith JF, Lau DTY, Yeung DKW, Wong MWN. High-resolution MR imaging of talar osteo-
chondral lesions with new classification. Skelet Radiol. 2012;41:387–99.
25. Astrand J, Skripitz R, Skoglund B, et al. A rat model for testing pharmacologic treatments of
pressure-related bone loss. Clin Orthop Relat Res. 2003;409:296–305.
26. Chuckpaiwong B, Berkson EM, Theodore GH. Microfracture for osteochondral lesions
of the ankle: outcome analysis and outcome predictors of 105 cases. Arthroscopy.
2008;24(1):106–12.
27. Cuttica DJ, Smith WB, Hyer CF, et al. Osteochondral lesions of the talus: predictors of clini-
cal outcome. Foot Ankle Int. 2011;32(11):1045–51.
28. Choi WJ, Park KK, Kim BS, et al. Osteochondral lesion of the talus: is there a critical defect
size for poor outcome? Am J Sports Med. 2009;37(10):1974–80.
29. Christensen JC, Driscoll HL, Tencer AF. Contact characteristics of the ankle joint. part 2. The
effects of talar dome cartilage defects. J Am Podiatr Med Assoc. 1994;84(11):537–47.
30. Giannini S, Ceccarelli F, Girolami M, et al. Biological osteosynthesis in osteochondral
lesions of the talus. Ital J Orthop Traumatol. 1989;15(4):425–32.
31. Dombrowski ME, Yasui Y, Murawski CD, Fortier LA, Giza E, Haleem AM, Hamid K, Tuan
R, Zhang Z, Schon LC, Hogan MV; International Consensus Group on Cartilage Repair
of the Ankle. Conservative Management and Biological Treatment Strategies: Proceedings
of the International Consensus Meeting on Cartilage Repair of the Ankle. Foot Ankle Int.
2018;39(1_suppl):9S–15S. https://doi.org/10.1177/1071100718779390. Erratum in: Foot
Ankle Int. 2021 Feb;42(2):248. Erratum in: Foot Ankle Int. 2022 Jan;43(1):NP3. PMID:
30215314.
32. Ramponi L, Yasui Y, Murawski CD, Ferkel RD, DiGiovanni CW, Kerkhoffs GMMJ,
Calder JDF, Takao M, Vannini F, Choi WJ, Lee JW, Stone J, Kennedy JG. Lesion Size
Is a Predictor of Clinical Outcomes After Bone Marrow Stimulation for Osteochondral
Lesions of the Talus: A Systematic Review. Am J Sports Med. 2017;45(7):1698–705.
https://doi.org/10.1177/0363546516668292. Epub 2016 Nov 16. PMID: 27852595
33. Furukawa T, Eyre DR, Koide S, et al. Biochemical studies on repair cartilage resurfacing
experimental defects in the rabbit knee. J Bone Joint Surg Am. 1980;62(1):79–89.
34. Choi WJ, Choi GW, Kim JS, Lee JW. Prognostic significance of the containment and location
of osteochondral lesions of the talus: independent adverse outcomes associated with uncon-
tained lesions of the talar shoulder. Am J Sports Med. 2013;41:126–33.
35. Choi WJ, Jo J, Lee JW. Osteochondral lesion of the talus: prognostic factors affecting
the clinical outcome after arthroscopic marrow stimulation technique. Foot Ankle Clin.
2013;18(1):67–78.
36. Raikin SM, Elias I, Zoga AC, Morison WB, Besser MP. Osteochondral lesions of the talus:
localization and morphologic data from 424 patients using a novel anatomical grid scheme.
Foot Ankle Int. 2007;28(2):154–61.
37. Deol P, Berlet GC, Hyer CF, et al. Age stratification of outcomes for osteochondral lesions of
the talus. AOFAS Summer Meeting, Vancouver, July, 2009.
38. Knutsen G, Engebretsen L, Ludvigsen TC, et al. Autologous chondrocyte implanta-
tion compared with microfracture in the knee. A randomized trial. J Bone Joint Surg Am.
2004;86(3):455–64.
39. Becher C, Thermann H. Results of microfracture in the treatment of articular cartilage defects
of the talus. Foot Ankle Int. 2005;26(8):583–9.
40. Choi WJ, Kim BS, Lee JW. Osteochondral lesion of the talus: could age be an indication for
arthroscopic treatment? Am J Sports Med. 2012;40(2):419–24.
41. Baxter MA, Wynn RF, Jowitt SN, Wraith JE, Fairbairn LJ, Bellantuono I. Study of telomere
length reveals rapid aging of human marrow stromal cells following in vitro expansion. Stem
Cells. 2004;22(5):675–82.
42. Banfi A, Muraglia A, Dozin B, Mastrogiacomo M, Cancedda R, Quatro R. Proliferation kine-
matics and differentiation of ex vivo expanded human bone marrow stromal cells: implica-
tions for their use in cell therapy. Exp Hematol. 2000;28(6):707–15.
43. Giannini S, Vannini F. Operative treatment of osteochondral lesions of the talar dome: current
concepts review. Foot Ankl Int. 2004;25(3):168–75.
44. Ferkel RD, Zanotti RM, Komenda GA, et al. Arthroscopic treatment of chronic osteochon-
dral lesions of the talus: long-term results. Am J Sports Med. 2008;36(9):1750–62.
45. Robinson DE, Winson IG, Harries WJ, et al. Arthroscopic treatment of osteochondral lesions
of the talus. J Bone Joint Surg Br. 2003;85(7):989–93.
46. Han SH, Lee JW, Lee DY, et al. Radiographic changes and clinical results of osteochondral
defects of the talus with and without subchondral cysts. Foot Ankle Int. 2006;27(12):1109–14.
47. Yoshimura I, Kanazawa K, Takeyama A, Angthong C, Ida T, Hagio T, Hanada H, Naito
M. Arthroscopic bone marrow stimulation techniques for osteochondral lesions of the talus
prognostic factors for small lesions. Am J Sports Med. 2013;41(3):528–34.
48. Choi WJ, Youn HK, Park YJ, Lee JW. Osteochondral lesions of the talus: are there any differ-
ences between osteochondral and chondral types? Am J Sports Med. 2013;41(3):504–10.
49. Lee D, Lee K, Jung S, Seon J, Kim M, Sung H II. Comparison of early versus delayed
weightbearing outcomes after microfracture for small to midsized osteochondral lesions of
the talus. Am J Sports Med. 2012;40(9):2023–8.
50. Gill TJ, McCulloch P, Glasson SS, et al. Chondral defect repair after the microfracture proce-
dure: a nonhuman primate model. Am J Sports Med. 2005;33(5):680–5.
51. Cuttica DJ, Shockley JA, Hyer CF, et al. Correlation of MRI edema and clinical outcomes fol-
lowing microfracture of osteochondral lesions of the talus. Foot Ankle Spec. 2011;4(5):274–9.
52. Goldstone RA, Pisani AJ. Osteochondritis dissecans of the talus. N Y State J Med.
1965;65(19):2487–94.
53. Easley ME, Latt LD, Santangelo JR, et al. Osteochondral lesions of the talus. J Am Acad
Orthop Sur. 2010;18(10):616–30.
54. Tol JL, Struijs PA, Bossuyt PM, et al. Treatment strategies in osteochondral defects of the
talar dome: a systematic review. Foot Ankle Int. 2000;21(2):119–26.
55. Shearer C, Loomer R, Clement D. Nonoperatively managed stage 5 osteochondral talar
lesions. Foot Ankle Int. 2002;23(7):651–4.
56. Mei-Dan O, Maoz G, Swartzon M, et al. Treatment of osteochondritis dissecans of the ankle
with hyaluronic acid injections: a prospective study. Foot Ankle Int. 2008;29(12):1171–8.
57. Sánchez M, Anitua E, Azofra J, Aguirre JJ, Andia I. Intra-articular injection of an autologous
preparation rich in growth factors for the treatment of knee OA: a retrospective cohort study.
Clin Exp Rheumatol. 2008;26(5):910–3.
58. Deol PPS, Cuttica DJ, Smith WB, Berlet GC. Osteochondral lesions of the talus: size, age and
predictors of outcomes. Foot Ankle Clin. 2013;18:13–34.
59. David TS, Shields CL. Radiofrequency and articular cartilage. Tech Knee Surg.
2004;3(3):193–7.
60. Taranow WS, Bisignani GA, Towers JD, et al. Retrograde drilling of osteochondral lesions of
the medial talar dome. Foot Ankle Int. 1999;20(8):474–80.
61. Qin-wei G, Yue-lin H, Chen J, Chang-long Y, Ying-fang AO. Arthroscopic treat-
ment for osteochondral lesions of the talus: analysis of outcome predictors. Chin Med
J. 2010;123(3):296–300.
62. Alford JW, Cole BJ. Cartilage restoration, part 1: basic science, historical perspective, patient
evaluation, and treatment options. Am J Sports Med. 2005;33(2):295–306.
63. Nehrer S, Spector M, Minas T. Histologic analysis of tissue after failed cartilage repair pro-
cedures. Clin Orthop Relat Res. 1999;365:149–62.
64. Donnenwerth MP, Roukis TS. Outcome of arthroscopic debridement and microfrac-
ture as the primary treatment for osteochondral lesions of the talar dome. Arthroscopy.
2012;28(12):1902–7.
65. Verhagen RA, Strujis PA, Bossuyt PM, van Dijk CN. Systematic review of treatment strate-
gies for osteochondral defects of the talar dome. Foot Ankle Clin. 2003;8:233–42.
66. Zengerink M, Struijis PAA, Tol JL, van Dijk CN. Treatment of osteochondral lesions of the
talus: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2010;18:238–46.
67. Savva N, Jabur M, Davies M, et al. Osteochondral lesions of the talus: results of repeat
arthroscopic debridement. Foot Ankle Int. 2007;28(6):669–73.
68. Lee KB, Bai LB, Park JG, et al. A comparison of arthroscopic and MRI findings in
staging of osteochondral lesions of the talus. Knee Surg Sports Traumatol Arthrosc.
2008;16(11):1047–51.
69. Doral MN, Bilge O, Batmaz G, Donmez G, Turhan E, Demirel M, Atay OA, Uzumcugil
A, Atesok K, Kaya D. Treatment of osteochondral lesions of the talus with microfracture
technique and postoperative hyaluronan injection. Knee Surg Sports Traumatol Arthrosc.
2012;20(7):1398–403.
70. Milano G, Sanna Passino E, Deriu L, et al. The effect of platelet rich plasma combined with
microfractures on the treatment of chondral defects: an experimental study in a sheep model.
Osteoarthr Cartil. 2010;18(7):971–80.
71. Fortier LA, Potter HG, Rickey EJ, et al. Concentrated bone marrow aspirate improves full-
thickness cartilage repair compared with microfracture in the equine model. J Bone Joint
Surg Am. 2010;92(10):1927–37.
72. Saw KY, Hussin P, Loke SC, et al. Articular cartilage regeneration with autologous mar-
row aspirate and hyaluronic acid: an experimental study in a goat model. Arthroscopy.
2009;25(12):1391–400.
73. Jung HG, Carag JA, Park JY, Kim TH, Moon SG. Role of arthroscopic microfracture for
cystic type osteochondral lesions of the talus with radiographic enhanced MRI support. Knee
74. Anders S, Lechler P, Rackl W, Grifka J, Schaumburger J. Fluoroscopy-guided retrograde
core drilling and cancellous bone grafting in osteochondral defects of the talus. Int Orthop.
2012;36(8):1635–40.
75. Assenmacher JA, Kelikian AS, Gottlob C, Kodros S. Arthroscopically assisted autologous
osteochondral transplantation for osteochondral lesions of the talar dome: an MRI and clini-
cal follow-up study. Foot Ankle Int. 2001;22:544–51.
76. Mendicino RW, Catanzariti AR, Hallivis R. Mosaicplasty for the treatment of osteochondral
defects of the ankle joint. Clin Podiatr Med Surg. 2001;18:495–513.
77. Hangody L, Kish G, Modis L, et al. Mosaicplasty for the treatment of osteochondritis dis-
secans of the talus: two to seven-year results in 36 patients. Foot Ankle Int. 2001;22:552–8.
78. Al-Shaikh RA, Chou LB, Mann JA, Dreeben SM, Prieskom D. Autologous osteochondral
grafting for talar cartilage defects. Foot Ankle Int. 2002;23:381–9.
79. Kreuz PC, Steinwachs M, Erggelet C, et al. Mosaicplasty with autogenous talar autograft for
osteochondral lesions of the talus after failed primary arthroscopic management: a prospec-
tive study with a 4-year follow-up. Am J Sports Med. 2006;34(1):55–63.
80. Emre TY, Ege T, Cift HT, Demircioğlu DT, Seyhan B, Uzun M. Open mosaicplasty in osteo-
chondral lesions of the talus: a prospective study. J Foot Ankle Surg. 2012;51(5):556–60.
81. Latt LD, Glisson RR, Montijo HE, Usuelli FG, Easley ME. Effect of graft height mis-
match on contact pressures with osteochondral grafting of the talus. Am J Sports Med.
2011;39(12):2662–9.
82. Hangody L, Fules P. Autologous osteochondral mosaicplasty for the treatment of full-
thickness defects of weight-bearing joints: ten years of experimental and clinical experience.
J Bone Joint Surg Am. 2003;85(S2):25–32.
83. Al-Shaikh RA, Chou LB, Mann JA, et al. Autologous osteochondral grafting for talar carti-
lage defects. Foot Ankle Int. 2002;23(5):381–9.
84. Scranton PE Jr, Frey CC, Feder KS. Outcome of osteochondral autograft transplantation for
type-V cystic osteochondral lesions of the talus. J Bone Joint Surg Br. 2006;88(5):614–9.
85. Woelfle JV, Reichel H, Nelitz M. Indications and limitations of osteochondral autologous
transplantation in osteochondritis dissecans of the talus. Knee Surg Sports Traumatol
Arthrosc. 2013;21(8):1925–30. https://doi.org/10.1007/s00167-013-2483-2.
86. Gobbi A, Francisco RA, Lubowitz JH, et al. Osteochondral lesions of the talus: randomized
controlled trial comparing chondroplasty, microfracture, and osteochondral autograft trans-
plantation. Arthroscopy. 2006;22(10):1085–92.
87. Kim YS, Park EH, Kim YC, Koh YG, Lee JW. Factors associated with the clinical outcomes
of the osteochondral autograft transfer system in osteochondral lesions of the talus : second-
look arthroscopic evaluation. Am J Sports Med. 2012;40:2709–11.
88. Reddy S, Pedowitz DI, Parekh SG, et al. The morbidity associated with osteochondral harvest
from asymptomatic knees for the treatment of osteochondral lesions of the talus. Am J Sports
Med. 2007;35(1):80–5.
89. Schottle PB, Oettl GM, Agneskirchner JD, et al. Operative therapy of osteochondral lesions
of the talus with autologous cartilage-bone transplantation. Orthopade. 2001;30(1):53–8.
90. Woelfle JV, Reichel H, Javaheripour-Otto K, Nelitz M. Clinical outcome and magnetic reso-
nance imaging after osteochondral autologous transplantation in osteochondritis dissecans of
the talus. Foot Ankle Int. 2013;34:173–9.
91. Paul J, Sagstetter A, Kriner M, Imhoff AB, Spang J, Hinterwimmer S. Donor-site morbidity
after osteochondral autologous transplantation for lesions of the talus. J Bone Joint Surg Am.
2009;91:1683–8.
92. Iwasaki N, Kato H, Kamishima T, Suenaga N, Minami A. Donor site evaluation after autolo-
gous osteochondral mosaicplasty for cartilaginous lesions of the elbow joint. Am J Sports
Med. 2007;35(12):2096–100.
93. McCollum GA, Myerson MS, Jonck J. Managing the cyst osteochondral defect. Allograft or
autograft. Foot Ankle Clin. 2013;18:113–33.
94. Tasto JP, Ostrander R, Bugbee W, Brage M. The diagnosis and management of osteochondral
lesions of the talus: osteochondral allograft update. Arthroscopy. 2003;19(S1):138–41.
95. Williams SK, Amiel D, Ball ST, et al. Prolonged storage effects on the articular cartilage of
fresh human osteochondral allografts. J Bone Joint Surg Am. 2003;85(11):2111–20.
96. Kim HT, Teng MS, Dang AC. Chondrocyte apoptosis: implications for osteochondral
allograft transplantation. Clin Orthop Relat Res. 2008;466:1819–25.
97. Berlet GC, Hyer CF, Philbin TM, et al. Does fresh osteochondral allograft transplantation of
talar osteochondral defects improve function? Clin Orthop Relat Res. 2011;469(8):2356–66.
98. El-Rashidy H, Villacis D, Omar I, et al. Fresh osteochondral allograft for the treatment of carti-
lage defects of the talus: a retrospective review. J Bone Joint Surg Am. 2011;93(17):1634–40.
99. Gortz S, De Young AJ, Bugbee WD. Fresh osteochondral allografting for osteochondral
lesions of the talus. Foot Ankle Int. 2010;31(4):283–90.
100. Hahn DB, Aanstoos ME, Wilkins RM. Osteochondral lesions of the talus treated with fresh
talar allografts. Foot Ankle Int. 2010;31(4):277–82.
101. Raikin SM. Fresh osteochondral allografts for large-volume cystic osteochondral defects of
the talus. J Bone Joint Surg Am. 2009;91(12):2818–26.
102. Haene R, Qamirani E, Story RA, Pinsker E, Daniels TR. Intermediate outcomes of fresh talar
osteochondral allografts for treatment of large osteochondral lesions of the talus. J Bone Joint
Surg. 2012;94(A):1105–10.
103. El-Rashidy H, Villacis D, Omar I, Kelikian AS. Fresh osteochondral allograft for the
treatment of cartilage defects of the talus: a retrospective review. J Bone Joint Surg Am.
2011;93(17):1634–40.
104. Kadakia AR, Espinosa N. Why allograft reconstruction for osteochondral lesion of the talus?
The osteochondral autograft transfer system seemed to work quite well. Foot Ankle Clin.
2013;18:89–112.
105. Bugbee WD, Khanna G, Cavallo M, McCauley JC, Görtz S, Brage ME. Bipolar fresh osteo-
chondral allografting of the tibiotalar joint. J Bone Joint Surg Am. 2013;95(5):426–32.
106. Brittberg M, Anders L, Anders N, et al. Treatment of deep cartilage defects in the knee with
autologous chondrocyte transplantation. N Engl J Med. 1994;331(14):889–95.
107. Giannini S, Buda R, Grigolo B, et al. The detached osteochondral fragment as a source of
cells for autologous chondrocyte implantation (ACI) in the ankle joint. Osteoarthr Cartil.
2005;13(7):601–7.
108. Johnson B, Lever C, Roberts S, Richardson J, McCarthy H, Harrison P, Laing P, Makwana
N. Cell cultured chondrocyte implantation and scaffold techniques for osteochondral talar
lesions. Foot Ankle Clin. 2013;18:135–50.
109. Baums MH, Heidrich G, Schultz W, et al. Autologous chondrocyte transplantation for treat-
ing cartilage defects of the talus. J Bone Joint Surg Am. 2006;88(2):303–8.
110. Koulalis D, SchultzW HM. Autologous chondrocyte transplantation for osteochondritis dis-
secans of the talus. Clin Orthop Relat Res. 2002;395:186–92.
111. Nam EK, Ferkel RD, Applegate GR. Autologous chondrocyte implantation of the ankle: a
2- to 5-year follow-up. Am J Sports Med. 2009;37(2):274–84.
112. Whittaker JP, Smith G, Makwana N, et al. Early results of autologous chondrocyte implanta-
tion in the talus. J Bone Joint Surg Br. 2005;87(2):179–83.
113. Giannini S, Battaglia M, Buda R, et al. Surgical treatment of osteochondral lesions of the
talus by open-field autologous chondrocyte implantation: a 10-year follow-up clinical and
magnetic resonance imaging T2-mapping evaluation. Am J Sports Med. 2009;37(S1):112–8.
114. Henderson I, Gui J, Lavigne P. Autologous chondrocyte implantation: natural history of
postimplantation periosteal hypertrophy and effects of repair-site debridement on outcome.
Arthroscopy. 2006;22(12):1318–24.
115. Wood JJ, Malek MA, Frassica FJ, et al. Autologous cultured chondrocytes: adverse events
reported to the United States Food and Drug Administration. J Bone Joint Surg Am.
2006;88(3):503–7.
116. Niemeyer P, Salzmann G, Schmal H, Mayr H, Südkamp NP. Autologous chondrocyte implan-
tation for the treatment of chondral and osteochondral defects of the talus: a meta-analysis of
available evidence. Knee Surg Sports Traumatol Arthrosc. 2012;20:1696–703.
117. Lee KT, Kim JS, Young KW, Lee YK, Park YU, Kim YH, Cho HK. The use of fibrin matrix-
mixed gel-type autologous chondrocyte implantation in the treatment for osteochondral
lesions of the talus. Knee Surg Sports Traumatol Arthrosc. 2013;21(6):1251–60.
118. Saris DB, Vanlauwe J, Victor J, et al. Characterized chondrocyte implantation results in bet-
ter structural repair when treating symptomatic cartilage defects of the knee in a randomized
controlled trial versus microfracture. Am J Sports Med. 2008;36(2):235–46.
119. Giza E, Sullivan M, Ocel D, et al. Matrix-induced autologous chondrocyte implantation of
talus articular defects. Foot Ankle Int. 2010;31(9):747–53.
120. Schneider TE, Karaikudi S. Matrix-induced autologous chondrocyte implantation (MACI)
grafting for osteochondral lesions of the talus. Foot Ankle Int. 2009;30(9):810–4.
121. Anders S, Goetz J, Schubert T, Grifka J, Schaumburger J. Treatment of deep articular talus
lesions by matrix associated autologous chondrocyte implantation—results at five years. Int
Orthop. 2012;36:2279–85.
122. Giannini S, Buda R, Vannini F, Di Caprio F, Grigolo B. Arthroscopic autologous chondrocyte
implantation in osteochondral lesions of the talus. Am J Sports Med. 2008;36:873–80.
123. Aurich M, Bedi HS, Smith PJ, Rolaufs B, Muckley T, Clayton J, Blackney M. Arthroscopic
treatment of osteochondral lesions of the ankle with matrix-associated chondrocyte implanta-
tion: early clinical and magnetic resonance imaging results. Am J Sports Med. 2011;39:311–9.
124. Cho HJ, Lee N, Lee JY, et al. Role of host tissues for sustained humoral effects after endothe-
lial progenitor cell transplantation into the ischemic heart. J Exp Med. 2007;204(13):3257–69.
125. Phinney DG, Prockop DJ. Concise review: mesenchymal stem/multipotent stromal cells.
The state of transdifferentiation and modes of tissue repair: current views. Stem Cells.
2007;25(11):2896–902.
126. Pittenger MF, Mackay AM, Beck SC, et al. Multilineage potential of adult human mesenchy-
mal stem cells. Science. 1999;284(5411):143–7.
127. Giannini S, Buda R, Vannini F, Cavallo M, Grigolo B. One-step bone marrow-derived cell
transplantation in talar osteochondral lesions. Clin Orthop Relat Res. 2009;467(12):3307–20.
128. Giannini S, Buda R, Cavallo M, Ruffilli A, Cenacchi A, Cavallo C, Vannini F. Cartilage repair
evolution in post-traumatic osteochondral lesions of the talus: from open field autologous
chondrocyte to bone-marrow-derived cells transplantation. Injury. 2010;41(11):1196–203.
129. Giannini S, Buda R, Battaglia M, Cavallo M, Ruffilli A, Ramponi L, Pagliazzi G, Vannini
F. One-step repair in talar osteochondral lesions: 4-year clinical results and t2-mapping capa-
bility in outcome prediction. Am J Sports Med. 2013;41(3):511–8.
130. Buda R, Vannini F, Cavallo M, Grigolo B, Cenacchi A, Giannini S. Osteochondral lesions of
the knee: a new one-step repair technique with bone-marrow-derived cells. J Bone Joint Surg
Am. 2010;92(S2):2–11.
131. Kim YS, Park EH, Kim YC, Koh Y. Clinical outcomes of mesenchymal stem cell injection
with arthroscopic treatment in older patients with osteochondral lesions of the talus. Am J
Sports Med. 2013;41:1090–9.
132. Sakaguchi Y, Sekiya I, Yagishita K, Muneta T. Comparison of human stem cells derived from
various mesenchymal tissues: superiority of synovium as a cell source. Arthritis Rheum.
2005;52(8):2521–9.
133. Koh YG, Choi YJ. Infrapatellar fat pad-derived mesenchymal stem cell therapy for knee
osteoarthritis. Knee. 2012;19(6):902–7.
134. Haleem AM, Singergy AA, Sabry D, et al. The clinical use of human culture-expanded
autologous bone marrow mesenchymal stem cells transplanted on platelet-rich fibrin glue in
the treatment of articular cartilage defects: a pilot study and preliminary results. Cartilage.
2010;1(4):253–61.
135. Nejadnik H, Hui JH, Feng Choong EP, et al. Autologous bone marrow-derived mesenchymal
stem cells versus autologous chondrocyte implantation: an observational cohort study. Am J
Sports Med. 2010;38(6):1110–6.
136. Filardo G, Madry H, Jelic M, Roffi A, Cucchiarini M, Elizaveta K. Mesenchymal stem cells
for the treatment of cartilage lesions: from pre-clinical findings to clinical applications in
orthopaedics. Knee Surg Sports Traumatol Arthrosc. 2013;21:1717–29.
137. Giannini S, Buda R, Bataglia M, Cacallo M, Ruffilli A, Ramponi L, Pagliazzi G, Vannini
F. One-step repair in talar osteochondral lesions: 4-year clinical results and T2-mapping
capability in outcome predictor. Am J Sports Med. 2013;41(3):511–8.
138. Behrens P, Bitter T, Kurz B, et al. Matrix-associated autologous chondrocyte transplantation/
implantation (MACT/MACI): 5-year follow-up. Knee. 2006;3(3):194–202.
139. Gille J, Schuseil E, Wimmer J, et al. Mid-term results of autologous matrix-induced chon-
drogenesis for treatment of focal cartilage defects in the knee. Knee Surg Sports Traumatol
Arthrosc. 2010;18(11):1456–64.
140. Walther M. Treatment option in osteochondral lesions: open ACT/AMIC. 18th annual meet-
ing of German Society of Foot and Ankle Surgery. Dresden, Germany, March 23, 2012.
141. Wiewiorski M, Barg A, Valderrabano V. Autologous matrix-induced chondrogenesis in
osteochondral lesions of the talus. Foot Ankle Clin. 2013;18(1):151–8.
142. Valderrabano V, Miska M, Leumann A, Wiewiorski M. Reconstruction of osteochondral
lesions of the talus with autologous spongiosa grafts and autologous matrix-induced chon-
drogenesis. Am J Sports Med. 2013;41(3):519–27.
143. McCormick F, Yanke A, Provencher MT, et al. Minced articular cartilage-basic science, sur-
gical technique, and clinical application. Sports Med Arthrosc Rev. 2008;16:217–20.
144. Mithoefer K, McAdams TR, Scopp JM, et al. Emerging options for treatment of articular
cartilage injury in the athlete. Clin Sports Med. 2009;28(1):25–40.
145. Adams SB, Yao JQ, Schon LC. Particulated juvenile articular cartilage allograft transplanta-
tion for osteochondral lesions of the Talus. Tech Foot Ankle Surg. 2011;10(2):92–8.
146. Farr J, Yao JQ. Chondral defect repair with particulated juvenile cartilage allograft. Cartilage.
2011;2(4):346–53.
147. Coetzee JC, Giza E, Schon LC, Berlet GC, Neufeld S, Stone RM, Wilson EL. Treatment
of osteochondral lesions of the talus with particulated juvenile cartilage. Foot Ankle Int.
2013;34(9):1205–11.
148. van Bergen CJA, Reilingh ML, van Dijk CN. Tertiary osteochondral defect of the talus
treated by a novel contoured metal implant. Knee Surg Sports Traumatol Arthrosc.
2011;19:999–1003.
149. Mologne TS, Ferkel RD. Arthroscopic treatment of osteochondral lesions of the distal tibia.
Foot Ankle Int. 1007;28:865–72.
150. Athanasiou KA, Niederauer GG, Schenck RC Jr. Biomechanical topography of human ankle
cartilage. Ann Biomed Eng. 1995;5:697–704.
151. Elias I, Raikin SM, Schweitzer ME, et al. Osteochondral lesions of the distal tibia plafond:
localization and morphological characteristics with an anatomical grid. Foot Ankle Int.
2009;30:524–9.
152. Cuttica DJ, Smith WB, Hyer CF, Philbin TM, Berlet GC. Arthroscopic treatment of osteo-
chondral lesions of the tibial plafond. Foot Ankle Int. 2012;33:662–8.
153. Battaglia M, Vannini F, Buda R, Cavallo M, Ruffilli A, Monti C, Galletti S, Giannini
S. Arthroscopic autologous chondrocyte implantation in osteochondral lesions of the
talus: mid-term T2-mapping MRI evaluation. Knee Surg Sports Traumatol Arthrosc.
2011;19:1376–84.
154. Battaglia M, Rimondi E, Mont C, Guaraldi F, Sant’Andrea A, et al. Validity of T2 mapping
in characterization of the regeneration tissue by bone marrow derived cell transplantation in
osteochondral lesions of the ankle. Eur J Radiol. 2011;80:132–9.
155. Zwingmann J, Südkamp NP, Schmal H, Niemeyer P. Surgical treatment of osteochondritis
dissecans of the talus: a systematic review. Arch Orthop Trauma Surg. 2012;132(9):1241–50.
156. Buda R, Pagliazzi G, Castagnini F, Cavallo M, Giannini S. Treatment of osteochondritis dis-
secans of the talus in skeletally immature population. Foot Ankle Spec. 2016;9(3):265–70.
157. Perumal V, Wall E, Babekir N. Juvenile osteochondritis dissecans of the talus. J Pediatr
Orthop. 2007;27:821–5.
158. Heyse TJ, Schüttler KF, Schweitzer A, Timmesfeld N, Efe T, Paletta JR, et al. Juvenile osteo-
chondritis dissecans of the talus: predictors of conservative treatment failure. Arch Orthop
Trauma Surg. 2015;135(10):1337–41.
159. Lam KY, Siow HM. Conservative treatment for juvenile osteochondritis dissecans of the
talus. J Orthop Surg (Hong Kong). 2012;20:176–80.
160. Siparsky PN, Kocher MS. Current concepts in pediatric and adolescent arthroscopy.
Arthroscopy. 2009;25:1453–69.
161. Masquijo JJ, Ferreyra A, Baroni E. Arthroscopic retrograde drilling in Juvenile osteochondri-
tis dissecans of the talus. J Pediatr Orthop. 2016;36(6):589–93.
162. Pagliazzi G, Baldassarri M, Perazzo L, Vannini F, Castagnini F, Buda R. Tissue bioengineer-
ing in the treatment of osteochondritis dissecans of the talus in children with open physis. J
Pediatr Orthop. 2018;38(7):375–81.
163. Vannini F, Cavallo M, Baldassarri M, Castagnini F, Olivieri A, Ferranti E, Buda R, Giannini
S. Treatment of juvenile osteochondritis dissecans of the talus: current concepts review.
Joints. 2015;2(4):188–91.
Posterior Ankle Impingement
Daniel Baumfeld and Tiago Baumfeld
Synopsis
Posterior Ankle Impingement (PAI) refers to a chronic painful mechanical limita-
tion of ankle motion caused by soft-tissue or osseous abnormality affecting the pos-
terior tibiotalar joint. Impingement can be associated with single traumatic event or
repetitive microtrauma. This syndrome is one of the possible etiologies of persistent
ankle pain. Nowadays, arthroscopic approach to this pathology, when indicated, is
consider as the gold standard with its high safety and low complication rates. In this
chapter, we describe the clinical and potential imaging features, as well as the
arthroscopic/endoscopic management strategies for PAI.
Key Points
• Posterior Ankle Impingement is a clinical syndrome of end-range joint pain or
motion restriction caused by the direct mechanical impact of bone or soft tissues.
• Imaging studies can show osseous and soft-tissue diseases and anatomic varia-
tions that can help diagnose and treat impingement syndromes.
• Soft-tissue impingement occurs more frequently on the lateral side as a conse-
quence of synovial scarring, inflammation, and hypertrophy in the anterolateral
recess of the tibiotalar joint, but it can also occur in PAI.
• Advantages of the arthroscopic treatment over open arthrotomy include reduced
recovery time and earlier return to sports activities.
D. Baumfeld (*)
Federal University of Minas Gerais, Felicio Rocho Hospital, Belo Horizonte, MG, Brazil
T. Baumfeld
Felicio Rocho Hospital, Belo Horizonte, MG, Brazil

Switzerland AG 2022
1108 D. Baumfeld and T. Baumfeld
1 Introduction
Posterior Ankle Impingement (PAI) refers to a chronic painful mechanical limita-

tion of the ankle caused by soft-tissue or osseous abnormalities [1]. Post-traumatic
synovitis, intra-articular fibrous bands/scar tissue, capsular scarring, or develop-
mental and acquired bony spurs or prominences are the most common causes [2].
Single traumatic event or repetitive microtrauma are also associated with this syn-
drome [1]. Although PAI is largely a clinical diagnosis, imaging is often used to
evaluate suspected ankle impingement in order to confirm the presence of typical
changes and as a tool for preoperative planning. Imaging can also help differentiate
impingement from alternative diagnoses that may have overlapping clinical presen-
tations [3]. Currently, the surgical approach to this pathology, when indicated, is
performed with arthroscopic/endoscopic assistance. This method provides a highly
accurate means of locating and treating intra-articular abnormality [3, 4].
In this chapter, we describe the clinical and potential imaging features, as well as
the arthroscopic/endoscopic management strategies for PAI.
2 Etiology
Posterior impingement arises from compression of the soft tissues between the pos-
terior process of the calcaneus and the posterior tibial border on plantar flexion of
the ankle [5–7]. The soft tissues compressed include the tibiotalar capsule, posterior
talofibular, intermalleolar, and tibiofibular ligaments. The flexor hallucis longus
(FHL) and the lateral posterior process of the talus are also important because addi-
tional bony impingement with these structures can occur as a consequence of prom-
inent os trigonum [8, 9] (Fig. 1a–c).
The lateral process of the talus initially forms as a secondary ossification center
between the ages of 7–13 years and usually fuses with the main body of the talus
within 1 year [7, 8, 10, 11]. If there is a failure of fusion, the ossicle is known as an
os trigonum and articulates with the talus via a synchondrosis (incidence 7–14%)
[12]. If the lateral talar process is unusually large or prominent, it is termed as Stieda
process.
The posterior ankle impingement can develop after a significant acute injury
such as avulsion of the posterior talo-fibular ligament, talar fracture, or fracture of
the os trigonum [13]. However, this is relatively rare and the syndrome usually
arises insidiously in predisposed athletes. It is believed that repetitive forced plantar
flexion of the foot results in chronic injury to the posterior osseous and soft tissues
[14]. Ballet dancers are especially prone to this injury, as the ankle is commonly at
the extremes of its full range of movement and is maintained in these positions for
relatively prolonged periods [13, 15]. Professional soccer players are also at
increased risk because ball kicking leads to repeated sudden forced plantar
flexion [4].
Posterior Ankle Impingement 1109
a c
Fig. 1 (a) Os trigonum syndrome. (b) Sagittal MRI (T1 and T2) images. The arrowheads point to
the os trigonum. (c) T1 cross section. White arrowheads point to os trigonum; the black arrowhead
points at the FHL tendon and the dashed line circumscribes the NAV bundle
3 Imaging Studies
The imaging assessment of PAI initiates with conventional radiography.

Anteroposterior (AP) ankle view typically does not reveal abnormalities related to
posterior impingement. On the lateral view, a prominent Stieda’s process or os tri-
gonum may be identified in the posterolateral aspect of the ankle; however, these
findings are commonly seen in asymptomatic individuals [4, 9].
Computed Tomography (CT) allows evaluation of anatomical details of osseous

structures of the posterior ankle and detection of fractures, loose bodies, and osteo-
chondral lesions that may be associated with posterior impingement. Ultrasound
has its main role as a tool for ultrasound-guided therapeutic injection of steroids and
anesthetics. In most patients, ultrasound will show hypoechoic, nodular capsular
thickening localized on the lateral aspect of the lateral talar process or the os tri-
gonum [5].
Nuclear medicine bone scintigraphy has been used as an adjunct to radiography
since it shows increased radiotracer uptake due to hyperemia and bone repair in the
posterior ankle in the setting of impingement. Although highly sensitive, bone scin-
tigraphy lacks specificity and cannot distinguish between radiotracer uptake related
to fracture, pseudarthrosis, bone contusion, or posterior subtalar arthritis. In com-
parison to bone scintigraphy, SPECT-CT allows superior anatomical correlation of
radiotracer activity and symptoms. Use of SPECT-CT has been described for poste-
rior ankle pain [16].
Magnetic Resonance Imaging (MRI) is the optimal modality as it can define
osseous and non-osseous abnormalities. Osseous findings associated with posterior
impingement include bone marrow edema pattern within a Stieda process or os tri-
gonum and the adjacent talus and/or fluid signal at the synchondrosis in the context
of an os trigonum. MRI in the sagittal plane using T1-weighted and fat-suppressed
PDW or STIR sequences can afford optimal visualization of an os trigonum, a
Stieda process. Soft-tissue abnormalities can consist of prominent fluid distending
the posterior joint recess, posterior ganglia, posterior synovial thickening, edema-
like signal within the surrounding soft tissues, and FHL tenosynovitis. MRI imag-
ing also allows accurate assessment of the remainder of the tibiotalar joint and
surrounding tendons, which can aid treatment and surgical planning [17, 18].
The diagnosis of PAI is based primarily on the clinical history and physical exam.
The patient usually reports chronic or recurrent posterior pain caused by forced
plantar flexion or push-off activities, such as dance, kicking sports, walking or run-
ning downhill, and wearing high heels. The pain is usually deep and may have a
mechanical component. Symptoms can develop 4–6 weeks after the initial ankle
injury, in which presumably thickening of the posterior capsule and adjacent soft
tissues develop. It may also arise secondary to loose avulsion fragments of bone
posterolaterally following a previous ligamentous injury. PAI syndrome more com-
monly arises in individuals with the previously described osseous anatomical vari-
ants who are exposed to repetitive forced plantar flexion resulting in compression of
the osseous and soft tissues behind the ankle [19–23].
On physical examination, there typically is posteromedial or posterolateral ten-
derness. Passive terminal plantar flexion may reproduce the patient’s symptoms.
The Posterior Impingement test consists of quickly forced hyper plantar flexion
causing the posterior talar process or the os trigonum to be compressed between the
posterior rim of the tibia and the calcaneus. A positive result causes pain-reproducing
symptoms; there may be a block to full plantar flexion [24].
If passive hallux motion causes pain, flexor hallucis longus abnormality may also
be present. Many patients being treated for an os trigonum can have symptomatic
involvement of the FHL. Patients with posterior ankle impingement syndrome sec-
ondary to FHL problems usually report posteromedial ankle pain during forced plan-
tar flexion of the ankle. Clinically, the pain may be reproduced by asking the patient
to repeatedly flex and extend the great toe with the ankle in 20-degree equinus while
palpating the tendon behind the medial malleolus. In more chronic cases, crepitus and
occasionally a nodule within the tendon may be felt. Triggering can be also found [25].
It was described that athletes affected by posterior impingement may attempt to
compensate for the loss of plantar flexion by assuming an inverted foot position.
This may predispose to frequent ankle sprains, calf strains and contractures, plantar
foot pain, and toe curling [26].
5 Approaches to Treatment
The initial treatment of choice for PAI is generally conservative [27, 28]. Potential
options include rest, physical therapy, ankle bracing or taping, shoe modification,
local corticosteroid injection, and the avoidance of extreme ankle plantar flexion.
Immobilization is indicated if there is evidence of an acute fracture. Subsequent
physical therapy and protective dorsiflexion taping may be helpful. Frequently, con-
servative treatment fails and surgery is recommended.
Open surgical techniques have been used with moderate success, but current
guidelines consider endoscopy as the gold standard surgical approach with its high
safety and low complication rates [26]. Open approach can be either posteromedial
or posterolateral, being the first the choice when FHL pathology has to be addressed.
It has been well documented with 75% successful results and a mean time to return
to sporting activities or dancing at 3–5 months but has a complication rate of
15–24%. With improvements in endoscopy techniques, arthroscopic treatment now
offers improved success rates with a shortened recovery time (average resumption
of sporting activities at 9 weeks) and reduced complication rate (1–9%).
6 Endoscopic Anatomy of the Posterior Ankle
Endoscopic approach for diagnosis and treatment of posterior ankle pathology has been
proven to be an effective and safe procedure for bony posterior ankle impingement due
different causes. The knowledge of particular anatomy of the posterior ankle joint is
imperative to achieve good results and perform a safe procedure. There are some par-
ticular anatomic issues of the posterior ankle joint that may help [25, 29] (Fig. 2a-f):
a b c
d e f
Fig. 2 Posterior ankle endoscopy: (a) The most important safety and reference point for posterior
ankle arthroscopy is the FHL. The tibial nerve bundle beam is 2 mm from this reference point in
the medial direction. (b) FHL can be arthroscopically evaluated distally within its own sheath. (c)
The central portion of the subtalar joint. (d) The medial “shoulder” of the calcaneus at the subtalar
joint. (e) The concavity of the talar articular surface and the convexity of the calcaneal articular
surface at the subtalar joint. (f) The lateral “shoulder” of the calcaneus at the subtalar joint.
Legends: FHL flexor hallucis longus, Ta talus, Ca calcaneus
1. The synchondrosis of the os trigonum may vary in orientation from coronal to

oblique sagittal plane.
2. There are unusual muscles that can cause posterior impingement including pero-
neus quartus, flexor accessories digitorum longus, accessory soleus, peroneus-
calcaneus internus muscle, tibiocalcaneus internus, and low-lying flexor hallucis
longus muscle belly; all of those can be identified by arthroscopic procedures.
3. The deep transverse ligament of the posterior inferior tibiofibular ligament is
considered a true labrum of the posterior ankle joint and has been implicated in
posterior ankle impingement.
4. When a tight and thickened crural fascia is present, this can hinder the free
movement of instruments. It can be helpful to enlarge the portals deep in the
fascia by means of a punch or shaver.
7 Endoscopic Treatment of the Posterior Ankle Impingement
When addressing posterior ankle impingement, hindfoot conventional endoscopic

portals with the patient in prone position are recommended [25]. This consists of
the posterolateral and posteromedial portals located at the junction of the tip of the
lateral malleolus and the medial and lateral borders of the calcaneal tendon.
Creation of these portals does not have a risk for injuries when performed close to
the Achilles tendon; however, the creation of a working area during hindfoot
endoscopy has a high potential risk of injury to the posterior neurovascular struc-
tures. A systematic technique when creating this space and working lateral to the
flexor hallucis longus tendon are both recommended in order to avoid
complications.
The initial posterior ankle debridement is often done in a blind fashion. Once the
bone can be visualized, the arthroscope and shaver can be advanced medially to
identify the FHL tendon. There is often a large amount of fibrous soft tissue and
capsule that makes initial visualization difficult. The key is to be patient with shaver
dissection and to always be aware of instrument position in the posterior ankle,
especially in relation to the FHL tendon. The safe initial working zone is midline to
lateral to avoid the tendon and deeper rather than superficial to avoid the Achilles
tendon. After the fatty tissue overlying the posterior ankle capsule, lateral from the
FHL tendon is resected, the possible posterior anatomic structures causing impinge-
ment can be identified [12, 26]:
• Hypertrophic posterior joint capsule
• Synovitis
• Os trigonum
• Hypertrophic posterior talar process
• Entrapment of the flexor hallucis longus
A 4.0-mm aggressive soft-tissue shaver is typically used for soft-tissue debride-
ment and a 3.5 or 4.0 mm barrel burr is typically used for bony resection.
Synovectomy may be safely performed with the shaver and a radio frequency abla-
tion instrument. The surgeon should be careful with radio frequency when working
around the flexor hallucis longus tendon to avoid thermal injury to the tibial nerve
and vascular structures. If there is also FHL tenosynovitis, or a distal insertion of the
FLH muscle belly, then the shaver or a punch can be used to release the flexor reti-
naculum from the medial border of the talus and to resect the distal portion of the
muscle belly. The FHL can be thoroughly debrided, and a smooth excursion of the
tendon can be directly verified with the arthroscope. Identifying the os trigonum or
Stieda process before initiating burring is also an important recommendation [13,
22] (Fig. 3a–f).
8 Specific Condition Regarding Posterior

Impingement Syndrome
Approaches described above are the usual treatment that surgeons can follow to
manage this pathology, but there are special presentations in daily practice that
make the decision hard and, in many times, different than usual.
a b c
d e f
Fig. 3 Posterior ankle impingement – os trigonum syndrome: (a) Regularly the limits between the
talus and the os trigonum are not so easy to find (dotted line). (b) After removal the fibrous tissue
(symphysis) or cartilage (synchondrosis) existing in the contact zone the os trigonum can be
removed. (c) After the os trigonum removal, the FHL runs completely free. (d) The dotted white
line delimits the area from which the os trigonum was removed. (e) Osteochondral lesions of the
posterior aspect of the talus could be accessed from the posterior arthroscopy. (f) Symptoms of
posterior impingement may be due to low FHL muscle belly implantation. These fibers can be
removed with the aid of soft-tissue shaver. Legends: OT os trigonum, FHL flexor hallucis longus,
Ta talus, Ca calcaneus
Athletes during season can be conducted with non-validated biological treat-

ments such as PRP or PRF, with injection solution of homeopathic combination
drugs or even with lidocaine just allowing them to participate during training or
official games. During season, we usually start with lidocaine and/or homeopathic
injection; if this option presents with a relatively good result that allows the athlete
to play, 10 days later a PRP or PRF injection is planned. Another possibility that may
help is Percutaneous Electrolysis Therapy (PET); this treatment involves applying a
modulated direct electrical current directly to damaged soft tissue via an acupunc-
ture needle, that may induce tissue’s recovery. Shock wave therapy is also another
possibility that can be used. Both of these modalities intend to stimulate fast soft-
tissue healing and pain relief, but, until now, they do not have prospective studies.
Normally, the decision to move on the treatment to surgery is discussed with the
team executive, coaches, and the athlete. Regarding posterior ankle impingement,
the most common seen scenario is the management of a typical ballet dancer with
posterior pain. How do we manage this? Inject or not? How often? Corticoid injec-
tions should be used as single shots or be avoided; first of all, they are considered
doping in some sports, and second they may lead to local consequences as tendon
ruptures, skin problems, and local adhesion41. It is preferable to use shock wave
therapies, injections with hyaluronic acid, PRP, or PRF and even homeopathic sub-
stances as Arnica Montana. The use of PET or shock wave therapy can also be used
as nonsurgical treatments.
9 Evidence and Final Considerations
Endoscopic management of posterior ankle impingement is associated with a low

morbidity, a short recovery time, and provides good/excellent results at 2 years fol-
low-up in 80% of patients [6, 20, 26, 27]. The theoretical advantages of posterior
ankle arthroscopy include better visualization of the posterior ankle and subtalar
joint, earlier return to activity due to less dissection and smaller incisions, and lower
complication rates. The disadvantages are that this technique is complex and
demanding with a steep initial learning curve and longer operating times. Comparing
open and arthroscopic os trigonum excision, there was no significant difference in
American Orthopaedic Foot and Ankle Society (AOFAS) visual analog scale scores
reported in the literature; however, the time for return to sports was almost 6 weeks
earlier for the arthroscopic patients (6 vs 11.9 weeks) [22, 26, 28]. The overall com-
plication rate was reported to be 3.8–8.5% after posterior hindfoot endoscopy for
posterior ankle impingement, FHL tenosynovitis, os trigonum syndrome, or a frac-
tured Stieda process while the rate of complications in open posterior hindfoot and
ankle surgery for the same pathologies ranged from 10% to 24% [25, 26]. The
potential for nerve injury appears to be similar for both open and arthroscopic tech-
niques. Ribbans et al. [29] compared open and arthroscopic debridement. Open
cases had a 4.2% incidence of nerve injury and a wound complication and infection
rate of 2.8%. Arthroscopic cases had a 3.7% incidence of nerve injury and 0.96%
incidence of wound complication and infection rate. Although rare, injury to the
tibial nerve and its branches for procedures around the posterior talar process has
been reported [13, 22]. This procedure has proven to be particularly effective in
patients with overuse injuries that have frequent plantar flexion activities, such as
dancers and soccer players. The main complication, sural nerve neuropraxia, can be
minimized by correct portal placement and instrumentation.
Correct diagnosis and treatment are essential on the management of PAI, espe-
cially in professional athletes. Endoscopic treatment is minimally invasive and suit-
able for athletes and nonathletes who desire an early return to sports and a lower
complications rate.
References
1. Lavery KP, McHale KJ, Rossy WH, Theodore G. Ankle impingement. J Orthop Surg Res.
2016;1–7 https://doi.org/10.1186/s13018-016-0430-x.
2. Tol JL, van Dijk CN. Anterior ankle impingement. Foot Ankle Clin N Am. 2006;11(2):297–310.
https://doi.org/10.1016/j.fcl.2006.02.002.
3. Ross KA, Murawski CD, Smyth NA, et al. Current concepts review: arthroscopic treatment
of anterior ankle impingement. Foot Ankle Surg. 2017;23(1):1–8. https://doi.org/10.1016/j.
fas.2016.01.005.
4. LiMarzi GM, Khan O, Shah Y, Yablon CM. Imaging manifestations of ankle impingement
syndromes. Radiol Clin NA. 2018;56(6):893–916. https://doi.org/10.1016/j.rcl.2018.06.005.
5. Robinson P. Impingement syndromes of the ankle. Eur Radiol. 2007;17(12):3056–65. https://
doi.org/10.1007/s00330-007-0675-1.
6. Niek van Dijk C. Anterior and posterior ankle impingement. Foot Ankle Clin N Am.
7. Dimmick S, Linklater J. Ankle impingement syndromes. Radiol Clin NA. 2013;51(3):479–510.
https://doi.org/10.1016/j.rcl.2012.11.005.
8. Zbojniewicz AM. Impingement syndromes of the ankle and hindfoot. Pediatr Radiol.
2019:1–11. https://doi.org/10.1007/s00247-019-04459-5.
9. Donovan A, Rosenberg ZS. MRI of ankle and lateral hindfoot impingement syndromes. AJR
Am J Roentgenol. 2010;195(3):595–604. https://doi.org/10.2214/AJR.09.4199.
10. Hess GW. Ankle impingement syndromes: a review of etiology and related implications. Foot
Ankle Spec. 2011;4(5):290–7. https://doi.org/10.1177/1938640011412944.
11. Larciprete M, Giudice G, Balocco P, Faletti C. [Ankle impingement syndrome]. Radiol Med.
2000;99(6):415–19.
12. Buchhorn T, Koch M, Weber J, Ziai P. [Ankle impingement. Indications and arthroscopic ther-
apy]. Unfallchirurg. 2016;119(2):115–19. https://doi.org/10.1007/s00113-015-0135-3.
13. Heier KA, Hanson TW. Posterior ankle impingement syndrome. YOTSM. 2017;25(2):75–81.
https://doi.org/10.1053/j.otsm.2017.03.005.
14. Hayashi D, Roemer FW, D’Hooghe P, Guermazi A. Posterior ankle impingement in athletes:
pathogenesis, imaging features and differential diagnoses. Eur J Radiol. 2015:1–11. https://
doi.org/10.1016/j.ejrad.2015.07.017.
15. Kudaş S, Dönmez G, Işık Ç, Çelebi M, Çay N, Bozkurt M. Posterior ankle impingement
syndrome in football players: case series of 26 elite athletes. Acta Orthop Traumatol Turc.
2016;50(6):649–54. https://doi.org/10.1016/j.aott.2016.03.008.
16. Zwiers R, Baltes TPA, Opdam KTM, Wiegerinck JI, van Dijk CN. Prevalence of os trigonum on
CT imaging. Foot Ankle Int. 2018;39(3):338–42. https://doi.org/10.1177/1071100717740937.
17. Spiga S, Vinci V, Tack S, et al. Diagnostic imaging of ankle impingement syndromes in
athletes. Musculoskelet Surg. 2013;97 Suppl 2(S2):S145–53. https://doi.org/10.1007/
s12306-013-0280-1.
18. Hayashi D, Roemer FW, D’Hooghe P, Guermazi A. Posterior ankle impingement in athletes:
pathogenesis, imaging features and differential diagnoses. Eur J Radiol. 2015;84(11):2231–41.
https://doi.org/10.1016/j.ejrad.2015.07.017.
19. Hong C, Pearce C, Ballal M, Calder JDF. Management of sports injuries of the foot and ankle.
Bone Joint J. 2016;98(B):1–13. https://doi.org/10.1302/0301-620X.98B10.
20. Berman Z, Tafur M, Ahmed SS, Huang BK, Chang EY. Ankle impingement syndromes: an
imaging review. Br J Radiol. 2017;90(1070):20160735. https://doi.org/10.1259/bjr.20160735.
21. Epstein DM, Black BS, Sherman SL. Anterior ankle arthroscopy. FCL. 2015;20(1):41–57.
https://doi.org/10.1016/j.fcl.2014.10.001.
22. Carreira DS, Vora AM, Hearne KL, Kozy J. Outcome of arthroscopic treatment of pos-
terior impingement of the ankle. Foot Ankle Int. 2016;37(4):394–400. https://doi.
org/10.1177/1071100715620857.
23. Dalmau-Pastor M, Vega J, Malagelada F, Manzanares MC. Surgical arthroscopic anatomy.
In: Arthroscopy and endoscopy of the foot and ankle, Principle and practice, vol. 21. 2nd ed.
Singapore: Springer Singapore; 2019. p. 13–27. https://doi.org/10.1007/978-981-13-0429-3_2.
24. Templeton-Ward O, Solan M. Posterior ankle and hind foot arthroscopy – how do you respon-
sibly learn this new technique? Foot Ankle Surg. 2014;20(4):229–30. https://doi.org/10.1016/j.
fas.2014.09.005.
25. Lui TH. Arthroscopy and endoscopy of the foot and ankle: indications for new techniques.
Arthroscopy. 2007;23(8):889–902. https://doi.org/10.1016/j.arthro.2007.03.003.
26. Beimers L, Frey C, van Dijk CN. Arthroscopy of the posterior subtalar joint. Foot Ankle Clin
N Am. 2006;11(2):369–90. https://doi.org/10.1016/j.fcl.2006.03.006.
27. Wang L, Gui J, Gao F, et al. Modified posterior portals for hindfoot arthroscopy. Arthroscopy.
2007;23(10):1116–23. https://doi.org/10.1016/j.arthro.2007.04.015.
28. Calder JD, Sexton SA, Pearce CJ. Return to training and playing after posterior ankle
arthroscopy for posterior impingement in elite professional soccer. Am J Sports Med.
29. Ribbans WJ, Ribbans HA, Cruickshank JA, Wood EV. The management of posterior
ankle impingement syndrome in sport: a review. Foot Ankle Surg. 2014:1–10. https://doi.
org/10.1016/j.fas.2014.08.006.
Common Stress Fractures Around the Foot
and Ankle
Roberto Zambelli and Nacime Salomão Barbachan Mansur
1 Introduction
The concept and pathophysiology of stress fractures (SF) have changed dramati-
cally in recent years. The traditional association between these disorders and high-
performance athletes (particularly women) is insufficient to explain the complex
universe of what is now considered an overload syndrome.
Any imbalance in the relationship between catabolism and bone metabolism can
lead to a SF. The complex physiology of the skeletal system and its constant interac-
tion with nutritional and hormonal factors add more complexity to the scenario. The
analysis of the lesion by overload under the mechanical and biological optics is
essential for the prevention, diagnosis, and success of the treatment employed.
2 Physiopathogenesis
The delicate symbiosis between bone formation and resorption can be altered by
intrinsic and extrinsic factors [1, 2]. The increase (commonly sudden) in the pattern
of physical activity and the decline in mineral matrix production are the main
R. Zambelli
Serviço de Ortopedia da Rede Mater Dei de Saúde, Belo Horizonte, MG, Brazil
Faculdade de Ciências Médicas de Minas Gerais, Belo Horizonte, MG, Brazil
N. S. B. Mansur (*)
Grupo de Medicina e Cirurgia do Pé e Tornozelo, Departamento de Ortopedia e Traumatologia,
Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brazil

Switzerland AG 2022
1120 R. Zambelli and N. S. B. Mansur
general causes for the occurrence of bone overload injuries [3, 4]. This definition,
therefore, incorporates both the professional sportsman in the middle of the season,
the sedentary individual who begins sports practice, and the elderly patient with
very low skeletal stock [5–7].
The non-gradual increase in mechanical demand on bone tissue, generally asso-
ciated with repetitive cycles and with a short period of rest, causes micro-lesions
that exceed the basal body healing speed [1, 6, 8]. The interference of one or more
skeletal metabolism factors in this response may be the triggering factor of the lesion.
The reaction to exaggerated stress in the region increases osteoclastic activity,
overcoming osteoblastic production and weakening the structure [9]. Normally, the
cavitations formed by the osteoclasts are filled with new bone by the osteoblasts, a
remodeling process that can last from 2 to 8 months [5, 9, 10]. The first 10 to
14 days are characterized by bone weakness, given the latency period between
resorption and bone formation. The continuity in mechanical stimulus causes micro-
fractures in the trabeculae, which may coalesce and form a macroscopic frac-
ture [3, 9].
3 Ethiopathogenesis
The skeletal tissue is an organism that suffers constant biological influence from
other systems as well as interacting directly with the local muscular, tendinous, and
ligamentous framework [1, 6, 11]. Thus, several agents may be involved in the
development of a bone overload lesion (Fig. 1).
Training History b
Nutritional History
Endocrinological History Bone Load
Genetics Stiffness
Bone Metabolism Diseases
Frequency a
Intensity
Duration
Adaptive Gait Mechanics
Bone Strain Sport Gesture
Formation Footwear
Training Surface
Deformity
Caloric | Nutritional Deprivation Muscular Strength
Endocrinopathy Fatigue
NSAID | Corticoid | Steroids Sarcopenia
Osteocyte
Sleep Deprivation Stimulation
Psychological Stress c
Fig. 1 Risk factors for stress fracture can be categorized according to their relationship to the load
applied to the bone (a), the effect on basal stiffness of the tissue (b) and the impact on adaptive
bone neoformation (c)
Common Stress Fractures Around the Foot and Ankle 1121
Evidently, factors such as training regimen, surface, and equipment are directly
related to the condition [6, 9]. Walking abnormalities, sports gesture errors, defor-
mities such as flat foot, cavus foot, and insufficiency of the first ray were also asso-
ciated with the condition in an attempt to justify hyperpressure points [6, 12].
The biological reserve of the individual plays a fundamental role in this genesis,
not only because of the healing contribution, but also because of the neuromuscular
preparation. The musculature has the capacity to dissipate and balance forces that
cross anatomical regions. Individuals with athletic unpreparedness or elderly people
with sarcopenia are considered risk populations for SF [5, 13].
Vitamin D acts on the absorption of the intestinal calcium and its transport to the
bone tissue. The decline in sun exposure of the urban adult population, mainly in the
subtropical regions, decreases the bioavailability of its active form [3, 14].
Gastrointestinal diseases and tract resection surgeries can also potentially decrease
the amount of serum calcium to be presented to the bone. Energy restriction, rang-
ing from insufficiency because of high consumption or eating disorders, also
depletes the supply of important essential nutrients such as protein, vitamin D, and
calcium [3, 15].
Endocrinopathies directly modify the skeletal metabolism by its direct action on
the cellular component [3]. Estrogen, progesterone, parathormone, and thyroid hor-
mone influence osteoclastic and osteoblastic activity [16]. The triad of female ath-
letes is characterized by the occurrence of at least one of the following factors:
menstrual dysfunction, reduction of bone density, and low caloric intake. They
incorporate the overload skeletal lesion as one of its outcomes. It shows that the
interaction between hormonal, mechanical, and nutritional factors is very important
in the genesis of SF [3, 15, 17].
Genetic inheritance, sleep deprivation, psychological stress, diabetes, smoking,
alcoholism, and use of anti-inflammatory drugs (hormonal and nonhormonal) are
also elements related to the etiology of overload bone lesions [1, 9, 18].
4 Clinical Picture
Even in the professional athletic population, SF can be difficult to diagnose. They

represent up to 20% of the complaints of a specialized orthopedic care service [12,
19]. Commonly, patients complain of diffuse pain over a topographic region, usu-
ally at the beginning or end of physical activity that becomes more localized over
time. Rest usually improves the pain complaint [6, 9]. A complete anamnesis should
be performed, including questions about the history of overload injury, current
training regimen, changes in technique or equipment, calorie intake, sun exposure,
hormonal and menstrual condition. These lesions must always be considered in the
treatment of musculoskeletal complaints, mainly in the sports scenario, due to the
usual negligence of the patients and the very high morbidity related to their natural
evolution.
The physical examination must contemplate the search for deformities, changes
in gait and movement limitations. The directed evaluation, based on the presence of
pain on palpation, presents high sensitivity and low specificity [6, 10]. Edema and
other inflammatory signs could be found as well. In more advanced cases, bone cal-
lus may be felt during the exam. Tests and specific clinical maneuvers are described
and are explained in the sections below.
5 Imaging Studies
Patients with a hypothesis of SF should have a radiographic evaluation. This evalu-

ation is important not only for diagnostic confirmation, but also for the exclusion of
differential diagnoses, lesion staging, prognosis, and therapeutic planning [6, 20]. In
clinical suspicion of high-risk fractures, imaging study is mandatory [13, 19].
Weight-bearing radiographs of the affected region in at least three projections,
even lacking good specificity, identify deformities and anatomical characteristics
that may predispose the patient to an overload injury [4, 5]. SF-compatible images
are generally seen only 2–4 weeks from the onset of the condition, and are charac-
terized by radiolucency areas, which may be bordered by sclerotic bone. Late pre-
sentations may demonstrate fracture lines and bone callus healing attempts [6].
Ultrasonography plays a role in the investigation of possible differential diagno-
ses, in particular tendinopathies, muscle lesions, and vascular compressive syn-
dromes. Conventional computed tomography has its utility restricted to cases where
magnetic resonance imaging is contraindicated [3, 9]. Cone-beam weight-bearing
CT images may add a more complete assessment of patient alignment. Scintigraphy,
previously an essential examination, is now reserved only for specific cases.
The gold standard exam to study SF is magnetic resonance imaging (MRI) [3, 5,
8, 9]. The exam presents high resolution, ability to confirm the lesion and exclude
others, besides not offering ionizing radiation. Findings can be identified early, up to
1 or 2 days from the onset of symptoms. Endosteal changes, periosteal reactions, and
bone marrow edema can be found. The latter, also called stress reactions by some
authors, should be interpreted with caution, because in asymptomatic individuals
they are related to the simple physiological response of the bone to exercise [5, 6].
The MRI assists in the staging of the SF and its treatment plans (Tables 1 and 2).
Table 1 Fracture classification according to magnetic resonance imaging [9, 15]

Grade RNM findings
I Moderate periosteal edema in T2. Normal bone marrow.
II Advanced periosteal edema on T2. Bone marrow with edema on T2.
III Advanced periosteal edema on T2. Bone marrow with edema on T2- and T1-weighted
sequences
IV Advanced periosteal edema on T2. Bone marrow with edema on T2- and T1-weighted
sequences. Fracture line.
Table 2 Stages of Arendt and Griffiths for bone lesions secondary to stress and necessary rest
time for healing, based on magnetic nuclear resonance images [22]
Grade RNM findings Time for healing
I STIR positive 3 weeks
II STIR and T2 positive 3–6 weeks
III T1 and T2 positive without cortical rupture 12–16 weeks
IV T1 and T2 positive with cortical rupture 16 weeks
and visible fracture
An adequate laboratory evaluation of these patients usually involves the initial

request of the serum dosage of Vitamin D, calcium, parathormone (PTH) and thy-
roid hormones [1, 3]. Other specific tests (such as estrogen, progesterone, albumin,
etc.) should be requested in patients with clinical suspicion of endocrinopathies or
high recurrence of SF. Bone turnover markers (IGF-1) and other cytokines are cur-
rently experimental, but may represent a future alternative [3, 21].
6 Differential Diagnosis
Rheumatic diseases may manifest primarily in the foot and ankle region, through
pain associated with low or moderate inflammation at the site [5, 11]. This can be
established in the dorsal region of the forefoot, mimicking the clinic of a metatarsal
SF (rheumatoid arthritis), in the territory of the hindfoot, confusing a calcaneal SF
(Reiter, ankylosing spondylitis) or in the sesamoid region, resembling a SF of these
bones (gout, pseudogout).
Reflex Sympathetic Dystrophy Syndrome or complex regional pain syndrome
(CRPS) may have a similar clinical presentation in selected cases. Neuropathic patients,
especially diabetics, should always be investigated for the possibility of Charcot’s
arthropathy. Superficial infection (infectious tenosynovitis, cellulitis, erysipelas) and
deep infection (osteomyelitis, infectious arthritis) need to be considered, particularly in
the immunosuppressed patients who may present a mild infectious clinic.
Musculoskeletal neoplasms can also present imaging findings that confuse them with
SF [12, 20].
Depending on the SF topography, other conditions should always be considered.
In the leg, the tibial overload injury should be confronted with chronic compartment
syndrome, muscle injury, and vasculopathies (compression of the popliteal artery in
the soleal arch, deep vein thrombosis, between others). In the calcaneus, plantar
fasciopathy, tarsal tunnel syndrome, and insertional tendinopathy should be
excluded. Talonavicular arthritis and Muller-Weiss disease are possible diagnoses in
the analysis of a navicular SF. Long-term fibular tendinopathy and fracture of the os
peroneum are possible if suspecting a cuboid SF. In the forefoot, other causes of
metatarsalgia (plantar plate injury, Morton’s neuroma, Freiberg’s osteochondritis)
and tenosynovitis of the extensors are differentials of metatarsal SF. For sesamoid
SF, the presence of hallux rigidus, sesamoiditis, osteochondral lesions, and tendi-
nopathy of the hallux flexors need to be excluded [6, 20].
Table 3 Classification of stress fractures according to their prognosis
High risk Low risk

Tibia anterior cortex Tibia posterior cortex
Medial malleolus Lateral malleolus
Talus Calcaneus
Navicular Cuboid
Proximal diaphysis fifth metatarsal Cuneiforms
Second metatarsal base 2–4 metatarsal diaphysis
Sesamoids 3–4 metatarsal bases
7 Classification
Stress fractures can be classified according to their prognosis, in low and high risk
(Table 3) [3, 9, 20]. The anatomical, vascular, and biomechanical characteristics of
each bone (or bone region), as well as the clinical course of their SF, define them for
these stages.
The graduation of the lesions according to the RNM findings by Fredericson
et al. (Table 1) suggests that treatment of grades I and II are conservative with a
shorter time of evolution (6–8 weeks) [9, 15]. The degrees III and IV would be of
more aggressive treatment because of the longer healing time (20 weeks). This clas-
sification inspired other authors to incorporate new RNM sequences for staging and
healing time prediction (Table 2) [22].
8 Principles of Stress Fracture Treatment
The adequate treatment of overloaded bone lesions starts with an adequate diagno-
sis of the lesions as early as possible, as these are known to be important factors in
the treatment success [3, 6, 10]. The chronicity of the condition worsens the local
biological healing conditions and may lead the patient to a complete and deviated
fracture with a slower recovery [6].
Once the SF is identified, physical demand (training or day-to-day activities)
should be reduced or stopped [3, 9, 22]. In low-risk fractures, a simple reduction in
intensity can be considered. In high-risk fractures, the complete cessation of exer-
cise and the removal of the load are recommended in some scenarios [6, 9]. The
return to the sport must respect the particularity of each fracture and take place at
least 14 days after the complete cessation of pain [23].
Nutritional and hormonal replacement should be performed when indicated.
Even in patients with normal serum levels of 25(OH)D, 800 IU of vitamin D3 per
day (2000 IU at high risk) is recommended [3, 14]. In cases of more severe deficien-
cies, this dose may be increased. The inclusion of 2 g of calcium in the diet is rec-
ommended by some studies, a number that should be higher if this mineral is
Table 4 Recommendations for prevention and management of stress fractures

Objective Recommendations
Prevention Good nutrition, including calcium, vitamin D, and proteins
Avoid negative energy balance
Training under supervision and with gradual increase of intensity
Women: maintain normal menstrual periods
Diagnosis Radiography and MRI
Biochemical panel, 25(OH)D, PTH, TSH, T4L, 24 h urinary calcium
Treatment Reduction of training until healing
Pain control
Replacement of vitamin D and calcium. Magnesium
Adequacy of caloric and proteinic intake
Bisphosphonates and teriparatide: not established or approved.
Adapted from: Moreira and Bilezikian [3]. Permission required
lacking. The use of drugs active in bone metabolism, such as bisphosphonates and
teriparatide, has no scientific support or approval from regulatory agencies for the
treatment of SF [3, 21].
Analgesic drugs can be used on demand. The use of anti-inflammatory drugs
should be avoided because of their potential to harm bone tissue scarring [18].
Hyperbaric oxygen, platelet-rich plasma, bone morphogenic proteins, ultrasound, and
shock wave therapy have anecdotal reports of good results but lack support in the lit-
erature [6, 24]. The intake of calories and proteins needs to be corrected when insuf-
ficient. Systemic diseases and other factors that may contribute to the syndrome, such
as sleep deprivation and psychological stress, need to be managed accordingly [1].
In both primary and relapse prevention, athletic surveillance is fundamental [25].
Physical activities should, whenever possible, be supervised by a qualified physical
educator and performed gradually and with adequate rest periods [6, 26]. Correction
of sports gesture errors, equipment, and training places are fundamental. Of course,
good control of body and nutritional factors plays a crucial role in prophylaxis of
overload injuries. The daily intake of 2 g of calcium and 800UI of vitamin D is
considered by some studies a good protective measure [3, 6, 14] (Table 4).
9 Main Stress Fractures
9.1 Talus
Stress fractures of the talus are rare, with an incidence of 4.4/10,000 person-years,
with 10% bilaterality [27]. Most of the studies present a series of cases, with few
patients included and little information regarding follow-up and final outcomes
[28]. Despite initially considered as low-risk fractures, recent studies consider that
the risk of delayed healing makes them high risk, with potential unsatisfactory
results [19].
The profile of the affected patient is usually athletes and military [27, 29]. Some
rare cases are reported, such as stress fractures of the talus body after talocalcaneal
coalition resection and adult acquired flat foot [30, 31].
The patient complains of nonspecific pain around the ankle, without apparent
ecchymosis, but with edema present [28, 32]. Pain on palpation may be more evi-
dent for talus head fractures (direct palpation) and talar body fractures (pain distal
to the medial malleolus tip). The time to diagnosis can vary from 3 weeks to
3 months, due to low suspicion [28, 32].
The image evaluation includes the first evaluation radiographs in the anteropos-
terior, lateral, and oblique views of the foot and ankle. Computed tomography
assists in the diagnosis by documenting the extension of the fracture line, mainly
after scintigraphy exams, which show nonspecific uptake in the ankle region [33].
MRI study presents extensive bone edema on T2-weighted sequences in the affected
and low or no signal in T1 [28] (Fig. 2). The most affected region is the head of the
talus in more than two thirds of the cases, followed by the body and eventually the
posterior region of the talus [27]. Stress changes in adjacent bones can also be
observed, with calcaneal lesions appearing in stress fractures of the talar body
(78%) and navicular lesions in SF of the talar head (60%) [28].
The treatment is usually nonsurgical in non-displaced fractures. It can range
from load reduction in physical activities in less symptomatic patients to complete
unloading of the affected extremity with the use of crutches and/or immobilization
for a period of 4 weeks in those who complain severe pain, associated with the use
of analgesics drugs and cryotherapy [10, 34]. After 4 weeks, a partial load is allowed
with crutches, finishing the period of weight-bearing restriction and removing the
immobilization, on average, at 6 weeks [32, 34].
a b
Fig. 2 Stress fracture of the talus head with innocent presentation on the lateral radiograph (a) and
clearer on the RNM (b)
In displaced fractures, the surgical treatment must be performed, with anatomic

reduction and rigid stabilization. Arthroscopic approach with percutaneous fixation
can be used when possible, minimizing surgical aggression and promoting earlier
patient recovery [29].
The evolution is usually favorable with most patients returning to their daily
activities. Patients may present minor symptoms in the affected region several years
after the end of conservative treatment, besides half of the patients presenting
degenerative signs in the evaluation by MRI [28].
9.2 Calcaneus
SF of the calcaneus are relatively common lesions, with their incidence being
approximately 20% among lower limb stress fractures, with bilaterality ranging
from 33% to 75% in the largest series of cases [35]. The most affected portion is the
posterior region of the calcaneus, but the anterior process may also be a site of
involvement [36].
Most calcaneal SF occur in healthy individuals due to an acute onset or increase
in volume and/or intensity of physical activity, or to significant weight gain [35, 37].
Use of inappropriate footwear during sports practice, biomechanical changes during
gait, cavus foot, and limb length discrepancy may also be related to injury occur-
rence [35]. A case series was reported with five stress fractures of the calcaneus
after lower limb arthroplasties, four patients after total knee arthroplasty, and one
after total hip arthroplasty, all fractures being on the same side of the arthroplasty
[37]. However, all of these patients had bone densitometry with a diagnosis of
osteoporosis.
The clinical presentation can be quite varied, the most common symptom being
plantar or diffuse pain in the hindfoot region, often confused with plantar fasciitis,
due to its more posterior and plantar location, but with rapid relief with rest [34, 35].
Usually, there is no history of related trauma. Unlike plantar fasciitis, it is not a pain
that worsens at the first touch of the foot on the ground after rest (like plantar fasci-
itis) but intensifies as the patient wanders longer or remains in a standing position
[38]. In clinical examination, the most sensitive test is the latero-lateral compression
of the calcaneus, compressing its lateral and medial walls between the thumb and
forefinger [35]. The edema may not be localized, and hematoma or ecchymosis are
usually not observed due to cortical integrity [35].
Radiographic evaluation is poor in the first 3 weeks, since to visualize lesions in
the cancellous bone, 50% of bone density change is required [35, 39]. The authors
also found that the lateral view of the calcaneus is the best when the lesion is visible
[35]. The ultrasound can be used, presenting the periosteum as an irregular
hypoechoic band, as a cortical thickening of 1–3 mm [40]. The three-phase bone
scintigraphy is an exam that reaches 100% sensitivity; however, as it is an invasive
exam, it has given rise to magnetic resonance imaging as the exam of choice to
confirm the diagnosis [35]. MRI offers a much more accurate evaluation of bone
and soft tissue contours [38]. Bone edema is observed with a hypersignal on T2 and
STIR sequences [35] (Fig. 3).
Treatment is imminently conservative, with rapid response to rest. The use of
analgesic and anti-inflammatory medication should be prescribed in cases where
pain relief is refractory to rest. The use of crutches can be more effective in the short
term, but the immobilizing boots, with their rigid soles, greatly help by distributing
load on the foot, besides keeping the patients vigilant with rest [35]. The symptoms
start to relieve after the second week and, usually, the treatment takes 6 weeks.
Surgical treatment can be indicated if the symptoms do not regress in 3 months,
mainly in the most marginal fractures, as in the anterior calcaneus process [36].
9.3 Navicular
Stress fracture of the navicular, although relatively rare in the general population, is
frequent among professional athletes. It represents 25% to 35% of all stress frac-
tures, usually in young male athletes, around 20 years old [41, 42].
The navicular is a bone of great cartilaginous coverage, with its blood contribu-
tion coming from small branches of the anterior tibial artery dorsolaterally and the
posterior tibial artery medially. Thus, the most central third is a more avascular
region, being more vulnerable to stress fractures [43, 44]. Biomechanical alterations
that limit ankle dorsiflexion forces the midfoot compensate, increasing its pressure
and excursion in the naviculocuneiform joint. The factors that may result in these
alterations would be cavus foot, subtalar joint motion restriction, first short metatar-
sal, second long metatarsal, and metatarsus adductus [43].
The clinical picture is usually poor, what makes the diagnosis late in most cases,
often up to 6 months of delay [41]. The pain is nonspecific, often in the dorsal
region of the midfoot. The pain can be aggravated with tiptoe walking, pulling, and
jumping [43]. Static inspection may reveal a cavovarus foot deformity which, due to
its more rigid biomechanical nature, has a lower impact absorption during ground
accommodation [44].
Imaging evaluation should begin with standing radiographs of anteroposterior,
lateral, and oblique views of the foot. However, the changes are usually not visible
because the fractures are in the sagittal plane and incomplete, being visualized only
after some osteoclastic resorption [45]. Three-phase bone scintigraphy presents a
100% sensitivity for the diagnosis of navicular stress fractures; however, they do not
clarify the fracture pattern [41]. MRI also presents great sensitivity, besides demon-
strating the extent of bone edema; however, CT is the exam with the greatest ability
to define the fracture pattern and guide definitive treatment.
Saxena and collaborators proposed a tomographic classification: Type 1 is a frac-
ture only of the navicular dorsal cortex, type 2 the fracture line extends to the navic-
ular body, and type 3 the line penetrates the navicular plantar cortex. The presence
of cysts, sclerosis in the fracture line and avascular necrosis of the navicular are
modifiers of worse prognosis [46]. Later type 0.5 was included as the stress reac-
tion, where there is signal alteration at MRI, without any fracture line at CT [46].
a b
Fig. 3 Stress fracture of the anterior (cervical) region of the calcaneus as seen on the axial (a),
coronal (b), and sagittal T2 MRI views
The treatment must be defined based on three pillars: tomographic findings, level
of sports participation, and functional status of the patient [41]. The type 0.5 and 1
lesions can be conservatively treated in immobilization without support for a mini-
mum period of 6 weeks and can go up to 12 weeks of immobilization if there is no
consolidation. After 12 weeks, if there is no consolidation, surgical treatment is
indicated.
Non-displaced type 2 fractures in non-athletic patients can be treated nonsurgi-
cally. However, in case the patient is an athlete or there was a failure in the conserva-
tive treatment, the surgical option is chosen, with compression screw fixation,
normally in a percutaneous way. In displaced fractures, type 3 fractures or type 2
fractures with sclerotic edges, the best indication is open surgical treatment, with
bone grafting and internal fixation with compression [41].
Despite efforts to find a treatment type that allows earlier mobilization and
weight-bearing, conservative treatment with non-weight-bearing presents results
comparable to surgical treatment both for fractures with and without displacement
[47]. However, when the time of return to sports is evaluated, the surgical treatment
is more effective, since it presents an earlier return (16.4 weeks) when compared to
the conservative treatment (21.7 weeks) [48].
9.4 Cuboid
Stress fractures of the cuboid are extremely rare, with few reports in the litera-
ture [49].
Most of these lesions occur due to the relationship of the cuboid with the long
fibular tendon, as the cuboid serves as the fulcrum for the long fibular to plantar flex
the first ray, stabilizing it [38]. In cases where there is greater instability in the mid-
foot, as in valgus deformities, the cuboid becomes a less stable fulcrum, becoming
vulnerable to overload and possible stress injury. Few patients remember the occur-
rence of trauma related to the onset of symptoms [50].
Clinically, stress fractures of the cuboid resemble calcaneus lesions, but due to
anatomical proximity to the sinus tarsi and fibular tendons, the picture may be
somewhat less clear [38]. Most patients have a significant history of sports activities
[51]. The nutcracker test, where the midfoot is abducted with the hindfoot stabilized
compressing the cuboid between the lateral metatarsals and the calcaneus, may
cause pain and help with diagnosis [50].
Complementary imaging evaluation should begin with weight-bearing antero-
posterior and lateral X-rays, as well as an oblique view. The fractures are usually
hidden, but appear as a radiopaque, sclerotic line, perpendicular to the bone trabecu-
lae [38]. Three-phase bone scintigraphy can be used, although it is invasive, where
we will observe uptake in the three phases in acute fractures. MRI, besides offering
great sensitivity for the diagnosis, also assists in orientation regarding prognosis and
return to activities [38]. They present with great bone edema, and usually of lateral
location [20].
The nonsurgical treatment, with immobilization and eventual support restriction,

is very effective, since displaced fractures that need surgical treatment are rare
[20, 34].
9.5 Metatarsals
After the tibia, stress fractures of the metatarsals are the most common, correspond-
ing to 38% of all stress fractures, being more frequent in the second and third meta-
tarsals [12, 34]. The fifth metatarsal fractures will be treated separately in another
chapter. The most affected region is the metatarsal neck; however, more proximal
fractures are described in dancers [44]. It is important to emphasize that the distal
fractures are benign, with favorable evolution, but the proximal fractures, mainly of
the base of the second and fourth metatarsals can evolve to nonunion or delayed
healing [20].
The injury mechanism is repetitive impact with the foot in plantar flexion [34].
Other factors that may contribute to the occurrence of this lesion are a second long
metatarsal, pronated foot, and limitation of ankle plantar flexion, which would lead
to a Lisfranc joint hyperflexion.
The patient complains of nonspecific pain in the forefoot and/or midfoot region,
with edema and eventually erythema [34]. The patient reports increased volume or
intensity of training, but also a change in sports shoes or ground type [39]. Many
times, the clinical picture presents itself with weeks of evolution until the search for
specialized evaluation, mainly for nonathletes. The differential diagnosis must be
made with metatarsalgia, Morton’s neuroma, metatarsophalangeal synovitis, among
others [39].
The initial radiographs should be made with loading in the anteroposterior, lat-
eral, and oblique incidences. The first images may not present alterations, but in the
subacute phase, after 3–4 weeks, a periosteal reaction can already be seen, and later,
an exuberant bone callus can be observed [44]. The ultrasound early reveals perios-
teal changes, and MRI is the exam that sooner demonstrates medullary edema-like
bone changes, even before the appearance of the fracture line, which can be very
useful in the management of these lesions in athletes [44] (Fig. 4).
The treatment is usually nonsurgical, with modification of activities until relief
of symptoms, with the use of postoperative shoes or immobilizer boots [39]. The
use of crutches with support restriction for the affected lower limb may be useful in
the most refractory cases to conservative treatment. Modifications in sports activi-
ties may be necessary, such as adjustment in the volume and intensity of the train-
ing, as well as of the sports shoes [20]. The return to sports activities can happen
according to the remission of symptoms, usually between 4 and 6 weeks [39].
Fractures in the metatarsal bases and distal fractures that evolve with delayed heal-
ing should be approached surgically, with rigid internal fixation to promote bone
healing [20, 52].
a b
Fig. 4 RNM of a stress fracture of the fourth metatarsal neck, showing medullary, periosteal, and
endosteal edema on the axial (a), coronal (b) and sagittal (c) T2 views
9.6 Sesamoid
Sesamoid stress fractures are one of the important possible diagnoses in the ath-
lete’s painful forefoot [53]. They correspond to between 1% and 3% of all stress
fractures, the medial sesamoid being the most affected [54].
The suggested mechanism of trauma are repeated impacts and/or movements of
forced hallux dorsiflexion, such as what occurs in runners, dancers, and gym-
nasts [53].
The patient complains of pain in the forefoot plantar region related to sports
practice, particularly under the head of the first metatarsal [53]. Some degree of
edema can be observed in the medial region of the forefoot [55]. The pain is caused
by passive dorsiflexion of the first metatarsophalangeal joint and relieved with rest
[34]. The mean time from the onset of symptoms to diagnosis ranges from 16 weeks
to 15 months [53].
Imaging evaluation begins with axial sesamoid, lateral, oblique, and anteropos-
terior foot radiographs. It can be difficult to distinguish a bipartite sesamoid from a
stress fracture [20]. If no changes are observed, MRI is requested to confirm the
diagnosis [53]. Computed tomography can also be useful for diagnosis, especially
in axial sections [56].
The initial treatment is always conservative for non-displaced fractures. A rest

period and change of activities from 2 to 6 months are necessary for symptom relief,
together with analgesic measures and rehabilitation [53].
If the symptoms persist for a period of 6 months, surgical treatment should be
indicated [20]. Sesamoidectomy is the most performed procedure, always remem-
bering to repair the short flexor of the hallux to restore the correct biomechanics of
the joint [53]. Internal fixation, percutaneous or open, with or without placement of
bone graft, is the second most performed procedure [53]. The postoperative period
should keep the patient with restriction of support for a period of 1–6 weeks in a
removable or plastered boot, followed by progressive support and rehabilitation
[53]. Comparing the different treatment methods, there is no difference in the rate
of return to sports activities with conservative treatment, sesamoidectomy, or inter-
nal fixation. But the time to return to sports activities is much shorter in surgical
treatment than in conservative treatment, and among the forms of surgical treat-
ment, sesamoidectomy presents an earlier return than osteosynthesis of fragments
[34, 53].
References
1. Hughes JM, Popp KL, Yanovich R, Bouxsein ML, Matheny RW Jr. The role of adaptive bone
formation in the etiology of stress fracture. Exp Biol Med (Maywood). 2017;242(9):897–906.
2. Faienza MF, Lassandro G, Chiarito M, Valente F, Ciaccia L, Giordano P. How physical activity
across the lifespan can reduce the impact of bone ageing: a literature review. Int J Environ Res
Public Health. 2020;17(6):1862.
3. Moreira CA, Bilezikian JP. Stress fractures: concepts and therapeutics. J Clin Endocrinol
Metab. 2017;102(2):525–34.
4. Fredericson M, Jennings F, Beaulieu C, Matheson GO. Stress fractures in athletes. Top Magn
Reson Imaging. 2006;17(5):309–25.
5. Mandell JC, Khurana B, Smith SE. Stress fractures of the foot and ankle, part 1: biomechanics
of bone and principles of imaging and treatment. Skelet Radiol. 2017;46(8):1021–9.
6. Astur DC, Zanatta F, Arliani GG, Moraes ER, Pochini ADC, Ejnisman B. Stress fractures:
definition, diagnosis and treatment. Revista Brasileira de Ortopedia (English Edition).
2016;51(1):3–10.
7. Al-Ashqar M, Panteli M, Chakrabarty G, Giannoudis PV. Atypical fractures: an issue of con-
cern or a myth? Injury. 2018;49(3):649–55.
8. Elias I, Zoga AC, Raikin SM, Peterson JR, Besser MP, Morrison WB, et al. Bone stress
injury of the ankle in professional ballet dancers seen on MRI. BMC Musculoskelet Disord.
2008;9:39.
9. Warden SJ, Davis IS, Fredericson M. Management and prevention of bone stress injuries in
long-distance runners. J Orthop Sports Phys Ther. 2014;44(10):749–65.
10. Romani WA, Gieck JH, Perrin DH, Saliba EN, Kahler DM. Mechanisms and management of
stress fractures in physically active persons. J Athl Train. 2002;37(3):306–14.
11. Peris P. Stress fractures. Best Pract Res Clin Rheumatol. 2003;17(6):1043–61.
12. Boden BP, Osbahr DC, Jimenez C. Low-risk stress fractures. Am J Sports Med.
2001;29(1):100–11.
13. McInnis KC, Ramey LN. High-risk stress fractures: diagnosis and management. PM
R. 2016;8(3 Suppl):S113–24.
14. Lawley R, Syrop IP, Fredericson M. Vitamin D for improved bone health and prevention of
stress fractures: a review of the literature. Curr Sports Med Rep. 2020;19(6):202–8.
15. Joy EA, Campbell D. Stress fractures in the female athlete. Curr Sports Med Rep.
2005;4(6):323–8.
16. Lanyon L, Armstrong V, Ong D, Zaman G, Price J. Is estrogen receptor alpha key to control-
ling bones’ resistance to fracture? J Endocrinol. 2004;182(2):183–91.
17. Daily JP, Stumbo JR. Female athlete triad. Prim Care. 2018;45(4):615–24.
18. Kidd LJ, Cowling NR, Wu AC, Kelly WL, Forwood MR. Selective and non-selective cyclooxy-
genase inhibitors delay stress fracture healing in the rat ulna. J Orthop Res. 2013;31(2):235–42.
19. Boden BP, Osbahr DC. High-risk stress fractures: evaluation and treatment. J Am Acad Orthop
Surg. 2000;8(6):344–53.
20. Mandell JC, Khurana B, Smith SE. Stress fractures of the foot and ankle, part 2: site-specific eti-
ology, imaging, and treatment, and differential diagnosis. Skelet Radiol. 2017;46(9):1165–86.
21. Kazmers NH, McKenzie JA, Shen TS, Long F, Silva MJ. Hedgehog signaling mediates woven
bone formation and vascularization during stress fracture healing. Bone. 2015;81:524–32.
22. Royer M, Thomas T, Cesini J, Legrand E. Stress fractures in 2011: practical approach. Joint
Bone Spine. 2012;79:S86–90.
23. Carter CW, Ireland ML, Johnson AE, Levine WN, Martin S, Bedi A, et al. Sex-based differ-
ences in common sports injuries. J Am Acad Orthop Surg. 2018;26(13):447–54.
24. Nelson BJ, Arciero RA. Stress fractures in the female athlete. Sports Med Arthrosc Rev.
2002;10(1):83–90.
25. Armstrong DW 3rd, Rue JP, Wilckens JH, Frassica FJ. Stress fracture injury in young military
men and women. Bone. 2004;35(3):806–16.
26. Korpelainen R, Orava S, Karpakka J, Siira P, Hulkko A. Risk factors for recurrent stress frac-
tures in athletes. Am J Sports Med. 2001;29(3):304–10.
27. Sormaala MJ, Niva MH, Kiuru MJ, Mattila VM, Pihlajamäki HK. Stress injuries of the cal-
caneus detected with magnetic resonance imaging in military recruits. J Bone Joint Surg Am.
2006;88(10):2237–42.
28. Sormaala MJ, Niva MH, Kiuru MJ, Mattila VM, Pihlajamäki HK. Outcomes of stress fractures
of the talus. Am J Sports Med. 2006;34(11):1809–14.
29. Kubo M, Yasui Y, Miki S, Kawano H, Miyamoto W. Stress fracture of the posterior talar pro-
cess in a female long-distance runner treated by osteosynthesis with screw fixation via two-
portal hindfoot endoscopy: a case report. BMC Musculoskelet Disord. 2019;20(1):401.
30. Stocker B, Bennett JT. Stress fracture of the talus following resection of a talocalcaneal coali-
tion: a case report. Foot Ankle Int. 2001;22(1):56–8.
31. Matsumoto T, Chang SH, Takeda R, Tanaka S, Juji T. Bilateral stress fractures of the talus
associated with adult-acquired flatfoot deformities. Case Rep Orthop. 2018;2018:5376384.
32. Kim YS, Lee HM, Kim JP, Moon HS. Fatigue stress fracture of the talar body: an uncommon
cause of ankle pain. J Foot Ankle Surg. 2016;55(5):1113–6.
33. Bradshaw C, Khan K, Brukner P. Stress fracture of the body of the talus in athletes demon-
strated with computer tomography. Clin J Sport Med. 1996;6(1):48–51.
34. Welck MJ, Hayes T, Pastides P, Khan W, Rudge B. Stress fractures of the foot and ankle.
Injury. 2017;48(8):1722–6.
35. Weber JM, Vidt LG, Gehl RS, Montgomery T. Calcaneal stress fractures. Clin Podiatr Med
Surg. 2005;22(1):45–54.
36. Taketomi S, Uchiyama E, Iwaso H. Stress fracture of the anterior process of the calcaneus: a
case report. Foot Ankle Spec. 2013;6(5):389–92.
37. Miki T, Miki T, Nishiyama A. Calcaneal stress fracture: an adverse event following total hip
and total knee arthroplasty: a report of five cases. J Bone Joint Surg Am. 2014;96(2):e9.
38. Dodson NB, Dodson EE, Shromoff PJ. Imaging strategies for diagnosing calcaneal and cuboid
stress fractures. Clin Podiatr Med Surg. 2008;25(2):183–201, vi.
39. Greaser MC. Foot and ankle stress fractures in athletes. Orthop Clin North Am.
2016;47(4):809–22.
40. Bianchi S, Luong DH. Stress fractures of the calcaneus diagnosed by sonography: report of 8
cases. J Ultrasound Med. 2018;37(2):521–9.
41. Gross CE, Nunley JA 2nd. Navicular stress fractures. Foot Ankle Int. 2015;36(9):1117–22.
42. Shakked RJ, Walters EE, O'Malley MJ. Tarsal navicular stress fractures. Curr Rev
Musculoskelet Med. 2017;10(1):122–30.
43. Lee S, Anderson RB. Stress fractures of the tarsal navicular. Foot Ankle Clin. 2004;9(1):85–104.
44. Hossain M, Clutton J, Ridgewell M, Lyons K, Perera A. Stress fractures of the foot. Clin Sports
Med. 2015;34(4):769–90.
45. Mann JA, Pedowitz DI. Evaluation and treatment of navicular stress fractures, includ-
ing nonunions, revision surgery, and persistent pain after treatment. Foot Ankle Clin.
2009;14(2):187–204.
46. Saxena A, Fullem B, Hannaford D. Results of treatment of 22 navicular stress fractures and a
new proposed radiographic classification system. J Foot Ankle Surg. 2000;39(2):96–103.
47. Torg JS, Moyer J, Gaughan JP, Boden BP. Management of tarsal navicular stress fractures: con-
servative versus surgical treatment: a meta-analysis. Am J Sports Med. 2010;38(5):1048–53.
48. Mallee WH, Weel H, van Dijk CN, van Tulder MW, Kerkhoffs GM, Lin CW. Surgical versus
conservative treatment for high-risk stress fractures of the lower leg (anterior tibial cortex,
navicular and fifth metatarsal base): a systematic review. Br J Sports Med. 2015;49(6):370–6.
49. Franco M, Albano L, Kacso I, Gaïd H, Jaeger P. An uncommon cause of foot pain: the cuboid
insufficiency stress fracture. Joint Bone Spine. 2005;72(1):76–8.
50. Joo SY, Jeong C. Stress fracture of tarsal cuboid bone in early childhood. Eur J Orthop Surg
Traumatol. 2015;25(3):595–9.
51. Yu SM, Dardani M, Yu JS. MRI of isolated cuboid stress fractures in adults. AJR Am J
Roentgenol. 2013;201(6):1325–30.
52. Rongstad KM, Tueting J, Rongstad M, Garrels K, Meis R. Fourth metatarsal base stress frac-
tures in athletes: a case series. Foot Ankle Int. 2013;34(7):962–8.
53. Robertson GAJ, Goffin JS, Wood AM. Return to sport following stress fractures of the great
toe sesamoids: a systematic review. Br Med Bull. 2017;122(1):135–49.
54. Iwamoto J, Takeda T. Stress fractures in athletes: review of 196 cases. J Orthop Sci.
2003;8(3):273–8.
55. Biedert R, Hintermann B. Stress fractures of the medial great toe sesamoids in athletes. Foot
Ankle Int. 2003;24(2):137–41.
56. Li X, Shi L, Liu T, Wang L. Progress in the clinical imaging research of bone diseases on ankle
and foot sesamoid bones and accessory ossicles. Intractable Rare Dis Res. 2012;1(3):122–8.
Achilles Tendon Ruptures
Diego Zanolli and Rubén Radkievich
1 Acute Achilles Tendon Ruptures
1.1 Introduction
From the mythical warrior Achilles, from Homer’s famous Greek Iliad, derives the
eponym of the “Achilles tendon” (AT), or calcaneal tendon according to classical
anatomy publications. It is the strongest and longest tendon in the human body, but
at the same time represents one of the most frequent tendon ruptures in the body.
This tendon is part of the Achilles-calcaneal-plantar system, has played a funda-
mental role in the development and individualization of the bipedal gait, and acts as
the main plantar flexor of the ankle, fundamental during the takeoff of the human
gait [1–3].
Because of its function and participation in activities of daily living, the AT is
subjected to high tensile loads. These demands increase considerably during physi-
cal activity and sports, reaching up to 6–12 times the body weight in impact activi-
ties such as running or jumping [4, 5].
There are still several controversies in the treatment of ruptures of the AT (ATR),
shifting over time from an open surgical approach as the dominant method, to spe-
cific protocols of conservative treatment in the last decade, and in recent years shift-
ing again back to surgical treatment as the predominant method, with the emergence
D. Zanolli (*)
Clínica Alemana, Santiago, Chile
Hospital Militar, Santiago, Chile
R. Radkievich
Clínica Alemana, Santiago, Chile
Hospital DIPRECA, Santiago, Chile

Switzerland AG 2022
1138 D. Zanolli and R. Radkievich
of various methods of percutaneous surgery, reducing the risks of complications

associated with classic open surgery.
There is no doubt that these ruptures can have important sequelae if they are not
treated with awareness, both for daily life activities and for recreational and elite
athletes; their prevention, early diagnosis, treatment, and rehabilitation must be very
timely, treated methodically and with understanding, both by the patient and by the
orthopedist.
1.2 Etiology and Pathophysiology
The incidence of ATR has been on a frank increase in the last decades, between 9 to
37/100,000 in different series. Also, the average age of people who suffer an ATR
has increased, possibly related to a greater participation and access to recreational
physical activities and sports of the population, the popularization of the fitness
culture, in the context of a longer life expectancy. These ruptures are more frequent
in men (2.9:1 to 12:1 male: female ratio), between the fourth and fifth decade of life,
in sedentary professions, and mostly occur during physical activities or recreational
sports [6–9].
Since it affects adults in their most productive stage, we must keep in mind the
considerable economic and social costs and absenteeism from work in these injuries.
Regarding ATR in professional athletes, it is worth bearing in mind that these
injuries can be catastrophic: decreasing performance, shortening the years of per-
formance, or even ending the athlete’s career.
If we want to anatomically locate the pathology of the Achilles tendon, it can
occur at different levels:
• Insertional
• Pre-insertional
• Myotendinous junction (proximal)
Regarding the frequency and location of acute ruptures of the AT, most of these
(83%) occur in the pre-insertional region, between 2 to 6 cm proximal to its inser-
tion at the level of the calcaneus; 5% are insertional and 12% are lesions at the level
of the myotendinous junction [6, 10, 11].
We can also classify them according to their time of presentation or diagnosis in:
acute, those that appear within the first 2 weeks, subacute from 3 to 4 weeks, and
chronic after 4 to 6 weeks according to the consulted bibliography [12, 13].
Another way of classifying them is in open or closed lesions, depending on
whether or not there is a penetrating wound with solution of continuity in the skin
and tendon.
ATR, like tendinopathies, has a multifactorial etiology. Local, biomechanical,
histological, pharmacological, genetic, and even environmental factors are taken
into account.
Achilles Tendon Ruptures 1139
At rest, the fibers of the main tendon component, type I collagen, are arranged in a
wavy and relaxed manner. Under physiological loads, when the tendon fibers undergo
a stretch of less than 4%, they recover their original arrangement when the tension
ceases. Between 4% to 8%, of stretch certain failures in the collagen cross-links and
molecular ruptures begin to occur. When the tension and elongation of its fibers
exceeds 8%, macroscopic failures and ruptures of the AT begin to be seen [14–16].
When we evaluate tendinopathic tendons or tendons that have suffered a rupture,
they show a decrease in the percentage of type I collagen and an increase in the pres-
ence of type III collagen. This gives the tendon a lower resistance to tensile forces,
which could predispose to rupture in diseased tendons under repair [17].
According to the “degenerative” theory, tendon wear and tear and weakness
occur with aging, and at the same time the capacity to respond to injury decreases.
Vascularization is impoverished in an area already considered hypovascular.
Therefore, the tendon’s resistance to rupture decreases, as does its regenerative
capacity, and the stress and overloading of the tendon increases, and so does the risk
of suffering ATR.
There are several risk factors for ATR: systemic inflammatory diseases such as
rheumatoid arthritis, gout, collagenopathies, diabetes, and neurological diseases. A
relationship has also been found with the use of certain drugs such as quinolones
and corticosteroids [6].
Both local infiltrations with corticoids, as well as their prolonged oral use, can
help mask an already pathological tendon, and have deleterious effects on it, which
is why corticosteroids have been associated with an increased risk of ruptures.
Quinolones are antibiotic drugs that can interact with some tenocyte regulatory
proteins and cause structural damage to the tendon. The risk of suffering an ATR
increases substantially with the concomitant use of corticosteroids, and in elderly
people [18, 19].
There are also studies that highlight genetic factors such as an increased expres-
sion of MMP3 (matrix metalloproteinases family), in relation to the increased risk
of ATR, but they are not conclusive, or their scientific evidence is low [6].
As for the mechanical theories, there are several factors that can alter the func-
tioning of the Achilles-calcaneal-plantar system. When there are limb deformities,
the tendon fibers are subjected to oblique traction instead of symmetrical linear
traction, and they can accumulate an eccentric load and suffer overload and degen-
eration. This is the case in patients with imbalances such as valgus flat feet or prona-
tors, pes cavo-varus, generally associated with a short or rigid gastrosoleus complex.
In the case of athletes, it is important to take into account alterations such as the
aforementioned imbalances, ankle or subtalar stiffness or instabilities, dysfunction
of the gastrosoleus complex, body mass index, and poor vascularization; these
intrinsic factors have been related to the production of tendinopathy at the level of
the AT. There are also modifiable extrinsic predisposing factors such as type of
footwear, hard, slippery or sloping surfaces, overtraining or poor technique, or pre-
vious injuries.
A “vascular” theory has been proposed and widely studied as an existing risk
factor in ATR, since there are anatomical regions that could be considered
hypovascular and more prone to injury. The irrigation of the AT is predominantly at

the muscular/myotendinous and insertional level, leaving an intermediate zone of
hypovascularity in the pre-insertional region, between 2 to 6 cm from the calcaneus,
the region most frequently affected in ATR [20, 21].
1.3 Anatomy
The triceps suralis is composed of three muscle masses arranged superiorly in two
distinct layers: a superficial one composed of the medial and lateral head of the
gastrocnemius, and a deep one corresponding to the soleus muscle.
Regarding the muscular function of the triceps suralis, in addition to plantar flex-
ion, the soleus muscle contributes greatly to gait and posture, as well as acting as a
peripheral vascular pump. It is mostly composed of slow twitch fibers. As for the
gastrocnemius, mostly composed of fast twitch fibers, it provides a dynamic con-
traction force to plantar flexion during various activities such as running, jumping,
and walking [22–24].
The AT results from the attachment of the terminating tendons of the triceps
suralis. This is the longest and most voluminous tendon in the body. On average, it
can measure up to 2.5 cm in diameter and 15 cm in length.
It is mainly composed of type I collagen, which in normal conditions represents
70% of the dry weight of the tendon. With a lower percentage in its composition,
collagen types III and V are found. At the molecular level, the parallel arrangement
and covalent bonds of the collagen molecules within the fibrils give the tendon a
high tensile strength (50–100 N/mm).
The AT does not have a true synovial sheath covering it; instead there is a
paratenon of areolar tissue, which facilitates its sliding and function, also providing
vascular support to the surrounding tissue.
Another particular characteristic of the AT is that as its fibers converge, from
proximal to distal, they rotate in a spiral form, with a 90° rotation from medial to
posterior, and posterior to lateral, achieving a passive storage of elastic energy,
which allows a greater efficiency of action in the different phases of the gait.
This rotation is maximal at distal level, between 2 to 5 cm from the calcaneal
insertion, which could add an area of mechanical stress to this zone, already men-
tioned as a region with certain “vascular weakness.”
1.3.1 Vascularization
The calcaneal tendon has a dual irrigation, by the posterior tibial artery medially
and by the peroneal artery laterally. In cadaveric studies that have analyzed the irri-
gation patterns of the tendon, three regions have been identified:
• Distal region: Irrigated by the posterior tibial artery, it involves the insertional
region and the distal 4 cm of the tendon.
• Medial region: Between 4 to 7 cm from the distal insertion, irrigated by the pero-
neal artery.
• Proximal region: From 7 cm from the calcaneal insertion, proximal to the myo-
tendinous junction, supplied by the posterior tibial artery.
The area of the medial region of the tendon, irrigated by the peroneal artery, is
the region with the least vascularization; it has the least amount of extrinsic and
intrinsic vessels, both in histological and angiographic analysis [20].
1.3.2 Innervation
The Achilles tendon is innervated mainly by branches of the sural nerve (saphenous
minor). At an average distance of 8–10 cm from the calcaneal insertion, the sural
nerve crosses the lateral border of the Achilles tendon. It is important to keep this
close anatomical relationship in mind when planning our surgical approaches and to
avoid any nerve injury.
The tibial nerve is responsible for innervating the sural triceps, and to a lesser
extent gives some branches to the Achilles tendon.
1.4 Diagnosis
In spite of the vast knowledge, study, and treatment of the tendinopathies of the
Achilles tendon, a fact is that most of the patients who suffer a ATR do not have
prodromal symptoms.
The urgency in making a proper diagnosis is also important not only because of
the sequelae that may be left by an undiagnosed rupture, but also because the sooner
the chosen treatment is defined and executed (especially in conservative treatment),
the better outcomes will be obtained.
About 15–25% of ATR are not detected in their acute stage, either because of a
late consultation by the patient, or because of an underdiagnosis by the medi-
cal team.
Despite the preexisting tendinopathy and tendon degeneration in ATR, most
patients are asymptomatic prior to the acute injury.
More than 80% of ATR occurs during sports practice, mostly by an indirect,
noncontact mechanism, in sports that require jumping and rapid changes of direc-
tion [6]. The patient reports a sudden pain in the calf, “rocking” or “whiplash” from
behind, even to an audible snap.
This is followed by difficulty in walking, with functional impotence, weakness
in plantar flexion, local edema, and associated ecchymosis.
They usually occur during an eccentric contracture, with a forced dorsiflexion of

a foot in plantar flexion; in a push off or take off action with knee in extension;
although we can also find them in low-demand activities, descending a step, before
a trip or false step, or even spontaneous ruptures without apparent cause. Whatever
the scene of the rupture, the common denominator is to find a tendon with long-
standing degenerative changes present, acting as a focal “zone of weakness” in the
tendon, with low tissue quality and regenerative capacity, without the need for a
previous prodrome as a condition [11, 12].
The diagnosis of ATR is fundamentally clinical (anamnesis and physical exami-
nation) [25, 26].
There are several tests that can be performed in the acute physical examination
for its diagnosis; among the most frequently used are the following:
• Palpation of the GAP: The path of the tendon is gently palpated, and it is classi-
fied as palpable or absent gap. In this case, the time of evolution of the lesion and
the anatomical region in which we determine its presence are very important. A
subacute presentation may make it difficult to find a GAP in the area of the ten-
don lesion, since fibrotic or scar tissues may be present. On the other hand, in the
presence of a lack of continuity in the path of the tendon at the insertional level,
and not in the most frequent area of injury, we should request imaging studies to
rule out an avulsive calcaneal injury, which will determine another type of treat-
ment or therapeutic approach.
• Squeeze test or Thompson’s test: Initially described by Simmonds [27] and later
by Thompson [28], this test is performed with the patient in prone position, with
the feet protruding from the stretcher; the examiner compresses the calf just
below the region with the greatest circumference of the leg. If the Achilles ten-
don is in continuity and there is no previous stiffness or injury, plantar flexion of
the ankle occurs in response to compression. In the presence of an acute Achilles
tendon rupture, we expect to find a lack of plantar flexion in response to com-
pression. A positive Thompson’s Test (+) describes a lack of tendon continuity
and therefore plantar flexion of the ankle associated with compression is not
observed [29].
There are some false negatives in this test for ATR (i.e., presence of thin plantar,
flexor muscles, partial ruptures), in which the rest of the clinical picture is compat-
ible with an acute injury, but when performing this maneuver we obtain some
degree of response in plantar flexion of the ankle; it is essential to perform this test
comparatively with the contralateral limb to determine different degrees of
asymmetry.
• Matles test: With the patient in prone position and 90 degrees flexion of both
knees, the position of the ankle is observed. The foot and ankle remain in a slight
plantar flexion when the calcaneal tendon is intact and in continuity; in cases of
acute ruptures (or even chronic ruptures or patients with elongated tendons), the
ankle tends to adopt a neutral position or with a slight dorsal flexion. Always
remember to scan both lower limbs comparatively for asymmetries [30].
There are other clinical tests described for the study of ATR, such as the Copeland
Test [31] or the O’Brien Test [32]; these tests tend to generate a certain degree of
discomfort, or because they are invasive for patients, they are not used very often.
The most frequently used in clinical practice are the Thompson Test, Matles test,
decreased plantar flexion strength, and gap palpation. These are noninvasive meth-
ods, generally well tolerated by the patient, plausible to perform in the acute setting
of the injury, and fully reproducible.
According to the AAOS (American Academy of Orthopaedic Surgeons) clinical
practice guideline, with a consensus recommendation, the clinical diagnosis of ATR
should include two or more of the following tests as positive:
• Squeeze test or Thompson test
• Increased passive ankle dorsiflexion to gentle manipulation
• Decreased plantar flexion strength
• Presence of a gap or palpable defect [33]
The use of routine complementary examinations in the diagnosis of ATR, such as
radiography, ultrasound, and Magnetic Resonance Imaging (MRI), can lead to mis-
diagnosis (i.e., false negatives in ruptures reported as partial by untrained sonogra-
phers, or even in MRI reports) as well as to a delay in the initiation of the relevant
treatment, whether surgical or conservative, in addition to the associated cost [32].
Complementary imaging methods should be reserved for specific cases, or precise
diagnostic doubts (e.g. distal avulsive lesions, proximal tears in the myotendinous
junction, subacute or chronic late presentations, re-ruptures, uncooperative patients,
or in poor general condition, etc.) [25, 26].
Dynamic ultrasound and MRI are used in some working groups to determine
whether to perform surgical or conservative management of the lesion, according to
the findings obtained at the level of the gap, apposition of the tendon ends and the
distance between them, both statically and dynamically. Its use is also described for
the study and monitoring of tendon healing after treatment.
1.4.1 Treatment
When faced with an acute rupture of the Achilles tendon, the treatment alternatives
can be surgical and nonsurgical (conservative). Surgical treatment can be open,
minimally invasive or percutaneous, and all of these techniques use some type of
internal suture that provides extra protection to the tendon repair process, but at the
same time may alter some of the local blood supply with the surgical procedure.
The benefits observed with surgical repairs are protection from minor forces to
the tendon that may elongate or re-rupture it during rehabilitation, but there are also
described risks such as operative wound infections and dehiscence, deep infections,
symptomatic scarring, sural nerve injury, and deep vein thrombosis.
Conservative treatment does not alter the local biology of the repair produced by
surgery, but requires strict medical control and patient adherence to achieve the best
results and avoid tendon elongation and residual weakness.
Thus, all these considerations should be taken into account when deciding the
indicated treatment for our patients, since both surgical and conservative treatment
can have excellent clinical and functional results and without statistical differences
in the long term. It should be considered that if there is difficulty in implementing
the conservative treatment protocol, or poor adherence to treatment by the patient,
surgical treatment should be implemented [34].
1.4.2 Conservative Treatment
Conservative treatment is described in several ways. Some classic treatment tech-

niques, with prolonged immobilization in equine, have described re-rupture rates
that in some series reach up to 20%. However, the use of orthoses and functional
rehabilitations with controlled ranges of motion and early progressive partial loads
have been able to decrease re-rupture rates and achieve long-term functional results
similar to surgical treatment. One of the latest functional protocols is the one pro-
posed by Dr. Mark Glazebrook of Halifax, Canada, called GAPNOT, which we will
review below [35].
Inclusion criteria: Complete body rupture of the Achilles tendon (clinically diag-
nosed, and with imaging confirmation with MRI), commitment to adhere to conser-
vative treatment protocol, start treatment within the first 7 days of injury, signature
of informed consent.
Exclusion criteria: Achilles end injuries (proximal muscle tear or calcaneal avul-
sion, failure to be immobilized with cast in maximum plantar flexion within 48 hours
of injury), open Achilles tendon ruptures, presence of additional involved leg inju-
ries, previous re-ruptures or significant previous Achilles tendon injuries, presence
of physical or mental impairments that do not allow good adherence to conservative
treatment protocol, presence of risk factors for tendon re-ruptures (diabetes, use of
immunosuppressive therapies, recent use of corticosteroids or fluoroquinolones).
At the time of diagnosis, they should be immobilized with a cast boot with the
ankle in maximum plantar flexion, maintained in unloading for 2 weeks. At the
2-week check-up, patients are fitted with a specific walking boot for Achilles tendon
rupture, with a 40-degree posterior heel lift, and the rehabilitation protocol is started
in conjunction with a kinesiologist, clearly establishing the weekly kinesiology ses-
sions, the time of progression of the load and progressive decrease of the ankle
equinus, and the removal of the boot.
Medical checkups are usually performed at 6, 12, 26, and 52 weeks post-injury.
In these controls, the inflammatory signs, progression of the activity, and disappear-
ance of the palpable gap are evaluated. It is important to evaluate the elongation of
the Achilles, which is done in relation to the contralateral ankle, with the knee in a
90-degree flexion position.
The GAPNOT protocol considers progressive loading, increasing 25% of body
weight weekly from week 3 to week 6. It also initiates an ankle range of motion, not
exceeding 90 degrees of dorsiflexion between week 2 and week 8. Cane removal is
achieved after approximately week 6. During this time, direct communication
between the patient, the traumatologist, and the kinesiologist is essential to avoid or
treat possible complications such as re-ruptures, tendon elongation, nonadherence
to the kinesic protocol, and the appearance of deep vein thrombosis.
Between week 6 and week 8, full loading is achieved, and the posterior heel lift
and then the immobilizing boot are progressively removed. And between week 8
and week 12, active ankle exercises are started avoiding dorsiflexion over 90
degrees. Exercises such as cycling or closed-chain physical activities are also indi-
cated at that time, as well as bipodal elevation. Between week 12 to 16, muscle
strengthening progresses. This is also the stage of greatest care, since it has been
described that most of the re-ruptures occur in patients who feel well and exceed
their activity, between weeks 10 and 16.
Between the fourth and sixth month, the patients already go to a gym or do sports
at home, and can even achieve a gentle jogging. From the sixth month, they resume
their usual sports, avoiding impact sports or high-intensity sports. The return to
normal sports activity is achieved between 9 and 12 months post-injury.
Among the main complications described are complete rupture (4%), partial rup-
ture, tendon elongation (mainly when there is no strict adherence to the protocol),
muscle atrophy and loss of strength, and deep vein thrombosis [35].
It should be noted that conservative management is not synonymous with “no
treatment,” but represents a viable alternative to surgery, and requires proper patient
selection, intensive rehabilitation, established protocols methodically followed in a
transdisciplinary team, close follow-up and monitoring, with clear consent, under-
standing and compliance by the patient and his medical team.
1.4.3 Surgical Treatment
Proponents of surgical treatment have demonstrated lower rates of tendon re-

rupture, and also in the medium term, greater significant plantar flexion strength
than patients treated nonsurgically, and earlier return to work and sport. In addition,
the rigorousness of the nonsurgical protocol is not always met by all patients, so in
many cases surgical treatment offers a better and more predictable functional
outcome.
The surgical treatment alternatives are open techniques, minimal approach or
“mini-open” techniques, and percutaneous or minimally invasive techniques, the
latter being the most popular in recent years [36].
1.4.4 Open Surgical Techniques
Open tenorrhaphy through a posteromedial para-Achilles approach to reduce the

possibility of damage to the sural nerve allows complete identification of the proxi-
mal and distal ends and restoration of the correct tendon length, thus obtaining bet-
ter functional results. The most common sutures for open tenorrhaphy are the
modified double Kessler suture or the Bunnel suture, reinforced with coronal sutures
from the tendon periphery. Open techniques have lower re-rupture rates than non-
surgical and minimally invasive treatments, but have higher rates of superficial and
deep infections and operative wound dehiscence [37].
1.4.5 Minimally Invasive Techniques: Percutaneous and Mini-Open
Due to the complications described in open tenorrhaphy, and the difficulties and
complications of conservative treatment, mini-open and percutaneous surgical treat-
ments appear as a good treatment alternative for patients with acute Achilles rupture.
Ma and Griffith described the first percutaneous technique in 1977 [38] with
good results, but in later studies it presented the risk of entrapment of the sural nerve
due to the cross-linking of the sutures, and also the inability to ensure the position-
ing of the rupture ends and the consequent repair with elongated gastrosoleus
complexes.
Among the so-called mini-open options, at the beginning of this century, the
Dresden group, led by Dr. Amlang, devised a new technique for the repair of the
ruptured sutures. Amlang designed a technique with important modifications to
those previously described, where through a single approach, 3 cm proximal to the
rupture, a specially designed reusable instrumental material (Dresden instruments)
is inserted between the crural fascia and the paratenon, taking the sutures percutane-
ously in the distal end and rescuing them through the proximal approach without
crossing them and performing the tenorrhaphy to the proximal end. This technique
has shown reproducible results, with a low rate of re-rupture and damage to the sural
nerve, which has made it very popular in Europe and Latin America [39, 40]. Some
modifications have been described by our group, for some sports patients or patients
where the Achilles rupture is insertional, the use of metallic anchors at the level of
the calcaneus and repeating the Dresden technique, using the anchor sutures to
make the tenorrhaphy (Figs. 1, 2, and 3).
Mini-open techniques also include techniques that involve direct visualization of
the focus of the Achilles tendon rupture through an incision of up to 2 cm in the
longitudinal axis of the leg, directly in the area of the rupture. The plane of the fascia
is identified, and both the proximal and distal strands are grasped with a Kocher
forceps, and specially designed devices are placed to trap both strands (proximal
first and then the distal strand) and allow passage of three sets of sutures through the
strands, then knotting the three sutures of each strand separately, those most proxi-
mal to the focus together and following with those most distal to the focus of rup-
ture. This allows direct control of our repair [41, 42].
The authors recommend the indication of minimally invasive repair with the
modified Dresden technique for all patients with ruptures between 2 to 8 cm distal
to the Achilles tendon, with less than 21 days of evolution [43]. In athletes, we also
prefer the mini-open option, often with some modification to the distal anchorage,
since we have observed in isokinetic tests an ad integrum recovery of joint torque
and muscle strength in the operated leg, demonstrating that it is not necessary to
submit this subgroup of patients to open surgery (research in the process of
Fig. 1 Dresden surgical

technique, showing a
posteromedial approach
proximal to the Achilles
tendon defect
publication). We refer readers interested in a modification to the distal and proximal

anchorage to the following reference [44]. In re-ruptures, subacute injuries (more
than 21 days), and open injuries, we prefer open surgical treatment.
We conservatively manage non-ambulatory patients or patients with a very low
functional threshold and patients with poor soft tissue conditions (burns, ulcers, etc).
Regarding the rehabilitation of our surgical patients, all our patients undergo
antithrombotic prophylaxis with oral anticoagulants for 10 days. The ankle is kept
in equinus in a removable boot, allowing immediate partial loading with the help of
Fig. 2 Dresden
instruments inserted from
proximal approach, with
transfixing needles in distal
end, each with a loaded
suture, passing through the
instrument holes distally
two crutches. Passive dorsiflexion up to 90 degrees is encouraged from the seventh

day and active plantar and dorsal flexion movements from the third week.
Kinesiotherapy begins at the third week, and from that moment on, the equinus
inside the boot is reduced by 1 cm per week, until the boot is removed at the sixth
Fig. 3 Sutures retrieved

through proximal
approach. These sutures
are tied to the proximal
Achilles segment
week. Gentle jogging is allowed around the third month, when patients are able to
perform monopodal elevation of the operated heel.
2 Complications
Both orthopedic and surgical treatment have potential complications described.

Conservative treatment has mainly described complete re-rupture, which can be
seen from 3%, up to 20% in other series [37], and partial re-ruptures. Both compli-
cations are important to reevaluate in order to define the need for surgical repair.
The most frequent complication of conservative treatment is elongation of the gas-
trosoleus complex, especially in patients who do not respect nonsurgical manage-
ment protocols and mainly observed between week 10 and 16, where patients feel
well but healing is still evolving. Of these patients, we reoperate those who have a
significant clinical functional compromise of the Achilles complex, which prevents
a normal development of their activities of daily living or sports (refer to the section
on chronic ruptures of the AT). Other described complications of this treatment are
deep vein thrombosis and pulmonary thromboembolism, muscle atrophy, and loss
of twin strength [34].
Surgical treatment also has complications described. There are classic risk fac-
tors for developing complications, which are chronic use of corticosteroids, smok-
ing, diabetes, and late treatment of ruptures.
Open repair significantly decreases the risk of rupture, but increases the risk of
deep and superficial infection, and the risk of operative wound dehiscence. These
should be treated aggressively, with surgical cleansing and antibiotics, and in the
case of deep infections it is necessary to evaluate the need for removal of suture
materials and consider chronic deferred repair, such as a hallux flexor tendon trans-
fer among some reconstruction alternatives. Wound dehiscence may benefit from
the use of negative pressure therapy, and in some cases flaps and coverage by plastic
surgery [45].
Percutaneous repair, designed to reduce operative wound complications and
achieve faster reintegration, achieves its objectives by presenting low rates of opera-
tive wound complications and superficial and deep infections. However, in some
series, it presents slightly higher re-rupture rates than open repair. In addition, sural
nerve injuries have also been described.
Finally, it should not be forgotten that deep venous thrombosis of the lower
extremities and pulmonary thromboembolism may also occur in surgical treatment.
2.1 Chronic Achilles Tendon Ruptures
2.1.1 Summary
In chronic ATR, there is a broad consensus that surgical treatment is the treatment
of choice. Depending on the characteristics and demands of the patient, and preop-
erative planning, end-to-end suturing techniques, local tissue, allografts, or syn-
thetic elements can be used for reconstruction. Conservative treatment is reserved
for patients with low demand or with basic contraindications for surgery.
2.1.2 Introduction
Both the temporal transition from what is considered an acute to a chronic rupture,
as well as the difference in the results and the surgical techniques chosen for its
treatment, is somewhat variable and arbitrary according to the literature consulted.
Despite this, there is some consensus that AT ruptures diagnosed after the fourth or
sixth week of evolution are considered chronic ruptures [46–49].
Strictly related to the increase in the frequency of acute AT ruptures, chronic
ATRs have also become more frequent in daily practice. Delay or error in the diag-
nosis of acute AT ruptures occurs in 20–25% of cases [46, 47], in which it is not
diagnosed in the acute period, either due to clinical misdiagnosis or lack of consul-
tation by some patients who may not seek medical services initially, with their
known sequelae and considerable functional morbidity [13, 50, 51].
The diagnosis of these lesions is also fundamentally clinical, with a physical
examination and directed anamnesis. As we are dealing with different evolution
times and within an ongoing repair and healing process, imaging diagnostic meth-
ods become more important and meritorious.
High-resolution ultrasound and magnetic resonance imaging are the most com-
monly used methods, both for diagnostic support and surgical planning.
In contrast to acute lesions, in chronic lesions there is a broad consensus that the
relevant treatment is surgical.
There are many methods described for ATR repair or reconstruction surgery;
depending on the case, the characteristics and demands of the patient, and the pre-
operative planning, techniques with terminal suture can be used as in acute injuries,
or local tissues, allografts, or synthetic elements can be used for reconstruction. In
patients with concomitant underlying pathologies, with low functional demand, or
with contraindications for surgery, conservative treatment with orthosis and kinesic
rehabilitation can be chosen.
2.1.3 Etiology and Pathophysiology
An inflammatory response and reparative processes are triggered by a tendon rup-

ture. In the days following the injury, granulation and scar tissue begins to develop
between the ends of the affected tendon, which makes it difficult to oppose the
tendon in a closed manner, and consequently alters the results and prognosis of any
attempt at conservative treatment [52, 53].
If the patient continues with activities of daily living, maintaining mobility and
contraction of the gastrocnemius apparatus, elongation of the gap and poor-quality
fibrous scar tissue will eventually occur, which may increase the length of the AT
over time. The tendon can heal and fill the defect in an elongated and thickened
form, with fibrosis and adhesions, a retraction of the proximal end and shortening of
the gastrocnemius; this elongation that is generated in the gastrosoleus complex has
repercussions at the molecular level in the sarcomere unit, producing a change in its
length, with the respective sequelae in the functioning, loss of strength and
mechanical efficiency of the triceps suralis, with weakness for plantar flexion and
alterations in gait [54–56].
2.1.4 Diagnosis
Chronic AT ruptures are the consequence of acute injuries with an erroneous, unrec-
ognized, or delayed diagnosis. The patient may or may not report the history of a
previous episode of acute injury. In these cases, and especially in patients with low
functional demand, nonathletes, the patient usually presents with difficulty in per-
forming activities of daily living, such as walking on slopes or climbing stairs, feel-
ing of fatigue or weakness, inability to get up on tiptoe, or persistent pain or swelling
at the site of injury, if it occurs in a subacute stage.
We have to keep in mind that in chronic injuries the rupture injury site begins to
be replaced by fibrous/scar tissue; clinical tests for physical examination and diag-
nosis of ATR may be difficult to interpret and less sensitive.
Depending on the time of evolution and activity of the patient, in some cases we
can still find the existence of a tendon gap; in others, although of lower tissue qual-
ity, there may be continuity at the injury site. The Matles test is also useful in chronic
injuries, as it can be seen asymmetrical with elongated AT and increased passive
dorsiflexion of the ankle.
The contour of the AT is frequently altered, somewhat thickened and without
precise definition. There may be a calcaneal gait with weakness for toe-off, and
atrophy at the calf level noted with respect to the contralateral healthy side.
Active plantar flexion, although weak, may be maintained by the action of other
muscles such as the posterior tibialis, flexor hallucis longus, common flexor digito-
rum, and peroneus [57]. Some patients may even maintain the ability to stand on
their toes in a monopodal manner, but it is difficult for them to resist or succeed in
performing this elevation for several repetitions in a row.
With regard to Thompson’s test, widely used and reproducible in acute AT rup-
tures, it does not retain its high sensitivity for chronic injuries, as the tendon may be
maintained in continuity by scar tissue and be negative for a rupture or only be
somewhat attenuated in its response.
These residual functions and repair tissue present can make it difficult to make
an accurate diagnosis by clinical examination alone, so a high index of suspicion is
required, and it is useful to rely on imaging studies to complement the diagnosis.
Radiography could be useful to evaluate avulsive lesions in the calcaneus, and
sometimes findings of calcifications at the tendon level.
Ultrasound can be used both statically and dynamically and explore the tendon
to evaluate the quality of its tissues, the gap and the apposition of the ends with the
different ranges of mobility of the ankle.
The study of choice in chronic AT ruptures, both for diagnosis and preoperative
planning, is magnetic resonance imaging (MRI). In MRI it is possible to analyze the
characteristics and size of the tendon ends and the scar gap, the presence of fibrosis
or perilesional calcifications, and the state and quality of the muscular apparatus.
The evaluation and study under computed tomography or MRI of muscle atro-
phy and fatty degeneration in rotator cuff pathology can be extrapolated to chronic
AT injuries. Several studies highlight the negative effect that muscle atrophy and
fatty infiltration would have on functional outcomes and risks of tendon rupture.
The knowledge of the quality and potential recovery capacity of the muscle-tendon
unit in a long-standing rupture can be crucial to determine the therapeutic conduct;
this helps to decide whether to perform a repair, an isolated reconstruction, or to
decide on a tendon transfer [58–60].
2.1.5 Treatment
Most of the existing treatments for chronic ATR are planned according to the size of
the gap or existing separation between the ends, the quality of the tissues, the state
of the skin and previous approaches, muscular degeneration of the gastrocnemius,
characteristics and demands of the patient to be treated. In short, there are many
variables to take into account regarding surgical treatment, including the surgeon’s
expertise, and there is no high-level evidence to be able to recommend one over
the other.
Conservative treatment is only reserved for patients who have a contraindication
for surgery, with concomitant pathologies or morbidities, or those patients with low
functional demand, in which their activities of daily living are not affected. This
would consist in the use of a walking boot with initial enhancement, and its associ-
ated rehabilitation, to maintain good flexor function that helps counteract the deficit
of the gastrocnemius muscles.
Excluding these isolated patients, there is a consensus that these chronic AT inju-
ries require surgical treatment.
Classifications:
Myerson proposed a classification and treatment plan according to the size of the
defect at rupture [61].
• Defects of 1–2 cm in length. Their treatment consists in a terminal repair and
fasciotomy of the posterior compartment.
• Defects between 2 and 5 cm require a V-Y lengthening, with the possibility of
augmentation with tendon transfer.
• Defects larger than 5 cm, in which a bridge is performed with a tendon transfer,
isolated or combined with a V-Y advancement.
Kuwada classifies AT ruptures into four grades [62]:
• Partial ruptures, worthy of conservative treatment with immobilization.
• Complete ruptures with defects up to 3 cm, with terminal repair treatment.
• Lesions with defects of 3–6 cm after debridement of the ends, leaving healthy
tissue; these defects require an autologous tendon graft, which may or may not
be accompanied by a synthetic graft for reconstruction.
• Defects of more than 6 cm after debridement; gastrocnemius release, repair with
free tendon graft and/or augmentation with synthetic graft.
The main objective of surgical treatment is to restore adequate length and tension
of the TA, promote adequate healing of the lesion, and restore the overall function
of the complex. Most of the studies and techniques published in the literature are of
a low level of evidence, so we cannot make a single recommendation of one treat-
ment method over another [49, 63].
2.2 Tendon Mobilization and End-to-End Suturing
In patients in whom we find a gap of less than 2 cm in length, after resection of the
scar tissue, it is plausible to perform a termino-terminal suture, leaving the ankle in
a slight postoperative equinus to allow and protect adequate healing. One technique
described to gain some length is to perform an extensive soft tissue release around
the ends and fibrosis, place a few Krackow stitches in the proximal end, and perform
gentle traction held for several minutes intraoperatively to obtain some elongation
to gain a few millimeters of accessory length to allow union (Figs. 4 and 5).
Fig. 4 Open AT gap

debridement
Fig. 5 Open AT repair

using the Krackow
technique
2.3 Tendon Advancement with V-Y Flap
Initially described by Abraham and Pankovich [64], this procedure applied for
chronic inveterate ruptures of the AT. The aim of this procedure is to perform an
end-to-end anastomosis of each tendon ends, through a gliding flap, with the carv-
ing of a proximal flap in the shape of an inverted V. The apex of the V should be
pointing away from the end of the flap. The apex of the V should be made in the
central part of the proximal aponeurosis. The arms of the “V” are 1.5 times the
length of the gap, in order to close the remaining defect proximally in a “Y” shape.
Although its use has been described in extensive defects of up to 10 cm, it is
generally used in ruptures with a gap length of less than 5 cm, in order to preserve
the insertion of the posterior muscle group. These advancement flaps have the
advantage of allowing adequate healing with native tissue at the site of union,
decreasing suture tension, without the need to sacrifice other tendon autografts
(with the morbidity that this entails), and avoiding allografts or synthetic materials
(Figs. 6, 7, and 8).
2.4 Inverted Flaps (Turndown)
There are many variants of AT inverted flaps, which have been used for both repair
and augmentation of chronic AT ruptures. Christensen [65] describes their applica-
tion for both acute and chronic injuries. The technique consists of gap debridement,
with a flap carved on the proximal fragment, distally based 2 cm wide by 10 cm
long. Then it is inverted distally filling the defect, suturing it distally to the distal
tendon end, and closing the resulting proximal gap. Care should be taken in rein-
forcing the “corners” of the flap with sutures. There are some modifications to the
carving (two lateral and medial flaps, Pulvertaft type, 180° turn, among others), and
Fig. 6 V-Y flap. Tendon

defect debrided and
regularized, leaving tissue
of adequate quality.
(Courtesy of Dr. Emilio
Wagner, MD.)
Fig. 7 V-Y flap. V-Y flap

designed proximally, with
sutures, traction and
approximation of both ends
Fig. 8 V-Y flap. Transfer

of the FHL associated with
the previous repair
in the suture or distal anchorage of this flap described, as well as different proce-
dures that can be performed in a supplementary way.
2.5 Shortening for Elongated Tendons
There are some patients with chronic ATR, in whom a defect in the rupture is not
observed, and there is continuity, the gap being replaced by fibrous scar tissue with
an elongated tendon, and the consequent loss of mechanical efficiency and strength.
In these cases, a shortening Z-plasty, or scar resection and end to end-terminal
suture can be performed, crossing the edges and regularizing the ends with suture,
to recover the appropriate length, leaving the injured foot in a slight postoperative
equinus with respect to the contralateral one. This can be associated with additional
suturing use of scar fibrinous tissue as reinforcement of the union zone [54, 57].
There are studies which report that the longer the time of evolution from rupture
to surgery, the less vascularization of the lesion area, and therefore the lower the
quality of the tissue to be healed [53, 66].
2.6 Tendon Transfers
These surgical techniques are indicated when there is atrophy or degeneration of the
muscle-tendon unit and when the tendon defect to be covered exceeds 5 cm.
Multiple tendon transfers have been described for the treatment of chronic
Achilles tendon ruptures. Several authors have published the use of the peroneus
brevis (PB) for reconstruction surgery of a chronic ATR, with some variants of
anchoring distally through a trans-osseous tunnel in the calcaneus, in the distal
stump of the AT, and with the help or not of the plantaris longus as reinforcement
depending on its presence [67, 68]. When indicating a PB tendon transfer, besides
its morbidity and possible biomechanical affectation in gait, remember that it is a
Fig. 9 Clinical image of

patient with scar retraction
due to previous skin burn,
making a direct approach
for repair difficult,
deciding on a percutaneous
technique
Fig. 10 Planning of
chronic rupture repair with
percutaneous technique,
performing a peroneus
brevis transfer
Fig. 11 Peroneus brevis

transferred to the distal AT
stump
Fig. 12 Final image with

percutaneous portals for
peroneus brevis transfer
and modified Dresden
technique. Dresden repair
was used as an
augmentation for the
tendon transfer
tendon of a reduced force capacity, and that it is in another phase and tension line
(Figs. 9, 10, 11, and 12).
Regarding the flexor digitorum longus (FDL), there are some case reports [69],
where the authors perform a section of the FDL before the division in each digital
branch, and then suture the distal remaining end to the FHL. Then it is correspond-
ingly sutured to the distal and proximal stump of the TA to fill the injury defect.
Currently, the most commonly used tendon transfer in chronic ATR is that of the
flexor hallucis longus tendon (FHL), given its biomechanical strength, phase of
action, and line of tension. Initially described by Wapner [70], with a medial mid-
foot approach, it can now be performed with a single posterior approach or two
minor incisions, and even arthroscopically.
The patient is positioned in prone position, with the feet at the edge of the operating
table. Depending on the surgeon’s preference, the surgery is performed in an open fash-
ion using a medial or central para-Achilles approach, where Kager’s fat is rejected, the
posterior fascia is opened, and the muscle belly and tendon of the FHL are identified
(this can be easily identified by moving the patient’s hallux in flexion and extension).
Once the approach has been made, the hallux is taken in maximum plantar flex-
ion and a tenotomy is performed as distally as possible and the FHL tendon can be
inserted in the distal end of the Achilles by sutures or inserted directly into the cal-
caneus by means of bone tunnels, anchors, or biotenodesis screws [71]. This treat-
ment, which theoretically takes away plantar flexion strength from patients, does
not have great repercussions on their function, since the connections of the FHL
with the FDL in the Henry’s knot are preserved. When a longer graft is required to
perform a transosseous calcaneal tunnel to bridge the Achilles rupture defect, it is
recommended to perform a medial approach in the midfoot.
2.7 Minimally Invasive and Endoscopic Procedures
Flexor hallucis longus tendon transfer has been described to be performed endo-
scopically, with its great benefits of less soft tissue damage, without sacrificing a
good surgical outcome. This is performed with traditional posterior ankle arthros-
copy, through two medial and lateral para-achilles portals; the FHL tendon is identi-
fied in the posteromedial aspect of the ankle and subtalar joints. Next, we debride
the insertion zone of our transfer, in the most dorsal and posterior area of the calca-
neus. The FHL tendon is identified, and in maximum plantar flexion of the hallux,
the tenotomy is performed as distally and securely as possible in its tunnel (in order
to obtain the greatest possible length of the tendon). It is taken with a suture, and
through a trans-osseous tunnel, as posterior and close to the insertion site of the
Achilles, it is inserted with the use of a biotenodesis screw with the ankle in 20
degrees of plantar flexion and taking the tendon as far into the bone tunnel as pos-
sible [72].
2.8 Graft Reconstruction
Reconstruction with grafts, unlike tendon transfers, takes advantage of the fact that
the muscle-tendon unit is still functional, and the objective is to resolve the solution
of continuity of the rupture by means of the contribution of collagen, either autolo-
gous or allogenic. They are frequently indicated when the tendon defect to be cov-
ered exceeds 5 cm.
2.8.1 Autologous
Multiple reconstructions with autografts have been described, including the use of
hamstring and quadriceps tendon. The main indication is when collagen is needed
to fill the gap, especially when the tendon defects are greater than 6 cm. The other
indication is when it is not possible to perform a tendon transfer, or the muscle-
tendon unit is preserved, and it is not necessary to enhance a degenerated muscle
[71]. For this, an extensive posterior central approach or two approaches at each end
of the ends of the rupture are used. After resection of the fibrous and non-vital tis-
sue, the graft of choice is passed previously taken, and tenodesis is performed proxi-
mally at the proximal end of the Achilles, and distally at the distal end or directly to
the calcaneus, similar to the anchor described for transfers (Fig. 13).
2.8.2 Allografts
Reconstruction with allografts and synthetic grafts

Allograft reconstruction is also described in the literature, which allows recon-
struction in extensive deficits, without adding the morbidity of the graft donor site.
Achilles allografts with and without distal bone block can be used for reinsertion.
Fig. 13 Mini-open
technique using autologous
hamstring tendons.
Through the proximal
portal, the tendons were
sutured to the proximal
Achilles stump using a
Pulvertaft technique.
Subcutaneously, the
autograft was passed to the
distal stump and sutured
to it
The use of synthetic grafts has also been described, but in general their use is
described as an augmentation of some other reconstruction technique. For both
alternatives, the published series consist in few patients [71].
2.9 Authors’ Recommendation
As a working protocol, the authors recommend using the end-to-end suture tech-
nique for defects up to 2 cm in the end gap. In tendons with elongations up to 2 cm,
we use shortening and end-terminal suture. When we encounter defects of 2–5 cm,
we perform a V-Y advancement flap.
In the presence of defects larger than 5 cm and with a muscle-tendon unit of good
quality and excursion, we use allograft or tendon autograft; this can be associated to
tendon transfers according to the case, as a biological and functional contribution.
In the case that we have to perform a tendon transfer, either when we have a
poor-quality muscle, or we want to perform some augmentation, the one we prefer
is the FHL.
2.10 Rehabilitation
In the initial postoperative period, the patient is immobilized with a short boot, with
the foot in equinus, and is kept in unloading for 4–6 weeks. After this, progressive
partial loading and progressive reduction of the protective repair equinus is indi-
cated, and kinesic rehabilitation is started with controlled stretching of the Achilles,
strengthening, and gait re-education. At 12 weeks, the protective orthoses are
removed. All impact activity of sudden acceleration or jumping is restricted for
6 months after surgery to avoid re-rupture [73].
2.11 Complications
Among the potential complications described are dehiscence and necrosis for open
techniques, re-ruptures, elongation, and weakness of ankle plantar flexion, sural
nerve injuries, and deep vein thrombosis [73]. Following the same therapeutic
scheme, for re-ruptures, for a new reconstruction we consider the size of the new
tendon gap, and the condition of the effector muscle to decide between the use of a
graft or a tendon transfer, in addition to the surgical technique used in the first
surgery.
References
1. Arandes R, Viladot A. Biomecánica del calcáneo. Med Quir. 1954;21:25.

2. Maceira E. Manuel Monteagudo. Madrid: Mecánica Clínica y Terapéutica Pie y Tobillo; 2017.
3. Dederer KM, Joshua N. Tennant. Anatomical and functional considerations in Achilles tendon
lesions. Foot Ankle Clin N Am. 2019;24:371–85.
4. Komi PV, Fukashiro S, Järvinen M. Biomechanical loading of Achilles tendon during normal
locomotion. Clin Sports Med. 1992;11(3):521–31.
5. Fukashiro S, Komi PV, Järvinen M, Miyashita M. In vivo achilles tendon loading during jump-
ing in humans. Eur J Appl Physiol. 1995;71:453–8.
6. Claessen FMAP, de Vos RJ, Reijman M, Meuffels DE. Predictors of primary Achilles tendon
ruptures. Sports Med. 2014. https://doi.org/10.1007/s40279-014-0200-z.
7. Maffulli N, Waterston SW, Squair J, Reaper J, Douglas AS. Changing incidence of Achilles
tendon rupture in Scotland: a 15-year study. Clin J Sport Med. 1999;9(3):157–60.
8. Suchak AA, Bostick G, Reid D, Blitz S, Jomha N. The incidence of Achilles tendon ruptures
in Edmonton, Canada. Foot Ankle Int. 2005;26(11):932–6.
9. G. Ho, et al. Increasing age in Achilles rupture patients over time. Injury. 2017. https://doi.
org/10.1016/j.injury.2017.04.007.
10. Hess GW. Achilles tendon rupture: a review of etiology, population, anatomy, risk factors, and
injury prevention. Foot Ankle Spec. 2010;3(1):29–32.
11. Leppilahti J, Orava S. Total Achilles tendon rupture, a review. Sports Med. 1998;25:79–100.
12. Schipper O, Cohen B. The acute injury of the Achilles surgical options (open treatment, and,
minimally invasive surgery). Foot Ankle Clin N Am. 2017;22:689–714.
13. Jennings AG, Sefton GK. Chronic rupture of tendo Achillis. Long-term results of operative
management using polyester tape. J Bone Joint Surg Br. 2002;84:361–3.
14. O'Brien M. Functional anatomy and physiology of tendons. Clin Sports Med.
1992;11(3):505–20.
15. Maganarisa CN, Paul JP. Tensile properties of the in vivo human gastrocnemius tendon. J
Biomech. 2002;35:1639–46.
16. Williams JGP. Achilles tendon lesions in sport. Sports Med. 1986;3:114–35.
17. Eriksen HA, Pajala A, Leppilahti J, Risteli J. Increased content of type III collagen at the rup-
ture site of human Achilles tendon. J Orthop Res. 2002;20(6):1352–7. https://doi.org/10.1016/
S0736-0266(02)00064-5.
18. Persson R, Jick S. Clinical implications of the association between fluoroquinolones and ten-
don rupture: the magnitude of the effect with and without corticosteroids. Br J Clin Pharmacol.
2019;85:949–59.
19. Wise B, Peloquin C, Choi H, Lane N, Zhang Y. Impact of age, sex, obesity, and steroid use on
quinolone-associated tendon disorders. Am J Med. 2012;125(12):1228–e23.
20. Chen TM, Rozen WM, Pan W-R, Ashton MW, Richardson MD, Taylor GI. The arterial anatomy
of the Achilles tendon: anatomical study and clinical implications. Clin Anat. 2009;22:377–85.
21. Lagergren C, Lindholm A. Vascular distribution in the Achilles tendon; an angiographic and
microangiographic study. Acta Chir Scand. 1959;116(5–6):491–5.
22. Dalmau-Pastor M, Fargues-Polo B, Casanova-Martínez D, Vega J, Golanó P. Anatomy of the
triceps surae: a pictorial essay. Foot Ankle Clin N Am. 2014;19:603–35.
23. Rouvière H, Delmas A. Anatomía Humana. Descriptiva, Topográfica y Funcional. 11th ed.
Barcelona: Masson S.A; 2005.
24. O’Brien M. The anatomy of the Achilles tendon. Foot Ankle Clin N Am. 2005;10:225–38.
25. Maffulli N. The clinical diagnosis of subcutaneous tear of the Achilles tendon a prospective
study in 174 patients. Am J Sports Med. 1998;26(2):266–70. American Orthopaedic Society
for Sports Medicine.
26. Hutchison A-M, Evans R, Bodger O, Pallister I, Topliss C, Williams P, Nicola Vannet F,
Morris V, Beard D. What is the best clinical test for Achilles tendinopathy? Foot Ankle Surg.
2013;19:112–7.
27. Simmonds FA. The diagnosis of the ruptured Achilles tendon. Practitioner. 1957;179:56–8.
28. Thompson TC. A test for rupture of the tendo Achillis. Acta Orthop Scand. 1962;32:461–5.
29. Thompson TC, Doherty JH. Spontaneous rupture of tendon of Achilles a new diagnostic test.
J Trauma Acute Care Surg. 1962;2:126–9.
30. Matles AL. Rupture of the tendo Achilles. Another diagnostic sign. Bull Hosp Joint Dis.
1975;36:48–51.
31. Copeland SA. Rupture of the Achilles tendon: a new clinical test. Ann R Coll Surg Engl.
1990;72:270–1.
32. O’Brien T. The needle test for complete rupture of the Achilles tendon. J Bone Joint Surg.
1984;66A:1099–101.
33. Chiodo CP, et al. Diagnosis and treatment of acute Achilles tendon rupture. AAOS clinical
practice guideline summary. J Am Acad Orthop Surg. 2010;18:503–10.
34. Glazebrook M, Rubinger D. Functional rehabilitation for nonsurgical treatment of acute
Achilles tendon rupture. Foot Ankle Clin. 2019;24(3):387–98. https://doi.org/10.1016/j.
fcl.2019.05.001. Epub 2019 Jun 22.PMID: 31370992.
35. Willits K, Amendola A, Bryant D, Mohtadi NG, Giffin JR, Fowler P, Kean CO, Kirkley
AJ. Operative versus nonoperative treatment of acute Achilles tendon ruptures: a multi-
center randomized trial using accelerated functional rehabilitation. Bone Joint Surg Am.
2010;92(17):2767–75. https://doi.org/10.2106/JBJS.I.01401. Epub 2010 Oct 29.PMID:
21037028.
36. Patel MS, Kadakia AR. Minimally invasive treatments of acute Achilles tendon ruptures. Foot
Ankle Clin. 2019;24(3):399–424. https://doi.org/10.1016/j.fcl.2019.05.002. Epub 2019 Jun
18.PMID: 31370993.
37. Movin T, Ryberg A, McBride DJ, Maffulli N. Acute rupture of the Achilles tendon. Foot Ankle
Clin. 2005;10(2):331–56. https://doi.org/10.1016/j.fcl.2005.01.003. PMID: 15922923.
38. Ma GW, Griffith TG. Percutaneous repair of acute closed ruptured Achilles tendon: a new
technique. Clin Orthop Relat Res. 1977;128:247–55. PMID: 340096.
39. Amlang MH, Christiani P, Heinz P, Zwipp H. The percutaneous suture of the Achilles ten-
don with the Dresden instrument. Oper Orthop Traumatol. 2006;18(4):287–99. https://doi.
org/10.1007/s00064-006-1178-y. PMID: 17103128.
40. Keller A, Ortiz C, Wagner E, Wagner P, Mococain P. Mini-open tenorrhaphy of acute Achilles
tendon ruptures: medium-term follow-up of 100 cases. Am J Sports Med. 2014;42(3):731–6.
https://doi.org/10.1177/0363546513511418,
41. Assal M, Jung M, Stern R, Rippstein P, Delmi M, Hoffmeyer P. Limited open repair of Achilles
tendon ruptures: a technique with a new instrument and findings of a prospective multicenter
study. J Bone Joint Surg Am. 2002;84-A(2):161–70.
42. Hsu AR, Jones CP, Cohen BE. Clinical outcomes and complications of percutaneous Achilles
repair system versus open technique for acute Achilles tendon ruptures. Foot Ankle Int.
2015;36(11):1279–86.
43. Keller A, Mococain P, Wagner E, Wagner P, Zanolli D. Percutaneous repair in acute
Achilles tendon rupture. Our experience in Chile PerkutaneNaht der Achillessehnenruptur.
UnsereErfahrungen in Chile. Fuß&Sprunggelenk. 2019;17(4):204–9. https://doi.org/10.1016/j.
fuspru.2019.10.001.
44. Wagner E, Wagner P. Mini-open Achilles tendon rupture repair. JBJS Essent Surg Tech.
2019;9(4):e46.1–2. https://doi.org/10.2106/JBJS.ST.18.00139. PMID: 32051783; PMCID:
PMC6974314.
45. Liles J, Adams SB. Management of complications of Achilles tendon surgery Jr. Foot
Ankle Clin. 2019;24(3):447–57. https://doi.org/10.1016/j.fcl.2019.04.008. Epub 2019 May
29.PMID: 31370996.
46. Gabel S, Manoli A II. Neglected rupture of the Achilles tendon. Foot Ankle Int. 1994;15:
512–7.
47. Den Hartog B. Surgical strategies: delayed diagnosis or neglected Achilles’ tendon ruptures.
Foot Ankle Int. 2008;29:456–63.
48. Leslie H, Edwards W. Neglected ruptures of Achilles tendon. Foot Ankle Clin. 2005;10(357):70.
49. Maffulli N, Ajis A, Longo UG, et al. Chronic rupture of tendo Achillis. Foot Ankle Clin N Am.
2007;12:583–96.
50. Scheller A, Kasser J, Quigley T. Tendon injuries about the ankle. Orthop Clin North Am.
1980;11:801–11.
51. Ballas MT, Tytko J, Mannarino F. Commonly missed orthopedic problems. Am Fam Physician.
1998;57:267–74.
52. Carden DG, Noble J, Chalmers J, et al. Rupture of the calcaneal tendon. The early and late
management. J Bone Joint Surg Br. 1987;69:416–20.
53. Yasuda T, Kinoshita M, Okuda R. Reconstruction of chronic Achilles tendon rupture with the
use of interposed tissue between the stumps. Am J Sports Med. 2007;35:582–8.
54. Padanilam T. Chronic Achilles tendon ruptures. Foot Ankle Clin N Am. 2009;14:711–28.
55. Maganaris CN. Force-length characteristics of the in vivo human gastrocnemius muscle. Clin
Anat. 2003;16:215–23.
56. Maganaris CN. In vivo force--length characteristics of human skeletal muscle. Acta Physiol
Scand. 2001;172:279–85.
57. Maffulli N, Ajis A. Current concepts review. Management of chronic ruptures of the Achilles
tendon. J Bone Joint Surg Am. 2008;90:1348–60. https://doi.org/10.2106/JBJS.G.01241.
58. Leppilahti J, Lahde S, Forsman K, Kangas J, Kauranen K, Orava S. Relationship between
calf muscle size and strength after Achilles rupture repair. Foot Ankle Int. 2000;21(4):330–5.
59. Gerber C, Schneeberger AG, Hoppeler H, Meyer DC. Correlation of atrophy and fatty infiltra-
tion on strength and integrity of rotator cuff repairs: a study in thirteen patients. J Shoulder
Elbow Surg. 2007;16(6):691–6. https://doi.org/10.1016/j.jse.2007.02.122.
60. Goutallier D, Postel JM, Bernageau J, Lavau L, Voisin MC. Fatty muscle degeneration
in cuff ruptures. Pre- and postoperative evaluation by CT scan. Clin Orthop Relat Res.
1994;304:78–83.
61. Myerson MS. Achilles tendon ruptures. AAOS Instruction Course Lectures. 1999;48:219–30.
62. Kuwada GT. Classification of tendo-Achilles rupture with consideration of surgical repair
techniques. J Foot Surg. 1990;29(4):361–5.
63. Maffulli N, Peretti GM. Surgery or conservative management for Achilles tendon rupture?
BMJ. 2019;364:K5344.
64. Abraham E, Pankovich AM. Neglected rupture of the Achilles tendon. Treatment by V-Y ten-
dinous flap. J Bone Joint Surg. 1975;57-A(2):253–5.
65. Christensen I. Rupture of the Achilles tendon; analysis of 57 cases. Acta Chir Scand.
1953;106:50–60.
66. Porter DA, Mannarino FP, Snead D, et al. Primary repair without augmentation for early
neglected Achilles tendon ruptures in the recreational athlete. Foot Ankle Int. 1997;18:557–64.
67. Pérez TA. Traumatic rupture of the Achilles tendon. Reconstruction by transplant and graft
using the lateral peroneus brevis. Orthop Clin North Am. 1974;5:89–93.
68. Turco VJ, Spinella AJ. Achilles tendon ruptures—peroneus brevis transfer. Foot Ankle.
1987;7:253–9.
69. Mann RA, Holmes GB Jr, Seale KS, Collins DN. Chronic rupture of the Achilles tendon: a
new technique of repair. J Bone Joint Surg Am. 1991;73:214–9.
70. Wapner KL, Pavlock GS, Hecht PJ, Naselli F, Walther R. Repair of chronic Achilles tendon
rupture with flexor hallucis longus tendon transfer. Foot Ankle. 1993;14(8):443–9. https://doi.
org/10.1177/107110079301400803.
71. Chen C, Hunt KJ. Open reconstructive strategies for chronic Achilles tendon ruptures. Foot
Ankle Clin. 2019;24(3):425–37. https://doi.org/10.1016/j.fcl.2019.04.002. Epub 2019 Jun 18.
72. Syed TA, Perera A. Endoscopic management of chronic Achilles tendon rupture. Foot Ankle
Clin. 2019;24(3):459–70. https://doi.org/10.1016/j.fcl.2019.04.010. Epub 2019 Jun 13.
73. Raikin SM. Chapter 110, Chronic Achilles tendon ruptures using V-Y advancement and FHL
transfer. In: Operative techniques in foot and ankle surgery. Mark Easley; 2011. p. 918–25.
Ankle Fractures
Guillermo Arrondo and Florencio Pablo Segura
1 Introduction
Ankle or malleolar fractures include all those injuries of the distal ends of the tibia
and fibula without involvement of the central region of the tibial plafond. They are
among the most frequent injuries of the skeleton, accounting for 9% of the total [1].
2 Anatomical and Biomechanical Aspects
From an anatomical point of view, the ankle is characterized by a particular con-

figuration that makes it one of the most congruent joints of the lower extremity.
The tibio-peroneal mortise, formed by the two malleoli joined together by a syn-
desmosis, constitutes a hemi-cylindrical structure that fits exactly with the talar
trochlea, covering more than half of its surface (Fig. 1). Other capsulo-ligamentary
structures that increase joint stability and are part of the talar fixation mechanism
within the mortise “enclose” the talus in a ring made up of “bony stops” - the tibial
G. Arrondo (*)
Instituto Dupuytren, Ciudad Autónoma de Buenos Aires, Argentina
Department of Leg, Ankle and Foot, Dupuytren Institute,
Ciudad Autónoma de Buenos Aires, Argentina
F. P. Segura
Universidad Nacional de Córdoba, Nuevo Hospital San Roque,
Ciudad de Córdoba, Argentina

Switzerland AG 2022
1166 G. Arrondo and F. P. Segura
Fig. 1 Schematic
representation of the
coverage of the talus
trochlea by the tibio-
peroneal mortise (black
arrow). Note how it
corresponds to more than
half of its total surface (red
arrow)
pylon, the malleoli, and the subtalar joint - and flexible restrictors responsible for
the elasticity of the whole (the capsule and the ligaments of the tibio-fibular-talar
joint). From a biomechanical point of view, the ankle is a trochlear joint but not a
fixed hinge. Its primary mobility occurs mainly in the sagittal plane and at the
expense of the tibio-fibular-talar joint, with an average flexion-extension range of
43° to 63° of which 30° (10° of dorsal flexion and 20° of plantar flexion) are neces-
sary for a stable gait. However, the fact that the talar trochlea is wider in front than
behind in the horizontal plane means that during dorsal flexion, the peroneal mal-
leolus must perform a movement of separation or abduction, ascent and external
rotations that together widen the mortise between 1.25 to 2 mm, while in plantar
flexion the opposite occurs. These movements take place at the level of the tibio-
peroneal syndesmosis and are controlled by the tibio-peroneal ligaments, the inter-
osseous membrane, and the tone of the deep muscles of the posterior aspect of the
leg [2–4].
3 Contemporary Classifications
Two are the most widespread systems currently used to classify ankle fractures.
The Lauge Hansen classification (1948–1950) has been considered over time as a
useful tool for understanding ankle fracture pathophysiology. Based on the mecha-
nism of production, it divides them into four types that in the authors’ original work
were obtained based on experiments with cadaveric legs that were secured proximally
and manipulated distally at the level of the foot: (1) supination-adduction, (2)
Ankle Fractures 1167
supination-external rotation, (3) pronation-abduction, and (4) pronation-external rota-

tion. The first term indicates the position of the foot at the time the deforming force is
applied, while the second refers to the direction or type of force applied. Each of these
four types corresponds to a specific sequence and injury pattern, which allows predic-
tion of the anatomical structures involved in each scenario [5, 6].
The AO-Orthopaedic Trauma Association classification, published in 1996 with
revisions in 2007 and 2018, includes ankle fractures in segment 44 (leg location,
malleolar segment). Based on the Danis-Weber (1987) system, it divides them into
three main variants according to the height of the fibula fracture with respect to the
tibio-peroneal syndesmosis, which in turn correlates with the progressive instability
resulting from the mortise: type 44-A fractures are infra-syndesmotic injuries, type
44-B are trans-syndesmotic injuries, and 44-C correspond to supra-syndesmotic
fractures. Each of these types is further subdivided into groups according to certain
morphological characteristics associated with greater injury severity: types 44-A
and 44-B are subdivided into 3 groups according to whether the injury is only lateral
(44A1 or B1), whether there is associated medial injury (44A2 or B2), or whether
there is medial and posterior injury (44A3 or B3), while in type 44-C the subdivi-
sion is based on the pattern or location of the fibula fracture (simple: 44C1, wedge
or multifragmentary: 44C2, proximal: 44C3). In the description, certain “qualifiers”
associated with greater lesional complexity and therefore greater instability can also
be added, such as the presence of fracture of the anterolateral tubercle of Tillaux-
Chaput, avulsion fibular fracture of Wagstaffe-LeFort, rupture of the deltoid liga-
ment, or syndesmal instability (Fig. 2) [7].
For practical purposes, it is convenient to establish some relationships between
the two systems. Type 44-A or infrasindesmal fractures generally correspond to a
Types:
Fx of the fibula below the syndesmosis Fx of the fibula at the level of the Fx of the fibula above the
or infrasyndesmotic (A) syndesmosis or transindesmal (B) syndesmosis or suprasindesmal (C)
Groups:
Isolated With medial Isolated With medial Simple Wedge

lateral lesion lesion (2) lateral lesion lesion (2) fibular fracture or
(1) (1) fracture (1) multi- Proximal
With medial With medial fragmentary fibula
and posterior and posterior fibula (2) fracture (3)
lesion (3) lesion (3)
Fig. 2 AO-Orthopaedic Trauma Association classification of ankle fractures (2018).

Simplified version
supination-adduction mechanism, in which there is first a failure in tension of the

lateral complex generating an avulsion lesion of the peroneal malleolus (stage I). If
the inertia of the trauma continues, the vertex of the talus impacts the medial part of
the tibia causing a vertical fracture of the internal malleolus (stage II), to finally
produce a fracture of the posteromedial malleolus (stage III) which can be associ-
ated with osteochondral lesions by impaction. The type 44-B or trans-syndesmal
fractures, on the other hand, may correspond to two mechanisms. The most frequent
is that of external supination-rotation, in which there is first a failure in tension of
the anterior syndesmosis (stage I). If the energy of the trauma continues, a transyn-
desmal oblique fracture of the fibula is generated (stage II), a lesion of the posterior
syndesmosis or an avulsion fracture of the posterolateral malleolus (stage III), and
finally a transverse fracture of the medial malleolus or lesion of the deltoid ligament
(stage IV). The other mechanism involved is pronation-abduction, where first there
is medial failure of either the internal malleolus or the deltoid ligament (stage I).
Subsequently, there is a lesion of the anterior and posterior tibio-peroneal syndes-
mosis (stage II) and finally, in the third stage, a fracture in flexion of the lateral
malleolus with a transverse pattern and lateral comminution (stage III). Finally, the
type 44-C or suprasyndesmal fractures generally correspond to a high-energy exter-
nal pronation-rotation mechanism. The kinetics of this injury begin by tensing the
medial complex compromising the deltoid ligament or generating an avulsion frac-
ture of the medial malleolus (stage I), continue damaging the anterior capsule, then
the syndesmosis (stage II), pass through the interosseous membrane, and finally
produce the high fracture of the fibula above the syndesmosis that can even affect
the proximal third of the fibula (Maisonneuve fracture) (stage III). The mechanism
also causes injury to the posterior syndesmosis or fracture of the posterolateral mal-
leolus in most cases (80%) (stage IV), and although less frequently, osteochondral
lesions of the talar dome or lateral marginal fragmentation of the tibial plafond
(Fig. 3) [5–7].
AO-OTA 44 -A AO-OTA 44 -B AO-OTA 44 -C
III IV
II
III
III II
I
II III
I I
I II
IV
Lauge y Hansen Lauge y Hansen Lauge y Hansen

Lauge y Hansen
Supination– Pronation- Pronation–
Supination-adduction
external rotation abduction external rotation
Fig. 3 Correlation between the Lauge-Hansen and AO-OTA classification systems

4 Clinical and Imaging Diagnosis
From the clinical point of view, ankle fractures may present two different scenarios
according to the magnitude of the energy involved in the trauma of origin.
Injuries associated with a low or medium impact injury mechanism present a less
spectacular clinical picture similar to that of other traumatic injuries of the region,
with pain, swelling, and perimalleolar hematoma of different degrees and location
and some restriction of the active and passive range of motion of the ankle or subta-
lar joints (Fig. 4). This not so obvious picture implies the need to carry out a system-
atic evaluation of each bone and ligament structure potentially involved. On the
lateral side, the entire length of the fibula should be palpated because of the possibil-
ity of a fracture of the proximal portion of the fibula in the case of a Maisonneuve
injury. On the medial side, the presence of pain and hematoma over the bony promi-
nence of the internal malleolus may be suggestive of both a fracture of the internal
malleolus and a medial ligament injury, although it should be taken into account that
the deep bundle of the deltoid ligament is intra-articular and not accessible to palpa-
tion, so that a severe injury such as its rupture may be associated with little clinical
repercussion. The anterior syndesmosis, due to its more superficial location, is eas-
ily accessible on examination, unlike its deeper posterior component, which can be
compromised without producing major manifestations [8].
a b
Fig. 4 Ankle fracture of low energy due to domestic accident. (a) Rx. (b) Clinic medial side
a b
Fig. 5 Ankle fracture of high energy due to traffic accident. (a) Rx. (b) Clinical appearance
High-energy malleolar fractures are relatively frequently associated with a loss

of normal joint relations due to a major capsule-ligament injury. For this reason,
they usually present with severe deformity resulting from dislocation, dislocation
fracture, or severe displacement that jeopardizes local perfusion of the skin over the
bony prominences of the malleoli or directly compromises the soft tissue envelope
in the case of exposed injuries (Fig. 5) [8].
The initial diagnostic methodology in ankle fractures should include radio-
logical study in the two classic anteroposterior and lateral projections and a
mortise oblique with 15° internal rotation consisting of a true anteroposterior
projection taken in a plane parallel to the empirical intermalleolar axis. The
measurements that can be performed on them are multiple and include, on the
one hand, those that evaluate the length of the fibula such as: (1) the talo-crural
angle (Sarkisian, 1976) - which is obtained by drawing two tangent lines one to
the tibial plafond and the other to the ends of the two medial and lateral malle-
oli, its normal value being 83° +/− 4° or a difference with the contralateral not
greater than 12° -, (2) the bimalleolar angle (Rolfe, 1989) - which is obtained by
drawing two tangent lines one to the lateral cortex of the fibula and the other to
the ends of the two medial and lateral malleoli, its normal value being 78°
+/− 6° or a difference with the contralateral not greater than 12° -, and (3)
Weber’s circle - which is obtained by drawing a circle equivalent to a small coin
whose upper edge should pass flush to the lateral process of the astragalus and
the tip of the fibula indicating that there is no shortening of the lateral malleolus.
Some parameters that evaluate the degree of lateral displacement of the talus
within the mortise can also be considered in the measurement: the most wide-
spread is the medial clear space, distance that extends from the lateral face of
the medial malleolus to the medial face of the talar dome at 5 mm from the tibial
plafond and that should not be greater than 2 mm than that of the healthy side
(Fig. 6). Finally, indemnity or involvement of the syndesmosis can be observed
through two radiological markers of the distal tibio-fibular relationship: the
clear tibio-fibular space which corresponds to the distance between the posterior
tubercle of the tibia and the medial cortex of the fibula, whose normal value
should not exceed 6 mm; and the tibio-fibular overlap which corresponds to the
area of overlap of the anterior tubercle of the tibia over the fibula and which
should be maintained above 6 mm (Fig. 7) [9–11].
a b
76 77
㼻㼻 77
76 㼻
㼻
Fig. 6 Comparative radiological measurements to define conduct in unimalleolar fracture

AO-OTA 44B. (a) Healthy side. (b) Injured side. In red: talo-crural angle. In yellow: bimalleolar
angle. In light blue: medial clear space. In green; Weber's circle
a b c
b a a b
b>a a>b
b a
Fig. 7 Radiological markers of the distal tibio-fibular relationship in AO-OTA 44C fracture. (a)
Healthy side. (b) Injured side. Note the increased tibio-fibular clear space (a) and decreased tibio-
fibular overlap (b) on the injured side with respect to the healthy side. (c) Schematic representation
of both measurements
Dynamic radiographs with manual stress in external rotation, with gravitational

stress and under body weight load (considered below), may be useful in the case of
isolated lesions of the lateral malleolus to define the definitive conservative or surgi-
cal therapeutic approach [12–15].
Computed axial tomography has now become a mandatory study for preopera-
tive planning in the setting of complex ankle fractures. Thin section slices in the 3
planes of space provide valuable complementary information usually not objectified
by simple radiology, including among others the relationship of the fibula to the
tibia at the level of the syndesmosis in the transverse plane, the fit of the talus within
the mortise, or the extension and morphology of the posterior component in the case
of injuries of the three malleoli. The latest generation software also makes it possi-
ble to obtain three-dimensional (3D) reconstructions that provide representative
images that can even be visualized dynamically, which facilitates their interpreta-
tion and optimizes the planning of surgical tactics (Fig. 8) [16].
Nuclear magnetic resonance is not a routine study, although it has two clear indi-
cations: the diagnosis of deltoid ligament injury in patients with AO-OTA 44B or C
lesions and clinical signs suspicious of medial injury, and the confirmation of osteo-
chondral lesions of the talar dome in high-energy AO-OTA 44C fractures, whose
finding in Raikin zones 1 and 4 is not uncommon [17].
a b
Fig. 8 Standard imaging study of a complex ankle fracture with posterior component. (a) CXR in
both projections. (b) CT in the three planes plus 3D reconstruction
5 Initial Management
The presence of a high-energy injury with joint dislocation implies an active man-
agement in the emergency, where the primary objective is reduction to limit second-
ary soft tissue lesion induced by regional edema. Once achieved, it is advisable to
proceed immediately with joint stabilization. A splint guarantees effective preserva-
tion of the reduction obtained, which together with the elevation of the affected limb
considerably reduces the development of skin complications and provides the best
conditions for possible surgery (Fig. 9).
Severe edema, blisters, or superficial or deep abrasion or open ankle fractures are
treated acutely similarly as in tibial pylon fractures, by means of external fixation.
The most commonly used configuration is the unilateral modular frame with two
pins in the medial aspect of the tibia, one in the posterior tuberosity of the calcaneus
and one in the first cuneiform or base of the first metatarsal (Fig. 10) [8]. It is of
utmost importance to discuss with the patient the complication risk. Complication
for young patients is mainly osteoarthritis (treated in another chapter), and for older
a b c
Fig. 9 Initial management of an ankle fracture in a 57-year-old male patient. (a) X-ray in both
projections. (b) Clinical pre- and post-reduction. (c) Post-reduction x-ray control
patients, is infection, wound complication, and fixation failure [1–3]. As in all oper-
ated patients, the risk of deep venous thrombosis is not negligible.
6 Definitive Management
Decision making regarding the definitive management of ankle fractures involves

the need to accurately assess the structural integrity and stability of the tibio-
peroneo-talar mortise.
Those injuries that do not affect both aspects can be managed conservatively.
This includes most isolated infrasyndesmal fractures (44 A1) and stable trans-
syndesmal fractures (44 B1).
Regarding the latter, an adequate radiographic interpretation considering the
objective measurements mentioned above in the imaging diagnosis section and
comparing them with those of the healthy contralateral side is key to define the
a b c
Fig. 10 Initial management of an open ankle fracture in a 49-year-old female patient. (a)
Anteroposterior X-ray. (b) Pre-reduction picture (c) Post-reduction control X-ray
best therapeutic modality. In this sense, an isolated displacement of the fibula

fracture (regardless of the amount in millimeters) is not an absolute indication for
surgery as long as the mortise remains congruent and there is no evident increase
in the medial clear space indicating medial ankle instability [18]. In case of doubt
and to confirm or rule out medial involvement, it is advisable to add to the diag-
nostic algorithm one of the following dynamic studies in the anterior-posterior
projection: (1) manual stress radiography in external rotation - which is obtained
by stabilizing the tibia with one hand with the ankle in neutral position and 15° of
internal rotation, while with the other hand a force is applied to the forefoot in
external rotation -, (2) gravity stress radiography - which is obtained with the hori-
zontal beam and the patient in lateral decubitus on the injured side with an
enhancement under the leg and limb in 10° to 15° of internal rotation -, and (3)
radiography under body weight loading. The absence of medial diastasis greater
than 2 mm with respect to the healthy contralateral and the correct centering of the
talus in the mortise with any of these three options rule out medial instability and
joint involvement and incline the decision to orthopedic treatment (Fig. 11)
[12–15].
On the other hand, unstable trans-syndesmal fractures (44 B1) characterized by
2 mm or more lateral displacement of the talus in the mortise or shortening of the
fibula by more than 3 mm in static or dynamic comparative radiographs should be
treated surgically since they cause a significant decrease in the tibiotalar contact
a b
Fig. 11 Use of weight bearing radiography. (a) Unloaded X-ray. (b) Loaded Rx. Note in the sec-
ond one the appearance of medial diastasis and the loss of centering of the talus in the mortise. Sign
of fracture instability
surface (close to 40%) and an increase of up to four times in the loads supported by
the talus during walking, which inevitably leads to early degenerative arthritis [19].
In this situation, strict adherence to the principles of management of any joint injury
including achieving anatomical reduction, achieving stable internal fixation with
minimal soft tissue impingement, and allowing early mobility is key to success.
Similarly, the presence of a medial or posterior malleolus fracture should tip the
balance toward surgical resolution, with a few exceptions related to patient factors
such as nonambulatory status, severely decreased function, or high surgical risk.
6.1 Fractures of the Medial Malleolus
Fractures of the medial malleolus have basically two mechanisms: the AO-OTA
44B and 44C injuries (trans and suprasyndesmal) occur by failure of the medial
complex and bony avulsion by traction of the deltoid ligament; while the AO-OTA
44A (infrasyndesmal) originates in a mechanism of impaction of the internal vertex
of the astragalus that produces higher and generally vertical patterns, associated in
a high percentage with osteochondral lesions [8].
Their treatment is eminently surgical by open reduction and internal fixation,
since the rate of consolidation disorders can reach 15% due to the inclusion of peri-
osteum within the fracture line [8, 20, 21].
6.2 Fractures of the Posterior Malleolus
Several authors have shown that the presence of a posterior malleolar component in
an ankle fracture can lead to poor functional outcomes [22–24]. For this reason, the
management of these injuries is the subject of multiple investigations and continues
to be controversial, and there is still no agreement on the factors that determine the
best treatment. The current consensus is to consider not only the size, but also the
three-dimensional morphology of the posterior component, making computed axial
tomography the study of choice for its characterization, decision making, and plan-
ning of the surgical strategy.
Of the different tomographic classifications, those devised by Haraguchi (2006)
[25] and Bartonicek and Rammelt (2015) [26] are the most widespread. The first
describes three fracture patterns: a posterolateral oblique one that determines a
wedge or triangular fragment involving the posterolateral corner of the tibial pla-
fond (type I, 67% of cases); a transverse one with medial extension extending from
the fibular incisura of the tibia to the medial malleolus (type II, 19% of cases); and
a marginal one that determines one or more small fragments affecting only the
posterior rim of the tibial plafond (type III, 14% of cases). Bartonicek and Rammelt
add one more variant and divide these lesions into four types morphologically
similar to those of Haraguchi’s classification: type I (8% of cases) is an extrainci-
sural lesion; type II (52% of cases) involves a posterolateral fragment involving
the sindesmal incisura; type III (28% of cases) is a fragment with posteromedial
extension; and type IV corresponds to a large triangular posterolateral fragment
(Fig. 12).
Beyond these descriptions, the determining factor that guides the anatomical
reduction and stable fixation of the posterior malleolar fragment is the involvement
of the sindesmal incisura. The restitution of its normal morphology allows the
Type I: extraincisural Type II: Posterolateral Type III: fragment Type IV:
fragment that with posteromedial posterolateral
compromises the extension massive triangular
incisura fibularis fragment
Fig. 12 Bartonicek and Rammelt classification of posterior malleolus fractures (2015)

adequate “fitting” of the fibula inside it, which guarantees the reestablishment of the
width of the mortise and the correct centering of the talus inside it. It also restores
the length and “working length” of the posterior-inferior tibio-fibular ligament,
restoring stability to the distal tibio-fibular joint and making trans-syndesmal fixa-
tion unnecessary [26–28].
According to the authors, the posterior malleolar fragment is the reference from
which to perform the reconstruction of a complex ankle fracture and should always
be visualized directly to ensure its anatomical reduction and stable fixation, which
is not achieved with percutaneous methods [29]. This determines the position of the
patient at the time of surgery, the selection of the surgical approach, and the reduc-
tion and fixation tactics. The protocol in Fig. 13 based on a tomographic section in
the axial plane at 1 cm from the articular surface of the distal tibia in which each of
the components of the lesion are identified (Fig. 14) can be of help [29]. In this
scheme, the posterior malleolar component is prioritized and subdivided into A1,
A2, and A3 according to whether the involvement is posterolateral, posteromedial,
or posterolateral/posteromedial, respectively. The recommended surgical approaches
are the posterolateral (PL) in the case of A1 lesions, the posteromedial (PM) and
medial posteromedial (MPM) in A2 lesions, and the modified posteromedial
(PMMf) in A3 lesions with involvement of both posterior columns. The need for
other approaches will depend on the number and location of the lesions associated
Fig. 13 Surgical strategy protocol for fractures involving the posterior malleolus
Fig. 14 Axial CT scan at

1 cm of the articular Posterior maleolus: A
surface of the distal tibia B D A1=posterolateral column
where each of the D A2=posteromedial column
components of an ankle A3=both
C
fracture associated with A2 A1 Medial malleolus: B
posterior injury is
identified in capital letters Lateral malleolus: C
Chaput y/o Wagstaffe: D
A3
with the posterior component, taking into account that the posterolateral approach
can also resolve the lateral malleolar component (identified with the letter C) and
the modified posteromedial approach can fix a medial malleolar lesion (identified
with the letter B).
6.3 Syndesmosis Involvement
The distal tibio-fibular syndesmosis consists of three stabilizing elements: the ante-
rior-inferior tibio-fibular ligament (LTFAI), the posterior-inferior tibio-fibular liga-
ment (LTFPI), and the interosseous tibio-fibular ligament (LTFI). The strongest and
most resistant is the interosseous, since it is the one with the largest insertion area
compared to the other two, although the one that contributes most to overall syndes-
mal stability is the anterior-inferior [30, 31].
It is accepted that for an ankle fracture to be associated with syndesmotic insta-
bility, there must be more than one of these three ligaments injured or insufficient,
a situation extremely infrequent to be observed in infrasyndesmal AO-OTA 44A
fractures. In trans-syndesmal AO-OTA 44B injuries, on the other hand, the probabil-
ity is higher, which is why after the osteosynthesis of all the components of the
fracture is completed, it is mandatory to perform intraoperative tests to identify or
rule it out. Suprasyndesmal AO-OTA 44C fractures show the highest rate of syndes-
motic instability, especially if the fracture line of the fibula begins more than 4.5 cm
from the tibial plateau and if there is associated medial ligament injury. In this con-
text, the sequence is the same as in lower injuries: osteosynthesis of all bony com-
ponents is completed and syndesmal stability is assessed before the end of surgery
[32, 33].
The most widespread intraoperative tests to assess the indemnity or compromise
of the syndesmosis in the coronal and/or rotational plane are two. The external rota-
tion stress maneuver under fluoroscopy is performed by stabilizing the tibia with one
hand while applying an external rotation force to the foot with the other hand, evalu-
ating the medial tibiotalar clear space: it is considered positive if the latter is greater
than 5 mm. The Heim/Cotton or “hook test” consists of lateral traction of the lateral
malleolus with a hook-shaped instrument while keeping the tibia stabilized: it is
a b
no stress
with stress
Fig. 15 Intraoperative tests for evaluation of syndesmal stability. (a) Heim/Cotton test. (b)
External rotation stress maneuver
considered positive if more than 2 mm of lateral movement of the fibula is observed

under direct vision (Fig. 15). Both have excellent interobserver agreement and spec-
ificity, although their sensitivity is low, which is why they are not absolutely reliable.
Likewise, the possibility of instability in the sagittal plane should also be consid-
ered, which can be observed by moving the fibula with the thumb and index finger
backwards and forwards outside its usual location in the tibial incisura [33, 34].
7.1 Patient Positioning
The most frequently used position for surgical fixation of an ankle fracture is supine
decubitus, with the affected limb free in the surgical field and tourniquet on the
thigh. It is convenient to use a sandbag under the ipsilateral buttock to abolish the
rotation of the injured limb as well as to place the opposite limb in a position that
does not hinder the access to the medial side and the execution of the lateral projec-
tions with the image intensifier.
In case a posterior fixation is planned, the prone position should be used, either as
the only and definitive position during the whole surgical procedure or changing to
supine if there is an anterior component whose fixation requires it. As an alternative in
this situation, an intermediate positioning with a 45° tilt on the healthy side or a frankly
lateral decubitus can be used in such a way as to simultaneously access both regions [20].
7.2 Instrumentation
The necessary instrumentation consists of a basic set of reduction forceps of ade-

quate size and different morphology including at least three elements: the Weber
point clamp - useful for manipulating bone fragments in different planes with mini-
mal periosteal damage; the serrated or Spanish reduction clamp - which allows bet-
ter grasping in thin cortical bones such as the fibula; and the Verbrügge self-centering
bone grasping forceps - useful for aligning a plate to the bone (Fig. 16).
Regarding osteosynthesis systems, tubular plates of small 3.5 mm fragments
preferably in their locked screw version, allow to handle most of the lesion patterns
of the lateral and posterior malleoli providing sufficient stability with low soft tissue
impact. There are new designs of anatomical preformed plates for the fibula that
allow a combination of screws of different diameters (2.4, 2.7 and 3.5 mm) and offer
more holes in different directions in the distal part, which makes them more suitable
Fig. 16 Instrumentation in
ankle fractures. (a) Weber a
spike clamp in internal
malleolus fracture. (b)
Reduction clamp in fibula
fracture
b
for the fixation of small apical segments or multifragmentary patterns. 4.0 mm par-
tial thread screws and tension bands with 1–1.8 mm wires are the most commonly
used option for stabilization of the medial malleolus [21].
7.3 Surgical Approaches
The ankle region can be approached directly around its entire circumference.
The classic surgical approach to the fibula is through a simple direct lateral
approach with no specific hazards. The only structure at risk when tracing it more
proximally for the fixation of supra-syndesmotic patterns is the lateral branch of the
superficial peroneal nerve, for which reason it is convenient to dissect and isolate it
since its lesion can lead to painful neuromas associated with important dysesthesia
in the dorsum of the foot (Fig. 17) [21, 35].
Fig. 17 Direct lateral

a
approach to the fibula. (a)
Schematic representation.
In red dotted line: the two
possible incisions. (b)
Intraoperative view
b
The internal tibial malleolus is accessed through a direct medial approach, usu-
ally central and curved, extending from its most proximal end to 2 cm distal to its
apex, whose structures at risk are the internal saphenous vein and nerve located
anteriorly (Fig. 18) [21, 35].
The posterior malleolus can be accessed from either lateral or medial side. On
the lateral side, the option most often cited in the literature is the posterolateral
approach (PL) popularized by Tornetta III and Sanders. The approach, a lateral
para-achilles incision, is performed with the patient in prone (Fig. 19) or lateral
Fig. 18 Schematic
representation of the direct
medial approach to the
internal malleolus (in red
dotted line)
a b
Fig. 19 Posterolateral approach to the distal tibia. (a) Patient positioning. (b) Skin incision. Note
its lateral para-Achilles location
a b
Fig. 20 Posterolateral approach of distal tibia. (a) Schematic representation. (b) Identification of
the peroneal fascia. (c) Flexor hallux fascia retracted medially and access to the posterolateral
quadrant
position and begins with an incision made midway between the external border of
the Achilles tendon and the posterior border of the fibula. The sural nerve is dis-
sected and protected and the peroneal fascia is identified, and then the fascia of the
flexor hallucis longus muscle is incised, which is mobilized medially, directly
accessing the posterolateral quadrant of the distal tibia (Fig. 20) [21, 35, 36].
Although it is the least technically complex approach and also allows simultaneous
access to the distal fibula, it should be taken into account that it is the one that pro-
vides the least amount of exposure of the posterior malleolus, with a visualization
area of no more than 40% of its surface [36, 37].
On the medial side - where the deep plane is more complex anatomically as it
corresponds to the fascia that covers from inside to outside the posterior tibial ten-
don, the flexor digitorum longus, the posterior tibial vasculonervous bundle, and the
flexor hallucis longus - the range of possibilities for accessing the posterior malleo-
lus is much more varied and includes at least three options of medial para-achilles
incisions that should be performed with the patient in prone position and a more
medial option that can be performed in supine position.
Among the first, Assal et al. [36] describe a posteromedial access (PM) between
the posterior tibial and flexor digitorum longus medially and the muscle belly of the
flexor hallucis longus laterally, which provides excellent visualization of the medial
2/3 of the posterior malleolus but does not allow access to its lateral third (Fig. 21).
a b
Fig. 21 Posteromedial approach of distal tibia (Assal et al). (a) Schematic representation. (b) Skin
incision. (c) Posterior tibial and flexor digitorum longus remain on the medial side
The same authors describe a modified posteromedial access (PMMf) that uses the
same intertendinous plane, but dissects the neurovascular bundle to its full extent,
allowing it to be mobilized forward along with the tendons of the tibialis posterior
and flexor digitorum longus avoiding its traction or compression and providing
visual access to 90% of the malleolus (Fig. 22). Philpott et al. [37] describe another
medial para-achilles variant of posteromedial access by incising the fascia over the
flexor hallucis longus well laterally, elevating it off the posterior aspect of the tibia
from lateral to medial, and retracting it internally along with the rest of the elements
of the retromalleolar slide. The approach is thus placed outside the flexor hallucis
longus, which can be retracted medially protecting the neurovascular bundle (green
dotted line in Fig. 22).
The most medial option for access to the posterior malleolus is the medial pos-
teromedial approach (MPM). The slightly curved “J” incision following the poste-
rior tibial tendon begins proximal to the metaphyseal extension of the fragment and
wraps posteriorly around the medial malleolus. The flexor retinaculum and poste-
rior tibial tendon sheath are incised and the dissection is completed posterolaterally
and medially until the best possible exposure of the fracture is achieved. It is a par-
ticularly useful variant in patterns with a large posteromedial fragment of medial
vertex and can be performed in the supine position (Fig. 23) with external rotation
a b
Fig. 22 Modified posteromedial approach of distal tibia (Assal et al.). (a) Schematic representa-
tion. (b) Skin incision. (c) Posterior tibial bundle dissected and reclined medially entering the
posteromedial quadrant. The green dotted arrow corresponds to the variant of Philpott et al.
of the extremity and knee flexion. This approach provides excellent access to the
central and medial posterior malleolus. Access to a single small posterolateral
(Volkmann) component is somewhat more difficult (although possible) [37, 38].
Finally, the anterolateral region of the distal tibia corresponding to the Tillaux-
Chaput tubercle or the anterior rim of the distal fibula corresponding to the Wagstaffe
tubercle can also be approached directly through a straight incision in line with the
4th MTT, developing the deep plane between the anterior and lateral or peroneal
compartment [21].
7.4 Specific Surgical Strategies
7.4.1 Infrasyndesmal Fractures (AO 44A)
Infrasyndesmal fractures of the fibula (exceptionally surgical) can be fixed with one
of the following methods of osteosynthesis: “8” cerclage with 1.8 mm K-pins and
1.2 mm wire, 3.5 mm tubular plate with distal “hook” modification, and anatomi-
cally locked compressive hook plate (Fig. 24).
b e
a
c d
Fig. 23 Medial posteromedial approach (MPM). (a) Schematic representation. (b) Skin incision.
(c) Intraoperative view of the medial malleolar (MM) and posterior malleolar (MP) fragments. (d)
Medial and posterior plates positioned through this approach. (e) Fluoroscopy of image (d)
a b c
Fig. 24 Fixation alternatives in infrasintemal fibula fractures AO-OTA 44A. (a) Cerclage in figure
of 8. (b) Distal tubular hook plate. (c) Compression locked anatomical hook plate
In type 44A2 or 44A3 fractures with medial or posteromedial association, it is

important to start first with reduction and stabilization of the medial or posterome-
dial fragments to avoid varus or valgus reduction of the fibula [20].
7.4.2 Transindesmal Fractures (AO 44B)
Simple transindesmal fractures of the fibula are the paradigm of anatomical reduc-
tion and rigid fixation through a 3.5 mm screw in compression and a tubular plate to
neutralize the compressive force generated by the screw. The surgical technique
includes the carving of a smooth canal with a 3.5 mm drill bit perpendicular to the
fracture line in the nearest cortex and the placement of a 2.5 mm drill bit guide
through it, which allows drilling the opposite cortex with a drill bit of the same
diameter. After measuring the length of the canal, a 3.5 mm tap is passed and a
3.5 mm cortical screw is placed. Finally, the tubular plate is placed in neutralization
function, with at least two 3.5 mm proximal cortex screws and two 4 mm distal full
thread cancellous screws (Fig. 25) [20].
Fig. 25 Classic fixation of a transindesmal fibula fracture AO-OTA 44B. (a) Placement of 3.5 mm
cortical screw in compression. (b) Placement of tubular plate in neutralization function
a b c d e
Fig. 26 Schematic representation of an anti-slip posterior fibular plate. (a) Hole 2.5 mm at frac-
ture apex. (b) Pre-molded plate with posterior convexity. (c) Plate application on the posterior
cortex. (d) Placement of screw through previous hole. (e) Finalized fixation
Alternatively, a tubular plate can be used for anti-slip function. For this, the inci-
sion should be slightly more dorsal, centered on the posterior edge of the fibula. A
hole is first made in the fracture apex in the proximal fragment with a 2.5 mm drill
bit, the tubular plate is premolded with posterior convexity, and it is applied on the
posterior cortex adjusting the screw placed through the previously drilled hole,
which produces the reduction by implant interference and compression of the ante-
rior cortex. Finally, the fixation is completed with proximal screws, and if neces-
sary, a distal compression screw placed through the plate (Fig. 26). The advantages
of using this type of configuration include a bicortical fixation in good quality bone
along the entire length, a more biological technique since the fracture is reduced
with minimal manipulation of the fragments respecting the biology, and the lower
probability of joint invasion of the distal screws since they are placed in a postero-
anterior direction. The rate of peroneal synovitis is low as long as implant place-
ment is avoided beyond the junction of the proximal 1/3 with the distal 2/3 of the
peroneal malleolus, where the pulley that contains them begins [20].
7.4.3 Suprasyndesmal Fractures (AO 44C)
Suprasyndesmal lesions can be differentiated into two large groups according to the
morphology and location of the lateral lesion: low (Dupuytren’s lesion - AO-OTA
44C1 and C2) or high (Maisonneuve’s lesion - AO-OTA 44C3) (Fig. 27). They are
frequently associated with some degree of medial involvement, either ligamentous
(50% of cases) (AO-OTA 44C1.1, C2.1 and C3.1) or osseous (AO-OTA 44C1.2,
C2.2 and C3.2) (37% of cases), and often with fracture of the posterolateral malleo-
lus (80% of cases) (AO-OTA 44C1.3, C2.3 and C3.3) [7].
The treatment of medial ligament injury is controversial [39–41]. The authors’
preference is for direct open repair, if a medial clear space greater than 4 mm is
observed on initial radiology or intraoperative stress, using metal fixations anchored
a b
Fig. 27 The two groups of suprasyndesmosis fibular fractures: (a) low fracture (Dupuytren); (b)
high fracture (Maissoneuve)
to the malleolus or talar neck (Fig. 28). Other management trends include repair
with arthroscopic technique or no repair in the event that after stabilization of the
fibula and fixation of the syndesmosis, the medial clear space appears normalized
on the radioscopic image.
The treatment of the medial or posterior bony component offers less discussion
since the current trend is towards open reduction and stable internal fixation of both
associated injuries, either through wire locks, screws in compression, or posterior
plates as previously mentioned [26, 32, 42].
Regarding the fibula fracture, the authors’ preference is to perform rigid stabili-
zation of any injury that lies within the distal 2/3 of its anatomy. For this purpose, a
tubular plate is recommended in a self-compressive or neutralizing function in
AO-OTA 44C1 fractures or in a bridging function in the more complex patterns
characteristic of AO-OTA 44C2, leaving at its distal end a free hole to place a tran-
syndesmal tricortical screw to protect the syndesmosis if necessary (Fig. 29) or
making the reduction and direct open syndesmal fixation by a second distal approach
in the case of lesions of the middle 1/3. In the case of high AO-OTA 44C3 fractures
with a localized pattern in the proximal 1/3 (Maissoneuve fracture), the most wide-
spread tactic involves direct open reduction through a lateral approach at the level
of the syndesmosis without fibular osteosynthesis (Fig. 30). Syndesmotic stabiliza-
tion can be performed with rigid or flexible fixation methods, with the first option
a c
Fig. 28 Medial ligament repair technique preferred by the authors. (a) Placement of metal fixation
in the talar neck. (b) Passage of sutures through tunnels in internal malleolus. (c) Postoperative X-ray
being the most commonly used. The preference is for two 3.5 mm cortical screws of
full thread, taking 3 cortices each (tricortical screws), depending on position and not
in compression, parallel, the most distal one at 1.5 cm from the tibial plateau and the
proximal one at no more than 2.5 cm. The transyndesmal location is due to the fact
that technically they are easier to place, it has been demonstrated that they do not
produce articular synostosis, and they allow an earlier loading with less risk of rup-
ture. Alternatively, they can be placed through a tubular plate with 2 holes that col-
laborate in the resistance of the lateral cortex of the fibula. The most widespread
tendency is to remove them after 8 to 10 postoperative weeks, although there is the
possibility of leaving them and waiting for their osteolysis or rupture without gen-
erating any functional inconvenience. Another option for stabilization of the syn-
desmosis which is becoming more and more widespread and apparently more
physiological are the flexible button/suture type systems, which are associated
according to different series with better or equal functional results compared to
screws with a lower rate of hardware removal (Fig. 31) [43–46].
a
b
Fig. 29 Same patient in Fig. 27a stabilized with tubular plate in self-compressive function and
3.5 mm transindesmal screw. (a) Immediate postoperative X-ray. (b) Postoperative X-ray after
syndesmotic screw removal
7.4.4 Fractures of the Medial Malleolus
The fixation protocol used by the authors depends on the morphology of the frac-
ture, dividing the medial malleolus into 3 zones determined by the apex of the tibial
axilla which allows planning the type of osteosynthesis to be used: type 1 fractures
are located below the axilla and the suggested fixation system is the “in 8” wire
cerclage; type 2 fractures are located at the level of the axilla and the recommended
fixation is a 4 mm smooth shank, compressive cancellous screw associated with a
1.25 mm antirotational pin; while type 3 fractures can be differentiated into a high
a b
Fig. 30 Same patient as in Fig. 27b. (a) Open direct reduction of the syndesmosis. (b) Radioscopic
view of fixation with two cannulated 3.5 mm screws
a b
Fig. 31 Other transindesmal stabilization options in AO-OTA 44C3 fractures. (a) Two-hole tubu-
lar plate. (b) Flexible button-suture type system
a b
c d
Fig. 32 Different fixation options for medial malleolus fractures. (a) Figure of 8 cerclage (b)
4.0 mm screw + anti-rotation pin. (c) Two 4.0 mm screws. (d) Anti-slip medial plate + screw in
compression
avulsion pattern - where the preferred technique is two parallel 4 mm smooth shank
screws - and a vertical ascending impaction fracture line - where a tubular plate in
anti-slip function associated with a 4 mm smooth shank screw compressive through
the same plate is indicated (Fig. 32).
7.4.5 Fractures of the Posterior Malleolus
A1 injuries correspond to a posterolateral malleolar fragment. In this case, the rec-

ommended approach is the posterolateral approach, which also allows resolution of
the fibula fracture. If there is a bony lesion of the internal malleolus, the medial
approach should be used (Figs. 33 and 34).
A2 lesions correspond to a posteromedial malleolar fragment. In this case, the
recommended approach is the posteromedial approach or a medial posteromedial
approach. If there is a fibula fracture, a lateral approach should be added (Figs. 35
and 36).
Fig. 33 (a) Schematic representation of A1 + B + C lesion. (b) X-ray and CT
b c
Fig. 34 (a) Osteosynthesis of postero-lateral malleolus with tubular anti-slip plate and fibula with
plate in the same function. (b) Medial approach and stabilization with two 4 mm diameter cancel-
lous screws (patient in prone position). (c) Postoperative control
Fig. 35 (a) Schematic representation of A2 + C lesion. (b) X-ray and CT
b c
Fig. 36 (a) Posteromedial column osteosynthesis by Assal posteromedial approach: 3.5 cortical
compression screw and tubular plate. (b) Fixation of avulsive fibula fracture with 4 mm cancellous
screw and antirotational pin. (c) Postoperative control
Fig. 37 (a) Schematic representation of lesion A3 + B + C. (b) X-ray and CT
A3 lesions correspond to a posterolateral malleolar fragment with posteromedial

extension, i.e., there is involvement of both posterior columns. In this case, the rec-
ommended approach is the modified posteromedial approach, which also allows the
osteosynthesis of the internal malleolus by extending it distally and retracting the
posterior tibial bundle and the common flexor tendon of the toes outwards. If there
is a fibula fracture, a posterolateral approach must also be used (Figs. 37 and 38),
although if the fracture is comminuted or has a suprasyndesmal Dupuytren type pat-
tern (variants not contemplated in the protocol), a classic lateral approach to the
fibula can be combined using plates as a bridge (Figs. 39 and 40).
7.4.6 Quatrimalleolar Fractures
The term quatrimalleolar fracture, defined by Rammelt et al., refers to a trimalleolar

injury where there is additional involvement of the anterolateral tubercle of the tibia
(Chaput’s tubercle). The same authors describe a “quatrimalleolar equivalent”
injury that corresponds to a trimalleolar fracture where there is involvement of the
anterior rim of the distal fibula (Wagstaffe’s tubercle) [47]. Both injury patterns
would correspond to an A + B + C + D injury (Fig. 41).
The current management trend involves open anatomical reduction and stable
internal fixation of each of the lesional components as long as the size of the
a b
c d
Fig. 38 (a) Osteosynthesis with anti-slip plate of both columns through the modified posterome-
dial approach. (b) Intraoperative control after fixation of the lateral malleolus through posterolat-
eral approach with anti-slip plate. (c) Osteosynthesis of the medial malleolus through lateral
window retracting posterior tibial and common flexor digitorum package outward. (d)
Postoperative control
tuberosity fragment is greater than 6 mm. Stabilization of all the involved columns
restores the anatomical structure of the ankle mortise, ensuring adequate congru-
ence of the distal tibio-peroneal joint, which also recovers its stability without the
need for additional trans-syndesmal fixation techniques [47].
The approach of choice for osteosynthesis of the quatrimalleolar component,
whether tibial or peroneal, is the anterolateral approach and is performed as the last
step of surgery after having completed the synthesis of the other fracture compo-
nents. Regarding the operative tactic, there are two possibilities: either the patient’s
decubitus is changed from prone to supine (Fig. 42a–d) or the knee is flexed to 90
degrees maintaining the prone position and working with inverted anatomical refer-
ences (Fig. 42e, f).
7.4.7 Syndesmosis
Regarding its management, direct open reduction of the syndesmosis is the tech-
nique of choice since the most important prognostic factor is the anatomical posi-
tioning of the fibula within the incisura. As mentioned above in the section on the
Fig. 39 (a) Schematic representation of lesion A3 + B + C. (b) X-ray and CT
a b
c d e
Fig. 40 (a) Osteosynthesis of both posterior columns with anti-slip plates. (b) Osteosynthesis of
the medial malleolus. (c) Radioscopic control. (d) Classic lateral approach and fixation with tubu-
lar plate associated with wire cerclage for Wagstaffe fragment. (e) Postoperative X-ray and CT scan
Fig. 41 Quatrimalleolar lesions (A+B+C+D). (a) Schematic representation and CT scan of

Chaput lesion. (b) Schematic representation and CT of Wagstaffe lesion
treatment of supra-syndesmotic fractures, 3.5 mm screws are the preferred method

of fixation, although flexible button/suture systems are another increasingly accepted
option [33].
Alternatively, arthroscopy has emerged as a suitable method for the identification
and treatment of syndesmotic instability. Some series report a diagnostic accuracy
rate of 100% including other common associations such as deep bundle ruptures of
the deltoid ligament or osteochondral lesions of the talus or tibia [48]. It also allows
percutaneous reduction and stabilization with less impact on the soft tissues and the
same accuracy as the open technique (Fig. 43) [33, 49, 50].
a b c d
e f g
Fig. 42 Two fixation options in quatrimalleolar lesions. (a–d) After prone, change to supine position.
(e–g) using 90 degree knee flexion, keeping prone position, working with an “inverted anatomy”
8 Postoperative Management
The postoperative protocol in ankle fractures implies the possibility of early

mobility except in two specific situations: (1) association with medial ligamentous
injury, in which case it is protected with three weeks of splint immobilization; (2)
use of posterior approach routes, in which case it is protected with splinting at 90
degrees for two weeks to avoid antalgic equinus due to manipulation of the flexor
hallucis longus. The mobilization of the ankle if the patient does it in a very
aggressive way could produce a dehiscence of the operative wound, so it must be
controlled.
The unloading of the body weight is on demand according to the patient’s symp-
tomatology, although in the case of using rigid fixation systems for syndesmal sta-
bilization and if its removal is planned, the load is restricted to no more than 50%
during the first 8 weeks.
a b
c d
Fig. 43 Arthroscopic treatment of syndesmosis lesion in Maissoneuve fracture. (a) Identification

of distal tibioperoneal instability. (b) Control reduction of the fibula at the incisura. (c) Passage of
flexible fixation. (d) Radioscopic control
9 Complications
The complications can be separated into nonoperative and operative complications.

Regarding the former, the most frequent are muscle atrophy, cartilage degeneration,
blisters, deep vein thrombosis (and pulmonary embolism), malunion, nonunion,
joint stiffness (mainly dorsiflexion), and persistent pain [1–3, 51]. Among the latter,
the most frequent are soft tissue necrosis-wound dehiscence, infection, delayed or
nonunion, malunion, joint stiffness, muscle atrophy, complex regional pain syn-
drome type 1, among others.
Infection rates (deep infection) in patients undergoing open reduction and inter-
nal fixation range from 1% to 8%. Predisposing factors include open fractures, dia-
betes mellitus, high-energy trauma, fractures, compromised soft tissue, and
alcoholism. For operated ankle fractures which present with infection, debridement
should be performed, and cultures obtained. Hardware should be removed as
well [51].
Regarding joint stiffness, regional pain syndrome, weakness, and swelling, rapid
mobilization and early weight bearing decrease their severity and occurrence. For a
stable fracture, immediate weight bearing can be allowed. Use of a removable
walker boot is recommended for 3–4 weeks, and then exchanged by an ankle ortho-
sis. For operated ankle fractures, use of a walker boot is recommended for 6 weeks,
with progressive weight bearing starting at 4 weeks postoperatively if a posterior
and/or medial malleolus was operated. If only a lateral malleolus was operated,
immediate weight bearing can be allowed postoperatively. Postoperative osteoar-
thritis can occur as high as in 70% of ankle fractures after even 20 years [51, 52].
Recognized risk fractures for arthrosis are joint damage, malunited fibular fracture
(valgus, shortening), and ligamentous damage leading to joint instability [52, 53].
Conflicts of Interest The authors have no relationship with any commercial company that has a
direct financial interest in the subject or materials discussed in this article or that manufactures
products for the market.
References
1. Court-Brown CM, Caesar B. Epidemiology of adult fractures: a review. Injury.

2006;37(8):691–7.
2. Monteagudo M. Mecánica clínica y terapéutica pie y tobillo. Madrid; 2010.
3. Hamilton WC. Traumatic disorders of the ankle. New York: Springer-Verlag; 1984.
4. Viladot VA. Anatomía funcional y biomecánica del tobillo y el pie. Rev Esp Reumatol.
2003;30(9):469–77.
5. Lauge-Hansen N. Fractures of the ankle. Analytic historic survey as basis of new experimental
roentgenologic and clinical investigations. Arch Surg. 1948;56:259.
6. Lauge-Hansen N. Fractures of the ankle. II. Combined experimental-surgical and experimental-
roentgenologic investigation. Arch Surg. 1950;60:957.
7. Meinberg E, Agel J, Roberts C, et al. Fracture and dislocation classification compen-
dium—2018. J Orthop Trauma. 2018;32(Suppl 1):S1–S10.
8. Carr JB. Malleolar fractures and soft tissue injuries of the ankle. In: Browner BD, edi-
tor. Skeletal trauma - basic science, management and reconstruction. 3rd ed. Philadelphia:
Saunders; 2003. p. 2307–74.
9. Perera A, Myerson M. Surgical techniques for the reconstruction of malunited ankle fractures.
10. Mitchell MJ, Ho C, Howard BA, et al. Diagnostic imaging of trauma to the ankle and foot:
I. Fractures about the ankle. J Foot Surg. 1989;28:174.
11. Mitchell MJ, Ho C, Howard BA, et al. Diagnostic imaging of trauma to the ankle and foot: part
II. J Foot Surg. 1989;28:266.
12. Egol KA, Amirtharajah M, Tejwani NC, Capla EL, Koval KJ. Ankle stress test for pre-
dicting the need for surgical fixation of isolated fibular fractures. J Bone Joint Surg Am.
2004;86-A:2393–8.
13. Gill JB, Risko T, Raducan V, Grimes JS, Schutt RC Jr. Comparison of manual and gravity
stress radiographs for the evaluation of supination-external rotation fibular fractures. J Bone
Joint Surg Am. 2007;89-A:994–9.
14. Weber M, Burmeister H, Flueckiger G, Krause FG. The use of weightbearing radiographs to
assess the stability of supination-external rotation fractures of the ankle. Arch Orthop Trauma
Surg. 2010;130:693–8.
15. Hoshino CM, Nomoto EK, Norheim EP, Harris TG. Correlation of weightbearing radiographs
and stability of stress positive ankle fractures. Foot Ankle Int. 2012;33:92–8.
16. Fernandez A. 3D coloreado Interactivo, Htal Britanico Montevideo, ICUC. 2019. https://p3d.
in/gsR1g.
17. Koval K, Egol K, Cheung Y, Goodwin D, Spratt K. Does a positive ankle stress test indicate the
need for operative treatment after lateral malleollus fracture? A preliminary report. J Orthop
Trauma. 2007;21(7):449–55.
18. Van Den Bekerom M, Mutsaerts E, Van Dijk N. Evaluation of the integrity of the deltoid liga-
ment in supination external rotation ankle fractures: a systematic review of the literature. Arch
Orthop Trauma Surg. 2009;129(2):227–35.
19. Thordarson DB, Motamed S, Hedman T, Ebramzadeh E, Bakshian S. The effect of fibular
malreduction on contact pressures in an ankle fracture malunion model. J Bone Joint Surg Am.
1997;79(12):1809–15.
20. Daghino W, Massé A, Marcolli D. Malleolar fractures. In: Foot and ankle trauma injuries.
Atlas of surgical procedures. Cham: Springer International Publishing AG, part of Springer
Nature; 2018. p. 21–32.
21. Hahn DV, Chong K. Specific fractures: Malleoli. In: Buckley RE, Moran CG, Apivatthakakul
T, editors. AO principles of fracture management. 3rd ed. Thieme Medical Publishers; 2017.
p. 933–60.
22. Jaskulka RA, Ittner G, Schedl R. Fractures of the posterior tibial margin: their role in the prog-
nosis of malleolar fractures. J Trauma. 1989;29(11):1565–70.
23. Tejwani NC, Pahk B, Egol KA. Effect of posterior malleolus fracture on outcome after unsta-
ble ankle fracture. J Trauma. 2010;69(3):666–9.
24. Odak S, Ahluwalia R, Unnikrishnan P, Hennessy M, Platt S. Management of posterior mal-
leolar fractures: a systematic review. J Foot Ankle Surg. 2016;55(1):140–5.
25. Haraguchi N, Haruyama H, Toga H, Kato F. Pathoanatomy of posterior malleolar fractures of
the ankle. J Bone Joint Surg Am. 2006;88-A:1085–92.
26. Bartonıcek J, Rammelt S, Kostlivy K, Vanecek V, Klika D, Tresl I. Anatomy and classification
of the posterior tibial fragment in ankle fractures. Arch Orthop Trauma Surg. 2015;135:505–16.
27. Miller A, Carroll EA, Parker RJ, Helfet DL, Lorich DG. Posterior malleolar stabilization of
syndesmotic injuries is equivalent to screw fixation. Clin Orthop Relat Res. 2010;468:1129–35.
28. Fitzpatrick E, Goetz JE, Sittapairoj T, Siddappa VH, Femino JE, Phisitkul P. Effect of poste-
rior malleolus fracture on syndesmotic reduction. A cadaveric study. J Bone Joint Surg Am.
2018;100:243–8.
29. Arrondo GM, Joannas G. Complex ankle fractures: practical approach for surgical treatment.
30. Williams BT, Ahrberg AB, Goldsmith MT, Campbell KJ, Shirley L, Wijdicks CA, LaPrade RF,
Clanton TO. Ankle syndesmosis: a qualitative and quantitative anatomic analysis. Am J Sports
Med. 2014;43(1):88–97.
31. Ogilvie-Harris DJ, Reed SC. Disruption of the ankle syndesmosis: diagnosis and treatment by
arthroscopic surgery. Arthroscopy. 1994;10(5):561–8.
32. Bartonıcek J, Rammelt S, Kasper S, Malik J, Tucek M. Pathoanatomy of Maisonneuve fracture
based on radiologic and CT examination. Arch Orthop Trauma Surg. 2019;139:497–506.
33. Rammelt S, Obruba P. An update on the evaluation and treatment of syndesmotic injuries. Eur
J Trauma Emerg Surg. 2015;41:601–14.
34. Pakarinen H, Flinkkila T, Ohtonen P, Hyvonen P, Lakovaara M, Leppilahti J, Ristiniemi
J. Intraoperative assessment of the stability of the distal tibiofibular joint in supination-external
rotation injuries of the ankle: sensitivity, specificity, and reliability of two clinical tests. J Bone
Joint Surg Am. 2011;93:2057–61.
35. Hoppenfeld S, DeBoer P, Buckley R. Surgical exposures in orthopaedics: the anatomic
approach. 4th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health; 2009.
36. Assal M, Dalmau-Pastor M, Ray A, Stern R. How to get to the distal posterior tibial malleolus?
A cadaveric anatomic study defining the access corridors through 3 different approaches. J
Orthop Trauma. 2017;31:e127–9.
37. Philpott M, Jayatilaka M, Millward G, Molloy A, Mason L. Posterior approaches to the ankle –
an analysis of 3 approaches for access to the posterior malleolar fracture. Foot. 2020;45:1–6.
38. Zhong S, Shen L, Zhao J, Chen J, Xie JF, Shi Q. Comparison of posteromedial versus postero-
lateral approach for posterior malleolus fixation in trimalleolar ankle fractures. Orthop Surg.
2017;9:69–76.
39. Salameh M, Alhammoud A, Alkhatib N, Attia AK, Mekhaimar M, D’Hooghe P, Mahmoud
K. Outcome of primary deltoid ligament repair in acute ankle fractures: a meta-analysis of
comparative studies. International Orthopaedics (SICOT). 2019. https://doi.org/10.1007/
s00264-019-04416-9.
40. Woo SH, Bae SY, Chung HJ. Short-term results of a ruptured deltoid ligament repair during an
acute ankle fracture fixation. Foot Ankle Int. 2018;39(1):35–45.
41. Zhao HM, Lu J, Zhang F, Wen XD, Li Y, Hao DJ, Liang XJ. Surgical treatment of ankle frac-
ture with or without deltoid ligament repair: a comparative study. BMC Musculoskelet Disord.
2017;18:543.
42. Solan MC, Sakellariou A. Posterior malleolus fractures: worth fixing. Bone Joint
J. 2017;99-B:1413–9.
43. Jones CB, Gilde A, Sietsema DL. Treatment of syndesmotic injuries of the ankle. A critical
analysis review. JBJS Rev. 2015;3(10):e1.
44. Yuen CP, Lui TH. Distal tibiofibular syndesmosis: anatomy, biomechanics, injury and manage-
ment. Open Orthop J. 2017;11(Suppl-4, M7):670–7.
45. Dingemans SA, Rammelt S, White TO, Goslings JC, Schepers T. Should syndesmotic screws
be removed after surgical fixation of unstable ankle fractures? A systematic review. Bone Joint
J. 2016;98-B:1497–504.
46. Sanders D, Schneider P, Taylor M, Tieszer C, Lawendy AR. Improved reduction of the tibio-
fibular syndesmosis with TightRope compared with screw fixation: results of a randomized
controlled study. J Orthop Trauma. 2019;33(11):531–7.
47. Rammelt S, Bartonicek J, Kroker L, Neumann AP. Surgical fixation of quadrimalleollar frac-
tures of the ankle. J Orthop Trauma. 2020; ahead of print.
48. Takao M, Ochi M, Oae K, Naito K, Uchio Y. Diagnosis of a tear of the tibiofibular syndesmo-
sis. The role of arthroscopy of the ankle. J Bone Joint Surg Br. 2003;85:324–9.
49. Forschner PF, Beitzel K, Imhoff AB, Buchmann S, Feuerriegel G, Hofmann F. Five-year out-
comes after treatment for acute instability of the tibiofibular syndesmosis using a suture-button
fixation system. Orthop J Sports Med. 2017;5:2325967117702854.
50. Switaj PJ, Mendoza M, Kadakia AR. Acute and chronic injuries to the syndesmosis. Clin
Sports Med. 2015;34:643–77.
51. Mehta SS, Rees K, Cutler L, Mangwani J. Understanding risks and complications in the man-
agement of ankle fractures. Indian J Orthop. 2014;48(5):445–52.
52. Horisberger M, Valderrabano V, Hintermann B. Posttraumatic ankle osteoarthritis after ankle-
related fractures. J Orthop Trauma. 2009;23(1):60–7.
53. Valderrabano V, Hintermann B, Horisberger M, Fung TS. Ligamentous posttraumatic ankle
osteoarthritis. Am J Sports Med. 2006;34(4):612–20.
Tibial Pilon Fracture
Christian Bastias and Leonardo Lagos
1 Introduction
Fractures of the distal tibia with joint involvement are relatively infrequent, less
than 1% of lower extremity fractures, but at the same time one of the injuries that
most challenges the technical skill and clinical judgment of the orthopedic surgeon
in its management [1].
Initially called “tibial pilon” by Destot in 1911; it was Bonin who coined the
term “tibial plafond” in 1950, as a way of describing the ankle roof alteration [2].
One of the essential facts in which the complexity of its treatment lies is that in
addition to the existence of an often-severe bone involvement, it is associated with
soft tissue damage of a similar or greater magnitude.
It is an injury that is associated with a high rate of complications, particularly
those injuries of greater energy. Within these complications we can find: infection,
dehiscence of wounds, nonunion, mal-union, and arthrosis.
2 Aetiology/Injury Mechanism
The described lesional mechanism presents 2 great variants:

• One of relatively low energy and torsional mechanism associated with falls in
sports activities such as skiing.
• Another of high energy and more frequent, in which the talus impacts in axial
form on the distal tibia producing fractures with comminution at different levels,
usually associated with falls from height and traffic accidents, either car or
C. Bastias (*) · L. Lagos

Hospital Mutual de Seguridad C. Ch. C., Clínica Santa Maria, Santiago, Chile

Switzerland AG 2022
1208 C. Bastias and L. Lagos
motorcycle (50% of tibial pilon fractures are in the context of vehicular acci-
dents). In these high-energy injuries, one third to one half of the patients will
have other fractures or other compromised organs. In total, 10% to 50% may
present as an exposed fracture [3–5].
The fracture pattern will be determined by the position of the foot, and therefore
the heel, at the time of impact [6].
3 Classification
There are several classifications that have been developed over time, ideally seeking
to give a prognostic value and guide the treatment.
Lauge Hansen described the tibial pilon fracture as a pronation-dorsiflexion frac-
ture with a 4-stage progression. Rüedi and Allgöwer described, in their 1969 publi-
cation, three groups based on the degree of joint and metaphyseal comminution and
displacement [7] (Fig. 1).
In 1987, Müller described the best known and most used classification to date,
adopted by the AO; it is associated with prognostic factor. It is divided into 3 groups:
extra-articular group A, partial articular group B, and total articular group C. Each
one divided consecutively in subgroups, in which the prognosis worsens and the
complexity of the fracture increases.
All these classifications are based on imaging studies by X-ray, which presents
the problem of not allowing a real understanding of the fracture pattern, in its three
dimensions. In 2017, Leonetti presented his new classification based on computed
tomography (CT), with four main groups and respective subgroups [8]. The classi-
fication is based on the number of fragments displaced in the different CT cuts;
ranging from Type 1 not displaced, to Type 4 with at least four fragments and high
comminution. This classification has prognostic value, is reproducible, and better
orients the treatment to be carried out in the operating room.
4 Anatomical Concepts
In the works published by Rüedi and Allgöwer, they determined four treatment con-
cepts, associated to the restoration of the anatomy of segment [9]. They are:
1. Recovery of the fibular length
2. Reconstruction of the joint surface
3. Filling with bone graft from the metaphyseal region
4. Stabilization of the tibial fracture, with a medial plate
Although these concepts are still in force, they were developed based on studies car-
ried out with radiographs as a base image, but with the use of CT scans in the last
Tibial Pilon Fracture 1209
Fig. 1 Classification of Rüedi and Allgöwer’s Tibial Pilon Type I, non-displaced joint. Type II,
with joint comminution. Type III, with joint and metaphyseal comminution
decades, we have better understood the morphology and pattern of the fractures, which
has allowed us to develop anatomical concepts that better guide the treatment.
Cole in 2013 describes, based on a CT study in C3 tibial pilon fractures of the
AO, the existence of a constant fracture pattern at the joint level (over 90% of cases),
in which we find three main fragments: medial, anterolateral and posterolateral,
with a base “Y” shape at the level of the incisura fibularis (Fig. 2). In turn, the areas
of greatest comminution are usually central, coinciding with the central point of the
talus dome, and anterolateral [10] .
With respect to the concept of the columns, it refers to an anatomical and
mechanical complex, in which it is considered a continuity between the articular or
epiphyseal fragments, with their respective metaphyseal and diaphyseal tibial zones.
Assal in 2015 describes three columns, exclusively tibial: medial, lateral, and pos-
terior [11].
Fig. 2 Joint fragments in

tibial pilon. There are 3
main fragments: medial,
anterolateral, and
posterolateral, with a base
“Y” shape at the level of
the incisura fibularis. Note
the anterolateral
comminution
In more recent works, as is the case of Chen’s study in 2019, four columns are
already described, adding the distal fibula as one more column, which provides
reduction and stability, being shaped as follows [12] (Fig. 3):
• Lateral column: distal fibula
• Posterior column: posterior joint fracture feature and 1/3 distal-posterior tibia
• Anterior column: anterior joint fracture feature and 1/3 distal anterior tibia
• Medial column: 1/3 medial plafond and distal tibia.
The importance of these anatomical concepts is that by recognizing the articular
areas and columns of greater comminution, it allows us to plan more accurately
where we should use our implants to stabilize the fracture and the approaches that
we require for it.
5 Diagnosis
The clinical evaluation should first consider ruling out more serious or even life-
threatening injuries, particularly in the context of high-energy injuries. Of course, it
should also rule out other fractures related to axial loading such as tibial plateau,
acetabulum, and spine.
In the same segment of the ankle and foot, the quality of soft tissue, eventual
exposure areas, erosions, and bullas must be evaluated.
Sensitive and motor neurological evaluation, and the presence of pulses and dis-
tal perfusion based on capillary filling, is also fundamental.
In relation to the imaging study, this is based on ankle and leg radiographs, in
addition to the projections that are required by suspected fractures of other seg-
ments. The CT scan is essential for planning, but it is usually requested after exter-
nal fixation, in the context of staged treatment, which we will discuss later.
Fig. 3 The 4 columns of the tibial pilon. Medial, lateral, posterior, and anterior
6 Treatment
Conservative management in tibial pilon fractures is reserved only for patients with
comorbidity that contraindicates surgery, and for patients with non-displaced, stable
fractures. Treatment consists of immobilization with a cast and unloading at least
the first 6 weeks, and then orthopedic boot until radiological consolidation is
achieved [13, 14].
The surgical treatment, except for the cases already mentioned, is indicated for
every pilon fracture and depends mainly on the condition of the soft tissue and the
type of fracture (comminution severity and compromised column). We must also
take into account the comorbidities of the patient (diabetes, venous insufficiency,
rheumatoid arthritis, etc.), which may lead us to consider less invasive treatments to
avoid complications.
6.1 Acute Management of the Tibial Pilon
Currently, the Gold Standard for the acute management of tibial pilon fractures is
the staged management: as a matter of urgency, we must stabilize and align the
fracture with external fixation, considering the most stable configuration (in delta),
since this, sometimes, must maintain stability for a long time. The objective of this
staged management is to allow the improvement of soft tissue conditions, in order
to secondarily perform definitive osteosynthesis [15].
We do not recommend emergency fibular fixation for the following reasons:
• With high frequency, they are complex fractures; therefore they have high prob-
ability of being badly reduced (recurvatum, bad rotation, long or shortened);
which will affect tibial reduction and therefore obligate the surgeon to re-operate
the fibular fracture [16].
• It will affect the planning of our approaches.
• In some cases, it is recommended to start with the tibial synthesis, especially
when there is great fibular comminution.
Emergency external fixation is of greater value when we are faced with an
exposed fracture that may be associated with a lack of skin coverage, generally on
the medial tibial side.
Some recently published studies support immediate synthesis in tibial pilon frac-
tures, up to 72 hours postfracture, showing good results without presenting a higher
rate of complications [17, 18]. In our opinion, this is a valid option if it is performed
early, before a lot of edema of the limb is present; when there are no soft tissue
injuries (erosions, bullae, exposure) and when it is performed by a surgeon with
experience in this type of fracture.
6.2 Definitive Fracture Management
Once the soft tissues are in good condition, we proceed to perform the definitive
management of the fracture, 2nd stage of the staged management, where it is key to
evaluate:
• Fracture pattern, determining our zones of greatest conflict (columns or pillars
that are compromised and those with the greatest joint and metaphyseal commi-
nution) [11, 12].
• Segments with persistent soft tissue injury, which may require skin coverage
with flaps or grafts, as these are areas where we must avoid making approaches
or large dissections.
Once these two parameters are determined (bone and soft tissue involvement),
we can plan our approaches and type of synthesis to be used.
With respect to the fracture pattern, in our opinion we have two large groups of
tibial pilon fractures:
• Fractures where we have at least one column in continuity, which helps us con-
siderably in the reduction and stability of this fracture. In these cases, we gener-
ally use low-profile plates, without great rigidity, to obtain a neutralization or
buttress effect and achieve joint reduction [19].
• Fractures where we have compromise of all the metaphyseal and articular col-
umns. Very unstable fractures generally associated with important damage of soft
tissues, where we require osteosynthesis of greater rigidity and stability to achieve
a proper reduction of metaphyseal and joint, which is maintained over time
[20, 21].
With respect to the choice of our approaches, we consider the areas of greatest
bone conflict and soft tissue status. The zone of greatest bone conflict (key zone)
corresponds to the articular and/or metaphyseal area of greatest comminution that
we must reduce anatomically, where we will generally place our osteosynthesis of
greatest rigidity. Along with this, we must know that our approaches must be at least
5 cm apart to avoid complications [22].
Rüedi and Allgöwer’s principles are still valid, but we must consider some modi-
fications that have occurred over time [9]:
1. Recovery of the fibular length. We believe that this is fundamental since it helps
us to reduce the anterolateral and posterior tibial fragment by means of its liga-
mentous insertions. It gives us stability, but should not always be performed first,
especially in cases of great comminution, since not leaving it well reduced can
interfere with tibial reduction [23, 24].
2. Joint reduction. It is fundamental to obtain good functional results, but we must
understand that in this type of fracture, many times, there is already irreversible
joint damage, so we must judiciously achieve an anatomical reduction and not
perform further damage to soft tissue. On some occasions, it is preferable to sacri-
fice joint reduction in order to avoid greater damage, but it is better to focus on
achieving adequate stability and alignment of the fracture [25–27].
Joint reduction is not always the second goal to be achieved, especially when
there is great joint comminution where it will help us to start by the metaphyseal
reduction.
3. Metaphyseal filling with bone graft. We do it less and less, only in cases where
we have a defect of 1 or 2 metaphyseal pillars that we cannot fill with the same
bone fragments. In cases of great comminution of the whole metaphysis, we
prefer to perform percutaneous synthesis and evaluate the need for grafting in
the future. In cases of exposed fractures with metaphyseal defect or closed frac-
tures with a great bone defect, we consider the use of bone cement with antibiot-
ics which gives us more stability and mechanical support. We wait 4–6 weeks
and we remove the cement spacer and fill the defect with bone graft (Masquelet
technique), thus avoiding the risks of infection and failure of osteosynthesis [28].
4. Stabilization of the medial column. We believe that it is fundamental to fix this
column since it gives us great stability and should avoid the mal and nonunion in
varus that can be produced in time. Please consider fixation of the other columns
depending on whether they are compromised [20, 21].
6.3 Treatment According to Fracture Type
6.3.1 Fracture with 1 or 2 Columns Compromise, Always One Unscathed
Medial Pilon Fracture
This type of fracture generally presents a medial articular impaction with a shearing
feature [29]. In these cases, we perform a medial approach by inclining its distal
portion towards the anterior aspect of the tibia, we open the large medial fragment
which allows us to disimpact and reduce the articular surface, we return it to its
place, and we fix the medial column with a low-profile plate where we anchor the
screws in the anterior and posterior column. If there is a great impaction, we place
a bone graft. This type of fracture is usually associated with low transverse features
of the fibula which we usually fix with endomedullary screws (Fig. 4).
Fig. 4 Fracture with compromise and impaction of the medial column, key zone (circle). Fixation
with third tube plate and screws from medial to lateral pillars (arrows)
Anterior Pilon Fracture
This type of fracture presents impaction and articular comminution of the anterior
column. In these cases, we perform an anterior approach and fix with a low-profile
anterior plate, anchoring our screws in the unscathed posterior column. Sometimes
it is associated with less severe involvement of the medial column which we have to
stabilize with plate or screws depending on the fracture features (Fig. 5).
Posterior Pilon Fracture
This type of fracture with involvement of the whole posterior column can present a
split and impacted articular fragments (Bartoniceck type III - IV [30]), which must
be reduced anatomically. For this type of fracture, we have several options of
approaches, the most popular being the posterolateral one with patient in prone
position since it allows us to reduce and fix the fibula and the posterior tibial frag-
ment with plate, but we must associate a medial approach if it presents a medial
malleolus compromise. We have also described the posteromedial approach and its
modifications for the posterior fragments, in association with a direct lateral
Fig. 5 Fracture with compromise and impaction of the anterior column, key zone (circle), and
feature a simple medial malleolus. It was planned as an anterior approach and synthesis with an
anterior plate directing the screws to the posterior column (arrows)
Fig. 6 Bartoniceck III posterior pilon fracture with clear fragment interposed in the fracture line,
key zone (circle). Modified posteromedial approach (eye) and synthesis was planned with two
plates (arrows), a posterolateral buttress plate plus an anterior-posterior screw to achieve interfrag-
mentary compression of large posterolateral fragment and a posteromedial plate for posteromedial
fragment
approach for the fibula. Fixation is performed with low-profile plates with the
screws anchored in the anterior column (Fig. 6) [30].
6.3.2 Fracture with Comminution of All Metaphyseal Columns
As we mentioned before, these types of fractures are the most complex since they
are more frequently associated with soft tissue involvement, metaphyseal comminu-
tion, and the complications this entails. But they can also present simple, articular,
and metaphyseal features, having a much better prognosis.
In this type of fracture, we must evaluate the most compromised column (greater
articular and metaphyseal comminution) to determine our approaches and
osteosynthesis.
If possible, we always try to perform the fibular fixation with a plate first, since
it helps us to reduce the tibia (anterolateral and posterior fragment), to achieve the
length, anatomy, and stability of the distal leg segment, especially when we have a
great metaphyseal tibia comminution.
In cases of involvement of lateral soft tissue or very high transverse features, we
recommend fixation with endomedullary devices, trying to achieve a correct
rotation.
With respect to the choice of our approaches, we have several options depending
on the fracture pattern [11]:
• Anterior approach: it is key to avoid opening the anterior tibial sheath. The plane
of deep dissection goes between the tibialis anterior and the extensor hallucis
longus, mobilizing the neurovascular package to the side. It achieves a very good
visualization of the joints and the anterior and medial columns. Through this
approach, we can place without problems an anterior and anterolateral osteosyn-
thesis. If we wish to place a medial plate, we can do so through a small percuta-
neous medial incision.
• Anteromedial approach: characterized by the fact that its distal third is curved
towards medial, passing through the medial third of the joint and reaching 15 mm
below the medial malleolus, without opening the anterior tibial sheath. This
allows us to see very well the compromise of the medial column and to place
anterior and medial osteosynthesis.
• Anterolateral approach: unlike the previous ones, this one creates a big flap,
achieving a good soft tissue coverage of the osteosynthesis used. It allows a very
good view of the anterolateral column and fibula, and we can place a fibular and
anterolateral osteosynthesis without problems. It does not allow us a very good
visualization of all the articular surface and less of the medial column, so it
should generally be associated with a medial approach.
• Posterolateral posterior approach: very popular for the reconstruction of the tib-
ial pilon in 2 stages, starting in prone position for anatomical reduction of the
posterior column and fibula, and then anterior approach for anterior reconstruc-
tion. Its disadvantage is that it produces a great desperiostization of the entire
distal-posterior portion of the tibia, which has been associated with a higher
percentage of nonunion. This approach is also widely used in posterior pilon
fractures [31, 32].
Once our approach is done and the fibula is fixed, we continue with the tibial
reduction in the following order:
• In the absence of great metaphyseal comminution, we start with the reduction of
the fibula and then of the joint. First, we recommend the temporary fixation with
AK of the posterior column in an indirect way (through the anterior aspect of the
tibia) which we achieve, thanks to manual traction and the use of elevators, and
many times we use as a reference the medial column. Once we have the posterior
column reduced, we reduce the medial column, die punch fragment, and finally
the anterolateral one. In some occasions where we do not achieve an adequate
reduction of the posterior column, we can start with the reduction of the medial
column and then the posterior one (Fig. 7).
• In case of fractures with great metaphyseal comminution, where we do not have
a clear anatomical reference, we perform the joint reduction first and then we
solidify this joint block to the diaphysis with the help of anatomical plates.
Once the fracture has been reduced and maintained with Kirschner wires, we
check the reduction under fluoroscopy and proceed to definitive fixation with plates.
Fig. 7 Fracture with compromise of all columns, where the 4 characteristic fragments are observed
in the axial CT section (posterior, medial, anterolateral, and die punch). The order of reduction
goes in relation to their numbers by first indirectly reducing the posterior column (yellow line),
then directly reducing the medial column, die punch, and anterolateral
Column fixation:
• Non-comminuted posterior pillar: we fix it indirectly with screws coming from
the anterior or anterolateral plate. In very exceptional cases where we cannot
achieve the reduction (due to technical difficulty, a little comminution, or a pos-
terior dislocation to flexors and posterior tibial), we reduce it and synthesize it
with posterior plate by means of a modified posteromedial approach.
• Non-comminuted medial pillar: we fix it with reconstruction plate, DCP, or third
tubular plate. In case of important comminution, we use an anatomical locking
plate. We always fix this column, since it provides great stability to the fracture,
and would avoid the very frequent varus malalignment in these cases [33].
• Non-comminuted anterior pillar: we can fix it only with screws or third tubular
plate, but if it presents metaphyseal or articular comminution, we use a locking
anterior or anterolateral plate.
An isolated medial plate does not achieve adequate fixation of the anterolat-
eral fragment, and an isolated anterolateral plate does not achieve good fixation
of the medial fragment, so depending on the type of fracture we often have to use
2 or 3 plates to adequately stabilize all the compromised tibial pilon columns
(Fig. 8) [21].
Fig. 8 Fracture with compromise of all pillars, being the “key zone” (circle) the anterolateral
column. Anterior approach and fixation with locking anterolateral plate, of greater rigidity and
third tube plate to the non-comminuted medial column (arrows) was performed. Posterior pillar is
fixed with screws through the anterolateral plate
6.4 Percutaneous Techniques
In recent years, percutaneous techniques for this type of fracture have become popu-
lar. In our opinion, we have three main groups where they are an excellent option.
1. Patients with poor soft tissue condition, where making an extended approach
will bring a great risk of complications.
2. Patients with simple articular fractures that we can reduce with arthroscopic
assistance and fix them in a percutaneous way.
3. Patients with great comminution of all the metaphyseal pillars. We try to perform
percutaneous fixation of the joint with arthroscopic assistance or mini anterior
approach, and then we stabilize metaphysis with percutaneous plate or external
fixation depending on the soft tissue condition.
Arthroscopic assistance is fundamental to achieve the reduction of displaced
fractures: we perform it with manual traction, or we maintain the initial fixator, if a
good reduction was achieved with it thanks to ligamentotaxis [34].
With respect to fixation: we start with the fibula, which can be percutaneous or
open depending on the state of the lateral soft tissues (this helps us considerably
with tibial reduction); then fixation of the articular surface with percutaneous screws
and finally a percutaneous medial plate through a mini medial incision, or external
fixator (Fig. 9).
Fig. 9 Tobacco patient with significant soft tissue and all columns fracture compromise, but with-
out great joint displacement. Percutaneous joint fixation is performed with arthroscopic assistance
and percutaneous medial plate
6.5 External Fixation
External fixation is part of the percutaneous techniques and we consider it as a

definitive treatment in the following cases.
• Patients with “non-reconstructable” fractures that present a great joint comminu-
tion and severe metaphyseal compromise.
• Patients with important uncontrolled comorbidities, which give a great risk of
complications, and not susceptible to percutaneous fixation.
• Patients with significant soft tissue involvement, sometimes requiring skin cov-
erage, which makes internal fixation impossible.
In these cases, we use circular, hybrid, or monoplanar medial fixation, which we
associate with percutaneous fixation of the joint surface, if possible. Once a consoli-
dated articular block and completely improved soft tissues are achieved, we can
consider transfer to a medial percutaneous plate, which we usually do after the 6th
to 8th week, or we maintain external fixation until consolidation is achieved (Fig. 10)
[35, 36].
Fig. 10 Poorly controlled diabetic patient with exposed fracture with great metaphyseal commi-
nution of all pillars. Open fibula synthesis and circular external fixation to the tibia are decided,
achieving consolidation without complications
7 Postoperative Management
Depending on the type of fracture, the patient is left in the hospital for one or two days
after surgery with an immobilizing boot and a strictly elevated foot. At the time of
discharge, the patient is discharged with two crutches and an immobilizing boot, and
the foot is kept strictly elevated. We try to restrict the mobility of the ankle during the
first three weeks in patients with an anterior approach, to avoid any complications
with the approach. The first control is done in the third week, where we take out the
stitches and start with the rehabilitation. We keep the patient non-weight bearing and
with a boot for 6 to 8 weeks, depending on the type of fracture, and then we progres-
sively load the patient until we verify the bone consolidation with CT scan, which we
request at the second and third month or until consolidation is achieved.
8 Complications
The complications can be separated into three groups: from the injury, from the
surgical treatment, and long term [37].
Of the injury: they are those related to the accident itself, although they do not
necessarily manifest themselves immediately. Exposed fractures have a higher risk
of infection than closed injuries; loss of skin coverage or segmental bone defects in
high-energy injuries also increase the risk of infection. Neurovascular injury at the
time of the accident, although we can find it, is infrequent.
Surgical treatment: it is associated with surgical timing or surgical technique
itself. We emphasize that these fractures have to be resolved by an experienced
surgeon.
Beyond an intraoperative injury of a vessel or a nerve branch, or a segment of a
tendon, the main complications are associated with choosing a bad time for surgery
(“early” surgery even with soft parts in resolution), or having chosen an open tech-
nique when the severe damage of soft tissues favored the use of percutaneous tech-
niques or even external fixation. The most devastating consequences of this are skin
flap dehiscence and necrosis, and infection.
Nonunion usually occurs in fractures with severe metaphyseal or diaphyseal
comminution in which soft tissue and therefore irrigation was not respected at the
time of surgery. Malunion is associated with insufficient fixation, or lack of fixation
of a compromised column.
Long term: the most frequent is osteoarthritis, usually localized in relation to the
articular zone corresponding to the most severely compromised column, Over time
it can progress from initial localized osteoarthritis to diffuse osteoarthritis. In addi-
tion, this arthrosis can or cannot be associated with malalignment. It should be
noted that osteoarthritis without malalignment is better tolerated than osteoarthritis
with an associated deformity.
References
1. Barei D, Nork S. Fractures of the tibial plafond. Foot Ankle Clin N Am. 2008;13:571–91.
2. Barei DP, Nork SE, Bellabarba C, Sangeorzan BJ. Is the absence of an ipsilateral fibular
fracture predictive of increased radiographic tibial pilon fracture severity? J Orthop Trauma.
2006;20(1):6–10.
3. Ovadia DN, Beals RK. Fractures of the tibial plafond. J Bone Joint Surg Am. 1986;68:543–51.
4. Liporace FA, Yoon RS. Decisions and staging leading to definitive open management of pilon
fractures: where have we come from and where are we now? J Orthop Trauma. 2012;26:488–98.
5. Chen D, Li B, Aubeeluck A, Yang Y, Zhou J, Yu G. Open reduction and internal fixation of
posterior pilon fractures with butress plate. Acta Orthop Bras. 2014;22:48–53.
6. Gay R, Evrard J. Recent fractures of the tibial pestle in adults. Rev Chir Orthop Reparatrice
Appar Mot. 1964;49:397–512.
7. Rüedi TP. Allgöwer: fractures of the lower end of the tibia into the ankle joint. Injury.
1969;1:92–9.
8. Leonetti D, Tigani D. Pilon fractures: a new classification system based on CT scan. Injury.
2017;48:2311–7.
9. Rüedi TP, Allgöwer M. Fractures of the lower end of the tibia into the ankle joint: result 9 years
after open reduction and internla fixation. Injury. 1973;5:130–4.
10. Cole P, Merle R, Bhandari M, Zlowodski M. The pilon map: fracture lines and conminution
zones in OTA/AO type 43C3 pilon fractures. J Orthop Trauma. 2013;27:152–6.
11. Assal M, Ray A, Stern R. Strategies and surgical approaches in open reduction internal fixation
of pilon fractures. J Orthop Trauma. 2015;29:69–79.
12. Chen H, Cui X, Ma B, Rui Y, Li H. Staged procedure protocol based on the four-column concept
in the treatment of AO/OTA type 43-C3.3 pilon fractures. J Int Med Res. 2019;47:2045–55.
13. De Valentine S. Evaluation and treatment of ankle fractures. Clin Podiatr Med Surg.
1985;2(2):325–47.
14. Schatzker J, Tile M. The rationale of operative fracture care. Heidelberg: Springer; 1987.
15. Sirkin M, Sanders R, DiPasquale T, Herscovici D. A staged protocol for soft tissue manage-
ment in the treatment of complex pilon fractures. J Orthop Trauma. 1999;13:78–84.
16. Borrelli J Jr, Catalano L. Open reduction and internal fixation of pilon fractures [current con-
troversies in orthopaedic trauma]. J Orthop Trauma. 1999;13(8):573–82.
17. White T, Kennedy S, Cooke C, et al. Primary internal fixation of AO type C pilon fractures is
safe. Orthopaedic Trauma Association Proceedings; 2006.
18. Guy P, White T, Cooke C, et al. The results of early primary open reduction and internal
fixation for treatment of AO C-type tibial pilon fractures: a cohort study. J Orthop Trauma.
2010;24(12):757–63.
19. Borens O, Kloen P, Richmond J, Roederer G, Levine DS, Helfet DL. Minimally invasive treat-
ment of pilon fractures with a low profile plate: preliminary results in 17 cases. Arch Orthop
Trauma Surg. 2009;129(5):649–59.
20. Penny P, Swords M, Heisler J, Cien A, Sands A, Cole P. Ability of modern distal tibia plates
to stabilize comminuted pilon fracture fragments: is dual plate fixation necessary? Injury.
2016;47(8):1761–9.
21. Aneja A, Luo TD, Liu B, Domingo M 4th, Danelson K, Halvorson JJ, Carroll EA. Anterolateral
distal tibia locking plate osteosynthesis and their ability to capture OTAC3 pilon fragments.
Injury. 2018;49(2):409–13.
22. Howard JL, Agel J, Barei DP, Benirschke SK, Nork SE. A prospective study evaluat-
ing incision placement and wound healing for tibial plafond fractures. J Orthop Trauma.
2008;22(5):299–305.
23. Kumar A, Charlebois SJ, Cain EL, Smith RA, Daniels AU, Crates JM. Effect of fibular plate
fixation on rotational stability of simulated distal tibial fractures treated with intramedullary
nailing. J Bone Joint Surg Am. 2003;85(4):604–8.
24. Helfet DL, Koval K, Pappas J, et al. Intraarticular “pilon” fracture of the tibia. Clin Orthop
Relat Res. 1994;298:221–8.
25. McKinley TO, Rudert MJ, Koos DC, Brown TD. Incongruity versus instability in the etiology
of posttraumatic arthritis. Clin Orthop Relat Res. 2004;423:44–51.
26. Ovadia DN, Beals RK. Fractures of the tibial plafond. J Bone Joint Surg Am. 1986;68A:543–51.
27. Babis GC, Vayanos ED, Papaioannou N, Pantazopoulos T. Results of surgical treatment of
tibial plafond fractures. Clin Orthop Relat Res. 1997;341:99–105.
28. Masquelet A, Kanakaris NK, Obert L, Stafford P, Giannoudis PV. Bone repair using the
Masquelet technique. J Bone Joint Surg Am. 2019;101:1024–36.
29. Haller JM, Ross H, Jacobson K, et al. Supination adduction ankle fractures: ankle fracture or
pilon variant? Injury. 2020;51:759–63.
30. Bartonícek J, Rammelt S, Kostlivý K, et al. Anatomy and classification of the posterior tibial
fragment in ankle fractures. Arch Orthop Trauma Surg. 2015;135:506–16.
31. Ketz J, Sanders R. Staged posterior tibial plating for the treatment of Orthopaedic Trauma
Association 43C2 and 43C3 tibial pilon fractures. J Orthop Trauma. 2012;26:341–7.
32. Chan DS, Balthrop PM, White B, et al. Does a staged posterior approach have a negative effect
on OTA- 43C fracture outcomes? J Orthop Trauma. 2016;31:90–4.
33. Haller J, Githens M, Rothberg D, Higgins T, Nork S. Barei. Risk factors for tibial pla-
fond nonunion: medial column fixation may reduce nonunion rates. J Orthop Trauma.
2019;33:443–9.
34. Pellegrini M, Cuchacovich N, Lagos L, Henríquez H, Carcuroa G, Bastias C. Minimally-
invasive alternatives in the treatment of distal articular tibial fractures. Fuß & Sprunggelenk.
2012;10(1):37–4.
35. Galante VN, Vicenti G, Corina G, Mori C, Abate A, Picca G, et al. Hybrid external fixation
in the treatment of tibial pilon fractures: a retrospective analysis of 162 fractures. Injury.
2016;47(Suppl 4):S131–7. 30.
36. Kapoor SK, Kataria H, Patra SR, Boruah T. Capsuloligamentotaxis and definitive fixation
by an ankle-spanning Ilizarov fixator in high-energy pilon fractures. J Bone Joint Surg Br.
2010;92(8):1100–6.
37. Swords M. Distal tibia/pilon fractures. In: Rammel S, Swords M, Dhillon M, Sands A, edi-
tors. Manual of fracture management - foot and ankle. 1st ed. (AO Foundation). Davos Platz,
Switzerland. Thieme; 2020: 17–24.
Calcaneus Fractures
Stefan Rammelt and Christine Marx
1 Introduction
Calcaneus fractures are the most frequent fractures of the tarsus. The majority of
them are displaced and intra-articular [1, 2]. The patterns of injury are diverse and
the operative treatment is challenging with a considerable learning curve for the
surgeon [3, 4]. The calcaneus has an irregular shape and four joint facets with dif-
ferent slopes and curvatures [5]. The skin over the lateral calcaneal wall is thin and
at risk for wound healing problems. The unique plantar skin cannot be replaced with
like tissue in case of avulsion or severe damage [6]. On the medial wall of the cal-
caneus runs the posterior tibial neurovascular bundle with the long flexor tendons.
The muscular compartments at the hindfoot are at risk for pathological pressures in
case of haemorrhage and the deep plantar (calcaneal) compartment connects to the
deep posterior compartment of the lower leg with the inherent risk of a combined
compartment syndrome [7]. For these reasons, the management of calcaneal frac-
tures is demanding and has undergone multiple shifts of principles. The controver-
sial discussion continues to this day [8].
Over the last years, many studies have explored different surgical techniques and
examined the results of operative and nonoperative treatment of displaced intra-
articular calcaneus fractures. There is some consensus that there is no gold standard
for all calcaneal fractures. Rather, treatment has to be tailored to the individual
fracture pattern, soft tissue conditions, patient demands, comorbidities, and compli-
ance [8, 9]. If surgical treatment is chosen, only anatomic reduction of the joint
surfaces and restoration of heel alignment are imperative for obtaining favorable
functional results [10–12]. In an effort to reduce the rates of soft tissue
S. Rammelt (*) · C. Marx

University Center for Orthopaedics, Trauma and Plastic Surgery, University Hospital Carl
Gustav Carus at TU Dresden, Dresden, Germany

Switzerland AG 2022
1226 S. Rammelt and C. Marx
complications like wound edge necrosis and infections, numerous percutaneous and
minimally invasive techniques have been developed and are used increasingly [8, 9].
2 Surgical Anatomy and Pathomechanics
The calcaneus as largest bone of the foot acts as a strong lever arm in interaction
with the Achilles tendon, the plantar fascia, and the extrinsic and intrinsic foot mas-
cules. It constitutes the posterior part of the longitudinal arch and of the lateral
column of the foot.
The odd-shaped calcaneus has a strong cortex at the medial aspect, particularly
at the sustentaculum tali and at the tuberosity (Fig. 1). The thin cortical layer of the
lateral wall forms a typical bulge in case of compression fractures. The trabecular
architecture follows the trajectories of mechanical stress and leaves a neutral trian-
gle at the neck of the calcaneus that is prone to impaction in fractures. The so-called
‘thalamus calcanei’ designates the dense cancellous bone below the posterior facet.
The anatomical shape of the calcaneus in the lateral view is described with two
measures: Böhler’s angle between the superior edge of the tuberosity and the exten-
sion of the subtalar joint line (25–40°) and Gissane’s crucial angle between the
superior edge of the anterior process and the subtalar joint line (120–145°).
The calcaneus articulates with the talus via the subtalar joint. It is composed of
three facets: the posterior, medial, and anterior, whereby the medial and the anterior
facets are merged in about 20–67% of all cases [5]. The medial facet covers the
sustentaculum tali and the anterior facet is located on the superomedial aspect of the
anterior process. The posterior facet is separated from the anterior and medial facets
by the calcaneal sulcus, which forms the bottom of the canalis tarsi (medial) and
sinus tarsi (lateral). The biconvex posterior facet represents the largest joint surface
of the subtalar joint. It is involved in almost 90% of all intra-articular calcaneal frac-
tures [2]. The calcaneocuboid joint has a levelled saddle shape and is involved in
about two thirds of intra-articular fractures of the calcaneus [13]. The subtalar and
calcaneocuboid joints are part of the triple joint complex, which contributes to the
three-dimensional eversion and inversion motion of the foot around the
talocalcaneonavicular joint, or “coxa pedis” [5]. Malfunction of the subtalar joint
Fig. 1 Anatomic features of

the calcaneus in a lateral
radiograph
Böhler‘s Angle
Gissane‘s Angle
Thalamic portion
Sustentaculum tali
Neutral triangle
Tuberosity
Calcaneus Fractures 1227
impairs the global foot function and causes difficulties and pain, especially on
uneven ground, ladders, and stairs [14].
The typical mechanism leading to calcaneal fractures is an axial force as in the
case of a fall from a height or motor vehicle accidents. According to the injury
mechanism, predominately males are affected in the prime of their professional life
[3]. On the other hand, there is an increasing number of calcaneus fractures after
low-velocity injuries like a misstep on uneven ground in elderly people with osteo-
porosis or diabetes that are not easy to treat with a high risk of complications [15].
Due to the parallel offset of the vertical axes of talus and calcaneus, an axial
impaction force leads to an oblique primary fracture line between the sustentaculum
tali and the calcaneal body with the tuberosity when the robust lateral process of the
talus smashes into the predominantly cancellous calcaneal body. The fracture runs
sagittally and usually affects the posterior facet of the subtalar joint [13]. Typically,
the thin lateral wall is blown out and forms a bulge, which irritates the peroneal
tendons and can even irritate the tip of the fibula. Sharp fragments on the thick
medial wall may lead to open fractures. Progressing axial load generates secondary
fracture lines. They follow a reproducible pattern, beginning at Gissane’s angle, and
result in up to five main fragments (Fig. 2).
Isolated fractures of the sustentaculum tali or the anterior process are frequently
caused by a dislocation mechanism at the mid-tarsal (Chopart’s) joint and must
prompt the search for further ligamentous or bony injuries [16]. In adolescents, but
also in patients with osteoporosis or diabetes, avulsion fractures of the superior
aspect of the tuberosity may be observed [17]. These are called “beak fractures” due
to their appearance in the lateral radiograph. These are typically extra-articular, but
may lead to severe soft tissue incarceration over the Achilles tendon insertion in
cases of gross dislocation [18, 19].
3 Diagnosis
Patients with an acute calcaneal fracture present with an increasing swelling and
pain over the heel. They are unable to bear weight on the affected leg. Inversion and
eversion of the injured foot are restricted. Typically, the hematoma occurs beneath
the lateral malleolus and spreads to the sole. In polytraumatized or unconscious,
multiply injured patients, the clinical signs of calcaneus fractures may pass unno-
ticed [20]. Repeat clinical examinations are recommended in these settings in order
not to overlook relevant foot injuries in these patients.
The soft tissue conditions require special attention in the clinical examination
and a continuous monitoring. A shiny, tense skin with loss of wrinkling, blister for-
mation, and pain out of proportion to the injury, despite adequate rest, immobiliza-
tion, cooling, and elevation (RICE), indicate pressure from the inside by hematoma
or displaced fragments that may lead to a manifest compartment syndrome of the
Fig. 2 The reproducible

main fragments of
intra-articular fracture of
the calcaneus [4] are:
tuberosity (TU),
sustentaculum tali (SU),
lateral posterior facet (PF),
anterior process (PA), and
anteromedial (AM)
fragment. Further
fragmentation of all main
fragments is possible. The
number of posterior facet
fragments determines the
fracture classification
according to Sanders [3]
AM
PA
SU
PF
TU
foot. Tensioning of the skin from the inside by displaced fragments like in severe
tongue-type or beak fractures can progress rapidly to full-thickness skin necrosis
over the Achilles tendon insertion, which generates defects that are challenging
to treat.
Radiographs in case of a suspected calcaneal fracture include axial and lateral
projections of the hindfoot. Typically, if the origin of pain is not entirely clear, a
mortise view (anteroposterior projection with the foot 20° rotated internally) of the
ankle is performed (Fig. 3). The lateral view of the hindfoot shows the characteristic
features of displaced calcaneus fractures such as reduced height or other gross
deformity of the calcaneus, decreased Böhler’s angle or increased Gissane’s angle,
and the so-called “double density sign” of the depressed posterior joint surface. The
latter is even more pronounced in cases of fracture-dislocations [21]; however, the
overall shape of the calcaneal body appears unaltered, but there is a substantial
overlap with the talus (see also Fig. 10). In addition, the laterally displaced tuberos-
ity of the calcaneus directly abuts the tip of the fibula, often producing a distal fibu-
lar fracture that might be misinterpreted as a “Weber A” fracture [22]. Further
special projections like 45° oblique views of the subtalar joint with the tube tilted
10–40° caudally (Brodén series) and a dorsoplantar view of the calcaneocuboid
joint with the tube tilted 20° caudally are useful for intra-operative assessment of
joint reconstruction.
If standard radiographs show a calcaneus fracture or a fracture cannot be safely
ruled out, a CT scan has to be performed (Fig. 4). Multiplanar reconstructions are
mandatory and help to analyze the complex fracture anatomy. Present classification
systems are based on CT scans to determine the need for surgery and allow the
assessment of prognosis.
a b c
Fig. 3 (a) Lateral, (b) axial, and (c) anteroposterior view of a tongue-type displaced, intra-articular
calcaneal fracture
a b c
Fig. 4 (a) Sagittal, (b) coronal, and (c) axial CT reconstructions of a Sanders Type III fracture.
(same patient as in Fig. 3)
4 Classification
In 1952, Essex-Lopresti established a simple classification based on the lateral

radiograph categorizing in “joint depression type” and “tongue-type” fractures [23].
In “joint depression type” fractures, the fracture line runs through the impacted
posterior facet downward and posterior, exiting behind the subtalar joint. In “tongue-
type” fractures, it exits through the superior tuberosity producing a large fragment
which is pulled upwards by the Achilles tendon. Because these are frequent and
characteristic fracture patterns, these terms are still widely used.
Sanders [24] established the most widely used classification system, which is
based on the quantity of displaced fracture lines through the posterior facet of the
subtalar joint in the coronal CT scans. Type I includes extra-articular and non-
displaced fractures, type II designates fractures with one displaced fracture line,
type III with two, and type IV with three or more displaced fracture lines of the
posterior facet. Depending on the position of the fracture lines, they are additionally
coded with A for lateral, B for intermediate, and C for medial ones.
Zwipp introduced a 12-point fracture scale, which assembles the count of main
fragments (2–5) and affected joint surfaces (0–3), the extent of soft tissue trauma,
and concomitant fractures of adjoining bones (0–4) [4]. Both the Sanders and Zwipp
classifications have been shown to be of prognostic value in clinical studies [2, 3,
24, 25].
In the updated AO/OTA classification [26], the general AO principles of fracture
classification were adjusted to the irregular shape and multiple joint facets of the
calcaneus with reference to the Essex-Lopresti [23] and Sanders [24] classification
systems. Type A represents an extra-articular fracture, type B a “partial articular”
tongue-type fracture exiting into the posterior facet, and type C a complete articular
joint depression fracture. Type C is further subdivided into three subgroups accord-
ing to the Sanders classification.
5 Indications to Surgery
To this day, no general consensus on the indications for surgical treatment of calca-
neus fractures exists. However, the following advantages are commonly accepted:
anatomic reduction of the joint surfaces as well as restoration of height, axis, and
external shape of the calcaneus. Thus, the risk of posttraumatic arthritis in particular
of the subtalar joint and painful hindfoot deformities should be reduced.
Biomechanical experiments have shown that even small step-offs of 1–2 mm in the
posterior facet of the subtalar joint result in a significant load redistribution [27, 28]
and are accompanied by inferior outcomes in multiple clinical series [3, 4, 11, 14,
24, 25, 29–35]. Extra-articular fractures with substantial dislocation, if left unre-
duced, will lead to hindfoot deformities with subsequent functional limitations,
painful callosities, problems with shoewear, and soft tissue impingement [8, 36].
Due to these findings, surgical treatment is generally recommended for intra-

articular calcaneal fractures with joint displacement of 2 mm and more and extra-
articular fractures with a varus deformity of more than 5°, valgus deformity of more
than 10°, and those with significant (20% or more) flattening, broadening, or short-
ening of the calcaneus.
Consequently, nonoperative treatment is recommended in non- or minimally dis-
placed intra-articular fractures and extra-articular fractures without a substantial
hindfoot deformity [8]. Functional treatment with partial weight-bearing of 20 kg
on the injured foot and motion exercises aims at early rehabilitation in these patients.
Depending on the type of fracture and bone quality, a progression to full weight-
bearing is possible after 6–10 weeks. Nonoperative treatment is also indicated in the
presence of contraindications to surgery.
Contraindications to open reduction and internal fixation are local infections or
infection-prone wounds, systemic disorders with immunodeficiency such as chemo-
therapy or HIV, consuming diseases, poorly controlled diabetes mellitus (particu-
larly with neuropathy), neurovascular insufficiency, patient noncompliance, and
several preexisting deformities. Regardless of the patient’s age, the therapy should
be tailored to the functional demand, comorbidities, and compliance [18].
6 Treatment
6.1 Emergency Procedures
Open fractures, soft tissues at risk from the pressure of grossly dislocated bony frag-
ments, and fractures with an acute compartment syndrome require emergency sur-
gery. Open wounds require an early and adequate debridement followed by an
extensive lavage and gross reduction of the fracture as well as an appropriate antibi-
otic therapy [37]. Early, stable soft tissue coverage is of utmost importance in order
to avoid deep soft tissue and bone infection with its deleterious consequences [38].
In many instances, this will require local or free flap coverage [39]. With these
staged treatment protocols, complication rates could be reduced in more recent
studies [40].
Acute compartment syndrome is reported in 1–10% of all intra-articular calca-
neus fractures [41, 42]. The diagnosis is made clinically. In unconscious patients,
tissue pressure exceeding 25–30 mmHg as determined with multiple stick measure-
ments demands a medial fasciotomy [43, 44]. This will release the medial, lateral,
and central (deep posterior or calcaneal) compartments, which is mostly sufficient
in case of an isolated calcaneal fracture. In case of a more complex foot trauma, an
additional dorsal fasciotomy may be required which can be carried out as a single or
double incision [43]. Because there is a direct connection between the deep poste-
rior compartments of the lower leg and foot along the course of the deep flexor
tendons, the possible combination of a lower leg and foot compartment syndrome
has to be borne in mind [7]. The intrinsic foot muscles appear to be particularly
vulnerable to elevated compartment pressure, resulting in the development of claw
toes [44].
In closed fractures, imminent incarceration of the soft tissue by grossly displaced
fragments of the calcaneus also calls for an urgent reduction in order to avoid a full-
thickness skin necrosis [45]. A typical example is the so-called “beak” fracture. In
this extra-articular tongue-type fracture, the Achilles tendon pulls on the fragment
of the superior tuberosity and the severe dislocation leads to pressure by the frag-
ment to the skin over the dorsal aspect of the heel [18]. In a substantial number of
cases, these tuberosity avulsion fractures either produce an open wound or severe
soft tissue compromise requiring urgent surgery [19, 46]. Persistent pressure
through the displaced fragment will rapidly lead to skin necrosis over the Achilles
tendon insertion which is particularly difficult to treat. These mostly extra-articular
fractures are exposed through a vertical posterolateral approach lateral to the
Achilles tendon. Purely percutaneous lag screw fixation may lead to catastrophic
failure of fixation, particularly with osteoporotic bone quality in elderly patients or
diabetics [46]. Therefore, supplementary tension band wiring through cannulated
screws or lateral interlocking plates are preferred in these patients in order to achieve
a more stable fixation [47, 48]. Intercalary fragments from the medial plantar tuber-
osity may even require an additional small medial approach that will be described
below [49].
In open fractures, polytraumatized patients with calcaneal fractures or closed
calcaneal fractures with highly critical soft tissue conditions, percutaneous reduc-
tion, and temporary external and/or K-wire fixation are indicated for soft tissue
protection or recovery and to counteract soft tissue contracture [50]. An external
fixator can be applied tibiometatarsal in addition to the percutaneous K-wire fixa-
tion of the tuberosity into the talus and/or cuboid. Alternatively, a three-point exter-
nal fixator is introduced from medial into the calcaneal tuberosity, the talar head,
and the navicular or medial cuneiform. With these procedures, restoration of the
overall geometry of the calcaneus is maintained until definite internal fixation
becomes feasible.
In closed fractures, the initial treatment aims at reduction of the initial swelling
and hematoma with ice, rest, and elevation of the foot. If open reduction and internal
fixation via an extensile lateral approach are planned, definite surgery is delayed
until the soft tissue conditions are improved. This is mostly achieved within 2 weeks
following the injury.
With less invasive reduction techniques, the time to surgery has become signifi-
cantly shorter and even acute fixation is safe when using a sinus tarsi approach for
calcaneal fracture fixation [48, 51]. When using percutaneous techniques, early
reduction and fixation is generally advised because delayed reduction may become
difficult if not impossible with purely percutaneous methods once fibrous healing
has set in [52].
7 Operative Treatment
7.1 Percutaneous Fixation
Besides temporary measures as outlined above, percutaneous reduction and screw

fixation are the treatment of choice for displaced extra-articular fractures and
Sanders type IIC fractures, i.e., simple intra-articular fractures with the posterior
facet being displaced as a whole [50, 53]. With precise control of joint reduction
with the use of subtalar arthroscopy, this technique can also be applied to simple
(Sanders types IIA and IIB) intra-articular fractures with just one displaced fracture
line across the subtalar joint [52–55]. Percutaneous techniques also have a role in
patients with critical soft tissue conditions. However, performing percutaneous
reduction and fixation irrespective of the type of calcaneal fracture and without
adequate control of reduction carries the risk of inadequate reduction and loss of
fixation [50].
The crucial step for most of these injuries is reduction of the displaced tuberosity
to the sustentacular fragment. This can be achieved with a Schanz screw with
T-handle introduced parallel the superior border of the tuberosity: the Westhues/
Essex-Lopresti manoeuvre [23, 56]. When the handle is moved downwards, the
tuberosity-joint angle is restored. Varus or valgus deformity can be corrected with
the same manoeuvre by moving the handle sidewards. For intra-articular simple
tongue-type fractures, this will also restore joint congruity [53]. In joint depression
fractures, the depressed articular fragment has to be manipulated separately with a
K-wire, elevator, or pestle [52].
Anatomic joint reduction is controlled with subtalar arthroscopy that is carried
out via the standard anterolateral and posterolateral portals [50]. This technique
requires a thorough understanding of the complex three-dimensional anatomy of the
calcaneus and expertise in small-joint arthroscopy. The surgeon should not be overly
zealous to achieve anatomic reduction by purely percutaneous methods. After two
or three failed attempts, conversion to a less invasive fixation using the existing
arthroscopic portals is advised in order not to exert too much strain on the soft tis-
sues while irrigating the joint for arthroscopy [50].
7.2 Less Invasive Fixation Via a Sinus Tarsi Approach
Over the last decade, less invasive reduction via a small oblique lateral approach
over the sinus tarsi has gained increasing popularity for less invasive reduction and
fixation of a wide range of calcaneal fractures [48, 57–59]. It allows a direct vision
on the displaced subtalar joint and manipulation of the articular fragments from the
sinus tarsi. This is combined with percutaneous reduction and fixation techniques.
It may also be used for direct access to the joint if an attempted percutaneous reduc-
tion proves impossible [50]. The sinus tarsi approach may be applied to all Sanders
type II and the majority of Sanders type III fractures. For Sanders type IV fractures,
an individual decision has to be made between internal fixation via an extensile
lateral or sinus tarsi approach and primary subtalar fusion if reconstruction of the
subtalar joint does not appear feasible [8, 10, 60].
The patient is placed in a lateral decubitus position on a beanbag on the uninjured
side. The operative limb is draped fully mobile and flexed at the knee. Protective
padding is placed beneath the extended contralateral limb for protection of the pero-
neal nerve, and an operating platform with padding is placed beneath the operative
limb [49]. A tourniquet is placed on the thigh and inflated until joint reconstruction
has been achieved and controlled.
The skin incision starts at the tip of the fibula above the peroneal tendons and
extends 2–3 cm distally towards the anterior process. It follows along the superior
aspect of the calcaneus to allow placement of a small plate at the end of the proce-
dure. The sural nerve and lateral calcaneal artery are situated below the incision and
the lateral branches of the superficial peroneal nerve are well dorsal. The sural nerve
has a communicating branch to the superficial peroneal nerve that may be injured
even with a sinus tarsi approach [61]. However, this branch seems to be present in
only half of the individuals and its clinical relevance remains unclear [62].
Several variants of the sinus tarsi approach have been described. In the authors’
preference, the incision is directed towards the fourth metatarsal. This way, the
approach can be extended distally along the “lateral utility” line [63] between the tip
of the fibula and the fourth metatarsal base if required. This will be particularly use-
ful if there is comminution at the anterior calcaneal process and involvement of the
calcaneocuboid joint. With an incision running towards the fifth metatarsal base,
more wound complications and sural nerve lesions are reported [64]. The peroneal
tendons are gently elevated off the lateral wall of the calcaneus and mobilized dis-
tally within their sheath. Dissection is carried down to the joint. The fat pad in the
sinus tarsi is removed to allow adequate visualization. The lateral capsule of the
subtalar joint, if still intact, is incised. Joint visualization can be improved by exert-
ing a varus stress on the heel or placing a collinear distractor via stab incisions into
the distal fibula and calcaneal tuberosity.
For direct manipulation of the tuberosity fragment, a 4.5 mm Schanz screw with
T-handle is introduced via a stab incision into the posterior tuberosity from either
posterior [4] or lateral [32]. Levering of the handle loosens the impacted intra-
articular fragments. The impacted superolateral articular fragment is carefully ele-
vated from the body of the calcaneus with either a posterior Schanz screw or a
periosteal elevator placed beneath the entire fragment for gentle disimpaction. Any
residual hematoma, debris, and small intercalary fragments are removed from the
joint and between the main fragments.
In a crucial first step, the main tuberosity fragment has to be brought downward
and medially beneath the sustentacular fragment with an elevator introduced as a
lever from the sinus tarsi between these two fragments. This manoeuvre restores the
medial wall and creates the room for the lateral articular fragments of the posterior
facet (Fig. 5). One or two K wires are inserted from the tuberosity just inside the
a b c
Fig. 5 Principle of tuberosity reduction and restoration of the medial wall as a prerequisite for
lateral subtalar joint reconstruction. (a) The superolateral joint fragment is gently disimpacted. (b)
The tuberosity fragment is levered medially and caudally thus restoring the medial wall. (c) This
manoeuvre allows fine reduction of the superolateral joint fragment(s). (From: Zwipp and
Rammelt [96])
medial wall up to the fracture. Following reduction of the main fragments, the
K-wires are advanced along the medial wall into the sustentaculum and reduction is
controlled with an axial x-ray. If the height of the tuberosity is not adequately
restored at this step, anatomic reduction of the lateral (and intermediate) joint frag-
ments will be difficult – if not impossible – later on. Both reduction of the tuberosity
and visualization of the subtalar joint can be facilitated by placing a collinear dis-
tractor between the tip of the fibula and the plantar aspect of the tuberosity via stab
incisions.
Congruity of the subtalar joint is then restored stepwise starting medially with
the sustentacular fragment. The latter was found to be either angulated, translated
medially, or fractured in 42% of intra-articular calcaneal fractures in one study [65].
However, the medial talocalcaneal ligaments remain intact and reduction of the
medial wall as outlined above will result in correct positioning of the sustentacular
fragment in most cases. If still tilted or shifted, reduction must be repeated until it is
congruent to the medial facet of the talus. In rare cases, comminute fractures of the
sustentaculum require an additional direct medial approach in order to anatomically
reduce the medial facet [2].
In Sanders type II joint depression fractures, the impacted lateral articular frag-
ment is lifted up gently with an osteotome or elevator and thus aligned to the medial
fragment under direct vision. K-wires are introduced from lateral up to the level of
the fracture and advanced into the medial fragment following reduction of the joint
surface. Drill sleeves inserted over the K-wires may be used to manipulate the frag-
ments [66]. In tongue-type fractures, the lateral joint fragment is connected to the
superior tuberosity and lifted and derotated with the help of the Schanz screw
(Fig. 6). In Sanders types IIA and IIB, the sinus tarsi approach allows for direct
a b
Fig. 6 (a) Visualization of the subtalar joint through the sinus tarsi approach is facilitated with a
collinear distractor placed percutaneously between the distal fibula and plantar tuberosity. (b) The
tongue fragment carrying the lateral part of the subtalar joint is manipulated with a Schanz screw
introduced from posterior (Westhues/Essex-Lopresti manoeuvre). (same patient as in Figs. 3 and 4)
control of reduction. Rotational reduction of the posterior component of the tongue

fragment is essential to prevent conflict with shoe wear which may result from a
prominent contour of the posterior tuberosity. In Sanders type III (and IV) fractures,
the intermediate joint fragment(s) are reduced to the sustentacular fragment and
fixed with one or two K-wires that are drilled through the medial cortex and the skin
until they are flush with the intermediate fragment laterally [2]. Small intermediate
fragments with an intact cartilage cover that are not amenable to screw fixation may
alternatively be definitely fixed with “lost” K-wires or absorbable pins [67]. The
depressed lateral portion of the posterior facet is reduced to the medial and interme-
diate fragment(s) and the K-wires are drilled back from medial to lateral (Fig. 7).
Anatomic reduction of the subtalar joint is controlled visually by tilting the
reconstructed joint block into varus or collinear distraction and with intraoperative
Brodén projections. Like with percutaneous reduction or open reduction via an
extensile approach, precise control of articular reduction can be achieved with dry
arthroscopy [68]. This is a quick and simple procedure using the sinus tarsi approach
as an anterolateral portal to introduce a small-joint arthroscope (2.7 mm, 30°) to
visualize the whole posterior facet (Fig. 8). It is particularly useful with multiple
fragmentation of the posterior facet or fracture lines that run far medially and there-
fore are hard to fully visualize via the sinus tarsi approach. If a residual intra-
articular step-off is found at this stage, the K-wires introduced from lateral are
removed and joint reduction repeated. After exact reduction is confirmed, one or
two independent screws are inserted from the lateral wall into the sustentaculum to
stabilize the articular portion of the calcaneus. To hit the sustentaculum, the screw
trajectory must start below the subtalar joint near the angle of Gissane and be aimed
approximately 10° upwards and anteriorly [59]. If a second screw is to be
a b c
Fig. 7 Principle of step-wise reduction of the posterior facet of the subtalar joint from medial to
lateral (left panel from: Zwipp and Rammelt [96]). (a) In the presence of a Sanders type III frac-
ture, (b) the central (intermediate) fragment is reduced under direct vision to the medial fragment
while applying joint distraction. The K-wire is pulled out medially until it is flush with the lateral
border of the central fragment. (c) The lateral fragment is then reduced to the central one and the
K-wire is driven back laterally. The medial (M), central (C), and lateral (L) joint fragments are
temporarily held with K-wires. Reduction is controlled by fluoroscopic Brodén projections (right
panel). (same patient as in Figs. 3, 4, and 6)
a b
Fig. 8 After anatomic reduction is confirmed by direct visualization (a) and dry subtalar arthros-
copy (b), if needed, independent screws are placed to hold the joint fragments. Further screws are
inserted longitudinally after fine reduction of the tuberosity and anterior process fragments (c).
Finally, a lateral plate is introduced along the crucial angle of Gissane through the sinus tarsi
approach. (same patient as in Figs. 3, 4, 6, and 7)
introduced into the posterior part of the joint block, the screw trajectory starts just
below the joint and is angled downwards. Correct screw positioning is controlled
fluoroscopically.
At this stage, fine alignment of the tuberosity fragment to the reconstructed sub-
talar joint block is checked and any residual loss of height, varus, or valgus of the
tuberosity is corrected by using the inserted Schanz screw as a lever. The tuberosity
is fixed temporarily to the joint block with K-wires.
In a next step, the anterior process is aligned with the posterior part and the cal-
caneus is fixed with axial K-wires. Reduction is checked at the strong cortical bone
that gives an accurate read at the crucial angle of Gissane [66]. If there is displace-
ment of the calcaneocuboid joint, the incision is extended along the lateral utility
line [63] in order to reduce the joint under direct vision. The articular fragments are
reduced from medial to lateral using the corresponding articular surface of the
cuboid as a template. The fragments are held temporarily with K-wires that are
introduced parallel to the joint into the subchondral bone. Restoration of the ana-
tomical shape of the calcaneus is confirmed fluoroscopically.
Definite fixation of the calcaneus supplements the independent screws that have
been introduced to hold joint reduction. This can be achieved with further percutane-
ous screws [8, 57, 59], an intramedullary nail with locking screws introduced percu-
taneously [69, 70], or a combination of screws and a small anatomic plate that is sled
in through the approach and tunnelled beneath the peroneal tendons [58, 66]. The
screws are typically placed into the medial wall and longitudinally from the poste-
rior tuberosity into the subchondral cortex of the anterior process. In joint depression
fractures, additional screws are introduced from the inferior tuberosity into the “tha-
lamic” portion of the calcaneus just beneath the subtalar joint [58]. In tongue-type
fractures, one or two screws are introduced from the superior portion of the tuberos-
ity into the inferior cortex of the calcaneal body. If warranted, these can be placed as
lag screws. The plates are typically locking plates with variable angle screw place-
ment [49]. They are positioned beneath and parallel to the angle of Gissane and
subtalar joint (Fig. 9). The decision on the kind of definite fixation is based on the
individual fracture anatomy, bone quality, and surgeon preference and experience.
a b c
Fig. 9 Reduction of the calcaneal shape and implant positioning is verified with fluoroscopic (a)
lateral, (b) axial, and (c) Brodén projections. (same patient as in Figs. 3, 4, 6, 7, and 8)
7.3 Open Reduction and Internal Fixation Via an Extensile

Lateral Approach
For many years, open reduction and plate fixation using an extensile lateral approach
have been the most widely used method for operative treatment of the majority of
displaced intra-articular calcaneus fractures. It offers a complete overview of the
lateral aspect of the calcaneus including the subtalar and calcaneocuboid joints with
direct control of the reduction [2–4, 32]. The major drawback of this approach lies
in the potential for soft tissue-related complications such as wound edge necrosis,
deep soft tissue, and bone infection as well as late problems including arthrofibro-
sis, adhesions of the peroneal tendons, and stiffness of the subtalar joint because of
the extensile soft tissue dissection even in the most experienced of hands [25, 71,
72]. It is still widely used and particularly useful for the treatment of complex frac-
tures with severe dislocation or comminution of the main fragments and blow-out
of the lateral calcaneal wall [10, 49]. A direct lateral approach [73] running
obliquely over the lateral calcaneal wall requires less soft tissue dissection but com-
promises the angiosome of the lateral calcaneal artery and may lead to irritation and
scarring of the peroneal tendons and the sural nerve. It is therefore discouraged.
In analogy to the sinus tarsi approach, the patient is positioned on the non-injured
side with the injured foot draped mobile on a pad. The L-shaped incision starts two
fingers proximal to the tip of the fibula and just lateral to the Achilles tendon and
posterior to the sural nerve and the lateral calcaneal artery. From there, the incision
runs downwards slightly oblique to the Achilles tendon. The horizontal limb of the
incision is placed along the junction of the hairy skin of the lateral foot and glabrous
skin of the heel pad. The demarcation between the two can be easily identified by
compressing the heel. In the angle when the two limbs meet, the incision is slightly
curved and carried out directly to the bone, while a layered incision is carried out
towards the proximal and distal end of the approach to protect the sural nerve and
lateral calcaneal artery in the subcutaneous tissue. Distally, the horizontal limb con-
tinues to a gentle anterior curve along the skin creases to allow access to the calca-
neocuboid joint [45]. Care is taken not to dissect the abductor digiti quinti muscle
that may be used as a local flap in case of wound edge necrosis.
A full-thickness fasciocutaneous flap is raised from the lateral calcaneal wall that
includes the peroneal tendons. The latter are mobilized within their sheath that is
dissected sharply only at the peroneal tubercle. The subtalar and calcaneocuboid
joints are exposed at full length and the capsule incised. The flap is held by bent
K-wires that are introduced into the lateral process of the talus and the cuboid.
The sequence of reduction is essentially the same as with the sinus tarsi approach.
A 4.5 mm Schanz screw with a handle is introduced via a stab incision into the
tuberosity either from lateral [32] or posterior [4], the latter resembling the tech-
nique popularized by Westhues in a German publication from 1935 [56] and later in
English by Gissane and Essex-Lopresti [23]. Lever movements of the handle loosen
the tuberosity and the impacted intra-articular fragments of the subtalar joint. The
bulged lateral wall is folded away and the depressed joint fragments become visible.
Loose fragments may be put on the back table or are secured with a suture.
The tuberosity fragment is pulled plantar and medially beneath the sustentacular
fragment with the help of the Schanz screw and an elevator introduced between the
two main fragments (see Fig. 5) and fixed temporarily with K-wires [45]. Reduction
of the medial wall is controlled fluoroscopically. This manoeuvre regularly realigns
the sustentacular fragment and the medial facet of the subtalar joint and creates
room for reduction of the lateral and intermediate joint fragments of the posterior
facet. These fragments are reduced starting from medial to lateral and temporarily
fixed with K-wires (see Fig. 7). Small intermediate fragments may be definitely
fixed with resorbable pins or “lost” K-wires [67]. If soft tissue restraints prevent
anatomic reduction of the lateral joint fragment in tongue-type fractures, anatomic
reduction can be facilitated by an osteotomy posterior the joint surface, turning the
tongue type into a joint depression type fracture [74].
Anatomic reduction of the subtalar joint is controlled visually and fluoroscopi-
cally with Brodén views. In cases of multiple fragmentation or fracture lines that are
situated far medially, the quality of reduction should be checked by open subtalar
arthroscopy as outlined above [75] or intra-operative 3D fluoroscopy [76]. If remain-
ing step-offs are found, the K-wires are removed and reduction repeated. Studies
have shown that this may be necessary in more than 20% of cases, even though the
2D fluoroscopic images have been judged as uneventful [75, 76].
After anatomic reduction of the subtalar joint has been confirmed, one or two
independent 3.5 mm screws are inserted underneath the posterior facet into the sus-
tentaculum. Fine reduction of the tuberosity fragment to the reconstructed joint
block, if necessary, is achieved by using the Schanz screw to correct any residual
loss of heel height and any varus or valgus deformity. The tuberosity is fixed tempo-
rarily to the joint block with K-wires.
The anterior process is reduced last. The calcaneocuboid joint is visualized in the
anterior part of the incision. In case of joint incongruity, the displaced articular frag-
ments are reduced congruently to the cuboid from medial to lateral by using the
joint facet of the cuboid as a template. A collinear distractor between the calcaneus
and cuboid may be helpful for restoring the length of the anterior calcaneal process
and controlling joint reduction. The articular fragments stabilized temporarily with
K-wires introduced from lateral into the cortex parallel to the joint surface. The
reconstructed anterior process, which is typically displaced upwards by the pull of
the bifurcate ligament, is then brought down as a whole, thus recreating the crucial
angle of Gissane and reducing the primary fracture line that should now fit anatomi-
cally along the strong superolateral cortex. The main fragments are retained with
additional K-wires along the longitudinal axis of the calcaneus and the anatomical
restoration of its overall shape is controlled fluoroscopically.
If the shape of the calcaneus has been restored anatomically, the bulged lateral
wall fragments should be without any overlap after being folded back. The impac-
tion force at the time of injury regularly leaves a bony defect beneath the subtalar
joint after reduction. However, this is the area where trabeculae are sparse physio-
logically at the neutral triangle. Consequently, there is no evidence for the need of
defect filling with autologous grafting or bone substitutes following reconstruction

of calcaneal fractures [45, 77].
Definite fixation is achieved with a lateral plate that should fit without bending
along its longitudinal axis. Various conventional, locking, or polyaxially locking
plates for internal fixation are available [45]. The plates are usually anatomically
shaped to fit the lateral aspect of the calcaneus. The plate is fixed to the calcaneus
with two screws each into the anterior process, the thalamic portion under the pos-
terior facet and the tuberosity [2]. The number and position of screws may vary
depending on the individual fracture anatomy and bone quality. There is no clear
evidence for superiority of locking over nonlocking plates based on biomechanical
studies [78]. The first screws should be inserted in a nonlocking manner in order to
increase friction of the plate to the underlying bone and avoid lateral protrusion with
irritation of the peroneal tendons [79]. Following fixation of the plate, all K-wires
(except for “lost” subchondral K-wires used for fixation of small articular frag-
ments) and the Schanz screw are removed. The final result is documented fluoro-
scopically with lateral, axial, dorsoplantar, and oblique (20° Brodén) of views. In
complex fracture patterns, intraoperative 3D fluoroscopy may provide a more reli-
able assessment of reduction and implant placement [76]. In case of doubt, a post-
operative CT scan provides better resolution and anatomical detail, particularly with
artifact suppression [80].
7.4 Lateral Utility Approach for Calcaneal

Fracture-Dislocations
For fracture-dislocations with the calcaneal body fragment carrying the tuberosity
and most of the subtalar joint being displaced as a whole superiorly and laterally
(Fig. 10), an extensile lateral approach is not useful because the lateral wall is com-
pletely intact and soft tissue dissection would have to be carried on even more
extensive over the distal fibula. In these rare cases, an extension of the sinus tarsi
approach starting over the distal fibula is used to allow access to the dislocated sub-
talar joint from above [2]. The approach can be extended posteriorly to access the
tip of the fibular and peroneal retinacle and anteriorly to access the anterior process
and calcaneocuboid joint along the lateral utility line (Fig. 11). This will be required
regularly because fracture-dislocations are frequently accompanied by direct com-
pression fractures of the distal fibula with avulsions of the peroneal retinaculum and
fractures of the anterior process running into the calcaneocuboid joint [22].
When performing the skin incision, the dislocated peroneal tendons will appear
subcutaneously in front of the lateral malleolus [59]. They are held away with a soft
strap. The articular surface of the dislocated lateral calcaneal fragment and the pri-
mary fracture line are identified (Fig. 11). The fracture line is entered through the
posterior facet with an osteotome or smooth elevator and the lateral portion of the
joint levered back under the talus. In cases of delayed presentation, a collinear
a b c
Fig. 10 (a) Lateral view of a calcaneal fracture-dislocation with enormous overlap of the lateral
contours of the talus and calcaneus (“double density sign”). (b) The anteroposterior view of the
ankle shows direct fracture of the distal fibula through impaction of the displaced calcaneal body
fragment. (c) A semicoronal CT image shows displacement along the primary fracture line
a b
Fig. 11 (a) The dislocation approach [2] allows direct access to the dislocated calcaneal body
carrying most of the subtalar joint facet. (b) It can be extended posteriorly to access the fractured
tip of the fibula and peroneal retinacle and anteriorly to access the anterior process and displaced
calcaneocuboid (CC) joint along the lateral utility line [63]. (same patient as in Fig. 10)
distractor with pins introduced into the distal fibula or talus and calcaneal tuberosity
may be helpful. The subtalar joint and fracture line are cleared from debris and
small fragments – above all from the lateral talar process that is fractured as a result
of the injury in about 70% of cases [22].
The intra-articular fracture of the posterior facet is then reduced under direct
visualization. Compression of the main fragments is achieved with a large pointed
reduction clamp that is placed over the lateral wall and the sustentaculum via a
medial stab incision across the sagittal fracture line [22, 59]. K-wires introduced
from lateral to medial provide provisional fixation.
The primary sagittal fracture is stabilized with lag screws introduced perpen-
dicular to the fracture line and parallel to the subtalar and calcaneocuboid joints, if
involved (Fig. 12). In case of significant comminution of the anterior process, an
additional small plate attached to the subchondral cortical bone is added for final
a b c
Fig. 12 (a) Internal fixation of facture-dislocations is achieved with lag screws introduced perpen-
dicular to the primary fracture line with the first screw being directed at the sustentaculum tali.
Further screws and K-wires (alternatively small plates) are used to fix fractures of the anterior
process involving the calcaneocuboid joint and the distal fibula including bony avulsions of the
superior peroneal retinaculum. (b) The anteroposterior view of the ankle shows decompression of
the fibular tip. (c) Postoperative CT scanning demonstrates anatomic reconstruction of the calca-
neal shape and subtalar joint
fixation [49]. In case of a dislocated fracture of the distal fibula from the direct com-
pression caused by the dislocated tuberosity fragment, the fragments are fixed with
small screws and/or plates [2]. Following fracture fixation, the peroneal tendons can
be easily rerouted into the retrofibular groove and the superior peroneal retinaculum
is reattached [22].
7.5 Sustentacular Approach
There are rare indications that warrant a medial approach. These include displaced
fractures of the sustentaculum tali and the medial plantar tuberosity. The classical
McReynolds approach that is centred over the medial calcaneal wall has a high risk
of damage to the tibial neurovascular bundle. For fractures of the sustentaculum tali
with a displaced medial joint facet, a small direct medial approach is preferred [44].
Because it is impossible to expose the posterior facet of the subtalar joint from
medial, this approach is reserved for isolated fractures of the sustentaculum tali or,
in addition to a lateral approach, in complex fractures with comminution of the
medial calcaneus.
A horizontal incision of about 3 cm is carried out directly over the sustentaculum
tali, which is palpable approximately 1.5 cm below and 1 cm anterior to the tip of
the medial malleolus [16, 49]. After subcutaneous dissection, the posterior tibial
and flexor digitorum longus tendons are held away with soft straps. The posterior
tibial neurovascular bundle lies plantar and usually is not exposed. If exposure of
the medial wall is needed, it is gently mobilized plantar and protected by the flexor
hallucis longus tendon without direct manipulation. The medial joint facet is
reduced under direct vision using the medial facet of the talus as a template [16]. A
pointed curved reduction clamp is applied in analogy to fracture-dislocations.
Simple fractures of the sustentaculum are fixed with compression fractures of the
medial plantar tuberosity screws from medial to lateral, while small plates may be
preferred in case of comminution [16, 81].
7.6 Medial Plantar Approach
Fractures of the medial plantar tuberosity may result from either direct plantar
impaction or avulsion of the plantar fascia. Surgery is indicated only in rare cases of
displaced fractures that may otherwise result in plantar pressure sores, conflict with
shoe wear, or even tarsal tunnel syndrome [45, 82, 83]. The medial process of the
calcaneal tuberosity is approached by a small medial incision of 3 cm parallel to the
sole at the transition to the glabrous skin – that should not be incised [49]. The sub-
cutaneous tissue is dissected carefully in order to avoid the terminal branches of the
lateral plantar nerve. The superior rim of the fracture is cleaned from debris. If there
is more than one plantar fragment, the lateral fragment is reduced first and the
medial one next to the calcaneal body. For reduction, the forefoot is held in maximal
plantar flexion to relax the pull of the plantar aponeurosis and Achilles tendon. The
fragments are fixed with small fragment screws placed from medial [45]. The screw
heads must be flush with the cortex in order to avoid irritation.
7.7 Primary Subtalar Fusion
The indications for performing a primary subtalar fusion are not entirely clear.
Some authors suggest it in all Sanders type IV fractures [10, 24]. A prospective
randomized study did not find significant differences in outcome between primary
fusion and internal fixation for Sanders type IV fractures, with only one secondary
fusion in the internal fixation group [60]. Others found no different secondary fusion
rates after internal fixation of Sanders type II, III, or IV fractures, although patients
with Sanders type IV fractures had inferior long-term outcome [25]. The results
after primary fusion for highly comminuted calcaneal fractures are mixed [84, 85].
In the authors’ preference, primary fusion is reserved for severely comminuted frac-
tures with almost complete loss of the articular surface or compound injuries with
severe soft tissue damage [22, 59]. After open reduction of the calcaneal shape and
internal fixation, the remaining cartilage is removed from the joint surfaces and one
or two large fragment cancellous screws are introduced via a stab incision from the
calcaneal tuberosity into the talar body. It is the authors’ approach to anatomically
reduce and fix even comminuted calcaneal fractures as long as there is a chance to
reasonably reconstruct the subtalar joint [25]. If a secondary subtalar arthrodesis
becomes necessary after primary open reduction and internal fixation, it can be
performed as an in situ fusion on a solidly healed and well-aligned calcaneus which
is easier to perform and associated with better results than corrective fusion for
malunited calcaneal fractures after nonoperative treatment [86].
8 Postoperative Care and Rehabilitation
Postoperatively, the leg is elevated and immobilized in a lower leg splint or cast
until the swelling recedes. Physical therapy aims at early functional rehabilitation
(Fig. 13) and starts at the second postoperative day with active and passive range-
of-motion exercises of the ankle and subtalar joints, if the soft tissue conditions
allow early motion. Patients are allowed to bear partial weight of about 20 kilo-
grams on the injured foot in their own shoes after soft tissue consolidation.
Noncompliant and unreliable patients are completely offloaded in an orthosis or
boot. Weight-bearing is gradually increased after 8–12 weeks, depending on the
type of fracture, bone quality, and radiologic evidence of union (Fig. 14). In case of
bilateral calcaneal fractures, special boots are recommended, which are supported
on the tibial head and eliminate pressure on the heel [2, 18].
Fig. 13 Functional result 8 weeks following surgery. (a) Anatomic axial alignment of the heel is
seen with the patient standing. (b) Range of motion is almost normal with unrestricted eversion,
inversion and dorsiflexion while plantarflexion is mildly restricted on the formerly injured side.
(same patient as in Figs. 3, 4, 6, 7, 8, and 9)
a b
Fig. 14 Standing lateral (a) and axial (b) radiographs and Brodén view (insert in A) 8 weeks fol-
lowing surgery. (same patient as in Figs. 3, 4, 6, 7, 8, 9, and 13)
Implant removal combined with subtalar arthrolysis and tenolysis of the peroneal
tendons 1 year after plate fixation is advised only in case of symptomatic hardware,
soft tissue impingement, or massive arthrofibrosis with restricted range of
motion [75].
9 Complications
9.1 Wound Healing Problems
Issues with wound healing are a common concern after open reduction of calcaneal
fractures in particular when using an extensile lateral approach. These include
delayed wound healing problems, wound edge necrosis, and superficial soft tissue
infections that are reported in up to one third of the patients [25, 71, 72, 76].
Considerably lower numbers are reported for minimally invasive or percutaneous
fixation [52, 57, 58, 70, 75, 87–89]. These wound-healing problems mostly heal
with local antiseptic care and only rarely require a surgical revision.
9.2 Infections
Deep soft tissue and bone infections requiring surgical revision are dreaded compli-
cations after surgical treatment of calcaneus fractures. The numbers provided in the
literature are not easy to interpret because not all authors distinguish between super-
ficial and deep or soft tissue and bone infections and the definitions are not always
clear. Deep infection rates account for up to 1–7% following open reduction via an
extensile approach and lateral plate fixation [25, 84] and increase up to 66.7% in
grade III open calcaneal fractures [37]. Besides open fractures, risk factors include
delay of surgery beyond 14 days after the injury, the number of persons in the oper-
ating room, a high body mass index, diabetes, and smoking [25, 30, 71, 90–92].
Because deep infections require radical, serial debridements of all infected and
necrotic tissue, functional deficits will remain in most cases even after successful
eradication of infection. Multiple studies including several meta-analyses have
demonstrated a significant reduction of wound complications and infections when
using a sinus tarsi approach which also translated into superior outcome in most of
these studies [57, 58, 88, 89, 93].
9.3 Malunions
An inadequate reduction or fixation including nonoperative treatment of displaced,

intra-articular calcaneus fractures regularly leads to painful malunions or nonunions
(Table 1) with serious deterioration of global foot function [8, 18, 45, 63, 86, 94–
96]. Residual step-offs in the subtalar joint aggravate the primary cartilage damage
at the time of injury and result in rapid progression to posttraumatic arthritis. The
typical flattening, broadening, and shortening of the calcaneus result in malalign-
ment of the hindfoot, conflict with shoewear, and soft tissue impingement. Bony
prominences may cause nerve irritation, painful callosities, and ulcerations at the
heel. The bulged lateral wall and a laterally shifted tuberosity result in an impinge-
ment or subluxation of the peroneal tendons, and in extreme cases, a direct abut-
ment of the fibula. Medially, the flexor hallucis longus tendon or tibial nerve might
be entrapped between displaced fragments. Severe malalignment of the calcaneus
leads to malpositioning of the talus in the ankle mortise with the development of
secondary arthritis at the ankle joint [94]. Finally, an unrecognized compartment
syndrome gradually results in rigid deformities like claw toes and cavus due to loss
of intrinsic muscle function [63].
In rare cases of extra-articular malunions and carefully selected patients with
simple, intra-articular malunions and preserved cartilage cover, a joint preserving
corrective osteotomy with lateral decompression, if needed, may be performed [36,
94, 95]. In the majority of cases, a corrective subtalar fusion is required which must
be combined with structural bone grafting, corrective osteotomies of the calcaneus,
Table 1 Classification of calcaneal malunions [94]

Type Quality
0 Any deformity without subtalar arthritis A. Solid malunion
I. Subtalar joint arthritis B. Nonunion
II. Additional hindfoot varus/valgus C. Necrosis
III. Additional loss of height
IV. Additional lateral translation of the tuberosity
V. Additional talar tilt at the ankle joint.
or revision of the ankle joint, according to the individual malunion pattern. While
solid unions (subtype A) require an osteotomy and corrective fixation, nonunions
(subtype B) warrant an additional debridement and cancellous bone grafting.
Avascular necrosis (subtype C) is rare but challenging to treat with resection of all
necrotic bone followed by bone augmentation with corticocancellous or vascular-
ized grafting. In addition, correction of the calcaneal malunion must always be com-
bined with a soft tissue balancing including Achilles tendon lengthening, tenolysis
and rerouting of the peroneal tendons, and tenotomies or transfers for the sequelae
of compartment syndrome [63].
References
1. Mitchell MJ, McKinley JC, Robinson CM. The epidemiology of calcaneal fractures. Foot
(Edinb). 2009;19:197–200.
2. Zwipp H, Rammelt S, Barthel S. Calcaneal fractures-open reduction and internal fixation
(ORIF). Injury. 2004;35 Suppl 2:SB46–54.
3. Sanders R, Fortin P, DiPasquale T, Walling A. Operative treatment in 120 displaced intraarticu-
lar calcaneal fractures. Results using a prognostic computed tomography scan classification.
Clin Orthop Relat Res. 1993;290:87–95.
4. Zwipp H, Tscherne H, Thermann H, Weber T. Osteosynthesis of displaced intraarticular frac-
tures of the calcaneus. Results in 123 cases. Clin Orthop. 1993;290:76–86.
5. Bartoníček J, Rammelt S, Naňka O. Anatomy of the subtalar joint. Foot Ankle Clin.
2018;23(3):315–34.
6. Firoozabadi R, Kramer PA, Benirschke SK. Plantar medial wounds associated with calcaneal
fractures. Foot Ankle Int. 2013;34(7):941–8.
7. Manoli A 2nd, Fakhouri AJ, Weber TG. Concurrent compartment syndromes of the foot and
leg. Foot Ankle. 1993;14(6):339–45.
8. Rammelt S, Sangeorzan BJ, Swords MP. Calcaneal fractures - should we or should we not
operate? Indian J Orthop. 2018;52(3):220–30.
9. Sharr PJ, Mangupli MM, Winson IG, Buckley RE. Current management options for displaced
intra-articular calcaneal fractures: non-operative, ORIF, minimally invasive reduction and
fixation or primary ORIF and subtalar arthrodesis. A contemporary review. Foot Ankle Surg.
2016;22(1):1–8.
10. Sanders R, Vaupel ZM, Erdogan M, et al. Operative treatment of displaced intraarticular cal-
caneal fractures: long-term (10–20 years) results in 108 fractures using a prognostic CT clas-
sification. J Orthop Trauma. 2014;28:551–63.
11. Makki D, Alnajjar HM, Walkay S, Ramkumar U, Watson AJ, Allen PW. Osteosynthesis of
displaced intra-articular fractures of the calcaneum: a long-term review of 47 cases. J Bone
Joint Surg Br. 2010;92(5):693–700.
12. Zhang W, Lin F, Chen E, Xue D, Pan Z. Operative versus nonoperative treatment of displaced
intra-articular calcaneal fractures: a meta-analysis of randomized controlled trials. J Orthop
Trauma. 2016;30(3):e75–81.
13. Miric A, Patterson BM. Pathoanatomy of intra-articular fractures of the calcaneus. J Bone
Joint Surg Am. 1998;80(2):207–12.
14. Dürr C, Apinun J, Mittlmeier T, Rammelt S. Foot function after surgically treated intraarticular
calcaneal fractures: correlation of clinical and pedobarographic results of 65 patients followed
for 8 years. J Orthop Trauma. 2018;32(12):593–600.
15. Rupprecht M, Pogoda P, Barvencik F, Münch C, Püschel K, Rueger JM, Amling M. The cal-
caneus as the site of manifestation for osteoporosis-associated fractures: age- and sex-specific
changes in calcaneal morphology correlate with the incidence and severity of intra-articular
calcaneal fractures. Unfallchirurg. 2007;110(3):197–204.
16. Dürr C, Zwipp H, Rammelt S. Fractures of the sustentaculum tali. Oper Orthop Traumatol.
2013;25(6):569–78.
17. Biehl WC 3rd, Morgan JM, Wagner FW Jr, Gabriel R. Neuropathic calcaneal tuberosity avul-
sion fractures. Clin Orthop Relat Res. 1993;296:8–13.
18. Rammelt S, Zwipp H. Calcaneus fractures: facts, controversies and recent developments.
Injury. 2004;35(5):443–61.
19. Gardner MJ, Nork SE, Barei DP, Kramer PA, Sangeorzan BJ, Benirschke SK. Secondary soft
tissue compromise in tongue-type calcaneus fractures. J Orthop Trauma. 2008;22(7):439–45.
20. Ahrberg AB, Leimcke B, Tiemann AH, et al. Missed foot fractures in polytrauma patients:
a retrospective cohort study. Patient Saf Surg. 2014;8:10. https://doi.org/10.1186/1754-
9493-8-10.
21. Kim DH, Berkowitz MJ. Double density sign variant in fracture-dislocation of the calcaneus:
clinical tip. Foot Ankle Int. 2012;33(6):524–5.
22. Rammelt S, Marx C, Swords G, Swords M. Recognition, treatment and outcome
of calcaneal fracture-dislocation. Foot Ankle Int. 2021;42(6):706–13. https://doi.
org/10.1177/1071100720980012.
23. Essex-Lopresti P. The mechanism, reduction technique, andresults in fractures of the os calcis.
Br J Surg. 1952;39:395–419.
24. Sanders R. Intra-articular fractures of the calcaneus: present state of the art. J Orthop Trauma.
1992;6(2):252–65.
25. Rammelt S, Zwipp H, Schneiders W, Dürr C. Severity of injury predicts subsequent func-
tion in surgically treated displaced intra-articular calcaneal fractures. Clin Orthop Relat Res.
2013;471:2885–98.
26. Meinberg EG, Agel J, Roberts CS, Karam MD, Kellam JF. Fracture and dislocation classifica-
tion compendium. J Orthop Trauma. 2018;32 Suppl 1:S1–S170.
27. Mulcahy DM, McCormack DM, Stephens MM. Intra-articular calcaneal fractures: effect of
open reduction and internal fixation on the contact characteristics of the subtalar joint. Foot
Ankle Int. 1998;19(12):842–8.
28. Sangeorzan BJ, Ananthakrishnan D, Tencer AF. Contact characteristics of the subtalar joint
after a simulated calcaneus fracture. J Orthop Trauma. 1995;9(3):251–8.
29. Buckley R, Tough S, McCormack R, et al. Operative compared with nonoperative treatment of
displaced intra- articular calcaneal fractures: a prospective, randomized, controlled multicenter
trial. J Bone Joint Surg Am. 2002;84-A(10):1733–44.
30. Rammelt S, Barthel S, Biewener A, Gavlik JM, Zwipp H. Calcaneusfrakturen-offene
Reposition und interne Stabilisierung. Zentralbl Chir. 2003;128(6):517–28.
31. Janzen DL, Connell DG, Munk PL, Buckley RE, Meek RN, Schechter MT. Intraarticular frac-
tures of the calcaneus: value of CT findings in determining prognosis. AJR Am J Roentgenol.
1992;158(6):1271–4.
32. Benirschke SK, Sangeorzan BJ. Extensive intraarticular fractures of the foot. Surgical man-
agement of calcaneal fractures. Clin Orthop. 1993;292:128–34.
33. Kurozumi T, Jinno Y, Sato T, Inoue H, Aitani T, Okuda K. Open reduction for intra-articular cal-
caneal fractures: evaluation using computed tomography. Foot Ankle Int. 2003;24(12):942–8.
34. Jardé O, Havet E, Alovor G, Carpentier P, Meunier W. Intra-articular calcaneal fractures: clini-
cal and radiological results of 54 cases with a minimum follow-up of 7 years. Med Chir Pied.
2005;21:107–17.
35. van Hoeve S, de Vos J, Verbruggen JP, Willems P, Meijer K, Poeze M. Gait analysis and func-
tional outcome after calcaneal fracture. J Bone Joint Surg Am. 2015;97(22):1879–88.
36. Ketz J, Clare M, Sanders R. Corrective osteotomies for malunited extra-articular calcaneal
fractures. Foot Ankle Clin. 2016;21(1):135–45.
37. Spierings KE, Min M, Nooijen LE, Swords MP, Schepers T. Managing the open calcaneal
fracture: a systematic review. Foot Ankle Surg. 2019;25(6):707–13.
38. Heier KA, Infante AF, Walling AK, Sanders RW. Open fractures of the calcaneus: soft-tissue
injury determines outcome. J Bone Joint Surg Am. 2003;85-A(12):2276–82.
39. Brenner P, Rammelt S, Gavlik JM, Zwipp H. Early soft tissue coverage after complex foot
trauma. World J Surg. 2001;25(5):603–9.
40. Beltran MJ, Collinge CA. Outcomes of high-grade open calcaneus fractures managed with
open reduction via the medial wound and percutaneous screw fixation. J Orthop Trauma.
2012;26(11):662–70.
41. Mittlmeier T, Machler G, Lob G, Mutschler W, Bauer G, Vogl T. Compartment syndrome of
the foot after intraarticular calcaneal fracture. Clin Orthop. 1991;269:241–8.
42. Park YH, Lee JW, Hong JY, Choi GW, Kim HJ. Predictors of compartment syndrome of the
foot after fracture of the calcaneus. Bone Joint J. 2018;100-B(3):303–8.
43. Sands AK, Rammelt S, Manoli A. Foot compartment syndrome – a clinical review. Fuss
Sprungg. 2015;13(1):11–21.
44. Zwipp H. Chirurgie des Fußes. Wien, New York: Springer; 1994.
45. Sanders R, Rammelt S. Fractures of the calcaneus. In: Coughlin MJ, Saltzman CR, Anderson
JB, editors. Mann’s surgery of the foot & ankle. 9th ed. St. Louis: Elsevier; 2013. p. 2041–100.
46. Mitchell PM, OʼNeill DE, Branch E, Mir HR, Sanders RW, Collinge CA. Calcaneal avulsion
fractures: a multicenter analysis of soft-tissue compromise and early fixation failure. J Orthop
Trauma. 2019;33(11):e422–6.
47. Giordano V, Godoy-Santos AL, de Souza FS, Koch HA, de Cesar NC, Rammelt S. Combined
lag screw and cerclage wire fixation for calcaneal tube rosity avulsion fractures. Case Rep
Orthop. 2018;2018:6207024. https://doi.org/10.1155/2018/620702.
48. Swords MP, Penny P. Early fixation of calcaneus fractures. Foot Ankle Clin. 2017;22(1):93–104.
49. Rammelt S, Swords M, Dhillon M, Sands A. AO Manual of Fracture Management: Foot &
Ankle. 2020; Stuttgart, New York: Thieme; and Davos: AO Foundation.
50. Rammelt S, Amlang M, Barthel S, Zwipp H. Minimally-invasive treatment of calcaneal frac-
tures. Injury. 2004;35 Suppl 2:SB55–63.
51. Joseph NM, Benedick A, McMellen C, Napora J, Wetzel R, Sontich J, Ochenjele G. Acute
fixation of displaced intra-articular calcaneus fractures is safe using the sinus tarsi approach. J
Orthop Trauma. 2021;35(6):289–29.
52. Rammelt S, Amlang M, Barthel S, Gavlik JM, Zwipp H. Percutaneous treatment of less severe
intraarticular calcaneal fractures. Clin Orthop Relat Res. 2010;468(4):983–90.
53. Tornetta P 3rd. Percutaneous treatment of calcaneal fractures. Clin Orthop Relat Res.
2000;375:91–6.
54. Woon CY, Chong KW, Yeo W, Eng-Meng Yeo N, Wong MK. Subtalar arthroscopy and fluro-
socopy in percutaneous fixation of intra-articular calcaneal fractures: the best of both worlds.
J Trauma. 2011;71(4):917–25.
55. Yeap EJ, Rao J, Pan CH, Soelar SA, Younger AS. Is arthroscopic assisted percutaneous screw
fixation as good as open reduction and internal fixation for the treatment of displaced intra-
articular calcaneal fractures? Foot Ankle Surg. 2016;22(3):164–9.
56. Westhues H. Eine neue Behandlungsmethode der Calcaneusfrakturen. Zugleich ein Vorschlag
zur Behandlung der Talusfrakturen. Zentralbl Chir. 1935;35:995–1002.
57. Weber M, Lehmann O, Sagesser D, Krause F. Limited open reduction and internal fixation of
displaced intra-articular fractures of the calcaneum. J Bone Joint Surg Br. 2008;90(12):1608–16.
58. Nosewicz T, Knupp M, Barg A, et al. Mini-open sinus tarsi approach with percutaneous screw
fixation of displaced calcaneal fractures: a prospective computed tomography-based study.
Foot Ankle Int. 2012;33(11):925–33.
59. Rammelt S, Zwipp H. Fractures of the calcaneus: current treatment strategies. Acta Chir
Orthop Traumatol Cechoslov. 2014;81(3):177–96.
60. Buckley R, Leighton R, Sanders D, Poon J, Coles CP, Stephen D, Paolucci EO. Open reduc-
tion and internal fixation compared with ORIF and primary subtalar arthrodesis for treatment
of Sanders type IV calcaneal fractures: a randomized multicenter trial. J Orthop Trauma.
2014;28(10):577–83.
61. Park JH, Chun DI, Park KR, Park GH, Park S, Yang J, Cho J. Can sural nerve injury be avoided
in the sinus tarsi approach for calcaneal fracture?: a cadaveric study. Medicine (Baltimore).
2019;98(42):e17611.
62. Smyth NA, Zachwieja EC, Buller LT, Miranda AD, Steinlauf SD. Surgical approaches to the
calcaneus and the sural nerve: there is no safe zone. Foot Ankle Surg. 2018;24(6):517–20.
63. Rammelt S, Zwipp H, Hansen ST. Posttraumatic reconstruction of the foot and ankle. In:
Browner BD, Jupiter JB, Krettek C, Anderson PA, editors. Skeletal trauma. 6th ed. Philadelphia:
Elsevier Saunders; 2019. p. 2641–90.
64. Li S. Wound and sural nerve complications of the sinus tarsi approach for calcaneus fractures.
Foot Ankle Int. 2018;39(9):1106–11.
65. Berberian W, Sood A, Karanfilian B, Najarian R, Lin S, Liporace F. Displacement of
the sustentacular fragment in intra-articular calcaneal fractures. J Bone Joint Surg Am.
2013;95(11):995–1000.
66. Swords MP, Rammelt S, Sands AK. Nonextensile techniques for treatment of calcaneus frac-
tures. In: Pfeffer GB, Easley ME, Hintermann B, Sands AK, Younger A, editors. Operative
techniques: foot and ankle surgery. Philadelphia: Elsevier; 2017. p. 319–26.
67. Min W, Munro M, Sanders R. Stabilization of displaced articular fragments in calcaneal frac-
tures using bioabsorbable pin fixation: a technique guide. J Orthop Trauma. 2010;24(12):770–4.
68. Park CH, Yoon DH. Role of subtalar arthroscopy in operative treatment of sanders type 2 cal-
caneal fractures using a sinus tarsi approach. Foot Ankle Int. 2018;39(4):443–9.
69. Goldzak M, Mittlmeier T, Simon P. Locked nailing for the treatment of displaced articular
fractures of the calcaneus: description of a new procedure with calcanail((R)). Eur J Orthop
Surg Traumatol. 2012;22(4):345–9.
70. Zwipp H, Paša L, Žilka L, Amlang M, Rammelt S, Pompach M. Introduction of a new locking
nail for treatment of intraarticular calcaneal fractures. J Orthop Trauma. 2016;30(3):e88–92.
71. Abidi NA, Dhawan S, Gruen GS, Vogt MT, Conti SF. Wound-healing risk factors after open
reduction and internal fixation of calcaneal fractures. Foot Ankle Int. 1998;19(12):856–61.
72. Harvey EJ, Grujic L, Early JS, Benirschke SK, Sangeorzan BJ. Morbidity associated
with ORIF of intra-articular calcaneus fractures using a lateral approach. Foot Ankle Int.
2001;22(11):868–73.
73. Palmer I. The mechanism and treatment of fractures of the calcaneus; open reduction with the
use of cancellous grafts. J Bone Joint Surg Am. 1948;30A(1):2–8.
74. Sanders R. Turning tongues into joint depressions: a new calcaneal osteotomy. J Orthop
Trauma. 2012;26(3):193–6.
75. Rammelt S, Gavlik JM, Barthel S, Zwipp H. The value of subtalar arthroscopy in the manage-
ment of intra-articular calcaneus fractures. Foot Ankle Int. 2002;23(10):906–16.
76. Rübberdt A, Feil R, Stengel D, Spranger N, Mutze S, Wich M, Ekkernkamp A. The clini-
cal use of the ISO-C(3D) imaging system in calcaneus fracture surgery. Unfallchirurg.
2006;109(2):112–8.
77. Longino D, Buckley RE. Bone graft in the operative treatment of displaced intraarticular cal-
caneal fractures: is it helpful? J Orthop Trauma. 2001;15(4):280–6.
78. Redfern DJ, Oliveira ML, Campbell JT, Belkoff SM. A biomechanical comparison of
locking and nonlocking plates for the fixation of calcaneal fractures. Foot Ankle Int.
2006;27(3):196–201.
79. Illert T, Rammelt S, Drewes T, Grass R, Zwipp H. Stability of locking and non-locking plates
in an osteoporotic calcaneal fracture model. Foot Ankle Int. 2011;32(3):307–13.
80. Beerekamp MSH, de Muinck Keizer RJO, Schepers T, Beenen LFM, Luitse JSK, Schep NW,
Ubbink DT, Goslings JC, EF3X-studygroup. The correlation between intra-operative 2D- and
3D fluoroscopy with postoperative CT-scans in the treatment of calcaneal fractures. Eur J
Radiol. 2019;112:222–8.
81. Della Rocca GJ, Nork SE, Barei DP, Taitsman LA, Benirschke SK. Fractures of the sus-
tentaculum tali: injury characteristics and surgical technique for reduction. Foot Ankle Int.
2009;30(11):1037–41.
82. Adams MR, Koury KL, Mistry JB, Braaksma W, Hwang JS, Firoozabadi R. Plantar
medial avulsion fragment associated with tongue-type calcaneus fractures. Foot Ankle Int.
2019;40(6):634–40.
83. Walley KC, Johns WL, Jackson JB, Gonzalez TA. Plantar medial avulsion fracture of the calca-
neus with acute tarsal tunnel: case report and technique tip. Foot Ankle Int. 2020;41(8):1002–6.
84. Schindler C, Schirm A, Zdravkovic V, Potocnik P, Jost B, Toepfer A. Outcomes of intra-
articular calcaneal fractures: surgical treatment of 114 consecutive cases at a maximum care
trauma center. BMC Musculoskelet Disord. 2021;22(1):234.
85. Schipper ON, Cohen BE, Davis WH, Ellington JK, Jones CP. Open reduction and primary
subtalar arthrodesis for acute intra-articular displaced calcaneal fractures. J Orthop Trauma.
2021;35(6):296–9.
86. Radnay CS, Clare MP, Sanders RW. Subtalar fusion after displaced intra-articular calcaneal
fractures: does initial operative treatment matter? J Bone Joint Surg Am. 2009;91(3):541–6.
87. Kwon JY, Guss D, Lin DE, et al. Effect of delay to definitive surgical fixation on wound
complications in the treatment of closed, intra-articular calcaneus fractures. Foot Ankle Int.
2015;36:508–17.
88. Kline AJ, Anderson RB, Davis WH, Jones CP, Cohen BE. Minimally invasive technique
versus an extensile lateral approach for intra-articular calcaneal fractures. Foot Ankle Int.
2013;34(6):773–80.
89. Seat A, Seat C. Lateral extensile approach versus minimal incision approach for open reduc-
tion and internal fixation of displaced intra-articular calcaneal fractures: a meta-analysis. J
Foot Ankle Surg. 2020;59(2):356–66.
90. Ding L, He Z, Xiao H, Chai L, Xue F. Risk factors for postoperative wound complications of
calcaneal fractures following plate fixation. Foot Ankle. 2013;34(9):1238–44.
91. Fischer S, Meinert M, Neun O, Colcuc C, Gramlich Y, Hoffmann R, Manegold S. Surgical
experience as a decisive factor for the outcome of calcaneal fractures using locking compres-
sion plate: results of 3 years. Arch Orthop Trauma Surg. 2021;141(10):1691–99. https://doi.
org/10.1007/s00402-020-03649-3.
92. Tennent T, Calder P, Salisbury R, Allen P, Eastwood D. The operative management of dis-
placed intra-articular fractures of the calcaneum: a two-centre study using a defined protocol.
Injury. 2001;32(6):491–6.
93. Steinhausen E, Martin W, Lefering R, Lundin S, Glombitza M, Mester B, Brinkmann N,
Dudda M. C-Nail versus plate osteosynthesis in displaced intra-articular calcaneal fractures-a
comparative retrospective study. J Orthop Surg Res. 2021;16(1):203.
94. Rammelt S, Zwipp H. Corrective arthrodeses and osteotomies for post-traumatic hindfoot
malalignment: indications, techniques, results. Int Orthop. 2013;37:1707–17.
95. Stephens HM, Sanders R. Calcaneal malunions: results of a prognostic computed tomography
classification system. Foot Ankle Int. 1996;17(7):395–401.
96. Zwipp H, Rammelt S. Tscherne Unfallchirurgie: Fuß. Berlin, Heidelberg, New York:
Springer; 2014.
Talus Fracture
Florencio Pablo Segura and Guillermo Arrondo
1 Introduction
Talar fractures are relatively uncommon, accounting for less than 1% of traumatic
injuries to the skeleton and 3–5% of all foot fractures [1]. A high energy mecha-
nism usually involved in a unique anatomical context with no musculotendinous
junctions, cartilage coverage on almost 60% of its surface and a single major
source vascular supply, make them challenging injuries with potentially
devastating clinical consequences and high rate of complications related to their
management [2–4].
2 Anatomical and Epidemiological Considerations
The talus is characterized by a particular morphology that includes five regions

divided into three main segments and two apophyses, all of which can be affected
by different traumatic injuries. Most of them are concentrated in two locations: the
neck, the narrowest and weakest region where 50% of the fractures are located; and
the body, the largest and predominantly articular segment, where up to 30% of the
fractures are produced. The remaining 20% corresponds to peripheral sectors of
the structure of the talus that includes the head. This segment constitutes, along with
F. P. Segura
Universidad Nacional de Córdoba, Nuevo Hospital San Roque,
Ciudad de Córdoba, Argentina
G. Arrondo (*)
Instituto Dupuytren, Ciudad Autónoma de Buenos Aires, Argentina

Switzerland AG 2022
1254 F. P. Segura and G. Arrondo
the navicular bone and the anterior and middle facets of the calcaneus, an area
denominated “acetabulum pedis” responsible for the rotatory movement of the mid-
foot on the rearfoot; the lateral process, a prolongation of the body that presents a
double articular surface for the distal fibula and for the lateral end of the posterior
facet of the calcaneus and it is the site of insertion of ligamentary structures involved
in the stability of the articulations of the ankle and subtalar [1–3]. The region less
frequently compromised corresponds to the posterior process, apophysis divided in
two tubers. Between both tubers lies the flexor hallucis tendon: the larger postero-
lateral and articular corresponding to the roof of the posterior subtalar joint and the
smaller posteromedial and extra-articular where the tibiotalar segment of the deltoid
ligament is inserted (Fig. 1) [2–4].
With respect to its vascular anatomy, talar irrigation depends on the posterior
tibial, peroneal perforator, and dorsal pedis arteries, which form a complex network
of extraosseous circulation [5–7]. The most important component of this network is
the connection between the artery of the tarsal canal – originating from the posterior
tibial artery 1 cm proximal to the emergence of the lateral and medial plantar arter-
ies – and the artery of the sinus tarsi – branch of the peroneal perforator – since
almost two-thirds of the body’s intraosseous circulation comes from it. This anasto-
mosis is located in the sulcus tali, a cleft that runs along the lower surface of the
a b
c d
Lateral processl
Posterior process
Fig. 1 Schematic representation of the bone anatomy of the talus. (a) Anterior view. (b) Superior
view. (c) Medial view. (d) Lateral and inferior view
Talus Fracture 1255
Deltoid
branches
a b Posterior
tibial
artery
Calcaneal
Perforating branches
Artery of the personal artery
tarsal canal
Artery of the
tarsal sinus
Posterior
tribial
artery Peroneal
artery
Artery of the
tarsal canal
Calcaneal
branches
Fig. 2 Schematic representation of extraosseous network around the talus. Big red arrows show
main retrograde flow to the body from connection between tarsal canal artery-artery of the tarsal
sinus. (a) Superior view. (b) Medial view
talus from posteromedial to anterolateral, narrower on the inside (tarsal canal) than
on the outside (sinus tarsi) and which, through small transcortical tunnels called
foramins, allows vascular entry. The second anastomosis in importance is located in
the region that surrounds the posterior process and is formed by calcaneal branches
dependent on the posterior tibial artery and branches coming from the peroneal
artery. Small vessels enter the body and establish communications with those com-
ing from the anastomosis of the sulcus talis determining a “anterograde flow” of
smaller quantitative value. Finally, there are minor contributions depending on the
deltoid branch, a direct tributary of the posterior tibial artery in charge of supplying
the medial third of the body, and from branches of the sinus tarsi artery that supplies
the lateral fifth of the astragaline dome (Fig. 2). In summary, most of the body’s
intraosseous circulation depends on the posterior tibial artery as its main source,
with a minor participation of the peroneal perforating artery. The irrigation of the
head, on the other hand, corresponds to branches coming from the dorsalis pedis
artery (Fig. 3) [7, 8].
3 Mechanism and Lesional Physiopathogenesis
The fractures of the three main segments of the talus share in their origin a high-
energy mechanism, because significant forces are needed to compromise structures
constituted fundamentally by highly resistant subchondral bone. Most of them result
from falls from heights or traffic accidents and a high percentage are produced in the
context of polytraumatized patients or with multiple injuries [1–3, 9]. For this reason,
they are usually also associated to different degrees of soft tissue compromise or to
other injuries of neighboring joints. Neck fractures are primarily caused by a mecha-
nism of forced ankle dorsiflexion which acts in stages. First, it leads to anterior tibia
a b
Anterior
tibial
artery Anterior
tibial
artery
Lateral Posterior
Anterior
Medial Perforating
Perforating Posterior
peroneal
peroneal tibial
Posterior artery
artery artery
tibial
artery
Fig. 3 Schematic representation of internal vascularity of the talus showing the posterior tibial
artery and branches as the major blood source to the body of the talus. (a) Dorsal view. (b)
Medial view
impaction. As the dorsiflexion force of the foot continues to act, the energy of the
trauma propagates through the neck and toward the subtalar joint, causing the pro-
gressive subluxation of the body with respect to the calcaneus progressing to disloca-
tion or complete enucleation from the ankle (Fig. 4a–c). This primary dorsiflexor
force usually has associated a secondary component of forced supination of the foot,
which produces a failure in tension of the lateral side of the neck and in compression
of its internal side, resulting in medial comminution, shortening and varus, and finally
the probable appearance of a vertical fracture of the medial malleolus [9–11]. The
fractures of the body generally result from a mechanism of axial compression of high
energy applied between the calcaneus and the tibial pilon, although also they can be
secondary to a mechanism of shearing similar to that of the injuries of the neck that
generates a more posterior line [11]. The fractures of the head can be related to two
mechanisms of high energy: a compression mechanism by an axial load transmitted
through the metatarsal-navicular-talar axis which results in a comminuted injury of
the medial portion of the head; or a shearing mechanism by a mediotarsal inversion-
adduction force in which the navicular bone impacts the head generating a simple
fracture line with two well-defined head fragments (Fig. 5a–c) [11].
Process fractures, on the other hand, are more frequently observed in the context
of medium-energy trauma produced during the practice of certain sports activities.
Lateral process fractures are characteristic of snowboarding (“snowboarder’s
Talus Fracture 1257
a b
Fig. 4 Schematic representation of the neck fracture mechanism. (a) Impact of the tibialis anterior
plafond on the neck of the talus. (b) Subtalar subluxation. (c) Complete dislocation/enucleation of
the body in lateral and medial view
fracture”) since the causal mechanism is an axial load or forward fall on an ankle in
dorsal flexion and forced external rotation or eversion of the hindfoot, a common
situation in this winter sport [12]. The fractures of the posterior process have been
associated with soccer and ballet dancing since they are generally secondary to a
direct mechanism of forced plantar flexion of the foot that causes compression of
the posterior tibial plafond against the posterolateral tubercle, or to an indirect
mechanism in forced dorsal flexion and inversion of the ankle that results in an avul-
sion fracture by traction of the posterior talofibular ligament [13, 14]. Both pro-
cesses can also be compromised in the context of high-energy trauma, particularly
when there is a history of subtalar dislocation [14, 15].
4 Clinical and Imaging Diagnosis
Clinical findings associated with high-energy neck or body fractures are evident
and include the presence of pain, swelling, and bruising of varying but usually
severe magnitude as well as some degree of deformity in the case of concomitant
a b c
Fig. 5 Schematic representation of the mechanism of fractures of the head of the talus. (a) Normal
relationship. (b) The navicular articulates around the talar head. (c) With an axial load, a shear
force is created that produces the fracture
peritalar dislocations. Similarly, different degrees of soft tissue injury can be

observed in relation to the energy of the trauma, which can include everything from
superficial abrasions or abrasions to coverage defects located in general on the
lateral face of the ankle or rearfoot. However, it is not uncommon for the diagnosis
to be delayed in the context of the polytrauma patient, which is why a thorough
physical examination is recommended in an unconscious patient in the intensive
care unit [15–17]. Process fractures, on the other hand, tend to present a less spec-
tacular clinical picture similar to that of other traumatic bone or soft tissue injuries
in the region, with pain, swelling, and perimalleolar hematoma and a certain degree
of restriction of the range of active and passive mobility of the ankle, subtalar, or
medial-osseous joints. This fact added to a more difficult radiological visualization
of the processes determines that its initial diagnosis can go unnoticed up to 50% of
the cases [12, 18].
The radiographic study in cases of clinical suspicion must include the two classic
anteroposterior and lateral projections of the ankle and, in the event that the contour
of the talus cannot be correctly visualized in the anteroposterior view, a mortise
oblique with internal rotation of 15°. Lateral radiography is usually the most useful
for interpreting the injury, since it shows a fracture of the body or neck with relative
ease, and in the case of fractures of the processes, it allows the suspicion of this
lesion (Fig. 6a, b) [12, 15–18]. X-rays of the foot in frontal, lateral, and oblique
projections should be requested routinely to correctly evaluate the head segment
and to rule out peritalar dislocations or other associated medial or forefoot injuries.
The specific Canale and Broden projections have lost relevance in the initial diag-
nostic phase, although they remain absolutely valid as methods of intraoperative
control of the quality of reduction achieved during surgical fixation. The Canale
projection allows control of the alignment achieved in the coronal plane especially
Talus Fracture 1259
a b
Fig. 6 (a) Clinical/radiological presentation characteristic of a high-energy fracture of the talar

neck. (b) Clinical/radiological presentation characteristic of a fracture of the lateral process of the
talus. Note how the lateral process loses its symmetrical V-shape contour and is projected in a
twisted or asymmetrical V-shape
in neck fractures: it is taken with the foot in maximum plantar flexion and 15 degrees
of pronation and the X-ray beam directed in a cephalic direction and pointing 75°
with respect to the horizontal (Fig. 7a). The Broden projection allows evaluation of
the congruence of the subtalar joint: it is taken with the foot in a neutral position and
internal rotation of 20–60° with respect to the vertical and the X-ray beam directed
in a cephalic direction of 10–40° with respect to the vertical (Fig. 7b) [1, 2, 11, 16].
Computed axial tomography is the study of choice for correct interpretation
and decision making in fractures of the talar neck and body. It allows evaluating
the exact location of the fracture, the degree of displacement, its morphological
pattern characterizing it as simple or comminuted, the involvement of the neigh-
boring joints, and the presence of associated injuries, key aspects to define the type
of treatment and plan the surgery if necessary. In the case of acute fracture-dislo-
cations, it is convenient to perform it after the reduction of the main fragments. In
the same way, the tomographic study with multiplanar cuts every 1–2 mm is espe-
cially useful to identify and characterize the fractures of the processes, defining
the size of the fragments, the degree of displacement, the presence of comminu-
tion, and the percentage of the subtalar or tibiotalar joint compromise [1–3, 15,
17, 18].
a b
Fig. 7 Specific projections for the talus and subtalar joint. (a) Canale projection. (b) Broden
projection
5 Management Criteria
5.1 Neck Fractures
Hawkins’ (1970) [19] radiographic classification, which divides these injuries into
four types according to the involvement of the surrounding joints, is a descriptive
system of prognostic value based on the body’s vascular involvement which, with
modifications and evolutions, has lasted over time as a useful tool for decision mak-
ing. Type I fractures are non-displaced fractures of the neck that do not affect any
joint surface and that in theory only interrupt anterolateral blood flow, for which
they are associated with a low risk of avascular necrosis of the body (AVN) that
ranges from 0% to 13%. They can be treated conservatively, with a protocol that
includes immobilization and unloading of body weight with two crutches for
8–10 weeks, biweekly radiographic control, and total weight load at full consolida-
tion, usually at 12 weeks. Alternatively, stable internal fixation with screws through
a minimal posterolateral incision may allow earlier functional rehabilitation by
reducing the risk of secondary displacement, vicious consolidation, or pseudoar-
throsis (Fig. 8) [16, 19]. Type II fractures involve displacement of the subtalar joint,
with the possibility of interruption of the circulation entering the neck both at the
Talus Fracture 1261
a b
Fig. 8 A 17-year-old female patient. Hawkins type I fracture. (a) Perioperative studies. (b)
Posterolateral route for percutaneous fixation. (c) Postoperative Rx
anterolateral level and through the sinus of the tarsus and a risk of AVN of the body
ranging from 20% to 50% according to Hawkins’ classic description. Recently,
Vallier et al. have divided them according to the degree of joint displacement into
two subtypes: IIa, where the joint is subluxated, the rate of VAP is similar to that of
type I, and the rates of subtalar and tibiotalar arthritis are lower (21% and 5.3%
respectively) (Fig. 9a); and type IIb, where the joint is dislocated, the rate of VNA
is high (25%), and the rates of subtalar and tibiotalar arthritis are higher (25% and
13% respectively) (Fig. 9b) [20]. Although they do not constitute a surgical emer-
gency since the delay in definitive fixation does not predispose to the development
of osteonecrosis [21, 22], the lesions associated with subtalar dislocation (IIb)
require active behavior in the emergency through closed manipulation and transi-
tory stabilization to protect soft tissues and preserve body’s vascularization. The
recommended technique for joint reduction includes the distraction of the ankle and
hindfoot from the calcaneus through a transfixed calcaneus wire of 2.5 mm followed
by a posterior translation looking for subtalar facet reduction. If necessary, a trans-
articular temporary stabilization can be applied (Fig. 10). Type III fractures – which
involve the dislocation of the talar body off the subtalar and tibiotalar joints with
posteromedial extrusion of the same given that it rotates around the deep deltoid
a b
Fig. 9 (a) A 27-year-old male patient. Hawkins’ type IIa fracture. (b) A 24-year-old male patient.
Hawkins’ type IIb fracture
a b
Fig. 10 Same patient as Fig. 9b. (a) Calcaneal K-wire for closed reduction. (b) Intraoperative
radioscopic vision after reduction and osteodesis
Talus Fracture 1263
Fig. 11 A 32-year-old female patient with Hawkins III astragalus neck fracture. Note the position
of the talus body outside the ankle mortise on the Rx (arrows)
ligament (Fig. 11) – and type IV fractures – category of injury added by Canale and
Kelly which involves the subluxation or dislocation of the talonavicular joint
(Fig. 12). Type III and IV can compromise all three sources of the talar body’s blood
supply, thus being associated with extensive circulatory involvement of the body
with a risk of VAS of 70–100% and possible vascular suffering of the head. They
both constitute a traumatic emergency and, like IIb lesions, must be reduced and
temporarily stabilized on admission, although unlike the latter, closed manipulation
is generally not effective and requires percutaneous procedures or formal open (usu-
ally medial) approaches for reduction. The use of a large fracture distractor can be
of great help, providing space for the reduction in a progressive way under radio-
scopic control avoiding forced manipulations of the body. In the case of open
lesions, the initial handling includes the immediate administration of antibiotics by
parenteral route and the irrigation and urgent debridement of the wound. The final
treatment follows the same principles of anatomical reduction and stable internal
fixation as for type II fractures.
The surgical technique at the time of definitive osteosynthesis in neck fractures
may include a single approach or a combined double access. The most frequently
cited single approach is the anteromedial approach, which begins on the anterior
margin of the medial malleolus and progresses into the tuberosity of the scaphoid,
running halfway between the anterior tibial and posterior tibial tendons and behind
Fig. 12 A 48-year-old male patient with Hawkins IV astragalus neck fracture. Note the talona-
vicular incongruence in the axial section of the CT
a b
Fig. 13 Anteromedial approach. (a) Conventional incision from the medial malleolus to the navic-
ular. (b) Intraoperative view of the fracture line (black arrows)
the nerve and saphenous vein, giving access to the more inferomedial side of the
neck (Fig. 13) [9, 21, 23–25]. Another alternative is the anterior approach that begins
about 3 cm proximal to the ankle joint outside the tibial crest and extends distally
Talus Fracture 1265
following the lateral margin of the anterior tibial tendon (ATT) in the interval
between the ATT and the extensor hallucis longus (EHL), allowing adequate expo-
sure of the dorsal surface of the neck, but very limited exposure of its two lateral
faces (Fig. 14) [24, 25]. The main disadvantage associated with the single-approach
technique is inadequate visualization: only the medial or superior cortex can be
directly accessed and verified, which may appear perfectly aligned but coexist with
an opening or loss of contact of the main fragments on the contralateral side
(Fig. 15). This situation can lead to inadequate compression of the fracture with
a b
Fig. 14 Anterior approach. (a) Incision between the tibialis anterior and extensor hallucis tendon.
(b) Intraoperative view of the dorsal neck region and fracture line (white arrows)
a b
Fig. 15 Area of direct visual control by a single approach. The (a) dorsal or (b) medial region of
the neck can be accessed but not the full extension of the fracture site
shortening of the neck or to an inclination of the fragment which inevitably has

functional repercussions: a poor dorsal or varus reduction of no more than 2 mm
alters the congruence and the subtalar movement and is associated with degenera-
tive phenomena in up to 30% of cases [19]. Similarly, the single-approach strategy
admits very limited reduction maneuvers and allows only screws to be placed for
fixation, which is why it is no longer used and is only suggested in the scenario of
simple fractures without comminution and with minimal initial displacement
(Fig. 16) [21, 23–25]. Combined lateral and medial access is the current modality
most recommended, especially in complex patterns (Fig. 17), since it is possible to
better visualize both sides of the segment and thus better control reduction by avoid-
ing residual displacement invariably associated with poor functional outcome. Of
the most frequently cited lateral approaches in the literature, Bohler’s classic sagittal
approach is apparently the most anatomical [21, 24, 26–29]: the incision is made
slightly curved from the anterolateral apex of the ankle joint in line with the exten-
sor digitorum longus and peroneus tertius tendons towards the sinus tarsi and the
base of the fourth metatarsal. Deep dissection continues up to the articular capsules
of the ankle and subtalar joints. The short toes extensor muscle (extensor digitorum
brevis) in a distal direction can be reflected plantarly, thus exposing the most distal
portion of the lateral neck (Fig. 18). For some authors, the lateral Ollier approach is
a c e
d f
b
Fig. 16 A 24-year-old male patient. (a, b) Preoperative CT showing simple vertical neck fracture
without comminution and with minimal initial displacement. (c, d) Intraoperative view of reduc-
tion and fixation by single anterior approach. (e, f) Anatomic reduction confirmed by radioscopy
Talus Fracture 1267
a b
c d
Fig. 17 Same patient as Figs. 9b and 10. (a–c) CT shows a complex pattern with extension to the
body. (d) Schematic representation of the fracture pattern
more effective [24, 30]: this incision extends from the tip of the lateral malleolus to
the neck of the talus, sectioning the inferior extensor retinaculum and identifying the
peroneus tertius and the short hallux extensor itself, which retract medially in the
superior part (distal) of the wound leaving the peroneal tendons in the inferior part
(proximal). After partial removal of the fat pad on the sinus tarsi, the entire lateral
talar neck can be accessed. In this dual strategy, the lateral approach is generally
performed first, since the lateral neck is the tension side and usually has no com-
minution allowing the displacement and rotational misalignment correction more
easily achieved. Similarly, in most cases there is a cortical bone spike on the lateral
neck that provides a reference to help achieve an accurate anatomical reduction by
means of a pointed clamp (Fig. 19) [24]. The temporary wire through the posterior
a b
c d
Fig. 18 Intraoperative view of the anterolateral approach of the patient from Figs. 9b, 10, and 17
(a) Skin incision. The displaced body fragment (b) was reduced and fixed with K-wires (c) and two
3.5 mm screws. Subsequently, the neck fracture is reduced with a Weber clamp (d)
a b
Fig. 19 Cortical bone spur (arrows) usually present on the lateral neck. (a) 3D CT image. (b)
Intraoperative view
Talus Fracture 1269
subtalar facet can be very useful in this instance by providing a fixed point on which
to adjust the distal fragment. Similarly, strong K-wires (2.5 mm.) can be used as a
“joy-stick” to correct some residual fragment pronation or supination [24]. Once the
lateral reduction has concluded, the anteromedial approach described above is initi-
ated from the anterior margin of the medial malleolus to the talonavicular joint and
the dorsal margin of the posterior tibial tendon sheath distally. The reduction
achieved must be visually verified so that if it is anatomical, definitive fixation can
proceed (Fig. 20). If there is severe medial comminution, the use of autografting is
suggested to maintain the medial length and prevent varus reduction. With respect
to the fixation technique for the simplest patterns, two 3.5 mm full-threaded screws
can be used, one on each side of the neck, placed from the margins of the head and
directed towards the body. It is recommended to insert the first screw laterally
because normally there is no comminution on that side of the neck and it is better to
grasp the denser cortical bone in that area and conveniently countersink the entry
site so that it is below the plane of the articular cartilage and subchondral bone.
Compression should be avoided especially in the presence of medial comminution
to avoid a varus or shortening neck malunion [24, 29, 31–33]. The antegrade
a b
c d
Fig. 20 Same patient as Figs. 9b, 10, 17, and 18. (a) Skin incision. (b) Anatomical reduction
control from the medial side. (c, d) Definitive fixation with two 3.5 mm posterior-anterior screws
placement of the screws by a small posterolateral approach lateral to the flexor hal-
lucis longus tendon from the lateral posterior process towards the head is biome-
chanically superior and provides a more rigid construct [34], but it is associated with
some difficulties that make its indication much more exceptional: instrumentation
more difficult since the patient is positioned in supine position, neuropraxia of the
sural nerve, posterior ankle impingement due to screw head conflict with the poste-
rior malleolus, and possibility of injury to the branches of the sinus tarsus anastomo-
sis (which may increase the risk of necrosis of the body) [32, 33]. In more complex
patterns associated with greater initial displacement and greater comminution, the
use of 2.7 mm diameter mini-fragment plates allows for a more rigid fixation than
that achieved with screws alone. Although they can be placed both on the compres-
sion face (medial) of the neck with a support function and on the tension face (lat-
eral) to maintain the length and alignment of the segment, the most frequently used
construct consists of a plate with four screw holes contoured to the lateral neck fixed
with unicortical screws (Fig. 21). The medial talar usually allows little space for the
placement of plates due to the wide footprint of the joint with the medial malleolus
[27–32].
The postoperative protocol includes immobilization of the ankle and foot in a
brace for 2 weeks, active and passive mobility exercises starting on day 15, and
a c e
b d f
Fig. 21 A 24-year-old female patient with complex talar fracture Hawkins II. (a) and (b) preop-
erative 3D CT. (c) Intraoperative view and (d) radioscopic image at the end of lateral time. (e) and
(f) Radioscopy image at the end of surgery
Talus Fracture 1271
unloading of the body weight for 10–12 weeks. Radiological controls are monthly
until healing, looking for around 6–8 weeks the appearance of “Hawkins’ sign”,
subchondral lucidity of the body that is a positive predictor of revascularization, and
therefore implies a low risk of avascular necrosis.
5.2 Body Fractures
From the descriptive/physiopathogenic point of view, three main patterns of body

fractures can be recognized, included within historical classifications, such as
Sneppen (1977) [35] or more modern ones such as AO/OTA (2018) [36] (1): Vertical
shear fractures including two fragments in the coronal or sagittal plane involving
only the ankle joint or the ankle and subtalar joint (2); multi-fragment compression
fractures involving only the ankle joint; and (3) multi-fragment compression frac-
tures involving the ankle and subtalar joints, also called crush fractures (Fig. 22).
The treatment of choice in any of these scenarios is open reduction and internal
a b c
Fig. 22 Main patterns of body fractures (a) Simple patterns. (b) Multifragmentary patterns involv-
ing only the ankle. (c) Multifragmentary patterns with tibiotalar and subtalar involvement
(crushing)
fixation with the aim of accurately restoring joint congruence and segment align-
ment. The initial management in the emergency implies the close or open reduction
of the associated dislocations, temporary stabilization if necessary, and the irriga-
tion and debridement in open lesions with the objective to preserve the soft tissues
and to avoid infection. Definitive treatment can be deferred for 1–3 weeks since, as
in neck lesions, there is no association between fixation time and the development
of osteonecrosis [9, 37].
The selection of the surgical approach is based on the location and the fracture
pattern, but generally implies the need to extend the visualization directly to the
back of the body by clearing the malleoli by means of an osteotomy. The most
commonly described is the medial malleolar osteotomy: first the medial malleolus
screws are positioned on the medial malleolus and then removed. Then, the oste-
otomy is made in 45° from the tibia axis, with its exit point at the tibial plafond
medial shoulder, reflecting the malleolus distally and preserving the deltoid liga-
ment (Fig. 23). In a similar way, a suprasindesmal transverse osteotomy of the
fibula can be performed to gain access to the posterior-lateral part of talar body,
after section of the anterior-inferior tibiofibular ligament and externally rotating the
bone segment, i.e., “open book”. Rigid fixation in shear fractures in the coronal
plane is achieved in the same way as in neck fractures through two 3.5 mm screws
placed from the medial and lateral edges of the talar head directed longitudinally
towards the body (Fig. 24). In case of associated involvement of the lateral process,
a medial screw and a lateral mini-fragmentation plate can be combined. For shear
fractures in the sagittal plane, fixation with countersunk traction screws at the entry
site is preferable to avoid protrusion of the implant. In case of partial or complete
a b
Fig. 23 Extended anteromedial approach by osteotomy of the medial malleolus (a) Chevron type-
osteotomy with the apex proximal to the tibial plafond (arrows). (b) Distal fragment mobilized
downwards giving access to the body
Talus Fracture 1273
a b c
Fig. 24 A 26-year-old female patient with talar body coronal fracture. (a) Preoperative studies. (b)
Intraoperative imaging. (c) Rx at 5 months postoperative
articular multi-fragment compression fractures, fixation of the main fragments is

obtained by mini-fragment implants (1.8 mm, 2.0 mm, 2.4 mm, 2.7 mm), while
devitalized fragments that do not contribute to joint stability or joint congruence
can be eliminated. The postoperative protocol is similar to that for neck fractures
with early mobility and deferred loading no earlier than 12 weeks postoperatively
[1, 2, 27–32, 38].
5.3 Fractures of the Head
The treatment of fractures of the talar head depends on the degree of compromise
of the talonavicular joint: a displaced injury generates joint incongruence and
secondarily limitation of subtalar mobility, shortening of the internal foot column,
and deformity in varus, so it must be surgically corrected by open reduction and
internal fixation. The preferred access route is anteromedial and fixation is per-
formed by 3.5 mm cortical screws in compression through the fracture focus
(Fig. 25). In the cases associated with comminution and substantial shortening of
a b
Fig. 25 A 29-year-old male patient. Single line fracture of the head. (a) Preoperative CT scan. (b)
Postoperative Rx
the medial column, small block grafts are used to recover the original length. A
mini external fixator anchored proximally in the body of the talus or in the calca-
neus and distally in the scaphoid or the medial cuneiform can be associated to help
avoiding talar shortening, which will be maintained until the radiological heal-
ing [39].
5.4 Fractures of the Processes
The treatment of process fractures is based on their anatomical morphology, which

is considered in all the classifications that try to protocolize their management and
that recognize for practical purposes three main types (1): an avulsive variant with
a small fragment (2); an intermediate or large single trace fragment variant; and (3)
an intermediate or large fragment variant with fragmentation, which can be only
articular, only metaphyseal, or affect the entire process (Fig. 26) [40–42].
Conservative management is reserved only for small avulsions without articular
commitment, with immobilization for 6 weeks with partial body weight loading
(10 kg). In the rest of the situations and due to the fact that displacement is usually
the rule, the treatment is surgical.
Talus Fracture 1275
a b c
Fig. 26 Main types of fractures of the lateral process of the talus: (a) avulsive, (b) simple, and (c)
with fragmentation
For the anterolateral process, arthroscopic access through two ventral and dor-
sal anterolateral portals can be an option both for resection-debridement of small
intra-articular lesions and for fixation of intermediate to large fragments with
minimal initial displacement [40]. Open surgery is the preferred technique for
larger lesions displaced through a transverse Ollier access or a slightly curved
anterolateral longitudinal access. The use of a universal distractor or a unilateral
external fixator with pins placed in the fibula and in the posterior tuberosity of the
calcaneus allows the creation of a certain space in the subtalar joint that facilitates
the visualization of the fracture. The single patterns can be fixed only with screws
since there is a uniform surface of bone contact between the main fragment and
the fracture bed (Fig. 27). The minimum size of a potentially “fixable” fragment
corresponds to three times the diameter of the screw head to be placed, which can
be 2.0, 2.4, or 2.7 mm (“rule of thirds”). Fragmentation patterns need augmenta-
tion with a plate, usually at ¨T¨ of 2.0 mm as a support, with the transverse plate
branch parallel to the subtalar joint with 3–4 screws in a subchondral “palisade”
shape and the vertical branch at the base of the neck immediately in front of the
articular facet for the fibula [41, 42]. In case of complete fragmentation of the
process, subtotal or total resection can even be considered, taking into account
that according to cadaveric studies, resecting a volume of between 5 and 10 cm3
of the segment is not associated with significant subtalar instability [43].
Regarding the posterior process fractures (posteromedial are called Cedell frac-
tures, posterolateral are called Shepherds fracture), although there are several
access options, the most widespread is the open way through a posterolateral
approach of 5 cm between the peroneal tendons and the Achilles tendon in the
superficial layer and lateral to the flexor hallucis longus tendon in the deep layer.
The fixation of the fragment is done only with microfragment screws (1.5, 2.0 or
a b c
Fig. 27 A 31 year old male patient with lateral process fracture with minimun metaphyseal frag-
mentation. (a) CT scan (b) Open reduction and fixation of main fragments by anterolateral
approach. (c) Final x-ray follow up
2.4 mm) since there is generally not enough space for plate placement (Fig. 28). In
case of resection, an arthroscopic approach can be used through two posterior por-
tals with the patient in prone position. The postoperative protocol in process frac-
tures includes early mobility with focus on the subtalar joint and deferred loading
from week 8 to 12 [40–42].
6 Results and Complications
The long-term functional outcomes of patients with neck fractures are variable and
there is no standardized modality for evaluating them, but in general and as
expected, the lower-grade injuries in Hawkins’ classification show better results
than the higher-grade ones. The most frequently reported complication is subtalar
arthritis, whose incidence varies widely from 4% to 100% of cases with a mean of
49% and is secondary to both chondral damage from the initial trauma and nonana-
tomical reductions, and is clinically well tolerated only in aligned fractures. In
symptomatic patients, subtalar arthrodesis as a rescue surgery is effective both for
Talus Fracture 1277
a b c
Fig. 28 A 42 year old male patient with posterior process fracture with metaphiseal fragmenta-
tion. (a) X-ray and CT scan (b) Open reduction and fixation of main fragments by posterolateral
approach. (c) Final x-ray follow up
pain relief and for foot shape. The talar body avascular necrosis (AVN) is another
common, although less frequent, sequel that can be conditioned by both the inter-
ruption of blood flow due to the trauma and by subsequent surgery. Its overall
incidence is approximately 25–30% for all types of fractures, although series pub-
lished after the year 2000 show lower rates of AVN in Hawkins type II and III
injuries probably related to an optimization of their initial and definitive manage-
ment. Focal AVN without collapse often occurs without significant functional
sequelae since in these cases the cartilage survives and the subchondral bone is
replaced over time by a “creeping substitution” mechanism. In cases with talar col-
lapse, tibio-talo-calcaneal arthrodesis is usually the main option. Symptomatic
nonanatomic healing is another reported complication, with an incidence of
between 20% and 37%. The most common malreduction includes leaving the talus
shortened and in varus (medial column shortening and varus), which significantly
changes the biomechanics of the peritalar joints. Another possibility is that the
body heals in excessive plantar flexion, which results in a dorsal prominent talar
neck conditioning a friction with the tibialis anterior tendon. Once a malunion is
detected, revision surgery of primary osteosynthesis in the acute or subacute sce-
nario or a corrective osteotomy in patients with healed injuries can correct the
problem. If left untreated, malunion leads to peritalar arthritis, which requires a
rescue arthrodesis to relieve pain and correct the associated deformity. Finally,
insufficient fixation of a neck fracture can lead to pseudoarthrosis, a rare complica-
tion that can reach up to 4–5% of cases. Rescue includes revision of fixation in the
absence of arthritis or a rescue arthrodesis in the case of associated arthritis or
insufficient remaining bone stock [44, 45].
Body fractures are potentially devastating injuries commonly associated with
complications. The most common is post-traumatic arthritis reported in up to
50–100% of patients, despite the use of modern reduction and fixation techniques.
The incidence of AVN, associated with the severity of the original injury and the
initial displacement of the fracture, is approximately 40%, and half are associated
with collapse. Classic series on immediate surgical treatment of body fractures also
report high rates of soft tissue complications of up to 77%, including wound dehis-
cence, skin necrosis, and infection [9, 10, 28, 46].
The literature on the outcomes of head fractures is sparse. Complications are
usually associated with hidden or initially unnoticed injuries, especially in the
context of patients with multiple injuries. Although the risk of osteonecrosis is
generally low and has been described as less than 10%, secondary arthritis is dif-
ficult to manage and is usually treated with arthrodesis of the talonavicular joint
[32, 39].
Early diagnosis and treatment are associated with the best results in process frac-
tures as they allow rapid normalization of subtalar function. In large single patterns
treated in a timely manner through open reduction and internal fixation, 80% of
patients return to their pre-trauma level of function. The most frequently reported
complication is arthritis with subtalar rigidity, which can be associated to any frac-
ture subtype even the simplest and with properly performed treatment. The most
frequently cited rescue procedures for the treatment of sequelae include subtalar
arthrodesis for symptomatic arthritis and partial or subtotal excision of the process
for friction syndromes [32, 40].
7 Total Extrusion of the Talus
The most extreme variant of talus dislocation is a total extrusion, uncommon injury
with controversial handling with guidelines based on only small case series.
Decision-making must weigh the benefits of maintaining the anatomical integrity of
the tibiotalar and subtalar joints by reimplanting the segment against the acute and
long-term risks of infection, body AVN, and post-traumatic arthritis potentially
associated with this procedure. Most authors recommend native talus reimplanta-
tion as long as conditions such as absence of gross contamination or severe joint
damage are favorable, reserving arthrodesis and talectomy for the treatment of post-
reimplantation complications [47, 48].
Talus Fracture 1279
References
1. Rammelt S, Zwipp H. Talar neck and body fractures. Injury. 2009;40(2):120–35.

2. Sanders R, et al. Fractures and fracture-dislocations of the talus. In: Mann’s surgery of the foot
and ankle. 9th ed. Philadelphia: Elsevier; 2014.
3. Zwipp H. Severe foot trauma in combination with talar injuries. In: Tscherne H, Schatzker J,
editors. Major fractures of the pilon the talus and the calcaneus. New York: Springer; 1993.
p. 123–35.
4. Sarrafian S. Anatomy of the foot and ankle. Philadelphia: Lippincott; 1983.
5. Mulfinger GL, Trueta J. The blood supply of the talus. J Bone Joint Surg Br. 1970;52(1):160–7.
6. Gelberman RH, Mortensen WW. The arterial anatomy of the talus. Foot Ankle. 1983;4:64–72.
7. Vani PC, Arthi G, Jessy JP, Rani N, Jhajhria SK. Vascular foramina of talus: an anatomical
study with reference to surgical dissection. Surg Radiol Anat. 2020;42(6):685–90.
8. Miller AN, Prasarn ML, Dyke JP, Helfet DL, Lorich DG. Quantitative assessment of the vas-
cularity of the talus with gadolinium-enhanced magnetic resonance imaging. J Bone Joint Surg
Am. 2011;93A:1116–21.
9. Lindvall E, Haidukewych G, Di Pasquale T, et al. Open reduction and stable fixation of iso-
lated, displaced talar neck and body fractures. J Bone Joint Surg Am. 2004;86A:2229–34.
10. Sneppen O, Buhl O. Fracture of the talus. A study of its genesis and morphology based upon
cases with associated ankle fracture. Acta Orthop Scand. 1974;45:307–20.
11. Penny JN, Davis LA. Fractures and fracture-dislocations of the neck of the talus. J Trauma.
1980;20:1029–37.
12. Kirkpatrick DP, Hunter RE, Janes PC, et al. The snowboarder’s foot and ankle. Am J Sports
Med. 1998;26:271–7.
13. Chen YJ, Hsu RW. Fracture of the posterior process of the talus associated with subtalar dislo-
cation: report of a case. J Formos Med Assoc. 1994;93(9):802–5.
14. Ebraheim NA, Skie MC, Podeszwa DA. Medial subtalar dislocation associated with fracture
of the posterior process of the talus. A case report. Clin Orthop Relat Res. 1994;303:226–30.
15. Rammelt S, Biewener A, Grass R, et al. Foot injuries in the polytraumatized patient.
Unfallchirurg. 2005;108:858–65.
16. Canale ST, Kelly FB Jr. Fractures of the neck of the talus: long-term evaluation of seventy-one
cases. J Bone Joint Surg Am. 1978;60:143–56.
17. Rammelt S, Bartonıcek J, Park KH. Traumatic injury to the subtalar joint. Foot Ankle Clin.
2018;23:353–74.
18. Ebraheim NA, Skie MC, Podeszwa DA, Jackson WT. Evaluation of process fractures of the
talus using computed tomography. J Orthop Trauma. 1994;8:332–7.
19. Fortin PT, Balazsy JE. Talus fractures: evaluation and treatment. J Am Acad Orthop Surg.
2001;9(2):114–27.
20. Vallier HA, Reichard SG, Boyd AJ, Moore TA. A new look at the Hawkins classification for
talar neck fractures: which features of injury and treatment are predictive of osteonecrosis? J
21. Vallier HA, Nork SE, Barei DP, Benirshcke SK, Sangoerzan BJ. Talar neck fractures: results
and outcomes. J Bone Joint Surg Am. 2004;86A:1616–24.
22. Patel R, Van Bergeyk A, Pinney S. Are displaced talar neck fractures surgical emergencies?. A
survey of orthopaedic trauma experts. Foot Ankle Int. 2005;26:378–81.
23. Ohl X, Harisboure A, Hemery X, Dehoux E. Long-term follow-up after surgical treatment
of talar fractures. Twenty cases with an average follow-up of 7.5 years. Int Orthop (SICOT).
2011;35:93–9.
24. Cronier P, Talha A, Massin P. Central talar fractures—therapeutic considerations. Injury, Int J
Care Injured. 2004;35:S-B10-S-B22.
25. Ahmad J, Raikin SM. Current concepts review: Talar fractures. Foot Ankle Int.
2006;27(6):475–82.
26. Fleuriau Chateau P, Brokaw D, et al. Plate fixation of talar neck fractures: preliminary review
of a new technique in twenty-three patients. J Orthop Trauma. 2002;16:213–9.
27. Rammelt S, Winkler J, Grass R, et al. Reconstruction after talar fractures. Foot Ankle Clin.
2006;11(1):61–84, viii.
28. Vallier HA. Fractures of the talus: state of the art. J Orthop Trauma. 2015;29:385–92.
29. Rammelt S, Pitakveerakul A. Hindfoot injuries how to avoid posttraumatic Varus deformity?
30. Maceroli MA, Wong C, Sanders RW, Ketz JP. Treatment of comminuted Talar neck fractures
with use of Minifragment plating. J Orthop Trauma. 2016;30:572–8.
31. Sangeorzan BJ, Wagner UA, Harrington RM. Contact characteristics of the subtalar joint: the
effect of talar neck misalignement. J Orthop Res. 1992;10:544–51.
32. He B, Krosin M. Talar neck fractures. In: Adams MR, Benirschke SK, editors. Fractures and
dislocations of the talus and calcaneus. Springer Nature Switzerland AG; 2020. p. 37–55.
33. Lemaire R, Bustin W. Screw fixation of fractures of the neck of the talus using a posterior
approach. J Trauma. 1980;20(8):669–73.
34. Swanson TV, Bray TJ, Holmes GB Jr. Fractures of the talar neck. A mechanical study of fixa-
tion. J Bone Joint Surg Am. 1992;74(4):544–51.
35. Sneppen O, Christensen SB, Krogsoe O, Lorentzen J. Fracture of the body of the talus. Acta
Orthop Scand. 1977;48(3):317–24.
36. Meinberg E, Agel J, Roberts C, et al. Fracture and dislocation classification compen-
dium—2018. J Orthop Trauma. 2018;32(Suppl 1):S1–S10.
37. Bellamy JL, Keeling JJ, Wenke J, Hsu JR. Does a longer delay in fixation of talus fractures
cause osteonecrosis? J Surg Orthop Adv. 2011;20(1):34–7.
38. Ziran BH, Abidi NA, Scheel MJ. Medial malleolar osteotomy for exposure of complex talar
body fractures. J Orthop Trauma. 2001;15(7):513–8.
39. Early JS. Management of Fractures of the talus: body and head regions. Foot Ankle Clin N
Am. 2004;9:709–22.
40. Boack D, Manegold S. Peripheral talar fractures. Injury. 2004;35:S-B23–35.
41. Valderrabano V, Perren T, Ryf C, Rillmann P. Snowboarder’s talus fracture treatment outcome
of 20 cases after 3.5 years. Am J Sport Med. 2005;33:871–80.
42. Tinner C, Sommer C. Fractures of the lateral process of the talus. Foot Ankle Clin N Am.
2018;23:375–95.
43. Sands A, White C, Blankstein M, et al. Assessment of ankle and hindfoot stability and joint
pressures using a human cadaveric model of a large lateral talar process excision: a biome-
chanical study. Medicine. 2015;94(14):e606.
44. Dodd A, Lefaivre KA. Outcomes of talar neck fractures: a systematic review and meta-
analysis. J Orthop Trauma. 2015;29(5):210–5.
45. Jordan RK, Bafna KR, Liu J, Ebraheim NA. Complications of talar neck fractures by Hawkins
classification: a systematic review. J Foot Ankle Surg. 2017;56(4):817–21.
46. Hawkins LG. Fractures of the neck of the talus. J Bone Joint Surg Am. 1970;52(5):991–1002.
47. Assal M, Stern R. Total extrusion of the talus. J Bone Joint Surg Am. 2004;86(A):2726–31.
48. Apostle KL, Umran T, Penner MJ. Reimplantation of a totally extruded talus. A case report. J
Bone Joint Surg Am. 2010;92(A):1661–5.
Midfoot Injuries
Leandro Casola and German Joannas
1 Introduction
Jaques Lisfranc (1790–1847), Napoleonic surgeon, described amputations at the

metatarsal-cuneal joint level for the treatment of necrotic forefoot and François
Chopart (1732–1795) determined the disarticulation of the hindfoot as an anatomi-
cal and functional method for the treatment of gangrene. Since then, these joints
have been named after him [1].
Lisfranc and Chopart joint lesions go unnoticed in 30–40% of cases [1], and this
is due to their rarity and the difficulty of their diagnosis [2]. The type and intensity
of the lesion of the joint complex is very variable, but the goal of treatment is the
same: to achieve a plantigrade, functional, painless, and stable foot.
2 Etiology and Physiopathology
In 44% of cases, the Chopart joint injury occurs in more than one bone [3]. In 40%
of cases, it is due to axial load on the foot [4] and the fracture pattern will depend
on the position of the foot at the moment of receiving the longitudinal load. If it is
L. Casola
Foot and Ankle Division, Dupuytren Institute,
Ciudad Autónoma de Buenos Aires (CABA), Argentina
G. Joannas (*)
Foot and Ankle Division “CEPP”, Dupuytren Institute,
Foot and Ankle Division, Centro Artroscópico Jorge Batista SA,
Foot and Ankle Division, Barrancas Institute, Buenos Aires, Argentina

Switzerland AG 2022
1282 L. Casola and G. Joannas
a b
Fig. 1 Schematic image taken from Rammelt and Schepers [12]. Where the stress on the joint in
adduction and abduction plus axial loading is schematized. While one side loads with compression
forces on the contralateral side the forces are distraction forces
in adduction, the result will be a medial stress and the lesion is produced in the head
of the talus and/or scaphoid. If it is in abduction, the stress will be lateral and as a
result we will have a lesion in the anterior process of the calcaneus and/or cuboid.
These compressive forces are accompanied by distraction forces on the contralat-
eral side, leading to ligament injuries or bone avulsions (Fig. 1). Less frequent but
no less devastating are injuries resulting from high-energy mechanisms (traffic acci-
dents, direct impact on the dorsum or sole of the foot), where injuries are more
obvious and the possibility of compartment syndrome, neurovascular injuries, and
exposed fractures should be contemplated.
3 Anatomy
The Chopart joint consists of two separate joints, which are closely related to each
other and move in concert with the subtalar joint: on the medial side the talonavicu-
lar and on the lateral side the calcaneocuboid.
The first corresponds to a type of diarthrodial joint where the talus offers an
oblong head and is received by a socket type structure covered with cartilage com-
posed of: the concave articular surface of the navicular, the dorsal and medial sur-
face of the Spring ligament, and the talar facet of the anterior calcaneus; this together
with the anterior sector of the subtalar joint make up the talus-calcaneus-navicular
Midfoot Injuries 1283
joint which, due to its anatomical and functional characteristics similar to the hip,
was named Coxa pedis [5].
In the second, the anterior tuberosity of the calcaneus presents a concave vertical
articular cartilage, and the cuboid presents a convex articular cartilage, forming a
joint of a reciprocal socket or saddle type [1].
Regarding ligaments, we can divide them in proper to each joint and ligaments
common to both [6].
The ligaments proper to the talonavicular joint are the superior talonavicular
ligament, which originates in the neck of the talus and is directed to the superior
edge of the scaphoid, and the inferior calcaneo-navicular ligament (hammock liga-
ment or spring ligament) which has three components: (1) the superomedial that
arises from the anterior margin of the sustentaculum tali and inserts broadly into the
tuberosity of the navicular and the tibiospring complex of the deltoid ligament deep-
ening the coxa pedis; (2) plantarly, the medioplantar oblique component, which
originates from the coronoid fossa of the calcaneus and projects medially in a fan
shape to insert into the medial aspect of the navicular; and (3) the thickest of the
three is the longitudinal inferoplantar, which has the same origin as the previous one
and projects more laterally and inserts in the peak of the navicular [5].
The ligaments of the calcaneocuboid joint are the superior calcaneocuboid liga-
ment, it is directed from the superior edge of the articular facet of the calcaneus to
the dorsal face of the cuboid, and the inferior calcaneocuboid ligament or “Great
Plantar Ligament,” which originates in front of the two inferior tuberosities of the
calcaneus and it is directed forward dividing in two branches, a superficial one,
which is fixed to the cuboid and then passes as a bridge over the osseous concavity
that this bone forms to the tendon of the peroneus longus muscle, ending by three or
four digitations in the posterior extremity of the 3 or 4 last metatarsals. The deep
branch, shorter and wider than the previous one, is fixed to the cuboid.
As for the common ligaments of the joint: there is the “Y” ligament, which starts
from the superior aspect of the calcaneus and bifurcates into an internal fascicle
towards the scaphoid and an external fascicle towards the dorsal aspect of the cuboid.
These two joints invert and evert together with the subtalar joint [7]. When the
heel is inverted, the two joints are not parallel and lock together to stabilize the
midfoot during the push-off phase of gait, along with the windlass mechanism given
by the plantar aponeurosis [7] (Figs. 2, 3, and 4).
4 Classification
Main and Jowett classified these injuries into five patterns based on the mechanism
of injury (Fig. 6):
• Longitudinal load: (40%) the foot is in plantar flexion and the force passes from
the metatarsal heads compressing the navicular between the talus and cunei-
forms (Fig. 5) and the cuboid between the base of the fourth and fifth metatarsal
Fig. 2 Diagram taken

from 3D anatomy of AO
Foundation, showing the
bifurcated ligament that
runs from the superior
aspect of the calcaneal
tuberosity towards the
scaphoid and cuboid and
the dorsal calcaneocuboid
ligament
Fig. 3 Representative
schematic taken from AO
Foundation 3D anatomy,
where the dorsal
talonavicular ligaments are
identified in yellow
and the anterior process of the calcaneus. They are high energy lesions resulting
in displaced fractures and may involve the Lisfranc joint. They possess the worst
prognosis within the indirect mechanisms.
• Medial load: (30%), the foot is in plantar flexion and inverted. Most are sprains,
although medial talus navicular dislocation and mild subtalar subluxation have
been described.
Fig. 4 Representative
schematic taken from AO
Foundation, where
Spring’s ligament or
Hammock ligament is
highlighted in red and
Great plantar ligament in
yellow
Fig. 5 Schematic image

taken from the article Main
and Jowett [4]. Where
longitudinal forces
transmitted along the
metatarsals (arrows) are
depicted (compressing the
scaphoid between the
cuneiforms and the head of
the talus, causing shear
forces as depicted)
• Lateral loading: (17%) occurs by forced abduction of the forefoot, resulting in a

fracture of the cuboid or anterior process of the calcaneus or avulsion.
Dorsolateral talonavicular dislocation and lateral subtalar subluxation may
occur by this mechanism. Avulsion fracture of the navicular tuberosity is a con-
stant injury in this mechanism [5]. It has a worse prognosis than medial loading
fractures.
• Plantar loading: (7%) resulting in sprains, talonavicular, and calcaneocuboid
plantar dislocation and dorsal avulsions.
• Crushing: are high-energy injuries that do not give a constant pattern.
Fig. 6 Schematic drawing of Zwipp’s classification according to the injured anatomical struc-
tures. (Rammelt et al. [3, p. 376])
• Zwipp et al. classified these injuries according to the anatomical structures

injured. Depending on the bones affected, Chopart fractures and dislocations are
classified as follows:
1. Pure transligamentous
2. Transtalar
3. Transcalcaneal
4. Transnavicular
5. Transcuboid
6. Combinations: 2–5 (more than 40% of the cases)
The distal bones (navicular and cuboid) are involved twice as often as the proxi-
mal bones (talus and calcaneus).
Eichenholtz [8] divides navicular fractures into avulsion fractures, tuberosity
fractures, and body fractures. Regarding the latter, Sangeorzan et al. [67] divide it
taking into account the direction of the fracture line, the pattern of injury of the sur-
rounding joints, and the direction of displacement of the foot:
• Type 1: fracture line in the coronal plane, with the proximal fragment less than
50% of the body (Fig. 7).
• Type 2: the most common, where the main fracture line is directed dorsolateral
to plantarmedial, the main dorsomedial fragment and the forefoot are displaced
medially (Fig. 8).
• Type 3: There is central or lateral comminution. The forefoot is displaced later-
ally (Fig. 9).
There is no universally accepted classification for cuboid bone fractures [9].
They can be grouped according to whether they are extra/intra-articular, displaced/
non-displaced, avulsive (often confused with ankle sprains), or “nutcracker” com-
pression fractures named after Hermel and Gershon-Cohen [10].
Fig. 7 Schematic drawing

of the Sangeorzan
classification taken from
Sangeorzan et al. [67].
Type 1, the dorsal fragment
consists of less than 50%
of the navicular and the
trace is evident on the
lateral radiograph

of the Sangeorzan
classification taken from
Type 2: The talonavicular
joint is most frequently
dislocated dorsally and
medially

of the Sangeorzan
classification from
Type 3: continuous
scaphoid injury and
forefoot deviation
5 Diagnosis
Clinical Examination: Lisfranc-Chopart joint injuries can present in a varied man-

ner depending on the mechanism of injury and the energy absorbed by the initial
trauma. We can find from localized pain with some edema and impossibility of
walking to large soft tissue injuries, neurovascular lesions, and bone disorganiza-
tion. The possibility of compartment syndrome and decubitus skin necrosis should
be kept in mind in dislocations where urgency is mandatory and should be resolved
immediately. The plantar hematoma described by Ross [11] (Fig. 10) is a suggestive
sign of acute tarsometatarsal injury and forces us to carefully evaluate injuries in the
midfoot, both bone and soft tissue (ligament).
Imaging: anteroposterior, lateral, and 45° oblique radiographs of the injured foot
are taken. For the anteroposterior view, it is recommended to place the beam of rays
at 30° to avoid bone overlapping in the Chopart joint and at 20° for Lisfranc lesions
[1]. In the lateral projection, the Chopart joint appears as a double harmonic curve
which, if interrupted, should be suspected to be injured [1, 12] (Fig. 11). The oblique
projection is useful to evaluate the cuboid as it shows its joints free of overlap-
ping [9].
If a fracture line is confirmed in the radiography, it should be evaluated with
tomography, in order to perform a correct planning. If a fracture is not identified in
the initial radiographs, but the suspicion of a bone lesion is high, CT, MRI, or bone
scintigraphy would confirm or rule out such lesion.
We perform conservative treatment in those stable ligament injuries and bone avul-
sions, with orthosis for 6 weeks allowing full support. In the case of non-displaced
fractures, we use an orthosis and non-weight bearing for 6 weeks avoiding joint
movements that could displace the fracture, followed by removal of the orthosis and
loading according to tolerance.
We indicate surgical treatment for intra-articular injuries that present 1 mm of dis-

placement or more, as well as for bony injuries that compromise the length of the
medial or lateral columns by 2 mm or more, which should be diagnosed on com-
parative foot radiographs.
In large dislocations, emergency reduction is mandatory to avoid soft tissue
necrosis and conversion of a closed fracture to an open fracture. Closed reduction is
usually difficult due to soft tissue interposition, in which case open reduction and
transitional fixation with Kirchner wires for 6 weeks would be indicated [1].

plantar hematoma “Ross
sign” indicative of acute
bone or ligament injury
In case of compartment syndrome, two longitudinal approaches should be made,

one in the first interosseous space and the other on the diaphysis of the fourth meta-
tarsal, with the possibility of adding a medial approach on the calcaneus to decom-
press this compartment. The wounds should be left open and closed once the edema
Fig. 11 Chopart’s joint

where the joint interlining
in the form of an
uninterrupted sigma is
highlighted.
has subsided. Exposed fractures should be treated with antibiotic therapy as appro-
priate and copious irrigation with physiological solution and removal of all devital-
ized tissue. The bony structure should then be stabilized with an external fixator
giving alignment and length to the medial and lateral columns until definitive osteo-
synthesis is performed.
The patient is placed in dorsal decubitus, after placing a hemostatic cuff on the
thigh and ipsilateral gluteal bump to position the foot in neutral. If bone grafting is
planned, the iliac crest should be left uncovered. Autologous bone can also be
obtained from the medial malleolus or proximal tibia.
Injuries involving the medial column (fractures of the talar head and/or tarsal
scaphoid): most fractures are accessed through a dorsomedial approach centered on
the talonavicular joint. The incision begins at the level of the ankle, medial to the
anterior tibial tendon, and reaches the body of the navicular. Hemostasis of the
tributaries of the great saphenous vein is performed, and with blunt dissection, we
take care not to injure nerve branches coming from the saphenous and superficial
peroneal nerve. According to the preoperative evaluation with CT, fracture lines
centered in the body of the navicular or head of the talus are approached in the
interval between the anterior tibial and common extensor of the toes; and more lat-
eral fractures are approached between the common extensor of the toes and the
extensor hallucis longus, tendon interval through which the anterior tibial neurovas-
cular bundle which has to be displaced laterally [9]. Accessorily, a percutaneous
medial approach can be added, accessing between the anterior tibial and posterior
tibial tendons, for the osteosynthesis of fractures of the scaphoid tuberosity.
In case of shortening of the medial column, its length can be restored by placing
a mini distractor (Hintermann distractor or AO tubular mini distractor) by inserting
pins in the medial cuneiform and the talar neck [1, 12]. Bone defects should be filled
with cancellous bone. In simple fracture lines, the reduction is obtained with a
clamp through the medial approach previously described. The fracture is fixed with
3.5–2.7 compressive screws (Fig. 12a, b).
a b
Fig. 12 (a) Avulsed scaphoid fracture. (b) long term follow-up, consolidation, and joint
congruence
a b
Fig. 13 Images showing (a) Axial CT scan with navicular fracture with plantar comminution. (b)
Extended dorsal approach to visualize the scaphoid and the Lisfranc joint, osteosynthesis on the
dorsal aspect of the scaphoid of the same patient
The bone fragments of the talar head should be reduced and fixed with 3.5–2.7 mm
screws depending on the size of the fragment. We must ensure that the heads of
these screws are not exposed on the articular cartilage. Therefore, headless screws
are used or headed screws should be countersunk to avoid protrusion. In case of
comminution, 2.7 mm locking plates are used (Fig. 13a, b).
In situations where comminution of the navicular is severe and osteosynthesis is
not feasible, it is indicated to place a plate as a bridge from the body of the talus to
the first cuneiform and/or base of the first metatarsal. It is performed percutane-
ously, thus taking advantage of the capsule as a means of indirect traction for the
reduction of the fragments. As the first metatarsal is mobile, its removal is recom-
mended once bone healing has been confirmed by CT scan (Fig. 14a–d).
Injuries involving the lateral column: (fractures of the anterior calcaneal tuberos-
ity and/or cuboid). They are approached through an anterolateral incision starting at
the level of the tarsal sinus [1] and extending towards the fourth metatarsal. The
peroneal tendons must be released from their retinaculum and, together with the
sural nerve, must be retracted downward. As in the medial column, we can apply a
mini distractor to achieve appropriate length. Pins can be placed between the body
a b
c d
Fig. 14 Intraoperative images of a comminuted scaphoid fracture. (a) clinical image where
Hinterman distraction is performed. (b) Radiological control of the distraction, see the pins placed
in the talar neck proximally and in the cuneiform distally. (c) Percutaneous placement of the recon-
struction plate. (d) Intraoperative radiological control of the result
of the calcaneus and the cuboid or between the anterior process of the calcaneus and
the fifth metatarsal if the cuboid is involved.
As for the cuboid, the osteoarticular fragments should be elevated and pinned in
order to anatomically reconstruct the articular surface, the bone defects are filled
with bone graft, and the osteosynthesis is performed with 2.7 mm premolded plates
(Fig. 15a, b).
Applying the same concepts as for the anterior calcaneal tuberosity, 2.7 mm
plates or 2.7–3.5 mm screws are placed in case of simple fracture lines. If the com-
minution does not allow osteosynthesis, the use of a plate is indicated as a bridge
from the calcaneus to the base of the fourth or fifth metatarsal, thus maintaining an
adequate column length, removing it at the fourth month after surgery. It is esti-
mated that in half of the Chopart joint lesions, more than two bones are involved, so
a 5 cm distance between the approaches must be respected to avoid devitalization of
the cutaneous bridge [12].
Primary arthrodesis of the involved joints will be the choice when there is great
involvement of the articular cartilage [12], since the fusion of one joint affects the
mobility of the other joint and of the subtalar joint. Talonavicular fusion limits
a b
Fig. 15 Intraoperative image of cuboid fracture. (a) Cuboid approach and visualization, with oste-
synthesis with perimetral plate. (b) Intraoperative radiological control showing the normal rela-
tionship of the cuboid with the anterior tuberosity of the calcaneus and the base of the fourth and
fifth metatarsal, fixed with a locked plate and interfragmentary screw
calcaneocuboid and subtalar joint motion by 90–92%, subtalar fusion limits talona-
vicular joint motion by 74%, and calcaneocuboid joint motion by 45%. Arthrodesis
of the calcaneocuboid joint has the least effect on the other two joints, with 33% of
the talonavicular joint and 8% of the subtalar joint [13].
8 Postoperative Care
In dislocations, osteodesis with transfixing pins should be left in place for 6 weeks
and foot mobility should be protected with a walker boot or cast. Once the pins are
removed, progressive loading and joint mobility should be started.
If osteosynthesis was performed, a removable walker boot should be placed to
allow passive mobility of the ankle and foot. Once the skin sutures are removed (at
2–3 weeks), physical therapy is initiated. Partial loading will be indicated from the
sixth week, and total loading from the eighth week. An objective decision tool to
know when to indicate weight bearing in bone lesions is the CT scan. When observ-
ing healing in at least 50% of the axial slices, weight bearing should be started.
9 Complications of Treatment
• Soft tissue injuries: 0–10%. Almost exclusively in case of open fractures [1]
where paresthesia or lack of sensitivity of the dorsal region may persist due to the
initial trauma.
• Post-traumatic arthrosis: more frequent in displaced fractures, due to the fact that
the talonavicular joint has greater movement and handles greater pressure than
the calcaneocuboid joint, which makes it more symptomatic than the latter.
Arthrodesis with bone graft is indicated, restoring length to the column both
laterally and medially.
• Avascular necrosis of the navicular: may occur despite early treatment. The navic-
ular collapses and extrudes dorsally, bringing the forefoot into adduction [12, 14].
The patient complains of persistent pain that increases with loading. Radio-
opacity is evident on conventional radiographs 4–6 months after initial treatment
[12]. For a more detailed diagnosis of necrotic extension, MRI should be requested.
• Collapse and shortening of the medial column is avoided by performing talona-
vicular arthrodesis with bone graft, also including the naviculocuneiform joint,
adding greater stability to the construct.
• Malunion and pseudoarthrosis: resulting in arthritis - early arthrosis and devia-
tions that can occur in all three planes, leading to an adducted or abducted fore-
foot (when there is shortening of the medial or lateral column) or to a flat or cavus
foot (when the dislocations are plantar or dorsal) or to a pronated or supinated
forefoot (when the dislocations are rotational). These deformities can occur in a
single plane or in combination with each other. Restoration of normal anatomy
can be accomplished by extra-articular corrective osteotomies if osteoarthritis is
not present [15] or by performing a joint fusion correcting the deformity.
10 Lesions of the Lisfranc Joint
10.1 Summary
The diagnosis of Lisfranc joint injury is difficult to make and goes unnoticed in many
cases. Patients should be studied with complementary studies in the presence of plan-
tar hematoma: conventional radiographs. In case of diagnostic doubt (occult lesions),
loading radiographs or stress radiographs (preferred by the authors) are extremely
useful. Computed axial tomography is very useful to differentiate simple or commi-
nuted fractures. We recommend the Arrondo et al. classification, as it allows not only
to classify the injuries, but also offers a protocolized treatment for each stage: 1A
(orthopedic treatment), 1B (percutaneous reduction and stabilization), 2A (open
reduction and internal fixation), and 2B (arthrodesis with or without bone graft).
Restoring normal anatomy and achieving a plantigrade and functional foot
should be the main objective of our treatment.
10.2 Introduction
Tarsometatarsal joint disorders occupy the second place in frequency of foot inju-
ries in athletes [16], accounting for about 0.2% of all fractures (1 per 55,000 people)
[17, 18]. Their clinical presentation can be varied, from evident to the eyes of any
orthopedist or hidden, leading to misdiagnosis in up to 20% of cases [19].
If the lesion is treated before the sixth week of the initial trauma, it will be con-
sidered acute, after this period of time it is chronic [7]. Acute injuries can be grouped
into two types: high and low energy. High-energy trauma corresponds to automobile
accidents (the most frequent mechanism, 40–45% of the cases [20]), motorcycle
accidents, crushing by direct trauma, and falls of more than 4 meters in height [21].
In these cases, the association with compartment syndrome is frequent. Low energy
injuries include those in sports activities produced by midfoot sprains and same
level falls [21].
10.3 Anatomy
The anatomy of the Lisfranc joint is complex. It presents a combination of liga-

ments and bony structures that give support to the longitudinal and transverse arches
of the foot. This joint is responsible for joining the midfoot to the forefoot. The first
(M1), second (M2) and third metatarsal (M3) articulate with the medial (C1), cen-
tral (C2), and lateral (C3) cuneiform, respectively; the fourth (M4) and fifth meta-
tarsal (M5) articulate with the proper facet provided by the cuboid. The three
cuneiforms articulating with their metatarsals form a trapezoidal configuration. The
articular interlining is not linear along its entire trajectory; it is interrupted by the
protrusion of the base of the second metatarsal proximally, at the level of the second
cuneiform, fitting as in a mortise between C1 and C3 [22–24], thus forming a trans-
verse or Roman arch structure [25], providing stability in the coronal plane (Fig. 16)
Three anatomical-functional areas can be differentiated: medial column, central
column, and lateral column. The medial column, composed of M1 and C1, presents
a range of mobility in the sagittal plane of 3.5 mm; the central column, composed of
M2 and M3 with C2 and C3, (more rigid column) with a range of mobility of
0.6 mm; and the lateral column composed of M4 and M5 with the cuboid, (the most
mobile column of the three) with 13 mm of dorsal-plantar mobility [26].
a b
Fig. 16 (a) Axial tomographic section showing a transverse or roman arch structure. (b) Top view
of anatomical preparation. See in yellow dotted lines the mortise made by the cuneiforms to the
second MTT. (de Palma et al. [22])
The dorsal ligaments have longitudinal, oblique, and transverse fibers. There are
seven tarsometatarsal ligaments [27]; those that join C1, C2 and C3 together, and
C3 with the cuboid, and ligaments that join the metatarsals together (with the excep-
tion of M1-M2 which does not have a dorsal ligament) [22]. They are weaker than
the plantar and interosseous ligaments. However, studies have shown that the dorsal
ligament joining C1 to M1 is stronger than previously thought and plays a very
important role in the stability of the medial column [28, 29] (Fig. 17).
The interosseous ligaments are the strongest ligaments of the Lisfranc joint, join-
ing the tarsal and metatarsal bones together except for the joint between M1 and M2
which has no proper interosseous ligament. C1 and M2 are joined by the strongest
ligament of the series, the interosseous ligament of Lisfranc. This extends from the
lateral aspect of C1, adjacent to the medial insertion of the C1-C2 intercuneiform
ligament [22] and runs laterally, distally and plantar inserting into the medial and
plantar half of M2, close to its articular surface. It is approximately 10 mm long and
between 5 and 7 mm thick [30, 31]. Its anatomy may be represented by a single
band in 73% of cases or by two bands in 27% of them [24].
Fig. 17 Dorsal ligaments

of the metatarsal tarsal
joint. In black the TMT
ligaments, in blue the
intertarsal ligaments, in
green the intermetatarsal
ligaments, and in red the
dorsal lisfranc ligament. M
metatarsals, C cradles, CU
cuboid
Fig. 18 Lateral ligament of lisfranc or Liverpool ligament. (From Mason et al. [32]; With permis-
sion of authors)
The plantar ligaments present longitudinal, oblique, and transverse fibers, variable
in number and course. The most important plantar ligament has an oblique course start-
ing from C1 and dividing into two bands, a superficial one for M3 and a deep one for
M2, thus joining the central column to the medial column. Mason et al. [32] described
a ligament which they called the lateral ligament of Lisfranc or Liverpool ligament. It
extends from the base of the fifth metatarsal to the plantar aspect of the second meta-
tarsal, lying below the tendon of the peroneus longus muscle. It has no connections
with M3 and M4, but is strongly attached to the large plantar ligament (Fig. 18).
10.4 Etiology
Lisfranc joint injuries can be caused by high or low energy mechanisms. High-
energy injuries are usually associated with direct trauma to the dorsum of the foot
displacing the base of the metatarsals to plantar, resulting in extensive soft tissue
involvement and vascular injury [31, 33, 34]. Those produced by indirect trauma are
of low energy, generated by an axial force vector applied to the limb with the foot in
plantar flexion, and are frequent in athletes or dancers [31, 35, 36] (Fig. 19).
10.5 Classification
Many classifications have been proposed for Lisfranc lesions. The most widespread
was the modification of Mark Myerson [34] in 1986 to the classifications of Quenu
and Kuss (1909) [37] and Hardcastle (1982) [38]. This classification divides the
lesions into three groups according to the direction of displacement:
Fig. 19 Direct mechanism. (From Myerson et al. [34]: with permission of authors). Indirect
mechanism. (From Myerson et al. [34]: with permission of authors)
• Total incongruence (Type A) includes displacement of all metatarsals (lateral or

dorsoplantar) with or without fracture of the base of the second metatarsal,
• Partial incongruence (Type B) is divided into two groups: B1, partial incongru-
ence with medial dislocation; and B2 partial incongruence with lateral
dislocation.
• Divergent (Type C) is further divided into C1 (partial) or C2 (total), where in
addition to the displacement of the first metatarsal medially, a lateral displace-
ment of some (C1) or all of the metatarsals (C2) is observed (Fig. 20).
However, this classification, with its modifications, does not include Lisfranc
occult lesions, a concept that became popular in the 1990s. Nunley and Vertullo
(2002) [39] in their research on sports patients incorporate the concept of “midfoot
sprain with diastasis”, classifying it into three stages according to clinical, scinti-
graphic, and loaded radiographic findings. Stage 1 is a sprain of the Lisfranc liga-
ment, with no displacement between the first and second metatarsal on loaded
radiographs and the scintigraphy is positive; stage 2 involves diastasis between the
first and second metatarsal (1–5 mm) without loss of the longitudinal arch of the
midfoot; and stage 3 are those cases where diastasis greater than 5 mm is evident
with loss of longitudinal arch of the midfoot.
Sivakumar et al. [31] add a lesion variant to Myerson’s classification (Type D)
considering hidden lesions. He subdivides this group into two: D1, those that do not
require surgery for fixation, and D2, those that do. The latter group, in turn, is sub-
divided into D2L, those with only ligament lesions, and D2B, those with bony avul-
sion. In contrast to the Nunley and Vertullo classification, subtype D of this
classification establishes the case of a stable lesion; those with diastasis of 2 mm or
less between the medial cuneiform and the base of the second metatarsal (C1M2).
Fig. 20 Classifications: A. Quenú and Kuss (1909), B. Hardcastle (1982) and C. Myerson (1986)
The previous classifications are based mainly on the degree of displacement of

the metatarsals involved. However, several authors classify Lisfranc injuries accord-
ing to their injury pattern. Haraguchi et al. in 2019 [40] examined 87 patients, in
which they collated intraoperative data and preoperative tomographic data (73
patients), and based on the concepts described by Kaar and colleagues in 2007 [41],
divided the lesions into two groups: simple or combined patterns. The simple ones
include the longitudinal type (38% of cases) instability between C1 and M2 and
between C1 and C2 and the transverse type (30% of cases) instability between C1
and M2 and between C2 and M2. The transverse type also includes lesions between
C3 and M3. Combined patterns include the transverse type and injury to the first
tarsometatarsal (TMT) joint (20%); longitudinal type plus transverse injury (7%);
longitudinal type and injury to the first TMT joint (3%); and longitudinal type plus
transverse injury and injury to the first TMT joint (2%). In 41 of the 73 patients
(56%) evaluated with CT scans, one or more associated fractures were found,
excluding bone avulsions.
Recently, Schepers and Rammelt [42] classified the severity of the lesions by
columns: Medial, Central, and Lateral, with the possibility of four levels that
increase the severity:
0. Does not include Lisfranc (includes extra-articular diaphyseal injuries of the
metatarsals).
1. Purely ligament injuries, including avulsive fractures (“fleck sign”)
2. Simple fractures of the metatarsal bases or cuneiform or cuboids of the respec-
tive TMT joint.
3. Comminuted fractures involving more than 50% of the TMT articular surface
(Fig. 21).
Fig. 21 Classification proposed by Rammelt and Scheppers
10.5.1 Classification Chosen by the Authors
The ideal classification is one that is easy to remember, composed of well-established

elements from other classifications. It should include occult ligamentous lesions
and bony lesions and present a treatment strategy. It should also improve communi-
cation between physicians with minimal interobserver and intraobserver variability.
Therefore, the classification of Arrondo et al. [43] (2008) is the one we use in our
team. It divides Lisfranc lesions into the following:
• Type 1 Hidden lesions (conventional radiographs without apparent bone lesion)
in turn are subdivided according to the changes observed in the weight bearing
radiograph or abduction stress radiograph test described by Coss [44] into the
following:
• Type (1A) “Stable hidden”: negative radiographic stress
• Type (1B) “ Unstable hidden” positive radiographic stress
• Type 2 Evident lesions (conventional radiographs with visible bone lesion). CT
is requested in order to subclassify them into the following:
• Type (2A) or simple
• Type (2b) or multifragmentary
Each type is further subdivided into three subtypes according to which column is
affected: (1) medial, (2) central, and (3) lateral column (Fig. 22).
Fig. 22 Classification proposed by Arrondo et al. Hidden: positive clinical findings without any
evident radiological abnormality (on standard non-weightbearing foot projections). Stable: no
radiological abnormalities under stress (weightbearing or manual adduction-abduction maneu-
vers). Unstable: radiological abnormalities under stress. Evident: positive clinical findings with
evident radiological abnormality (on standard non-weightbearing foot projections). Simple: tarso-
metatarsal dislocation-subluxation and/or dislocation-subluxation with one fracture line on one or
more metatarsal bases and/or cuneiforms. Comminuted: tarsometatarsal dislocation-subluxation
with comminuted fractures in one or more metatarsal bases and/or cuneiforms
10.6 Diagnosis
High-energy injuries present no major difficulty in diagnosis since they present with
deformity, large edema, and evident joint incongruence. Those caused by low
energy trauma are the most challenging to diagnose, not only because their clinical
presentation is not so evident but also because imaging studies are sometimes
almost normal. Failure to detect these lesions or misdiagnosis is frequent, and this
leads to poor functional results with chronic pain, functional impotence, and arthri-
tis. The misdiagnosis of these lesions can be as high as 50% [17, 45].
Plantar hematoma is highly associated with Lisfranc lesions [11] and its pres-
ence should alert the specialist to perform the corresponding diagnostic studies
which include conventional radiographies, stress radiographies (manual or with bi
or monopodal load), magnetic resonance, and tomography [46, 47].
Conventional X-rays: they are important and are the first to be requested; they
can diagnose 68.9% of Lisfranc lesions [48]. We must remember the Foster lines
[49] in conventional X-rays. In AP X-rays: The lateral border of the first MTT
should be aligned with the lateral border of the first cuneiform and the medial bor-
der of the base of the second MTT should be aligned with the medial border of the
second cuneiform. On oblique radiographs, the medial and lateral edges of the third
MTT should coincide with the edges of the third cuneiform, and the medial edge of
the base of the fourth MTT should be aligned with the medial edge of the cuboid [50].
A reliable indicator of Lisfranc injury is the lateral displacement of the base of
the second MTT [50] (diastasis greater than 2 mm between the first and second
tarsometatarsal joints) and avulsion of the base of the second MTT or first cunei-
form (“fleck sign”) is a pathognomonic sign [34, 50] (Fig. 23).
Fig. 23 Stress radiograph.

The “Fleck Sign” can be
seen in the red circle
We must remember that the measurement of distances will change according to

the position of the foot when the radiograph is taken, so the ideal is always to have
comparative radiographs in case of diagnostic doubt.
10.6.1 Weight-bearing Radiographs
In the face of diagnostic doubt, loaded radiographs can accentuate the degree of
displacement; they can be performed in two ways: bi-podalic or mono-podalic. We
believe that the mono-podalic evaluation allows to obtain more precise information,
since in the bi-podalic way, the patient can load more weight on the healthy side and
the information obtained is not completely reliable. They should be performed com-
paratively. Differences of alignment between the healthy and injured sides more
than 2 mm between C1-M2 and M1-M2 are diagnostic of instability.
In the lateral projections, it is important to observe the continuity of the dorsal
surface of the base of M1 and C1; and the plantar border of M1 should be seen
above the plantar border of 5 MTT [50] (Fig. 24).
Fig. 24 Radiographs with monopodal loading. The diastasis between M2 and C1 can be seen on
the injured side
Stress radiographs (abduction test)

In the presence of normal radiographs and clinical suspicion of instability, man-
ual stress radiographs are very useful to demonstrate instability or malalignment.
Karr and collaborators [41] in their cadaveric work showed that the radiographs
with manual stress present greater displacements in the evaluation of instability than
the radiographs with load. It is important that the maneuver be performed by a
trained person.
This test was described by Coss in 1998 and should be performed on both feet.
A tangential line is drawn through the medial border of the navicular and the first
cuneiform. In a healthy foot, this line should cross the head of the first MTT, while
in an injured foot it does not and passes medially to it [44]. Many publications do
not recommend this test because of the pain it causes at the moment of performing
it; however, we believe that it is a very reliable study to determine not only instabil-
ity in the Lisfranc region and surroundings, but also to be able to perform a correct
presurgical planning (Fig. 25).
10.6.2 Computed Axial Tomography (CT)
CT helps diagnose hidden fractures and some joint subluxations that are not seen on
conventional radiographs, and also allows us to plan surgery. However, since it is a
static study, it does not diagnose instabilities. Kennelly et al. compared loaded
Fig. 25 Stress X-rays. In the image on the left, see how the red line passing through the medial
border of the scaphoid and C1 crosses the 1 MTT through the center of its head. In the image on
the right, it can be seen how the red line passes medial to the head of the 1 MTT. Always perform
them bilaterally
X-rays and CT scans, reaching the conclusion that a significant number of unstable
lesions go unnoticed with CT [51].
10.6.3 Magnetic Resonance Imaging (MRI)
MRI is useful for detecting soft tissue and ligament injuries. It presents a sensitivity
and predictive value of 94% to determine Lisfranc instability. It is an expensive and
not always available study. It is also a static study, so that many of the lesions can be
underestimated or misinterpreted.
The following is the diagnostic protocol chosen by the authors [52] (Fig. 26)
Fig. 26 Diagnostic protocol for Lisfranc lesions. The black squares show the preference of the
authors of this chapter
10.7 Treatment
The treatment goal is to be able to achieve a pain-free, stable, and plantigrade foot,
with the least morbidity for the patient. As mentioned above, we will describe the
treatment for each of the stages following the protocol of the Arrondo et al. classifi-
cation (Fig. 27).
High-energy injuries should be treated as emergencies and an effective tactic
would be a staged protocol, including immediate treatment on the day of the trauma,
and then defer surgery 10–15 days after the trauma [53, 54]. In large bone disorga-
nizations, metatarsal alignment and reduction of dislocations should be achieved by
closed reduction and fixation with pins, in order to reduce pressure on the skin and
soft tissues, improving blood circulation and reducing the risk of compartment syn-
drome. Technically, the use of an external medium or small pinned fixator, placed
on either the external or internal side of the foot, has proven to be a useful tool [53].
The use of large pins in small bones is not recommended, since it may leave an
unstable assembly, with irritation of the soft tissues and thus increase infection rates
in the area of pin placement [53, 55, 56]. If a correct closed reduction is not achieved,
the lesion should be approached with the planning of definitive surgery in mind.
Fig. 27 Treatment protocol according to the classification of Arrondo et al. Hidden: positive clini-
cal findings without any evident radiological abnormality (on standard non-weightbearing foot
projections). Stable: no radiological abnormalities under stress (weightbearing or manual
adduction-abduction maneuvers). Unstable: radiological abnormalities under stress. Evident: posi-
tive clinical findings with evident radiological abnormality (on standard non-weightbearing foot
projections). Simple: tarsometatarsal dislocation-subluxation and/or dislocation-subluxation with
one fracture line on one or more metatarsal bases and/or cuneiforms. Comminuted: tarsometatarsal
dislocation-subluxation with comminuted fractures in one or more metatarsal bases and/or cunei-
forms. Conservative: no surgery needed. See text for details. Percutaneous: Surgery is performed
using cannulated percutaneous tarsometatarsal screws. No joint preparation is performed
If compartment syndrome is highly suspected, fasciotomies should be performed

in addition to the aforementioned procedures. The evolution of the soft tissues will
determine the optimal moment for definitive surgery, approximately 10–15 days is
the estimated term, time at which the edema decreases, the bullas heal, and the
wrinkle sign appears on the skin [55, 57].
10.7.1 Stage 1A: Stable Occult
We define a stable occult lesion as a lesion where stress radiographs maintain nor-
mal anatomical parameters.
The proposed treatment is nonsurgical, including walker boot for 6 weeks, the
first 3 weeks without support and then progressive loading is allowed. At the
sixth week, the immobilization is removed and physical therapy begins. The
progressive return to normal activities is according to pain tolerance. This type
of injury takes approximately 4–6 months to recover completely [17, 58, 59]. If
there is persistent pain, suspect associated injuries not diagnosed at the time of
the trauma.
10.7.2 Stage 1B: Occult Unstable
After clinical suspicion and positive data in dynamic imaging, treatment is decided.
We propose percutaneous fixation: It is effective, safe, and relatively simple in
experienced hands. This method has several advantages: less soft tissue dissection,
less surgery time, less hospitalization, and rapid mobilization [60]. If a correct
reduction cannot be achieved, it should be performed openly [61].
The patient is placed in dorsal decubitus, with an ipsilateral hip bump, to place the
foot in neutral position. The clamp tips are placed through two small incisions, one
at the lateral base of the 2 MTT and the other at the medial base of the first cunei-
form, covering the Lisfranc region. The clamp is compressed and controlled under
fluoroscopy. If the reduction is anatomic, we proceed with percutaneous fixation. We
use full thread cannulated screws of 4.0 mm diameter depending on the position. The
screw should be placed from the base of the second MTT towards the first cuneiform
(or vice versa). After this fixation, an intraoperative radiographic stress test is per-
formed. If instability is observed in any of the other columns, they are fixed percuta-
neously in the same way. If instability of the fourth and fifth ray is observed, fixation
is performed with pins. These are removed after 6 weeks [60] (Fig. 28).
10.7.3 Stage 2A: Simple Evident
In these cases, we request a CT scan. This allows us to differentiate simple lesions

(stage 2A) from comminuted lesions (stage 2B).
a b c
Fig. 28 (a) Intraoperative image: clamp placement for percutaneous reduction. (b) Intraoperative
fluoroscopy image showing reduction of the lisfranc joint. (c) Post screw placement image follow-
ing the direction of the lisfranc ligament
It is of utmost importance to analyze which columns are affected in order to cor-

rectly plan the approaches, select the correct implant, and perform the surgery.
The patient is positioned as previously described. A first approach is made in the
first interosseous space. The hallux extensor, pedicle artery, and deep peroneal nerve
are dissected together in one plane. The Lisfranc joint is thus exposed. Intraoperative
stress radiographs are performed to observe “live” instability of the Lisfranc joint
and/or other columns. If instability of the first column (C1 M1) is observed, it is
fixed temporarily with a pin to provide medial containment. Then we focus on the
Lisfranc joint. Scar tissue or small bony avulsions of the space are resected. This is
reduced with a spike clamp and the 4.0 full thread cannulated screw guide pin is
passed from the base of the second MTT to the first cuneiform position screw. We
believe that fixation from the cuneiform to the metatarsal is an option; however,
many injuries present fractures at the base of the second MTT, especially in the
plantar region, and if the screw seeks fixation in that area (in the cuneiform-MTT
direction), the fixation will not be sufficiently stable, therefore, our recommenda-
tion is fixation from the second MTT to the first cuneiform. After fixation of the
Lisfranc joint, we remove the pin that kept the first column stable and we perform
again intraoperative stress radiographs and thus evaluate which columns should
now be stabilized. The fixation of the columns can be done with trans-articular can-
nulated screws or 2.7 mm transitional bridging plates. The literature shows similar
results in terms of rigidity and stability with both methods [31, 62]; however, the use
of trans-articular screws reports joint injuries between 2% and 7.6% [31, 62, 63].
In a case of instability of the first column, we add a medial approach on the first
MTT and 1 cuneiform, in order to place the plate on the tension side of the joint. To
achieve a correct reduction of this joint, the hallux is manipulated: slight varus and
dorsiflexion while applying slight lateral pressure to the base of the first MTT. If we
observe instability of the third column, we perform another approach on the 3 space.
From there, we stabilize the joint and place another transitional bridge plate. In case
of instability of the fourth and fifth MTT, we stabilize with transitional pins (removal
at 6 weeks).
Our preferred method of fixation is with a position screw simulating the direction
of the Lisfranc ligament (from the 2 metatarsal to the cuneiform) and the use of
transitional plates for the rest of the columns (Figs. 29 and 30).
10.7.4 Stage 2B: Comminuted Evident
In this stage, joint derangement is evident on conventional radiographs. There is no

need to add dynamic radiographic studies for diagnosis. It is important to request a
CT scan in order to demonstrate joint involvement, as well as associated lesions.
The patient is placed in the same position already described for lesions 1 B and 2 A,
with the exception that in this lesion the use of bone graft may be required, so we
add in the surgical field the region of the homolateral iliac crest. If the injury pres-
ents instability and fractures in the first column, it is there where we should begin
the osteosynthesis process by means of a medial approach. It is important to
a b c
Fig. 29 (a) Fluoroscopy of an intraoperative yawn: medial, central, and lateral column instability.
(b and c) Clinical and fluoroscopy image: transitional stabilization of the medial column, reduction
with tip clamp of the Lisfranc joint, and pin passage of the cannulated screw in position of the
Lisfranc ligament
a b c
Fig. 30 (a) Intraoperative postoperative yawning fluoroscopy image post-reduction of the Lisfranc
joint with instability of the 3-column and stable first column. (b) and (c) Choice of two approaches
for stabilization with plate plus intra-op fluoroscopic imaging
reestablish the length of this column, since from there, the rest of the midfoot can be
reorganized. If the comminution is large, the placement of a tricortical graft helps to
give length. The central columns are then fixed after resection of the damaged artic-
ular surfaces. A single graft can be placed by fixing the bases of the second and third
MTT with their respective cuneiforms or individual grafts for each of the metatar-
sals (Fig. 31).
a b c
Fig. 31 (a) Anteroposterior foot X-ray with lesion 2B. (b) Intraoperative fluoroscopy with transi-
tional pin stabilization. (c) Postoperative radiograph showing medial and central column arthrod-
esis with tricortical graft plus lateral column fixation with pins
10.8 Removal of Material
The osteosynthesis material can be left permanently or be removed at 16 weeks [33,

64–66]. The percentage of screw breakage is low (5–25%), generally asymptom-
atic, and could cause future inconveniences in the event of having to convert the
osteosynthesis into an arthrodesis [20, 45, 66].
We routinely remove material from stages 1B and 2A at 16 weeks post-surgery.
We do not remove osteosynthesis material in arthrodesis Cases.
References
1. Rammelt S. Chopart and lisfranc fracture-dislocations. Eur J Orthop Surg Traumatol.

2014:3835–57.
2. Wei C-J, Tsai W-C, Tiu C-M, Wu H-T, Chiou H-J, Chang C-Y. Systematic analysis of missed
extremity fractures in emergency radiology. Acta Radiol. 2006;47(7):710–7.
3. Rammelt S, Grass R, Schikore H, Zwipp H. [Injuries of the Chopart joint]. Unfallchirurg.
2002;105(4):371–83; quiz 384–5.
4. Main BJ, Jowett RL. Injuries of the midtarsal joint. J Bone Joint Surg Br. 1975;57(1):89–97.
5. Walter WR, Hirschmann A, Alaia EF, Tafur M, Rosenberg ZS. Normal anatomy and trau-
matic injury of the midtarsal (Chopart) joint complex: an imaging primer. Radiographics.
2019;39(1):136–52.
6. Testut L, Latarjet A. Tratado de anatomía humana. 1964. Available from: http://www.sidalc.

net/cgi-bin/wxis.exe/?IsisScript=UNCPE.xis&method=post&formato=2&cantidad=1&expre
sion=mfn=000416.
7. Benirschke SK, Meinberg EG, Anderson SA, Jones CB, Cole PA. Fractures and dislocations
of the midfoot: Lisfranc and Chopart injuries. Instr Course Lect. 2013;62:79–91.
8. Eichenholtz SN, Levine DB. Fractures of the tarsal navicular bone. Clin Orthop Relat Res.
1964;34:142–57.
9. Clements JR, Randolph Clements J, Dijour F, Leong W. Surgical management navicular and
cuboid fractures [Internet]. Clin Podiatr Med Surg. 2018;35:145–59. Available from: https://
doi.org/10.1016/j.cpm.2017.12.001.
10. Hermel MB, Gershon-Cohen J. The nutcracker fracture of the cuboid by indirect violence.
Radiology. 1953;60(6):850–4.
11. Ross G, Cronin R, Hauzenblas J, Juliano P. Plantar ecchymosis sign: a clinical aid to diagnosis
of occult Lisfranc tarsometatarsal injuries. J Orthop Trauma. 1996;10(2):119–22.
12. Rammelt S, Schepers T. Chopart injuries: when to fix and when to fuse? Foot Ankle Clin.
2017;22(1):163–80.
13. Astion DJ, Deland JT, Otis JC, Kenneally S. Motion of the hindfoot after simulated arthrod-
esis. J Bone Joint Surg Am. 1997;79(2):241–6.
14. Ramadorai MUE, Beuchel MW, Sangeorzan BJ. Fractures and dislocations of the tarsal navic-
ular. J Am Acad Orthop Surg. 2016;24(6):379–89.
15. Rammelt S, Zwipp H, Schneiders W, Heineck J. Anatomic reconstruction of malunited
Chopart joint injuries. Eur J Trauma Emerg Surg. 2010;36(3):196–205.
16. Seybold JD, Coetzee JC. Lisfranc injuries: when to observe, fix, or fuse. Clin Sports Med.
2015;34(4):705–23.
17. Desmond EA, Chou LB. Current concepts review: Lisfranc injuries. Foot Ankle Int.
2006;27(8):653–60.
18. Cassebaum WH. 13 Lisfranc fracture-dislocations. Clin Orthop Relat Res. 1963;30:116.
19. Aronow MS. Treatment of the missed Lisfranc injury. Foot Ankle Clin. 2006;11(1):127–42, ix.
20. Thompson MC, Mormino MA. Injury to the tarsometatarsal joint complex. J Am Acad Orthop
Surg. 2003;11(4):260–7.
21. Ly TV, Coetzee JC. Treatment of primarily ligamentous Lisfranc joint injuries: primary
arthrodesis compared with open reduction and internal fixation. A prospective, randomized
study. J Bone Joint Surg Am. 2006;88(3):514–20.
22. de Palma L, Santucci A, Sabetta SP, Rapali S. Anatomy of the Lisfranc joint complex. Foot
Ankle Int. 1997;18(6):356–64.
23. Testut L, Latarjet A, Latarjet M. Tratado de Anatomia Humana, vol. 2. Barcelona: Salvat; 1958.
24. Panchbhavi VK, Molina D, Villarreal J, Curry MC, Andersen CR. Three-dimensional, digital,
and gross anatomy of the Lisfranc ligament [Internet]. Foot Ankle Int. 2013;34:876–80.
25. Watson TS, Shurnas PS, Denker J. Treatment of Lisfranc joint injury: current concepts. J Am
Acad Orthop Surg. 2010;18(12):718–28.
26. Ouzounian TJ, Shereff MJ. In vitro determination of midfoot motion. Foot Ankle.
1989;10(3):140–6.
27. Castro M, Melão L, Canella C, Weber M, Negrão P, Trudell D, et al. Lisfranc joint liga-
mentous complex: MRI with anatomic correlation in cadavers. AJR Am J Roentgenol.
2010;195(6):W447–55.
28. Crim J. MR imaging evaluation of subtle Lisfranc injuries: the midfoot sprain. Magn Reson
Imaging Clin N Am. 2008;16(1):19–27, v.
29. Kura H, Luo ZP, Kitaoka HB, Smutz WP, An KN. Mechanical behavior of the Lisfranc
and dorsal cuneometatarsal ligaments: in vitro biomechanical study. J Orthop Trauma.
2001;15(2):107–10.
30. Blouet JM, Rebaud C, Marquer Y, Duval JM, Husson JL, Jourdain R, et al. Anatomy of the
tarsometatarsal joint and its applications to dislocation of this articular interface. Anat Clin.
1983;5(1):9–16.
31. Sivakumar BS, An VVG, Oitment C, Myerson M. Subtle Lisfranc injuries: a topical review and
modification of the classification system [Internet]. Orthopedics. 2018;41:e168–75. Available
from: https://doi.org/10.3928/01477447-20180213-07.
32. Mason L, Jayatilaka MLT, Fisher A, Fisher L, Swanton E, Molloy A. Anatomy of the lateral
plantar ligaments of the transverse metatarsal arch. Foot Ankle Int. 2020;41(1):109–14.
33. Myerson M. The diagnosis and treatment of injuries to the Lisfranc joint complex. Orthop Clin
North Am. 1989;20(4):655–64.
34. Myerson MS, Fisher RT, Burgess AR, Kenzora JE. Fracture dislocations of the tarsometatarsal
joints: end results correlated with pathology and treatment. Foot Ankle. 1986;6(5):225–42.
35. Curtis MJ, Myerson M, Szura B. Tarsometatarsal joint injuries in the athlete. Am J Sports Med.
1993;21(4):497–502.
36. Makwana NK. (iii) Tarsometatarsal injuries—Lisfranc injuries. Curr Orthop.
2005;19(2):108–18.
37. Quenu E, Kuss G. Study on the dislocations of the metatarsal bones (tarsometatarsal disloca-
tions) and diastasis between the 1st and 2nd metatarsal. Rev Chir. 1909;39:281–336.
38. Hardcastle PH, Reschauer R, Kutscha-Lissberg E, Schoffmann W. Injuries to the tarsometatar-
sal joint. Incidence, classification and treatment. J Bone Joint Surg Br. 1982;64(3):349–56.
39. Nunley JA, Vertullo CJ. Classification, investigation, and management of midfoot sprains:
Lisfranc injuries in the athlete. Am J Sports Med. 2002;30(6):871–8.
40. Haraguchi N, Ota K, Ozeki T, Nishizaka S. Anatomical pathology of subtle Lisfranc injury. Sci
Rep. 2019;9(1):14831.
41. Kaar S, Femino J, Morag Y. Lisfranc joint displacement following sequential ligament section-
ing. J Bone Joint Surg Am. 2007;89(10):2225–32.
42. Schepers T, Rammelt S. Classifying the Lisfranc injury: literature overview and a new clas-
sification [Internet]. Fuß & Sprunggelenk. 2018;16:151–9. Available from: https://doi.
org/10.1016/j.fuspru.2018.07.003.
43. Arrondo G, Peratta M. Lesion tarsometatarsiana: Parte 1: Anatomia: Diagnostico: Clasificacion:
Tratamiento. Rev Asoc Argent Ortop Traumatol. 2008;73:302–6.
44. Coss LHS, Steven Coss LH, Usnr MC, Manos LRE, Usnr MC, Buoncristiani LTA, et al.
Abduction stress and AP weightbearing radiography of purely ligamentous injury in the tar-
sometatarsal joint [Internet]. Foot Ankle Int. 1998;19:537–41. Available from: https://doi.
org/10.1177/107110079801900806.
45. Kuo RS, Tejwani NC, Digiovanni CW, Holt SK, Benirschke SK, Hansen ST Jr, et al. Outcome
after open reduction and internal fixation of Lisfranc joint injuries. J Bone Joint Surg Am.
2000;82(11):1609–18.
46. Penev P, Qawasmi F, Mosheiff R, Knobe M, Lehnert M, Krause F, et al. Ligamentous Lisfranc
injuries: analysis of CT findings under weightbearing. Eur J Trauma Emerg Surg [Internet].
2020. Available from: https://doi.org/10.1007/s00068-020-01302-7.
47. Gunio DA, Vulcano E, Benitez CL. Dynamic stress MRI of midfoot injuries: measurable mor-
phology and laxity of the sprained Lisfranc ligament during mechanical loading: a case report.
JBJS Case Connect. 2019;9(3):e0228.
48. Rankine JJ. The diagnostic accuracy of plain radiographs in Lisfranc injury and the potential
value of a cranial caudal projection. Clin Radiol. 2011;66:S3.
49. Foster SC, Foster RR. Lisfranc’s Tarsometatarsal fracture—dislocation. Radiology.
1976;120(1):79–83.
50. Siddiqui NA, Galizia MS, Almusa E, Omar IM. Evaluation of the tarsometatarsal joint using
conventional radiography, CT, and MR imaging. Radiographics. 2014;34(2):514–31.
51. Kennelly H, Klaassen K, Heitman D, Youngberg R, Platt SR. Utility of weight-bearing radio-
graphs compared to computed tomography scan for the diagnosis of subtle Lisfranc injuries
in the emergency setting [Internet]. Emerg Med Australas. 2019;31:741–4. Available from:
https://doi.org/10.1111/1742-6723.13237.
52. Joannas G, Filippi J. How to identify unstable Lisfranc injuries? Review of diagnostic strate-
gies and algorithm proposal. Foot Ankle Clin. 2020;25(4):697–710.
53. Herscovici D, Scaduto JM. Acute management of high-energy lisfranc injuries: a sim-
ple approach [Internet]. Injury. 2018;49:420–4. Available from: https://doi.org/10.1016/j.
injury.2017.11.012.
54. Tarkin IS, Sop A, Pape H-C. High-energy foot and ankle trauma: principles for formulating an
individualized care plan [Internet]. Foot Ankle Clin. 2008;13:705–23. Available from: https://
doi.org/10.1016/j.fcl.2008.08.002.
55. Chandran P, Puttaswamaiah R, Dhillon MS, Gill SS. Management of complex open fracture
injuries of the midfoot with external fixation. J Foot Ankle Surg. 2006;45(5):308–15.
56. Bibbo C, Brueggeman J. Prevention and management of complications arising from external
fixation pin sites [Internet]. J Foot Ankle Surg. 2010;49:87–92. Available from: https://doi.
org/10.1053/j.jfas.2009.07.026.
57. Benirschke SK, Kramer PA. High energy acute Lisfranc fractures and dislocations
[Internet]. Tech Foot Ankle Surg. 2010;9:82–91. Available from: https://doi.org/10.1097/
btf.0b013e3181ecb117.
58. Mulcahy H. Lisfranc injury [Internet]. Radiol Clin N Am. 2018;56:859–76. Available from:
https://doi.org/10.1016/j.rcl.2018.06.003.
59. Rosenbaum A, Dellenbaugh S, DiPreta J, Uhl R. Subtle injuries to the Lisfranc joint [Internet].
Orthopedics. 2011;34:882–7. Available from: https://doi.org/10.3928/01477447-20110922-23.
60. Puna RA, Tomlinson MPW. The role of percutaneous reduction and fixation of Lisfranc inju-
ries. Foot Ankle Clin. 2017;22(1):15–34.
61. Abdelgaid SM. Closed reduction & percutaneous fixation of Lisfranc joints injuries: possibil-
ity, technique & results [Internet]. Clin Res Foot Ankle. 2013;01. Available from: https://doi.
org/10.4172/2329-910x.1000109.
62. Alberta FG, Aronow MS, Barrero M, Diaz-Doran V, Sullivan RJ, Adams DJ. Ligamentous
Lisfranc joint injuries: a biomechanical comparison of dorsal plate and transarticular screw
fixation. Foot Ankle Int. 2005;26(6):462–73.
63. Gaines RJ, Wright G, Stewart J. Injury to the tarsometatarsal joint complex during fixation
of Lisfranc fracture dislocations: an anatomic study [Internet]. J Trauma Injury Infection Crit
Care. 2009;66:1125–8. Available from: https://doi.org/10.1097/ta.0b013e318176c563.
64. Kalia V, Fishman EK, Carrino JA, Fayad LM. Epidemiology, imaging, and treatment of
Lisfranc fracture-dislocations revisited. Skelet Radiol. 2012;41(2):129–36.
65. Sands AK, Grose A. Lisfranc injuries [Internet]. Injury. 2004;35:71–6. Available from: https://
doi.org/10.1016/j.injury.2004.07.014.
66. Arntz CT, Veith RG, Hansen ST Jr. Fractures and fracture-dislocations of the tarsometatarsal
joint. J Bone Joint Surg Am. 1988;70(2):173–81.
67. Sangeorzan BJ, Benirschke SK, Mosca V, et al. Displaced intra-articular fractures of the tarsal
navicular. J Bone Joint Surg Am. 1989;71:1504–10.
Diaphyseal and Distal Tibia Fractures
Rodrigo Pesántez and Eduardo José Burgos
1 Introduction
Tibial shaft fractures have an incidence of 15 per 100,000 people [1, 2] and are
associated with different mechanisms of injury, ranging from low to high energy.
These fractures can be closed; nonetheless, open ones are more common due to the
bone subcutaneous location in the leg and its consequent involvement of soft tis-
sues. This is a risk factor for open tibial shaft fractures predisposing to high compli-
cation rates including infection, nonunion, or malunion leading to poor functional
outcomes in the long term [3, 4].
2 Etiology
Tibial shaft fractures have a bimodal distribution: low-energy patterns leading to

spiral fractures on older patients, and high-energy patterns leading to comminuted
transverse fractures on a younger and more active population. Among the most
common causes of low-energy fractures, same-height falls and sport injuries are
some examples. High-energy-associated fractures are most commonly due to motor
vehicle accidents, gunshot wounds, or falls from heights greater than 10 feet. As
previously mentioned, the subcutaneous location makes them prone to be open frac-
tures with an incidence between 12% and 47% according to different series [5, 6],
being the Gustilo-Anderson IIIB the most common [2, 7].
R. Pesántez (*)
Hospital Universitario Fundación Santa Fé, Universidad de Los Andes, Bogota, Colombia
E. J. Burgos
Hospital Universitario Fundación Santa Fé, Bogotá, Colombia

Switzerland AG 2022
1316 R. Pesántez and E. J. Burgos
The mechanism of action can be described also as direct or indirect. Direct

mechanisms include high-energy bending, producing a displaced, transverse, and
comminuted fracture. In cases of predominant comminution or segmental patterns,
there should be a high suspicion for soft-tissue injury with an underlying compart-
mental syndrome to rule out. Low-energy bending fractures present a short oblique
pattern or a transverse fracture associated with a butterfly fragment. Finally, direct
mechanisms can also include penetrating injuries as in gunshot wounds. The frac-
ture pattern is variable, but always with great comminution.
Regarding indirect mechanisms, they can include torsional patterns when the leg
rotates with the foot fixed on the ground, or low-energy falls producing spiral, non-
displaced fractures. Stress fractures can be included as an indirect mechanism, and
they occur mostly in the metaphyseal–diaphyseal union in soldiers or ballet dancers.
3 Anatomy
The tibia is a long tubular bone with a triangular shape in the axial plane. Its antero-
medial border is located subcutaneously and the remaining of its circumference is
covered by four muscular compartments: anterior, lateral, and posterior superficial
and deep. The fibula is located posterior and lateral to the tibia and they are con-
nected by the interosseous membrane. The distal tibia is normally externally rotated
about 20° compared with the proximal segment. This is known as tibial torsion.
Hence, a plain AP radiograph of the ankle cannot be obtained as a plain AP radio-
graph of the knee.
The tibial blood supply is given by a nutrient artery, a branch of the posterior
tibial artery, entering through the posterolateral cortex distally to the origin of the
soleus muscle. Once intramedullary it gives three ascending branches and one
descending branch which form the medullary blood supply. This medullary system
anastomoses with the periosteal blood supply originated from the anterior tibial
artery. If the nutrient artery is compromised by soft tissue stripping, outer cortical
viability is maintained by outward flow from the medullary system. This highlights
the importance of maintaining the vitality of the periosteum during dissection,
reduction, and fixation.
As mentioned earlier the musculature of the leg is divided into four compart-
ments. The anterior compartment is located anterolaterally and contains the main
dorsiflexors of ankle and toes. Important structures include the deep peroneal nerve
and anterior tibial artery. The lateral compartment contains the muscles in charge of
ankle eversion and also the superficial peroneal nerve. The superficial posterior
compartment contains the gastrocnemius soleus complex and the plantaris muscle.
On the other hand, the deep posterior compartment contains the tibialis posterior,
flexor hallucis longus and flexor digitorum longus, popliteus muscle, and the neuro-
vascular bundle which is formed by the peroneal artery, posterior tibial artery, and
tibial nerve.
Diaphyseal and Distal Tibia Fractures 1317
4 Diagnosis
History of present illness and a thorough physical exam are the cornerstones in
patients with a tibial shaft fracture. Questions should focus on mechanism of action,
time lapse since injury, location and quality of pain, and any additional symptom
like weakness or numbness of the limb. Past medical history should evaluate previ-
ous fractures, infections, tumors, or interventions in that leg. Likewise, chronic
medical history should be known for possible conditions the patient has that can
affect bone consolidation process or normal function of the limb. Given the high-
frequency tibial shaft fractures present in polytraumatized patients, injury to other
organs should be noticed and the physiological state of the patient should be assesed.
During physical examination, the characteristics of soft tissues are very impor-
tant for the treatment of future complications. Areas where the skin is tight or hard,
or even with signs of tension, imminent rupture, or a dimple sign because of contact
with a spike of bone, should direct our efforts to align the leg and put on a splint or
any other method for immobilization. One of the common complications on soft
tissues is skin necrosis, result of poor soft tissue management in the initial contact
with the patient. This can easily evolve into coverage defects requiring reconstruc-
tive procedures in the future. If stabilization cannot be obtained and soft tissues are
in danger, it is an indication for surgical intervention.
In case the limb has wounds, you should always assume it is an open fracture
until proven otherwise (Fig. 1). Always consider the different mechanisms described
previously, because the wounds may be more than a few centimeters apart from the
fracture site [8]. Wounds should be examined in the operating room to irrigate and
debride thoroughly. Afterward, the fracture should be reduced, the soft tissues cov-
ered with sterile gauze, and immobilized. Make sure to record the size of the
wounds, location, and degree of contamination to have a starting point for treatment
election.
Fig. 1 Soft tissue conditions on a distal tibia fracture. (a) Open wound on lateral side. (b) Closed
soft tissue conditions on medial side. (c) Lateral and (d) medial soft tissue conditions 1 year later
Once the soft tissues are evaluated, you should perform a detailed exam on the
vascular status proximally and distally right before doing any reduction of the frac-
ture. In cases with gross deformity of the leg, distal pulses may be diminished due to
compromise by some of the bone fragments. After reduction, vascular exam should
be repeated to check if pulses are back or there is still a deficiency. In this case, you
should continue with additional imaging diagnostic tools to rule out vascular injury.
Motor function is difficult to evaluate because pain limits the patient to help during
examination. Nonetheless, always have in mind that a motor dysfunction can be pro-
duced by pain, muscular or tendinous rupture, neurovascular injury, ischemia, or com-
partment syndrome. Additionally, a neurological exam should be performed including
areas of deep peroneal, superficial peroneal, saphenous, sural, and tibial nerves.
Finally, in the clinical evaluation, you must rule out compartmental syndrome as
one of the first and most common complications in tibial shaft fractures. If there are
doubts about this diagnosis, serial exam should be done to determine if it develops
or if it can be ruled out. Signs and symptoms include pain out of proportion, pain
with passive movement, paresthesia, paralysis, pulselessness, and poikilothermy.
The initial radiological diagnostic approach for fractures of the tibia should include
anteroposterior (AP) and lateral radiographs that show the entire length of the tibia. To
rule out any involvement of the knee or ankle joints, AP and lateral views should be
obtained. In the ankle, additionally, a mortise view should be taken. These views may
also help to diagnose any involvement of adjacent bones as the patella or talus. Besides
evaluating for evident fracture lines, soft tissue involvement with gas or edema sug-
gesting articular effusion can help in the diagnosis or suspicion of articular compro-
mise, prompting the use of additional imaging studies. For example, spiral distal third
tibial fractures are associated with posterior malleolar fractures and a high percentage
of them are not identified on plain radiographs [9, 10]. Furthermore, CT and MRI may
help with possible pathological fractures or irregular appearance of bone on X-ray.
In tibial shaft fractures there exists a variety of classifications. As we mentioned
earlier, soft tissue plays an important role in diagnosis and management. Therefore,
the first important classification to have in mind is the Tscherne classification for
closed fractures and the Gustilo classification for open fractures [11–13]. Tscherne
has shown to correlate with time to return to walking and recreational activities,
while Gustilo has shown a correlation with increased risk of nonunion, malunion,
and reoperation [14]. The most used fracture classification system of tibia is the AO/
OTA classification which describes three basic types, simple (type A), wedge (type
B), and multifragmentary (type C) [15]. This classification is most helpful for
research purposes and communication among surgeons.
5 Nonoperative Treatment
Traditionally tibial shaft fractures can be treated nonoperatively following

Sarmiento’s protocol [9]. The selection of the patient should be done according to
soft tissues and fracture pattern; usually this treatment is reserved for closed
fractures, low energy injuries, axially stable fracture patterns, alignment within 5°
in any plane, less than 2 cm of translation, and shortening less than 1 cm.
According to Sarmiento, this treatment has three stages. Stage 1: reduction and
immobilization in an above the knee cast, and this cast should immobilize the knee
in almost complete extension and the ankle in 90° of flexion and a walking heel; the
patient can start weight bearing as tolerated using crutches and also encourage toe
motion and isometric exercises of the quadriceps. Stage 2: once the patient can tol-
erate partial weight bearing without pain at the fracture site it is time to apply a
below the knee functional cast or a below the knee brace, allowing the patient to
increase weight bearing as tolerated using crutches. Stage 3: once pain and swelling
have subsided, below-the-knee cast can be changed for a below-the-knee brace that
will allow complete range of motion of all joints; weight bearing is increased as
tolerated and can discontinue the use of crutches. During the first 4 weeks, weekly
X-rays are taken to assess alignment and then once a month until radiological heal-
ing is observed (Fig. 2).
6 Surgical Management, Timing, and Postop Protocol
Operative treatment is indicated nowadays for most tibial fractures, shaft and distal.
Most of the indications for operative treatment are relative and include open frac-
tures, fractures in multiple trauma patients, fractures with articular extension, unsta-
ble fractures (shortening >1 cm, translation >50%, >10° of malalignment in any
plane), compartment syndrome, vascular injuries, loss of reduction following non-
operative treatment.
Once operative treatment has been selected, the timing for intervention is accord-
ing to the soft tissue conditions; open fractures should be operated on as soon as the
patient’s clinical conditions allow it, ideally in the first 6 hours after the injury. On
the other hand, closed fractures should wait until swelling subsides and the skin
wrinkles, especially if using plates and in distal tibia fractures.
Preoperative planning should include: radiolucent table, bumps under the ipsilat-
eral buttock, image intensifier, and surgical approach for nailing or plating; for nail-
ing conventional approach (medial, lateral, or transtendinous approach) or
semi-extended position (suprapatellar or parapatellar); for plating classic open
reduction and internal fixation or minimally invasive plating. Then plan the reduc-
tion technique to obtain length, alignment, and rotation, usually some traction using
a large distractor or an external fixator, plus use of percutaneous clamps, in case of
open reduction using pointed reduction forces to reduce simple oblique or spiral
fractures, use of the implant as a reduction aid in distal tibia fractures when using
anatomically contoured plates.
Patient is placed supine on a radiolucent table with a bump under the ipsilateral
buttock to neutralize the external rotation of the lower limb. Image intensifier com-
ing from the opposite side and the screens at the foot of the patient obtain perfect AP
and lateral views of the knee, ankle, and shaft before starting the procedure. Prep
Fig. 2 Nonoperative treatment of a proximal tibia shaft fracture. (a) Initial X-rays showing a mini-
mally displaced proximal tibia fracture. (b) 2 weeks later using a Sarmiento Brace. (c) A healed
tibial shaft fracture 4 months later
and drape the whole lower extremity and wrap the toes to minimize
contamination.
Most tibial fractures are treated with reamed locked intramedullary nailing. For
diaphyseal tibial shaft fractures, infrapatellar nailing is the preferred technique, and
for distal tibia, nailing semi-extended position is selected using a suprapatellar or
para patellar (medial or lateral) approach; the-semi-extended position is preferred

because it facilitates reduction in very distal tibia fractures. Draw on the skin the
patella, patella tendon, and tibial tubercle before marking the skin incision. To find
the correct entry point for tibial nailing the use of image intensifier on a true AP
view, using a wire to mark this point medial to the lateral tibial spine and toward the
center of the tibial shaft, mark this with a pen over the skin, and assess if the skin
incision in infrapatellar nailing is going to be lateral, medial, or transtendinous. For
extra-articular parapatellar approach in semi-extended position, evaluate patella
motion medial and lateral and then decide if the approach is going to be medial or
lateral, most of the time is lateral.
Infrapatellar approach:
• 3 cm skin incision from the inferior pole of the patella toward the tibial tubercle
• Identify paratenon and incise it as a separate layer for closure
• Palpate the patella tendon and incise it longitudinally in its mid-portion
• Separate tendon using Senn miller retractors
• Identify and retract fat pad to expose entry point in the proximal tibia
Semi-extended position:
• Flex the hip about 45° using bumps and flex the knee 30°
• This is the preferred position for nailing proximal and distal tibia fractures; in
proximal tibia fractures, it helps with the reduction and counteract the deforming
forces. In the distal tibia fractures, the distal fragment is usually small and diffi-
cult to manipulate in the flexed position, and in the semi-extended position, it is
easier to reduce it and use adjuncts to improve reduction (Fig. 3 nailing of a distal
tibia fracture in semi-extended position using a large distractor and a pointed
reduction clamp).
• Suprapatellar approach (Fig. 4): longitudinal skin incision above the superior
pole of the patella, identify quadriceps tendon and incise it longitudinally from
the proximal pole of the patella proximally, separate it using Senn miller retrac-
Fig. 3 Closed distal tibia fracture treated by reamed intramedullary nailing. (a) Initial X-rays
showing a spiral distal tibia fracture. A CT scan of the distal tibia was taken to rule out posterior
malleolus fracture. (b) Intraoperative imaging showing reduction technique with a medial large
distractor and a percutaneous pointed reduction forceps to fine-tune the spiral component reduc-
tion. (c) Postoperative X-rays
Fig. 4 Distal tibia fracture with medial malleolus. Suprapatellar approach. (a) Initial X-rays. (b)
Patient positioning Hip flexed 45° and knee flexed 30° and fracture reduction using a large distrac-
tor. (c) 2 cm proximal to the patella make a straight incision and identify the quadriceps tendon and
incise it. (d) Using the protection sleeves insert the guidewire, open the canal, and ream the tibia.
(e) Intraoperative imaging of the entry point, distractor as a reduction aid, and final position of the
guidewire before reaming and inserting the nail. (f) Final follow-up: X-rays and clinical result
tors, palpate the patellofemoral joint and insert the cannula to the selected entry
point in the proximal tibia, and assess position using image intensifier.
• Parapatellar extra-articular approach (Fig. 5): 5 cm longitudinal skin incision on
the lateral border of the patella, incise the lateral retinaculum without opening
the capsule, push the patella medially (dislocate), and identify the entry point
using image intensifier. We prefer this approach as it avoids entering into the
joint and allows the use of a regular nailing system.
Fig. 5 Para patellar approach. (a) Patient positioning Hip flexed 45° and knee flexed 30°. (b)
Assess patella laxity; in this case, it was lateral. (c) Using image intensifier identified the center of
canal and the perfect insertion point on the AP image. (d) Mark tibial shaft on the skin and the
ideal position of the nail. (e) 5 cm skin incision on the lateral border of the patella. (f) Incise the
lateral retinaculum without opening the capsule. (g) Position of the guidewire respecting the cap-
sule. (h) Capsule intact at the end of the procedure. Suture retinaculum, subcutaneous tissue,
and skin
Most of the time to reduce the tibia we use the large distractor or an external
fixator on the medial side. Schanz pins are positioned parallel to the proximal and
distal joints, and posteriorly in the sagittal plane; sometimes for very distal tibias
the distal Schanz pin can be positioned in the talus on the medial side, distal to the
anterior colliculus of the medial malleolus. In oblique or spiral fractures, percuta-
neous pointed reduction clamps to fine-tune the reduction is commonly used; be
careful to avoid crushing of the skin and assess the position using the image
intensifier.
Once the fracture is reduced, pass the guidewire and check its position center
(AP/center of talus) – center (lateral/center of talar dome) in the distal fragment
using the image intensifier. If the guidewire is not centered, then consider using
blocking screws to align the guidewire in the tibia. Once the guidewire is in the cor-
rect position proximal and distal then reaming can start, reaming should be done
using the reamed to fit technique and ream 1–1.5 mm above the diameter of the
selected nail. Finally insert the nail by hand and once in its place locked statically
proximal and distal using freehand technique (Fig. 3).
7 Plating Tibial Fractures
Plating can be done in the immature skeleton, narrow canal, periarticular injuries,
deformed or obliterated canal, malunion, or nonunion (Fig. 6).
Fig. 6 Closed distal tibia fracture treated by minimally invasive plating. (a) Initial X-rays of a
16-year-old male who sustained a closed tibial shaft fracture in a motorcycle accident. (b)
Intraoperative imaging showing medial soft tissue conditions and the use of a large distractor on
medial side as a reduction aid. (c) Intraoperative imaging showing the incision to slide the medial
plate using MIPO technique. (d) Fracture healed at final follow-up 1 year later
Surgical technique:
• Supine on a radiolucent Table.
• C arm.
• Reduction usually with a large distractor or external fixator on the opposite side
of plating.
• Minimally invasive plating can be done medially or laterally; laterally the plate
is covered by the muscles and medially the plate lies under the skin but the per-
cutaneous screws are easier to insert.
• If used in periarticular injuries, anatomical contoured plates are useful; in mid-

shaft plates, a regular straight plate can be used and contoured.
• In extra-articular distal tibia plating, the implant can be used as a reduction aid,
especially if using anatomically contoured plates.
• Once length, alignment, and rotation are corrected, the insertion of a percutane-
ous plate, as a bridging plate in complex fracture pattern, and fixation with proxi-
mal and distal screws can be done; the selection of locking or unlocking screws
depends on bone quality.
External fixation is usually indicated in open fractures or as a temporary fixation
in severe soft tissue injuries; it can also be used as a definitive treatment, but its use
has decreased in favor of internal fixation.
8 Complications
Some of the most common complications associated with tibial shaft fractures are:
compartment syndrome, malunion, nonunion, infection, symptomatic hardware,
and knee pain.
Rates of compartment syndrome associated with tibial shaft fractures are around
1.5% and 11% according to most series [16, 17]. The orthopedic surgeon must have
a high suspicion for this diagnosis in patients with tibial shaft fractures, due to the
devastating consequences it may have on the patient. As mentioned earlier, clinical
diagnosis is the main tool; nonetheless, intubated or unconscious patients are not
able to comply with the examination. If no clinical exam can be done, you can use
a pressure differential of <30 mm Hg between the intercompartmental pressure and
the diastolic blood pressure.
Other risk factors to consider for a patient to develop compartment syndrome are
male, young age, proximal tibia fracture, and gunshot wounds, among others.
There is no consensus on defining the parameters for the diagnosis of tibial mal-
union. This comes related to acceptable parameters for tibial alignment being within
ranges of varus/valgus <5–10°, recurvatum/antecurvatum <5–10°, rotation 0–10°,
and shortening of less than 2 cm. Some series show that greater degrees of malalign-
ment correlate with poor functional outcomes. Also, pain was a variable that showed
to be more prevalent in patients with malalignment >5°. Even though some series
show that even minimal angular deformities of the tibia can result in a significant
impact in functional outcomes, there are reports of no correlation between tibial
malunion and subsequent functional limitation.
The timeline for healing in long bones differs from 3 to 6 months. Tibial shaft
injuries heal in a different manner and may take more time, making it harder to
define a nonunion. Nonoperative tibial shaft fractures heal approximately in
20 weeks, while operative treatment decreases healing time regardless of the treat-
ment method. The mean time to union ranges between 16 and 36 weeks.
Nonunion rates for conservative treatment range from 1% to 10%, but some
series have reported values as high as 27%. Operative treatment may decrease this
number to 2%.
The most common definition for nonunion is incomplete healing between 3 and
6 months radiologically, associated with pain with weight bearing.
Risk factors for nonunion include open fractures, infection, malreduction with
gaps, distal fractures, and smoking.
Infection rates depend on fracture severity. Closed ones have rates around 2%,
while open fractures depending on Gustilo-Anderson classification range between
10% and even 40%. Staphylococcus aureus is the most common organism to cause
infections in tibial shaft fractures, but nosocomial pathogens have also been
reported. Risk factors include skin necrosis, external fixation use, severity of open
fracture, substance abuse, smoking, and soft tissue coverage complications.
After fracture management, reported rates of hardware removal vary from 10%
to 60%, regardless of plating or nailing system. Hardware-related pain is the main
cause of implant removal, besides infection.
Interlocking screws from tibial nails are one of the most common implants
removed, specifically when they are too long postoperatively. Implant removal has
shown a low complication rate and is associated with high patient-reported satisfac-
tion, improved pain, and improved functional outcomes.
References
1. Alho A, Benterud JG, Hogevold HE, Ekeland A, Stromsoe K. Comparison of functional brac-
ing and locked intramedullary nailing in the treatment of displaced tibial shaft fractures. Clin
2. Wennergren D, Bergdahl C, Ekelund J, Juto H, Sundfeldt M, Möller M. Epidemiology
and incidence of tibia fractures in the Swedish Fracture Register. Injury [Internet].
2018;49(11):2068–74. Available from: https://doi.org/10.1016/j.injury.2018.09.008.
3. Puno RM, Teynor JT, Nagano J, Gustilo RB. Critical analysis of results of treatment of 201
tibial shaft fractures. Clin Orthop Relat Res. 1986;212:113–21.
4. O’Malley O, Trompeter AJ, Krishnanandan S, Vesely M, Holt P, Goh G, et al. How com-
mon are vascular injuries in open tibial fractures? A prospective longitudinal cohort study.
Eur J Orthop Surg Traumatol [Internet]. 2019;29(5):1119–24. Available from: https://doi.
org/10.1007/s00590-019-02416-4.
5. Bhandari M, Guyatt G, Walter SD, Tornetta P, Schemitsch EH, Swiontkowski M, et al.
Randomized trial of reamed and unreamed intramedullary nailing of tibial shaft fractures. J
6. Weiss RJ, Montgomery SM, Ehlin A, Al DZ, Stark A, Jansson KÅ. Decreasing incidence of
tibial shaft fractures between 1998 and 2004: information based on 10,627 Swedish inpatients.
Acta Orthop. 2008;79(4):526–33.
7. He QF, Sun H, Shu LY, Zhan Y, He CY, Zhu Y, et al. Tibial plateau fractures in elderly people:
an institutional retrospective study. J Orthop Surg Res. 2018;13(1):1–8.
8. Foote CJ, Guyatt GH, Vignesh KN, Mundi R, Chaudhry H, Heels-Ansdell D, et al. Which
surgical treatment for open Tibial shaft fractures results in the fewest reoperations? A net-
work meta-analysis. Clin Orthop Relat Res [Internet]. 2015;473(7):2179–92. Available from:
https://doi.org/10.1007/s11999-015-4224-y.
9. Hou Z, Zhang Q, Zhang Y, Li S, Pan J, Wu H. A occult and regular combination injury:

the posterior malleolar fracture associated with spiral tibial shaft fracture. J Trauma.
2009;66(5):1385–90.
10. Purnell GJ, Glass ER, Altman DT, Sciulli RL, Muffly MT, Altman GT. Results of a computed
tomography protocol evaluating distal third tibial shaft fractures to assess noncontiguous mal-
leolar fractures. J Trauma. 2011;71(1):163–8.
11. Gustilo RB, Anderson J. Prevention of infection in the treatment of one thousand and twenty-
five open fractures of long bones (Gustilo-Anderson). J Bone Jt Surg. 1976;58(4):523–7.
12. Gustilo RB, Mendoza RM, Williams DN. Problems in the management of type III (severe)
open fractures: a new classification of type III open fractures. J Trauma. 1984;24:742–6.
13. Ibrahim DA, Swenson A, Sassoon A, Fernando ND. Classifications in brief: the tscherne clas-
sification of soft tissue injury. Clin Orthop Relat Res. 2017;475(2):560–4.
14. Gaston P, Will E, Elton RA, McQueen MM, Court-Brown CM. Fractures of the tibia. Can their
outcome be predicted? J Bone Joint Surg Br. 1999;81(1):71–6.
15. Marsh JL, Slongo TF, Agel J, Broderick JS, Creevey W, DeCoster TA, et al. Fracture and
dislocation classification compendium - 2007: Orthopaedic Trauma Association classifica-
tion, database and outcomes committee. J Orthop Trauma [Internet]. [cited 2017 Dec 4];21(10
Suppl):S1–133. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18277234.
16. O’Toole RV, Whitney A, Merchant N, Hui E, Higgins J, Kim TT, et al. Variation in diag-
nosis of compartment syndrome by surgeons treating tibial shaft fractures. J Trauma.
2009;67(4):735–41.
17. McQueen MM, Christie J, Court-Brown CM. Compartment pressures after intramedullary
nailing of the tibia. J Bone Joint Surg Br. 1990;72(3):395–7.
Metatarsal Fractures
Gabriel Khazen
1 Introduction
Fracture of the metatarsal bones is a frequent injury whose incidence has been
reported between 35% and 88.5% of all fractures of the foot [1, 2]. Jeffers et al. [3]
reported in their series that 49.1% of motorcycle accident foot fractures were meta-
tarsal fractures. Despite the high incidence and inherent risk of complications from
these fractures, there is very little literature reported on them [4], with the exception
of the proximal fracture of the fifth metatarsal.
Metatarsal fractures can be caused by direct trauma, fall from height, overload,
or inversion of the foot. Depending on the energy involved, they can be simple frac-
tures involving a single metatarsal or complex fractures that affect several metatar-
sals, soft tissues and neighboring joints.
The incidence of fractures is diverse and may vary according to the age group
and/or gender of the patient, with central metatarsal fractures, especially the third
metatarsal, being the most frequent in elderly women [5] and the fifth metatarsal in
young males [6]. In a demographic study, Cakir et al. [7] reported that the fifth MTT
was fractured in 56% of the patients studied for metatarsal fractures, 15.6% pre-
sented multiple fractures, and 75% were injured after inversion of the foot or fall
from height.
The inadequate treatment of metatarsal fractures can generate permanent
sequelae to the patient, such as metatarsalgia, functional limitation and deformity of
the forefoot (see Figs. 1 and 2); therefore, it is mandatory to preserve the forefoot
anatomy [4, 5, 7].
G. Khazen (*)
Hospital de Clinicas Caracas, Caracas, Venezuela

Switzerland AG 2022
1330 G. Khazen
Fig. 1 Image of a foot

with malunion of the third
metatarsal in plantar
flexion. The plantar
overload is seen through a
hyperkeratosis under the
third metatarsal
Fig. 2 Clinical photo of a

foot with malunion in the
frontal plane of the second
and third metatarsal that
originated deformities of
the lesser toes. In this case
lateral deviation of the
second toe and shortening
of the third toe
2 Diagnosis
The clinical presentation of patients with metatarsal fractures will depend on the
severity of the injury; it can range from mild pain to severe pain and/or signs of
compartment syndrome, which we must be aware of in high-energy fractures, in
fractures of multiple metatarsals and/or in forefoot/midfoot dislocations.
Metatarsal Fractures 1331
Imaging study is performed with anteroposterior, lateral, and oblique compara-

tive feet X-rays. It is very important to know the radiological anatomy and the
accessory bones to avoid confusion with an avulsion fracture [8].
In case of high energy injury or in an articular fracture, computed axial tomography
should be requested. In certain special circumstances that will be discussed later, it may
be necessary to indicate magnetic resonance imaging and/or other imaging studies.
3 Stress Fracture
The incidence of stress fracture of the metatarsals represents 38% of these frac-
tures in the lower limb [9]; it can occur in any metatarsal, but more attention has
been given to the fifth metatarsal due to its vascular anatomy.
Stress fractures of the second and/or third metatarsal are generated by repetitive
loading of the area. Dixson et al. [10] determined that aspects of foot type such as
low abduction and a low dynamic arch index, such as cavus and/or adductus,
increased the risk of these fractures in the second metatarsal. Patients with third
rocker metatarsalgia may increase the risk of third metatarsal fracture. Other risk
factors are repetitive exercises such as jumping or running performed without ade-
quate preparation [11]. Barrack et al. [12] report an increased risk of 30–50% inci-
dence of these fractures in female patients with low bone mineral density.
Patients with stress fractures usually present nonspecific pain in the affected
area and edema in the midfoot of sudden onset or preceded by a prodrome. The
history and clinical evaluation are important to diagnose this injury, since in the
initial radiological studies the fracture line may not be evident, if not weeks later
when the periosteal reaction, bone resorption, and/or signs of fracture healing are
evident, which can lead to doubt or misdiagnosis. In MRI, edema in periosteum and
bone marrow, fracture lines, and edema in surrounding soft tissues can be seen [13].
In central metatarsals, stress fracture can be proximal or distal [14]. Proximal
fractures are seen in patients with Achilles tendon contracture, significant dif-
ference in length between metatarsals and low bone mineral density, while dis-
tal fractures are more associated with training intensity.
4 Treatment
The treatment of the metatarsal fracture will depend on several factors but mainly it
is related to the displacement of the fracture. Non-displaced fractures or those with
slight displacement in the frontal or sagittal plane are treated nonsurgically. Shereff
[15] recommends reduction and fixation in fractures with displacement greater than
2 mm and/or angulation greater than 10° (although no biomechanical study so far
supports this criterion), to restore forefoot alignment.
Due to anatomical and biomechanical differences and different fracture mecha-
nisms [16], fractures of the first metatarsal, lesser metatarsals and proximal fracture
of the fifth metatarsal will be analyzed separately.
1332 G. Khazen
5 Fracture of the First Metatarsal
The incidence of this fracture depends on the age of the patient and the fracture
mechanism; of all metatarsal fractures, this fracture has an estimated incidence of
1.5–5% [2, 7] in adults, and a 28% in children [17].
The head of the first metatarsal carries twice the weight of the lateral metatar-
sals during stance [18], so malunion can lead to significant biomechanic changes.
Malunions in dorsiflexion can generate central metatarsalgia. Tranverse plane
malunions (medial or lateral deviations), can generate angular deformities such as
hallux valgus or varus; therefore, it is crucial to preserve the anatomy [19].
The fracture of the first metatarsal is usually generated by a high energy trauma
and can be unstable due to the constant traction of intrinsic and extrinsic muscle
groups. This fracture can present with some degree of comminution and/or proxi-
mal or distal joint compromise [20], which is better evaluated with a computerized
axial tomography (see Figs. 3, 4, and 5).
Fig. 3 AP radiograph of a
patient who suffered
frontal trauma to his left
foot. A fracture of the base
of the first metatarsal is
seen, with intra-articular
involvement and
displacement
Fig. 4 CT of the same

patient presented in Fig. 3,
with joint compromise
Fig. 5 Sagittal image of

the same previous patient,
showing the plantar
fracture extension
1334 G. Khazen
The treatment of this metatarsal fracture with a displacement of less than 2 mm

and/or angulation of less than 10° in the sagittal or coronal plane consists of plac-
ing the patient in a postoperative rigid sole shoe or walking boot. X-rays should be
performed at 2 weeks to verify that there has been no fracture displacement. The
patient is kept in this immobilization for 4–6 weeks.
Fractures with displacement greater than 2 mm and/or angulation greater than

10°, as well as the presence of proximal or distal articular fracture lines with
displacement greater than 2 mm require surgical treatment [15]. This will
depend on the type and anatomical location of the fracture. Fixation can be per-
formed exclusively with Kirschner wires [21]; however, the risk of inadequate
reduction or loss of reduction is very high with this technique and, therefore, the
suggestion is to perform anatomic reduction and fixation with 2.7 or 2.0 mm low
profile plates. For joint fractures, anatomical reduction with headless screws
should be performed, stabilizing the metatarsal with anatomical T or L plates
[21] (Figs. 6 and 7).

of the same patient
presented previously,
stabilized with plate and
screws
Fig. 7 AP X-ray of patient

presented in previous
image
Open fractures should be treated following the general recomendations, such as

irrigation, debridement, fasciotomy (if necessary), external fixation and antibiotic
therapy, between others.
6 Malunion of the First Metatarsal
The inadequate treatment of this fracture can lead to malunion. Malunions should
be treated with an osteotomy correcting all deformity planes. A stable fixation
should be perform using plate and screws (see Figs. 8, 9, 10, 11 and 12). If severe
load transfer is present, with lesser metatarsal overload, plantar plate damage and/
or stress fractures, additional lesser metatarsal elevation osteotomies could be
performed.
1336 G. Khazen
Fig. 8 First metatarsal

malunion, with shortening
and elevation of the
metatarsal head
7 Fracture of the Lesser Metatarsals
Lesser metatarsal fractures displacement and angulation can change the whole fore-
foot mechanics, generating pain and secondary fractures in adjacent bones. Medial
or lateral displacements can generate secondary toe deviations as well.
Displacements greater than 2 mm or angulation in the sagittal plane greater than
10° may require reduction and fracture fixation [18], to restore the length and angu-
lation of the metatarsal. Displaced transverse diaphyseal fractures may be more
unstable due to traction of the intrinsic and extrinsic musculature, mainly the flex-
ors. The isolated fracture of a central metatarsal will be more stable due to its intrin-
sic stability than multiple fractures.

the patient shown in the
previous image
Fig. 10 Long oblique

osteotomy was performed
in the fracture area to
lower the metatarsal head
and recover length
1338 G. Khazen
Fig. 11 Remote
postoperative AP
radiograph of previous
patient. Consolidated
remodeling osteotomy and
metatarsal parabola
recovered

of previous patient.
Recovery of the correct
plantar angulation of the
first metatarsal can be seen
The diaphyseal and distal fractures of the fifth metatarsal, known as the ballerina
fracture [22], have been the subject of discussion and debate, and a special classifi-
cation has even been described for this fracture [23]. The classification separates
between no displacement, displacement equal or less than 3 mm and greater dis-
placements with rotation and migration of the distal fragment. It is important to note
that the fourth and fifth metatarsals have greater mobility in the sagittal plane than
the other metatarsals. This may facilitate their adaptation to malunion of these bones.
Morgan et al. [24] reported good results for conservative treatment of diaphyseal
fractures of the fifth metatarsal with rigid sole shoe and full weight bearing, regard-
less of fracture displacement. Although it is true that O’Malley et al. [22] reported
in their study in 35 professional dancer patients similar results between the patients
treated surgically and those treated nonsurgically, regardless of the magnitude of
fracture displacement. The author has not had the same experience. Fifth metatarsal
malunions can generate 4th metatarsal transfer pain. Therefore, the author uses
same criteria for surgical indication as the fracture in other metatarsals, (Level V
evidence), despite the previously referred studies [22, 24].
Fractures with displacement equal to or less than 2 mm and/or angulation less than 10°
are treated conservatively. We indicate a postoperative shoe to avoid full weight b earing
[25]. X-rays are performed at 2 weeks to verify that no fracture displacement has
occurred. The patient is kept in this immobilization for 4–6 weeks.
Cakir [7] reported that metatarsal fracture displacement greater than 2 mm in any
plane is associated with poor results. Surgical treatment is indicated to restore the
length and/or angulation of the metatarsal.
Several reduction and fixation techniques have been described for diaphyseal
and metatarsal neck fractures, consisting of retrograde medullary pinning, ante-
grade medullary pinning and plate fixation. The retrograde medullary pinning tech-
nique is the most commonly used [26].
1340 G. Khazen
7.3 Retrograde Medullary Pinning
This procedure can be performed percutaneously, but often due to the technical dif-
ficulty of achieving the anatomical reduction of the fracture, it is necessary to per-
form a longitudinal dorsal approach. A 1.4–1.8 mm Kirschner wire is introduced in
an antegrade direction through the diaphysis of the distal fragment toward the meta-
tarsal head, exiting plantar in the MTF joint or through the base of the first phalanx.
This is followed by reduction of the fracture site and retrograde insertion of the wire
into the proximal diaphysis (Fig. 13).
It is important to note that endomedullary fixation with Kirschner wires does not
allow early mobilization of the joint. If the pin is passed through the base of the first
phalanx, it can cause joint damage and stiffness. If the pin is placed plantar to the
first phalanx, it will keep the metatarsophalangeal joint in dorsiflexion during the
fixation time, which can generate a claw deformity.
Fig. 13 Reduction and

synthesis of diaphyseal
fractures of the metatarsal
with retrograde
intramedullary pinning
7.4 Antegrade Medullary Pinning
Techniques have been described to attempt intramedullary fixation while avoiding

damage to the metatarsophalangeal joint. One option is to use wires perpendicular
to the fracture, which proved to be very unstable [27]. The antegrade fixation
described by Kim et al. [28], that inserts a pin with a double distal curvature that
reduces the fracture, avoiding joint damage. However, they clarify in their report
that it is a complex and demanding procedure, with a high rate of irradiation and a
high risk of iatrogenic fracture of the proximal fragment where the pin is inserted;
They reported a series of 30 patients followed for 5 years, where joint limitation was
seen in 2 patients, and a global AOFAS score of 83 was achieved.
Potential complications found with wire fixation are: joint stiffnes, cartilage
damagem infection, fracture displacemente, between others [29].
7.5 Fixation with Plates
Sánchez Alepuz et al. [4] did not show any difference when comparing 57 central
metatarsal fractures treated with Kirschner pins in 21 patients and with nonsurgical
treatment in 36 patients. They reported a 56.8% of metatarsalgia in cases of fracture
malunion. Factors that contributed to poor outcome were malunion, open fractures
and soft tissue injuries.
Bryant et al. [30] in their study of plate and screw fixation reported a 5% inci-
dence of coronal or sagittal angulation, and no patient had residual metatarsalgia,
nonunion, or discomfort.
Khazen et al. [31] compared the results with both fixation techniques in 47
patients. Eighteen patients were treated with open reduction and internal fixation
with K-wire through the metatarsophalangeal joint or distal phalanx, with 44%
showing some degree of loss of fracture reduction after implant removal, metatar-
salgia in six patients, and residual claw deformity in 33% of patients. Open reduc-
tion and internal fixation with plate and screws were performed in 29 patients, with
no evidence of loss of fracture reduction or metatarsalgia (Figs. 14 and 15).
Curtis et al. [32] biomechanically compared the resistance to failure between
intramedullary pins, transverse pins, and non-locked plates, showing a greater resis-
tance to failure and bending in fixation with plate and screws compared to intramed-
ullary wires.
Due to the above arguments, our suggestion is to perform open reduction and
internal fixation with 2.0 or 2.7 mm plates; this technique keeps an anatomical
reduction and stable fixation, allowing early mobilization and weight bearing with-
out distal joint damage.
1342 G. Khazen
patient with multiple
metatarsal fractures,
considering incomplete
fracture of the first
metatarsal, and complete
fractures of the second,
third, and fourth
metatarsals
7.6 Special Considerations
In subcapital fractures with evident displacement or dislocation, fixation using 2.0

or 1.5 mm screws is recommended.
In proximal articular fractures or proximal metaphyseal comminuted fractures, a
bridge plate (metatarsal-cuneiform) is the recommended option. In cases of moder-
ate or severe cuneometatarsal joint damage, it may be necessary to perform primary
arthrodesis, topic which will be discussed in another chapter.
Fig. 15 Open reduction

and internal fixation of the
fracture with plates,
allowing early mobilization
and support without distal
joint damage, guaranteeing
fracture reduction until
consolidation is achieved
The concept of column stabilization in multiple or complex fractures with soft

tissue involvement is interesting. If the fracture involves the medial (first metatarsal)
and middle (second and third metatarsal) column with a stable lateral column
(fourth and fifthh metatarsals), it is enough to stabilize the first and second (or third)
metatarsals. If there is a fracture of the lateral and middle columns, it is enough to
perform lateral column and second or third metatarsals fixation (Figs. 16, 17,
and 18).
1344 G. Khazen
Fig. 16 Stabilization by
columns in multiple or
complex fractures with soft
tissue involvement. AP
radiograph of foot with
multiple fractures of the
second, third, and fourth
metatarsals
In high energy trauma particular attention should be paid to the presence of com-
partment syndrome [33]. The respective fasciotomies should be performed together
with fracture stabilization. This topic will be treated extensively in another chapter
(Figs. 19, 20, and 21).
7.7 Malunion
Malunion can generate transfer metatarsalgia, plantar hyperkeratosis and toes defor-
mities. Corrective osteotomies [34] should be performed if conservative treatment
(insoles) failed.
Fig. 17 Oblique view of

previous patient, showing
comminution at the base of
the third metatarsal
8 Proximal Fifth Metatarsal Fracture
The proximal fifth metatarsal fracture is the most common fracture of the foot (68%
according to Petrisor [2]). The special characteristics of this area can generate a
torpid evolution and a delay in return to physical activities, especially in athletes,
[35, 36].
The fifth metatarsal is anatomically and biomechanically different from the other
metatarsals. It has great motion to be able to adapt to irregularities during stance and
gait [37]. Proximally it is stabilized by the plantar fascia, the insertion of the fifth toe
1346 G. Khazen
previous patient with
reduction and stabilization
of the second metatarsal,
with additional fixation of
the lateral column,
achieving stability mainly
stabilizing the second
metatarsal
abductor tendon as well as the peroneus brevis, the tarsometatarsal ligaments, and
the intermetatarsal ligaments that join it to the fourth metatarsal. These structures
stabilize the proximal part.
Fujitaka et al. [38] reported in a study in soccer players that the group of patients
with this fracture had a longer fifth metatarsal and its tuberosity was positioned
more proximal; they also reported cavus feet were more prone to have this fractures.
The blood suply is a key factor to understand why fracture healing may fail in
these fractures [39]. The main artery of the fifth metatarsal enters through the nutri-
tional foramen, located approximately in the middle of the diaphysis. It divides into
two branches, one proximal and one distal. In proximal fractures, the proximal
branch gets interrupted, which may cause delayed-unions or non unions. In
Fig. 19 Open midfoot and

forefoot fracture due to
high energy trauma.
Clinical image
contrast, the tuberosity receives blood supply from the metaphyseal arterioles,
which favors the healing of fractures in this zone. Lawrence and Botte [40], after
appreciating that the fractures distal to the tuberosity presented a higher incidence
of delayed healing or nonunion for the reason described, classified the fractures of
the proximal third of the fifth metatarsal in three zones; zone 1: tuberosity; zone 2:
at the fourth-fifth metatarsal joint; zone 3: proximal diaphysis. The fracture of the
tuberosity (zone 1) is an acute avulsion fracture generated by traction of the plantar
fascia [41], following a midfoot inversion movement. Jones fracture (zone 2) by
definition occurs at the level of the joint between the fourth and fifth metatarsals.
This fracture bears the eponym since Sir Robert Jones presented a series of four
cases of this metaphyseal fracture in 1902 [42], (including his own fracture, that
occured while dancing). In this area, fractures may be generated by an acute mecha-
nism after a forced inversion of the foot or by a chronic mechanism of axial load
with the foot in plantar flexion. Stress fractures (zone 3) occur in the proximal
diaphysis of the fifth metatarsal, distal to the joint between the fourth and fifth meta-
tarsals. They are generated by chronic repetitive overload or a sudden increase in
the level of activity. Carp [43] reported in 1927 that these metaphyseal fractures
distal to the tuberosity of the fifth metatarsal (zones 2 and 3) presented some
1348 G. Khazen
Fig. 20 X-ray of previous

patient, showing multiple
metatarsal involvement, in
addition to a Lisfranc
fracture
difficulty to consolidate reporting 24% of nonunion. Subsequent anatomical studies

confirmed the weak blood supply of this area, which can be interrupted by the frac-
ture and compromise fracture healing.
Based on the healing problems of zones 2 and 3, Torg et al. [41] published a
radiological classification, where they divide fractures into acute (type I), delayed
consolidation with medullary sclerosis (type II), and nonunion (type III), recom-
mending in their report surgical treatment only in the latter.
Clinically the patients with fracture in zones 2 or 3 refer pain in the fracture zone
that is exacerbated with exercise; it can be preceded by a prodrome of discomfort in
the same zone for several months, accompanied or not by edema and ecchymosis.
In the physical examination some degree of varus in the rearfoot or lateral foot bor-
der overload can be appreciated.
The radiological study is mandatory with anterolateral, lateral, and oblique foot
weight bearing X-ray [44]. MRI can help in decision making when there is any
doubt about the treatment. Porter [45] described that an MRI with a weak signal in
T1 in the area of a recent Jones fracture can be treated nonsurgically, but if there is
Fig. 21 X-ray of previous

patient, showing reduction
plus temporary
osteosynthesis with
Kirschner wires plus
isolated intercuneiform
screws
an increased signal in the same area, it should be treated surgically. Computed

tomography may be helpful to evaluate sclerosis in Torg II and III fractures, as well
as to evaluate fracture healing status.
9 Treatment
9.1 Zone 1
The tuberosity fracture (zone 1) is an acute avulsion fracture that should be treated
conservatively (Fig. 22). It has been clearly demonstrated that prolonged immobiliza-
tion leads to delayed recovery and worse outcomes [25]; therefore, functional reha-
bilitation is recommended. We recommend the use of a walking boot for 4–6 weeks
with immediate full weight bearing as tolerated. As previously discussed, this is an
1350 G. Khazen
Fig. 22 Fracture of the

fifth metatarsal tuberosity
(zone 1), treated
functionally with a
walking boot
area with good irrigation by the metaphyseal arterioles, which aids in the healing of
these fractures without the need for surgical treatment regardless of the degree of
displacement or comminution.
The author has one exception for zone 1 fractures treatment: in fractures with
metatarsal-cuboid joint compromise with more than 2 mm displacement, fracture
reduction and fixation is performed using a screw (no evidence in the literature)
(Figs. 23 and 24).
There are cases of non union in zone 1 fractures that are completely asymptom-
atic. If that is the case, the author does not recommend surgical treatment for this
non union.
9.2 Zones 2 and 3
The treatment of zone 2 and zone 3 fractures remains controversial and a matter of
debate. Reports of nonunion in these zones range from 7% to 67% [46], which led
to discussion about the need to indicate surgical treatment, especially in athletic
Fig. 23 Long oblique fifth

metatarsal fracture, with
articular compromise with
the cuboid and
displacement greater
than 2 mm
patients. Recent studies focus on improving fixation, biology and alignment correc-
tions to reduce failures [45], mainly hindfoot varus.
In a systematic review, Rouche and Calder [47] reported healing in 96% of
patients with Torg I fractures treated surgically, and 76% of those treated conserva-
tively. In chronic Jones fractures, 97% of those operated and 44% of those not oper-
ated were healed which is why they recommend surgical treatment in these fractures.
Baumbach et al. [48] recommend conservative treatment in zone 2 fractures with a
walking boot and surgical treatment in zone 3 fractures. The literature is full of stud-
ies supporting both options, but most seem to coincide in indicating surgical treat-
ment in zone 2 and zone 3 fractures in athletic patients, since it allows them to
reintegrate more quickly to their sporting activity and has a lower risk of nonunion
[35, 37, 40, 44–49].
Intramedullary screw fixation is the most accepted treatment for these fractures
[37]. Although it is still controversial, several sizes and types of screws have been
described. The ideal screw, is the one that completely fills the medullary canal
(Fig. 25).
1352 G. Khazen
Fig. 24 Reduction and

synthesis with screw in
fracture of previous case
Most studies report a low failure rate of intramedullary screw fracture stabiliza-
tion in the non-athlete population but a higher incidence of failure in athletes [50].
Larson also observed this tendency and reported nonunion in 40% of patients with
this type of fracture, in his series only one elite athlete healed his fracture, highlight-
ing that these patients start their high physical demand activity earlier, without
radiological evidence of fracture consolidation.
Fig. 25 The screw should

fill the intramedullary
canal and the threads
should pass the
fracture site
Multiple clinical and biomechanical studies comparing sizes, materials, and fixa-
tion methods have been reported. Although biomechanically it has been proven that
solid screws are more resistant [51], clinical studies have not been able to show
better fracture healing rates with any specific type of screw.
Sides [52] compared solid with cannulated screws, finding no difference between
them. Shah [53] compared 4.5 mm cannulated screws with 5.5 mm screws without
showing significant difference in the bending of both screws, while Porter [45] com-
pared them in athletic patients, reporting bent screw incidence in 12.5% of the
4.5 mm screws and none of the 5.5 mm screws.
Duplantier [54] compared fracture stabilization with lateroplantar locked plate
versus screws, reporting that plates had more resistance to failure than screws. Huh
[55] compared hooked plate and screws, reporting that screws showed more resis-
tance to bending and plates more resistance to fracture site rotation. Ismat [56]
described the fixation of this fracture with the Ulna hook plate reporting good
results.
1354 G. Khazen
9.3 Author’s Recommendation
In fractures of zone 1, we indicate conservative treatment with immediate weight

bearing in postoperative shoe or walking boot for 6 weeks. Pituckanottai et al. [57]
in a systematic review and meta-analysis reported that when immobilizing these
fractures with plaster, the risk of nonunion is 1.5 times higher than with immobiliza-
tion in a walking boot. In elderly patients we indicate vitamin D for 8 weeks [58].
In fractures of zones 2 and 3, Torg I, in non-athlete patients, we indicate conservative
treatment in postoperative shoe or walking boot, non weight bearing for 2 weeks and
then weight bearing as tolerated for another 4 weeks. After immobilization, if there is
any degree of varus of the rearfoot or lateral overload, a corrective orthosis is indicated
(with posterolateral elevation, low medial arch support and a depression for the first
metatarsal head).
In athletes with fractures in zones 2 and 3, Torg I, and in patients with fractures
in zones 2 and 3, Torg II type, surgical treatment is recommended.
Under sedation and regional ankle block, the surgical procedure is performed posi-
tioning the patient in lateral decubitus; the fracture is fixed using a cannulated par-
tially threaded screw that fills the intramedullary canal with its threads pass the
fracture focus, normally of 4.5 or 5.0 mm. The entry point should be “high and
inside” at the metatarsal base, to correctly align it to the metatarsal diaphysis.
Progressive weight bearing is allowed using a walker boot 4–6 weeks.
In cases of nonunion or refracture, screw exchange for a larger diameter is
recommended. In addition bone graft and/or demineralized bone matrix should
be added in the non union through a percutaneous lateral incision. If there is a
hindfoot varus, a lateral sliding calcaneal osteotomy is added. A first metatarsal
osteotomy is recommended depending on the flexibility of the varus deformity
(evaluated with Coleman test) (Fig. 26).This topic will be discussed elsewhere
in this book [44, 59].
In fractures Torg III (Fig. 27), surgical treatment is recommended including,

extensive riming of the medullary canal, autologous bone graft (depending on the
defect it can be taken from the calcaneus or tricortical from the iliac crest), demin-
eralized bone matrix, and fixation with a lateral plate or intramedullary screw
(Figs. 27, 28, 29, and 30). Non weight bearing for 2 weeks followed with weight
bearing as tolerated in a boot for another 6 weeks.
Fig. 26 In cases of fifth

metatarsal nonunion or
refracture in patients with
moderate to severe varus
hindfoot deformity,
a calcaneal valgus
osteotomy is recommended
Fig. 27 In cases of Torg

III fifth metatarsal stress
fractures, surgical
treatment is performed
with an approach to the
fracture site, extensive
riming of the medullary
canal, autologous bone
grafting, demineralized
bone matrix, and fixation
with a lateral plate or
intramedullary screw
1356 G. Khazen
Fig. 28 AP foot
radiograph showing a fifth
metatarsal stress fracture.
Please note the lateral
metatarsal cortex
thickening and fracture line
Fig. 29 AP foot
radiograph showing a fifth
metatarsal stress fracture,
magnified
Fig. 30 Oblique foot

radiograph (same patient
as Fig. 29) showing an
endomedullary screw with
a fully healed fifth
metatarsal stress fracture
References
1. Hasselman CT, Vogt MT, Stone KL, Cauley JA, Conti SF. Foot and ankle fractures in elderly
white women. Incidence and risk factors. J Bone Joint Surg Am. 2003;85-A(5):820–4.
2. Petrisor BA, Ekrol I, Court-Brown C. The epidemiology of metatarsal fractures. Foot Ankle
Int. 2006;27(3):172–4.
3. Jeffers RF, Tan HB, Nicolopoulos C, Kamath R, Giannoudis PV. Prevalence and patterns of
foot injuries following motorcycle trauma. J Orthop Trauma. 2004;18(2):87–91.
1358 G. Khazen
4. Sanchez Alepuz E, Vicent Carsi V, Alcantara P, Llabres AJ. Fractures of the central metatarsal.
Foot Ankle Int. 1996;17(4):200–3.
5. Samaila EM, Ditta A, Negri S, Leigheb M, Colò G, Magnan B. Central metatarsal fractures: a
review and current concepts. Acta Biomed. 2020;91:36–46.
6. Shuen WM, Boulton C, Batt ME, et al. Metatarsal fractures and sports. Surgeon. 2009;7:86–8.
7. Cakir H, Van Vliet-Koppert ST, Van Lieshout EM, et al. Demographics and outcome of meta-
tarsal fractures. Arch Orthop Trauma Surg. 2011;131:241–5.
8. Dameron TB Jr. Fractures and anatomical variations of the proximal portion of the fifth meta-
tarsal. J Bone Joint Surg Am. 1975;57:788–92.
9. Wilson E, Katz F. Stress fractures an analysis of 250 consecutive cases. Radiology.
1969;92:481–6.
10. Dixon S, Nunns M, House C, Rice H, Mostazir M, Stiles V, Davey T, Fallowfield J, Allsopp
A. Prospective study of biomechanical risk factors for second and third metatarsal stress frac-
tures in military recruits. J Sci Med Sport. 2019;22(2):135–9.
11. Aspa R. Common stress fractures. Am Fam Physician. 2003;68(8):1527–32.
12. Barrack MT, Gibbs JC, De Souza MJ, Williams NI, Nichols JF, Rauh MJ, et al. Higher inci-
dence of bone stress injuries with increasing female athlete triad- related risk factors: a pro-
spective multisite study of exercising girls and women. Am J Sports Med. 2014;42:949–58.
13. Mandell JC, Khurana B, Smith SE. Stress fractures of the foot and ankle, part 2: site-
specific etiology, imaging, and treatment, and differential diagnosis. Skeletal Radiol.
2017;46(9):1165–86.
14. Chuckpaiwong B, Cook C, Pietrobon R, Nunley J. Second metatarsal stress fracture in sport:
comparative risk factors between proximal and non-proximal locations. Br J Sports Med.
2007;41(8):510–4.
15. Shereff MJ. Complex fractures of the metatarsals. Orthopedics. 1990;13:875–82.
16. Boutefnouchet T, Budair B, Backshayesh P, Ali SA. Metatarsal fractures: a review and current
concepts. Trauma. 2014;16(3):147–63.
17. Singer G, Cichocki M, Schalamon J, Eberl R, Hollwarth ME. A study of metatarsal fractures
in children. J Bone Joint Surg Am. 2008;90(4):772–6.
18. Shereff MJ. Fractures of the forefoot. Instr Course Lect. 1990;39:133–40.
19. Becker A. First metatarsal malunion. Foot Ankle Clin. 2009;14(1):77–90.
20. Lee DK, Mulder GD, Scwartz AK. Hallux, sesamoid and first metatarsal injuries. Clin Podiatr
Med Surg. 2011;28:43–56.
21. Rammelt S, Heineck J, Zwipp H. Metatarsal fractures. Injury. 2004;35:SB77–SB86.
22. O’Malley MJ, Hamilton WG, Munyak J. Fractures of the distal shaft of the fth metatarsal:
“Dancer’s fracture”. Am J Sports Med. 1996;37(5):488–500.
23. Soave R, Bleazey S, Rudowsky A, Clarke R, Avino A Jr, Kuchar J. A new radiographic clas-
sification for distal shaft fifth metatarsal fractures. J Foot Ankle Surg. 2016;55(4):803–7.
24. Morgan C, Abbasian A. Management of spiral diaphyseal fractures of the fifth metatarsal: a
case series and a review of literature. Foot (Edinb). 2020;43:101654.
25. Zenios M, Kim WY, Sampath J, Muddu BN. Functional treatment of acute metatarsal frac-
tures: a prospective randomised comparison of management in a cast versus elasticated sup-
port bandage. Injury. 2005;36:832–5.
26. Sanders RW, Papp S. Fractures of the midfoot and forefoot. In: Coughlin MJ, Mann RA,
Saltzmann CL, editors. Surgery of the foot and ankle. 8th ed. Philadelphia: Mosby; 2007.
p. 2216–35.
27. Donahue M, Manoli A. Technical tip: transverse percutaneous pinning of metatarsal neck
fractures. Foot Ankle Int. 2004;25:438–9.
28. Kim H, Park Y, Kim G, Park Y. Closed antegrade intramedullary pinning for reduction and
fixation of metatarsal fractures. J Foot Ankle Surg. 2012;51:445–9.
29. Sammarco GJ, Carrasquillo HA. Intramedullary fixation of metatarsal fracture and nonunion.
Two methods of treatment. Orthop Clin North Am. 1995;26:265–72.
30. Bryant T, Beck D, Daniel J, Pedowitz D, Raikin S. Union rate and rate of hardware removal fol-
lowing plate fixation of metatarsal shaft and neck fractures. Foot Ankle Int. 2018;39(3):326–31.
31. Khazen G, Rondón F, Ruiz H. Comparación radiológica y clinica de dos métodos de fijación
de fractura diafisaria de metatarsiano. Tobillo y pie. 2015;7(1):26–30.
32. Curtis BD, Fajolu O, Ruff ME, Litsky AS. Fixation of metacarpal shaft fractures: biomechani-
cal comparison of intramedullary nail crossed K-wires and plate-screw constructs. Orthop
Surg. 2015;7(3):256–60.
33. Richter M, et al. Fractures and fracture dislocation of the midfoot: occurrence, causes and long
term results. Foot Ankle Int. 2001;22:392–8.
34. Murphy R, Fallat L. Surgical correction of metatarsal Malunion. J Foot Ankle Surg.
2012;51:801–5.
35. Hunt KJ, Anderson RB. Treatment of Jones fracture non unions in athletes sustaining proximal
fifth metatarsal stress fracture. Foot Ankle Int. 2010;31(3):203–11.
36. Lareau CR, Hsu AR, Anderson RB. Return to play in National Football League players after
operative Jones fracture treatment. Foot Ankle Int. 2016;37(1):8–16.
37. Lareau CR, Anderson RB. Jones fractures pathophysiology and treatment. JBJS Rev.
2015;3(7):e4.
38. Kohei Fujitaka K, Tanaka Y, Taniguchi A, Ogawa S, Isomoto S, Otuki S, Okubo M. Pathoanatomy
of the jones fracture in male university soccer players. J Sports Med. 2020;48(2):424–31.
39. Rath B, Notermans HP, Franzen J, et al. The micro-vascular anatomy of the metatarsal bones:
a plastination study. Surg Radiol Anat. 2009;31:271–7.
40. Lawrence SJ, Botte MJ. Jones’ fractures and related fractures of the proximal fifth metatarsal.
Foot Ankle. 1993;14(6):358–65.
41. Torg JS, Balduini FC, Zelko RR, et al. Fractures of the base of the fifth metatarsal distal to the
tuberosity: classification and guidelines for non-operative and operative management. J Bone
Joint Surg Am. 1984;66A:209–14.
42. Jones RI. Fracture of the base of the fifth metatarsal bone by indirect violence. Ann Surg.
1902;35:697–700.2.
43. Carp L. Fracture of the fifth metatarsal bone: with special reference to delayed union. Ann
Surg. 1927;86:308–20.
44. Karnovsky S, Rosenbaum A, DeSandis B, Johnson C, Murphy C, Warren R, Taylor S, Drakos
M. Radiographic analysis of National Football League Players’ fifth metatarsal morphology
relationship to proximal fifth metatarsal fracture risk. Foot Ankle Int. 2019;40(3):318–22.
45. Porter DA. Fifth metatarsal Jones fractures in the athlete. Foot Ankle Int. 2018;39(2):250–8.
46. Granata JD, Berlet GC, Philbin TM, Jones G, Kaeding CC, Peterson KS. Failed surgical man-
agement of acute proximal fifth metatarsal (Jones) fractures: a retrospective case series and
literature review. Foot Ankle Spec. 2015;8(6):454–9.
47. Rouche AJ, Calder JD. Treatment and return to sport following a Jones fracture of the fifth
metatarsal. Knee Surg Sports Traumatol Arthrosc. 2013;21(6):1307–15.
48. Baumbach SF, Prall WC, Braunstein M, Bocker W, Polzer S, Polser H. Fractures of the base of
the V metatarsal bone-current concepts revised. Unfallchirurg. 2018;121(9):723–9.
49. Jenkyn TR, Anas K, Nichol A. Foot segment kinematics during normal walking using a multi-
segment model of the foot and ankle complex. J Biomech Eng. 2009;131:034504.
50. Larson CM, Almekinders LC, Taft TN, Garrett WE. Intramedullary screw fixation of Jones
fractures: analysis of failure. Am J Sports Med. 2002;30(1):55–60.
51. Nunley JA, Gilsson RR. A new option for intramedullary fixation of Jones fracture. Foot Ankle
Int. 2008;29(12):1216–21.
52. Sides SD, Fetter NL, Glisson R, Nunley JA. Bending stiffness and pull- out strength of tapered,
variable pitch screws, and 6.5-mm cancellous screws in acute Jones fractures. Foot Ankle Int.
2006;27(10):821–5.
53. Shah SN, Knoblich GO, Lindsey DP, et al. Intramedullary screw fixation of proximal fifth
metatarsal fractures: a biomechanical study. Foot Ankle Int. 2001;22(7):581–4.
1360 G. Khazen
54. Duplantier NL, Mitchell RJ, Zambrano S, Stone AC, Delgado DA, Lambert BS, Moreno MR,
Harris JD, McCulloch PC, Lintner DM, Varner KE. A biomechanical comparison of fifth
metatarsal Jones fracture fixation methods. Am J Sports Med. 2018;46(5):1220–7.
55. Huh J, Glisson RR, Matsumoto T, Easley ME. Biomechanical comparison of intramedullary
screw versus low-profile plate fixation of a Jones fracture. Foot Ankle Int. 2016;37(4):411–8.
56. Ismat A, Rupp R, Knapp G, Heiss C, Szalay G, Biehl C. Treatment of proximal fifth metatarsal
fractures with an ulna hook plate. Foot (Edinb). 2020;42:101653.
57. Kwanchai Pituckanotai K, Arirachakaran A, Piyapittayanun P, Tuchinda H, Peradhammanon
P, Kongtharvonskul I. Comparative outcomes of cast and removable support in fracture fifth
metatarsal bone: systematic review and meta-analysis. J Foot Ankle Surg. 2018;57(5):982–6.
58. Clutton J, Perera A. Vitamin D insufficiency and deficiency in patients with fractures of the
fifth metatarsal. Foot (Edinb). 2016;27:50–2.
59. Fleischer AE, Stack R, Klein EE, Baker JR, Weil L Jr, Weil LS Sr. Forefoot adduction is a risk
factor for Jones fracture. J Foot Ankle Surg. 2017;56(5):917–21.
Compartment Syndrome of the Leg
and Foot
Omar Ituriel Vela Goñi and Luis Felipe Hermida Galindo
1 Introduction
The diagnosis of compartment syndrome of the leg (CS), as well as its treatment,
represents a highly complex situation on some occasions due to the challenge it
represents, as well as the complications or sequelae that this type of patient may
present [1, 2]. This is a surgical emergency [3]. Therefore, the following consider-
ations must be taken into account for the suspicion of this condition [2, 4]:
1. Presentation of highly variable signs and symptoms.
2. The patient may sometimes present cognitive alteration (substance abuse, seda-
tion, anesthetic blockade).
3. Compartment pressure monitoring is auxiliary, but not conclusive enough to
exclude the diagnosis [3, 5].
4. Definitive treatment is invasive and presents associated risks.
5. This diagnosis is associated with high transient and definitive morbidity (com-
plications) [4].
Having understood these points, we can understand that a delay or lack of diag-
nosis of this condition can be disastrous, not only in the clinical and functional
aspects of the patient (quality of life), but it can also represent a high risk of medical-
legal problems for the treating physician [1]. Since there are reports in which this
type of sequelae produces legal compensations between $136,000 and $460,000
O. I. Vela Goñi (*)

Orthopaedics and Traumatology Institute at Zambrano Hellion Hospital,
San Pedro Garza García, Nuevo León, México
L. F. Hermida Galindo
ABC Medical Center, Santa Fe Campus, Ciudad de México, México

Switzerland AG 2022
1362 O. I. Vela Goñi and L. F. Hermida Galindo
(dollars), it is also necessary to consider the costs related to the legal defense of the
medical personnel involved, with figures of up to $2 billion dollars annually [6].
In relation to the incidence of CS, in the lower extremity, it can occur in up to
30% of the cases of tibia fracture, (this being the most frequent presentation) [2, 3,
4, 7]. Its incidence reaches 0.7 cases per 100,000 women, and as high as 7.3 per
100,000 men in annual statistics [1, 5], a difference very marked by the type of
accidents suffered. It is important to highlight that up to 30% of the cases of acute
compartment syndrome are secondary to trauma without associated fracture [3, 8].
The age of presentation is 32 years old in men, and 44 years in women [2].
2 Physiopathology
Acute compartment syndrome is produced either by a decrease in the space con-

fined by fascia or by an increase in the pressure inside it, remembering that this
tissue (fascia) is not elastic, a situation that produces hemodynamic alterations [1, 3].
This circulatory alteration can be explained as follows [9, 10]:
• Arterial circulation presents a higher pressure in relation to venous circulation;
therefore, this pressure difference between both systems produces the arteriove-
nous pressure gradient.
• As a result of the decrease of this gradient, two situations arise: first, since the
supply of oxygenated blood is altered, the drainage of venous blood is also
decreased; second, this decrease in venous drainage produces extravasation of
liquid toward the muscular interstitium, a situation which causes an increase in
muscular edema, with the consequent elevation of the intracompartmental hydro-
static pressure [4].
• Faced with these local alterations, a vicious cycle generated, which produces the
obliteration of the lymphatic and arterial system, finally producing the necessary
changes to cause permanent alterations such as tissue necrosis (mainly muscle
and nerves).
• In summary, the necrosis suffered is a consequence of high hydrostatic pressure,
compression of arterioles, minimum perfusion pressure, hypoxia, oxidative
stress, cellular hypoglycemia, failure in cellular homeostasis, osmotic imbal-
ance, among others [10].
Once this vicious circle is understood, it is necessary to know the normal intracom-
partmental pressure, which is accepted to be between 8 and 10 mmHg in adults [3, 11]
and up to 15 mmHg in the pediatric population under normal conditions [10]. Pressures
above this threshold can orient the physician about the presence of CS, but should not
be excluded by finding a “normal” pressure taken on a single occasion [2].
It is important to highlight the reperfusion injury known as ischemia-reperfusion
injury in which there is tissue damage at the moment of restoring the vascular flow.
Several substances are released such as oxygen radicals, electrolytes, lactic acid,
TNF-α, IL-1β, MCP-1 between others [11], which can produce systemic alterations
such as arrhythmia, renal failure, and in severe cases, even death [4, 10].
Compartment Syndrome of the Leg and Foot 1363
It is important to highlight that the time of evolution translates into viability of

tissues, since they begin to present necrosis after 6 and 12 hours of hypoxemia [12].
Individually: muscle: reversible changes (3–4 hours), irreversible changes (8 hours);
peripheral nerve: conduction alteration (2 hours), neuropraxia (4 hours), irreversible
changes (8 hours) [10].
3 Anatomy
As mentioned initially, acute compartment syndrome is more frequent in the leg,

which is related to the type of trauma energy involved in the injury, as well as factors
related to the anatomy of this anatomical segment and other factors specific to the
patient.
The leg is made up of four compartments as follows [13]:
1. Anterior: tibialis anterior, extensor hallucis longus, extensor digitorum longus.
2. Lateral: peroneus longus and peroneus brevis.
3. Posterior Superficial: gastrocnemius and soleus.
4. Posterior Deep: tibialis posterior, flexor digitorum longus, and flexor hallucis
longus, in addition to the neurovascular bundle containing tibial-peroneal artery
and veins and tibial nerve.
These compartments are delimited by fascia or septum, an inelastic tissue that
does not allow changes in the volume they cover, a situation that is crucial in this
pathology [1, 8, 12, 14], as shown in Fig. 1.
Fig. 1 Diagram showing

the four compartments at
the level of the middle
third of the leg; the
numbers included in the
image are in relation to the
previous description of the
compartments
The knowledge of these anatomical relationships is of utmost importance, to be

able to suspect about this condition [1, 15].
4 Diagnosis
In spite of the technological advances, experience and clinical suspicion take greater
relevance at the moment of confirming this diagnosis.
Having said that, we should pay close attention to the following factors that can
be considered as risk or alarm factors [1, 2, 16]:
• Males, young (demographic) (most important factor)
• Penetrating trauma, crush injury (type of injury)
• Arterial or venous injury of the extremity
• Fractures associated with trauma (polytrauma)
• Use of anticoagulants, diuretics (base diseases)
• Systemic factors in the emergency room such as need for massive transfusion,
shock, and hypotension
• Patients difficult to evaluate due to cranial injury, spinal cord injury, and sub-
stance intoxication
• Application of peripheral anesthetic blocks as pain management in transferred
patients
As we can see, the evaluation of this type of patients is not always the simplest
or easiest, since several of these factors can be combined.
In general, the following signs are widely accepted as indicators of this syn-
drome: edema or swelling, pain on passive joint motion (ankle or toes), pain out of
proportion, paresthesia, paresis or paralysis, absence of pulses, and poikilothermy
[1, 10]. Pain out of proportion has a specificity of up to 97% in this diagnosis [10];
however, the diagnostic sensitivity of these signs and symptoms grouped together is
quite low, between 0.13 and 0.19. The physical examination presents a sensitivity of
0.54 and a specificity of 0.76 [1].
It is important to highlight that the absence of peripheral pulses, pallor of the
integuments, and diminished capillary return represent late signs in relation to acute
compartment syndrome, which requires vascular study, since the risk of amputation
can be very high in this context [1, 2].
Another diagnostic tool is to quantify or measure the intracompartmental pressure
of the segment under suspicion, especially when the patient is unconscious or with
alteration of the cognitive state [16].
To perform this measurement, there are three general monitoring methods: the
one proposed by Whitesides, described in the 70s, which uses common hospital
material (syringe, 3-way key for venoclysis, mercury manometer, needle), in which
the needle and venoclysis tube are inserted into the muscle of the compartment to be
measured and this pressure is detected by the manometer.
Another method of measurement is by means of an arterial line pressure monitor,

which implies having this equipment and being familiar with it.
There is also a specific monitor of different commercial brands such as Stryker®,
Rehacare®, C2Dx®, among others [5], which, in general, facilitate the measure-
ment of the compartments [1].
Once the decision to measure the compartment pressure has been made, the
question arises as to whether to do it intermittently or continuously, finding that the
latter modality presents a sensitivity of 0.94 and a specificity of 0.98, since it allows
the early detection of changes in pressure [1].
Whenever an intracompartmental pressure measurement is required, there are
two methods: absolute pressure and the differential pressure (Delta pressure).
Absolute pressure is the direct compartment measurement without any factors act-
ing upon it. Delta pressure is obtained when we subtract the compartment pressure
from the diastolic pressure. If this is less than 30 mmHg, it suggests a deficient tis-
sue perfusion, ischemia and even tissue necrosis; if there are doubts, measurements
should be repeated every hour to decide surgical treatment [1, 10, 16].
Another promising tool for this type of situation is near infrared spectroscopy
(NIRS), which is a noninvasive and easy-to-apply method that allows monitoring
oxygen variations in the tissues several centimeters deep; therefore, a decrease in
oxygen represents an indirect way of suspecting an increase in compartment pres-
sure [1, 2, 5, 10]. However, this diagnostic tool has not been validated [1, 2].
As for other studies measurement of CPK in peripheral blood (creatine phospho-
kinase), allows to have a better understanding of the tissue damage (biomarker),
presenting a considerable alteration 2 hours after trauma and remaining elevated for
up to 48 hours. After suffering an isolated tibia/peroneal fracture without associated
compartment syndrome, CPK can vary between 300 and 400 IU/L (being 200 IU/L
the normal maximum) [17]. In a major soft-tissue injury such as a high-speed car
crash, results higher than 2000u/L is highly suggestive of this syndrome. If the CPK
level is above 4000u/L, up to 92% of the cases already present an acute compart-
ment syndrome, especially in sedated patients or those in mechanical ventilation
[1, 18].
The authors stress the importance of a diagnosis based on history and physical
examination. Ancillaries such as pressure measurement and laboratory studies
should not delay the definitive treatment of the patient.
5 Treatment
The treatment for CS is to carry out the release of the compartment or compartments
involved by means of a fasciotomy. For this to be achieved, it is necessary that the
incision of the skin and subcutaneous cellular tissue allows the expansion of the
muscular tissue, a situation that will facilitate the evaluation of this tissue (color-
ation, consistency, and contractile capacity), in the understanding that all tissue with
a devitalized appearance must be debrided in order to avoid the risk of infection [8,
10, 12].
Therefore, once the compartment or compartments have been decompressed and
an adequate exploration of the involved tissues has been carried out, it is possible to
consider carrying out a partial closure of the surgical approach. Partial closure can
be performed using a few techniques (braided suture system, negative pressure sys-
tems, others) in order to facilitate a second revision [3, 14, 19].
Another important point to mention is that in the case of open fractures, it does
not exempt the risk nor exclude the diagnosis, so this lesion should not be a “distrac-
tor” that could delay the diagnosis and/or treatment [12, 15].
5.1 Four-Compartment Release – Two Incisions (Mubarak

and Hargens technique)
This modality or surgical technique (anterolateral and posteromedial approach) is

the most frequently performed in this clinical scenario, since the anterolateral
approach allows access to the lateral and anterior compartment, and the medial
approach to the superficial and deep posterior compartments.
To be able to perform these, it is important to have the following anatomical
references: head of the fibula and peroneal malleolus as well as the anterior border
of the fibula; and in the medial region of the leg, the anterior tuberosity of the tibia,
medial border of the tibia, and tibial malleolus; these references can sometimes be
somewhat difficult to identify, remembering that the leg will have significant
oedema and deformity (fracture of tibia-fibula for example).
The lateral approach is located between 2 and 3 centimeters anterior to the edge
of the fibula. Start 5–7 cm distal to the fibular head in order to avoid a lesion of the
common peroneal nerve. This incision ends 2–3 cm proximal to the lateral malleo-
lus, taking precaution to identify the superficial peroneal nerve of subcutaneous
trajectory in the distal lateral third [8, 10, 12, 14, 19].
In Fig. 2, an example of this wide approach can be seen where only the skin and
subcutaneous cellular tissue have been incised.
At this point, the anterior intermuscular septum is located, which separates the
lateral compartment from the anterior compartment. Once identified, the classic
“H” incision is made over the fascia and septum Figs. 3 and 4.
Regarding the medial approach the medial border or medial crest of the tibia is
located. The incision starts at the level of the anterior tuberosity, 2–3 cm posterior
to the medial tibial crest. The approach ends 3–4 cm proximal to the medial malleo-
lus. Once this approach has been performed, the fascia of the superficial posterior
compartment can be identified, which is incised longitudinally with scissors to com-
pletely free this compartment. Once this step is finished proceed to locate the pos-
teromedial border of the tibia and soleus muscle, which should be released from the
posterior aspect of the tibia. This will allow to observe the transverse intermuscular
septum, which should be incised longitudinally. This will allow the release or
decompression of the deep posterior compartment [15].

lateral view of fasciotomy,
where arrows in green
color point out the
anatomical references of
the anterolateral approach,
at proximal level the
fibular head and at distal
level the peroneal
malleolus
Fig. 3 Clinical image where the dissection of the fascia with scissors toward the proximal region
is observed; in addition, the arrow in yellow color shows us the conditions of the soft tissues at
proximal level of the leg, in which this specific patient presented a fracture of tibial plateau second-
ary to a motor vehicle accident

fasciotomy by anterolateral
approach, where the
opening of the lateral
compartment using curved
scissors can be appreciated
in order to protect the deep
soft tissues, being very
important the complete
opening of the same for its
complete decompression
5.2 Four-Compartment Release – One Lateral Incision

(Davey Technique)
In this single-incision technique, the lateral approach is performed in the same

fashion as in the two-incision technique as described in the Mubarak and Hargens
technique. After releasing the anterior and lateral compartments, it is dissected
posteriorly to release the superficial posterior compartment. At the posterior mar-
gin of the fibula, dettach the soleus and flexor hallucis longus. Once this step is
done, the peroneal vascular bundle can be identified which is reflected posteriorly
and the fascia of the posterior tibial muscle is observed, which must also be
incised longitudinally. In this way, it is possible to decompress the four compart-
ments of the leg as shown in Fig. 5; however, this technique may require greater
skill and knowledge of the anatomy, as well as greater caution with soft tissue
handling [14, 15, 19].
5.3 Selective Release of Compartments
Sometimes, after performing a thorough physical examination and having some

methods to quantify the pressure in the compartments of the leg, the scenario may
arise that only the anterior and/or lateral compartment is affected.
Fig. 5 Diagram showing

the direction (arrows in
blue) of the deep tissue
dissection to perform the
decompression of the four
compartments by means of
the single anterolateral
approach or Davey’s
technique; the numbers
included in the image
correspond to the
anatomical description of
the compartments
This situation has been described by Hatz and collaborators [20]. They found
that 80% of their patients were treated with selective fasciotomies. In that group, the
anterior compartment was decompressed in 100% of cases, the lateral compartment
in 88% and the deep posterior compartment in 2% frequent. They also reported that
there were no permanent complications, and only one of these patients required
conversion to a four compartments release.
In summary, if the treating physician has sufficient clinical data, in addition to
some method of pressure measurement, it could be a treatment modality for this
type of patients, remembering that the gold standard is the release of the four com-
partments by means of a double approach [1, 10, 12, 14, 19, 20].
6 Complications
The most feared complications include the following: systemic complications

(rhabdomyolysis, renal insufficiency for example) [7, 14], leg, amputation and/or
death [3, 21].
As for general complications, these can be related to the surgical procedure itself
(wide approaches), as well as to delayed tissue healing, infection, delayed local
fracture healing, residual pain, nerve damage, muscle weakness, vascular complica-
tions, and related to reconstruction procedures (osteotomies, arthrodesis, skin cov-
erage) [7, 20].
Compartment syndrome can sometimes go unnoticed despite the physician’s
skills. In this scenario, the patient may present with alteration of sensory and motor
nerve function, presence of neuropathic ulcers, distal deformity secondary to intrin-
sic muscles compromise such as claw toes, (Fig. 6) cavo-varus foot, as well as
alteration of gait biomechanics (Figs. 7 and 8) [1].
It is important to highlight that even in a perfectly timed treatment, these compli-
cations may appear [1, 3, 7, 15, 21].
Fig. 6 Clinical image

where we can observe: (a) a
in frontal view, rigid claw
toe deformity is observed
which includes the hallux
in addition to a tendency to
supination of the forefoot;
(b) in sagittal view a
combined deformity of the
middle and forefoot in
supination and cavus is
more easily appreciated,
where the contracture of
the tibialis anterior can
also be noted; it
corresponds to a patient
with sequelae of
compartment syndrome
secondary to a tibial
fracture who was managed
with external fixator and
the diagnosis went
unnoticed
7 Summary
The suspicion of compartment syndrome represents an emergency, which most of

the time requires surgical treatment. It frequently is a complicated situation, since
the symptoms and signs of CS may be very varied. Patient may present with an
altered state of consciousness and/or his pain perception may be altered, the reason
why, despite the CS, he may not report disproportionate pain, which could cause the
diagnosis to go unnoticed.
Therefore, it is important to keep in mind the following characteristics that are
seen more frequently in patients diagnosed with compartment syndrome: leg inju-
ries, young male patients, high energy trauma, good muscular condition, altered
Fig. 7 Clinical image in

relation to the surgical a
correction of the patient
illustrated in the previous
figure; (a) Tendon transfer
and interphalangeal
arthrodesis of the hallux
are performed, (b) superior
view of the tendon transfer
closure in hallux, where
percutaneous tenotomy of
flexors of the lesser toes
was also performed

the result of claw toe and
hallux correction as a
sequel of compartment
syndrome secondary to
tibial fracture of the
previous case illustrated
state of consciousness; these being the factors most frequently associated with the
diagnosis, but are not exclusive to it.
The diagnosis should be made in the first 6–12 hours of the injury, since this time
is when it has been shown by different studies that tissue necrosis begins, being a
major complication.
Once the compartment syndrome is diagnosed, surgical management involves
extensive approaches that allow adequate and sufficient decompression. Potential
complications include delay in healing/closure of the approaches, need of flaps to
provide coverage, delay in fracture healing, transient/definitive nerve damage, alter-
ation of gait biomechanics, amputation and death.
8 Compartment Syndrome of the Foot
8.1 Introduction
This is a rare entity, which is often undiagnosed and represents less than 5% of
compartment syndrome in the body [22–24]. The compartment syndrome of the
foot (CSF) should be identified and treated early to avoid severe and permanent
sequelae that alter the sensitivity and functionality of the foot and the entire limb,
which also has a negative impact on the patient’s quality of life.
8.2 Pathophysiology
High-energy trauma and crush injuries of the foot are well-identified causes of CSF,
(similar to the situation described in the section on compartment syndrome of the
leg). The most serious injury is peripheral nerve demyelination, followed by fibrosis
in addition to muscle necrosis causing claw toe due to plantar muscle damage. This
may occur during the first weeks or months after the ischemic event [25, 26].
Calcaneal fracture represents the most frequent cause of CSF, occurring in up to
10% of cases of such fracture. There are reports by Myerson, which describe up to
41% incidence with a foot fracture associated with a foot crush injury [27, 28].
Other known causes are pure soft tissue injuries (crush injuries), hindfoot and mid-
foot fractures, and/or dislocations, as well as multiple forefoot fractures [15, 27,
29], as shown in Fig. 9.
There are several published case reports of CSF secondary to an ankle sprain
[30], tibia fractures [31], minimally invasive surgery of “calcaneal spur” [26], bilat-
eral calcaneal fractures [32], forefoot revision surgery [33], recurrent CSF [34], in
addition to chronic compartment syndrome of the foot that was reported by
Middleton et al. [35]. Myerson describes a case in which, without apparent major
trauma, a 25-year-old young man develops a medial CSF after playing recreational
soccer [36].
a b
Fig. 9 Multiple metatarsal fracture, (a) clinical image showing tension edema of the dorsum of
the foot, diffuse ecchymosis, deviation of the toes as well as hallux nail injury; (b) anteroposterior
radiographic image of the foot, showing fracture of the 2,3,4,5 metatarsal
There is a case report on CSF due to ischemia-reperfusion following emergency

revascularization of the common femoral artery and distal popliteal artery for an
ischemic limb [37]. This is the only report of a non-traumatic cause and should be
taken into consideration in patients with vascular disorders submitted to procedures
of this nature.
It has been proposed that a risk factor for developing CSF is the antithrombotic
status of patients at the time of trauma. Park et al. found no significant statistical
relationship that could predict CSF in patients taking anticoagulants.
8.3 Anatomy
How many compartments does the foot have?

Throughout the years and from the first description of four compartments of the
foot in 1944 by Wood [38], there has been an evolution in the knowledge of the
number of compartments [39, 40].
In 1990, Manoli [41] questioned this number and carried out an investigation
through the injection of stained gelatin to determine that there are nine compart-
ments in the foot, including the calcaneal compartment which has communication
with the deep compartment of the leg. The latter has a clinical relevance demon-
strated in the report of eight cases of CSF concomitant with compartment syndrome
of the leg [42].
Ling and Kumar studied 13 cadaveric specimens where they found 3 very firm
vertical septum extending from the hindfoot to the midfoot. They proposed that
there were 3 compartments only. Unlike previous descriptions, the authors do not
find dense fasciae dividing the compartments of the forefoot that would cause a real
increase in pressure [43].
One of the major discrepancies of this study with respect to the rest of the publi-
cations is the presence of a dense fascia covering the abductor hallucis in the hind-
foot, which for them is absent in their dissections.
We have found this dense fascia not only in the dissections done for this chapter,
but also during the surgical releases.
So, based on the above, the compartments and their muscles are (Figs. 10 and 11)
as follows:
• Medial:
–– Adductor hallucis
–– Flexor hallucis brevis
• Superficial:
–– Flexor digitorum brevis
–– Tendons of Flexor digitorum longus
–– Lumbrical
• Lateral:
–– Abductor digiti minimi
–– Flexor digiti minimi brevis
• Abductor:
–– Abductor hallucis
• Four interossei:
–– Plantar and dorsal interossei.
• Calcaneus:
–– Quadratus plantae
–– Lateral plantar neurovascular bundle
–– Tibial nerve
Fig. 10 Clinical image of coronal cut at the level of the forefoot, in this dissection, carried out
approximately at half the length of the metatarsals, we can observe: (1) Interosseous compartments
[4], (2) Medial compartment (flexor hallucis brevis and abductor hallucis), (3) Central compart-
ment, (4) Superficial compartment (plantar aponeurosis), (5) Lateral compartment (flexor digiti
minimi brevis and abductor digiti minimi)
Fig. 11 Clinical image (cadaveric piece) of coronal cut in midfoot, observe the arrangement of the
compartments in this dissection performed transversely at the level of the naviculo-cuneal and
calcaneocuboid joint. The purple line depicts the septa (A. – medial, B. – lateral, C. – intermediate,
D. – plantar aponeurosis), in addition to the following structures: (1) abductor hallucis, (2) quadra-
tus plantae, (3) flexor digitorum brevis, (4) abductor digiti minimi, EDB extensor digiturom brevis
It is also important to keep in mind the opinion of Reach et al. [44], who propose
the skin as the 10th (tenth) compartment, arguing that, although it is not an osteo-
fascial compartment, there are descriptions of the increased pressure contained by
the skin and the immediate dermal fascia.
8.4 Diagnosis
Clinically, the patient has intense pain on palpation of the affected compartment, as
well as in passive flexion-extension of the toes that does not yield to analgesics. A
tense and painful edema is constant in these cases. Two-point discrimination is not
altered [45].
In the acute and early phase, pulses (posterior tibial artery and pedis artery) are
usually normal. An evident decrease or loss of sensation are conditions that appear
slowly if the patient is not treated [15].
Before the 1990s, most CSF fasciotomies were not preceded by a measurement
of intracompartmental pressures due to lack of equipment or training to perform
them [46], and patients were treated based on history and clinical assessment. In
these cases, the findings of devitalized muscle tissue confirmed the diagnosis.
As mentioned above, to objectively evaluate intracompartmental pressures, there
are several methods and systems for their measurement, as well as other indirect
measurements of tissue ischemia such as intramuscular pH. The latter is an early
diagnostic method with 80% specificity to detect acute compartment syndrome
based on pH less than 6.8, the latter proposed by Raza and Mahapatra [47].
Irreversible damage to a cell can be documented by finding mitochondrial and
lysosomal edema, in addition to damage to plasmatic membranes. Theoretically,
this could be measured with elevated tissue levels of glucose 6 phosphate, pyruvate,
and lactate. In this sense, the measurement of intramuscular pH comes closer than
any other method to documenting the presence of lactate and pyruvate in the injured
tissue, but it has not yet been validated as such [48].
That said, intracompartmental pressure greater than 30 mmHg is a pathological
indicator and suggests immediate surgical decompression [49].
Whitesides et al. report the use of a differential pressure that is calculated with
the diastolic pressure minus the intracompartmental pressure, proposing below 30
mmHg as diagnostic [16, 50].
In general, there is no consensus on how many compartments to measure, nor a
standard on whether to do it as a single or serial measurement. The traumatic history
and above all the patient’s clinical condition, should give us a diagnosis and above
all a guide to procee with the surgical decompression.
There is a report by Daniels et al. [52] in which they describe a patient with rhabdo-
myolysis and acute renal failure, who was treated with IV mannitol with resolution
of the problem after 5 days of treatment. Mannitol has been proposed as a conserva-
tive treatment for compartment syndrome in experimental work in dogs, but its
efficacy has never really been proven in humans [53].
Conservative treatment for acute CSF is proposed by some physicians who
weigh the possible complications of fasciotomies, such as: infections, need for skin
coverage, between others, and prefer to treat the CSF complications [54], i.e. not
decompressing an acute CSF.
In 1914, Murphy [55] was the first to speak of fasciotomy as a treatment to prevent
the consequences of compartment syndrome.
Once the CSF is installed, the emergency fasciotomy must be performed, and
although it is impossible to know the extension of the damage due to muscular isch-
emia, 12 hours is the time proposed, based on an experimental animal study, to find
muscular necrosis [56].
8.7 Fasciotomies in the Foot
It is recommended to make three incisions to decompress the nine compartments of

the foot. However, there are cases where only the affected compartment will be
decompressed in isolation [36] (Figs. 10 and 11).
8.7.1 Two Dorsal Approaches
In order to maintain a good distance between both incisions, the approach is made
on the medial border of the second metatarsal and on the lateral border of the fourth
metatarsal with a length of approximately 5 cm [27], starting just proximal to the
metatarsal heads. Through the medial approach, the first and second interosseous
compartments are decompressed, as well as the adductor compartment. Fasciotomy
over the fourth metatarsal decompresses the third and fourth interosseous compart-
ments, as well as the central and lateral compartments as shown in Fig. 12.
Fig. 12 The location of

the two dorsal approaches
(green lines) to perform
decompression of the
compartments described
above. Remember the
importance of performing
them as far apart as
possible so that the soft
tissue flap between the
approaches is as wide as
possible (red arrow)
8.7.2 Medial Approach
The dorsal border of the abductor hallucis muscle is identified and an approach of
approximately 6 cm is made starting 4 cm anterior to the posterior border of the heel,
directing the incision to the plantar border of the first metatarsal. Through this approach,
the abductor hallucis is dissected, retracting the muscle both plantar and dorsal to release
the intermuscular septum resulting in the herniation of the quadratus plantaris muscle
(calcaneal compartment). Releasing the quadratus plantaris is essential, as its injury is
associated with claw toe formation as the main sequelae [27, 36] (Fig. 13).
Once fasciotomies have been performed, the patient should be re-intervened for
wound closure in 5–7 days. Occasionally, plastic surgery intervention will be
required for skin coverage with partial-thickness grafting [49]. In cases of calcaneal
Fig. 13 Clinical image in

sagittal view showing the
orientation of the medial
approach (green line) used
to decompress the
previously described
compartments
fracture, it will be necessary to wait for skin closure. It can be approached laterally
for reduction and fixation 10–14 days after fasciotomy [15].
An alternative method preferred by the authors is to use negative pressure ther-
apy system at the fasciotomies, which has two objectives: reduce edema and avoid
retraction of the superficial tissues, which favors the subsequent direct closure of the
skin and reducing the need for a partial-thickness skin graft.
8.8 Complications of Nontreatment and Treatment
Untreated CSF results in muscle necrosis leading to muscle scarring which is

responsible for toes deformities and permanent neurological impairment [42].
The sequelae of CSF such as claw toes, decreased sensation, and nonspecific
discomfort may occur within weeks or months after the primary event [25, 26].
Pisan and Klaue [27] published a series of eight cases of CSF where the time
between trauma, measurement of pressures, and fasciotomy was a mean of
11.5 hours (4–20 hours). The only patient who had persistence of sensory deficit
was the one who was treated 20 hours after the CSF onset. In a case of “calca-
neal spur” surgery treated with minimally invasive surgery, severe pain was
described in the surgical area for some weeks that ended up resolving without
treatment. The patient developed claw deformity 3 months later [26].
In a study, Manoli et al. [42] described that three of eight patients who presented
falls from height or automobile accidents and who were treated with late fascioto-
mies (between 24 hours and 6 days after the accident), showed necrosis of the
abductor hallucis, flexor hallucis brevis, claw deformity of the lesser toes, and alter-
ation of the tibial nerve in all three patients, the sequelae were permanent. Myerson
reports a case with 18 hours of evolution of a CSF in the medial compartment,
reporting a necrosis of 50% of the abductor hallux muscle [36].
Fig. 14 Presence of claw

toes at 7 weeks after
calcaneal fracture.
Osteosynthesis of the
calcaneus was postponed
15 days after the fracture,
since the patient also
presented concomitant
cranioencephalic and
thoracic trauma
The compartment syndrome after a calcaneal fracture usually presents a

decrease in pressure in 48 hours spontaneously [57]. This may be the reason
why we often overlook this entity in these fractures specifically thinking that it
is an obvious pain due to the trauma.
The most frequent sequela of untreated or unnoticed CSF is the presence of
claw toes (Fig. 14). Flexor tenotomies with interphalangeal arthrodesis or resec-
tion arthroplasty are the methods of choice.
When cavus deformity and/or ulcerations are present, they should be treated
with usual methods such as tendon transfers, osteotomies, or arthrodesis in stra-
tegic sites. Nerve releases and medical treatment for neuropathic pain are also
an option. When pain is not treatable, amputation is a last resort [15, 58].
8.9 Treatment Complications
Up to 65% of patients with fasciotomies require a skin graft, which prolongs recov-
ery time and increases treatment costs. The return to pre-injury physical activity, as
well as the use of everyday footwear, becomes problematic after these procedures.
Only 10% of patients who undergo fasciotomy return to their presurgical state due
to pain, altered sensitivity, and stiffness of the foot [54].
8.10 Summary
CSF diagnosis need a high level of awareness and suspicion for a foot with high-
energy trauma, multiple fractures, fractures/dislocations (especially calcaneal frac-
tures) and even in clinical scenarios with severe and progressive foot pain. Close
and continuous physical examination in the first few hours after trauma is critical to
diagnosis.
Although the intracompartmental measurement will give us an objective param-
eter, this result is NOT essential to perform fasciotomies in the presence of a patient
with a clear history.
Wound closure or skin coverage should be planned and performed in conjunction
with plastic surgery 7 days after the fasciotomies.
Despite being a rare entity, compartment syndrome of the foot should be treated
as an emergency to avoid permanent sequelae in the patient.
Acknowledgments We are deeply grateful to Emilio and Pablo for their invitation and trust given
to us to develop this chapter, and especially to Dr. Felipe Vega Rivera, Coordinator of the Centro
de Enseñanza e Investigación en Cirugía (CEIC) of the Hospital Ángeles Lomas, for the invaluable
cooperation to carry out the cadaveric dissections and photographs included in this chapter.
References
1. Schellenberg M, Chong V, Cone J, Keeley J, Inaba K. Extremity compartment syndrome. Curr

Probl Surg. 2018;55:256–73.
2. Duckworth A, McQueen M. The diagnosis of the acute compartment syndrome - a critical
analysis review. JBJS Rev. 2017;5(12):e1.
3. Torlincasi A, Lopez R, Wassem M. Acute compartment syndrome. StatPearls (Internet); 2020.
4. Maher M, Mauffrey C. Diagnostic dilemma for the orthopedic surgeon. In: Mauffrey C, Hak
D, Martin-III M, editors. Compartment syndrome. Switzerland: Springer; 2020. p. 1–8.
5. Mortensen S, Vora M, Mohamadi A, Wright C, Hanna P. Diagnostic modalities for acute com-
partment syndrome of the extremities - a systematic review. JAMA Surg. 2019;154(7):655–65.
https://doi.org/10.1001/jamasurg.2019.1050.
6. Little M, Lin C, Vrahas M. Legal aspects of compartment syndrome. In: Mauffrey C, Hak D,
Martin III M, editors. Compartment syndrome. Switzerland: Springer; 2020. p. 9–16.
7. Du W, Hu X, Shen Y, Teng X. Surgical management of acute compartment syndrome and
sequential complications. BMC Musculoskelet Disord. 2019;20:98.
8. Owen C, Cavalcanti A, Molina V, Honoré C. Decompressive fasciotomy for acute compart-
ment syndrome of the leg. J Visc Surg. 2016;153:293–6.
9. Tapiwa N, Malahias M, Hindocha S, Khan W, Juma A. Acute compartment syndrome of the
lims: current concepts and management. Open Orthop J. 2012;6(Suppl 3:M7):535–43.
10. Papachristos IV, Giannoudis PV. Acute compartment syndrome of the extremities: an update.
Orthopaedics and Trauma. 2018.
11. Merle G, Harvey E. Pathophysiology of compartment syndrome. In: Mauffrey C, Hak D,
12. von Keudell A, Weaver M, Appelton P, Dyer G, Heng M, Jupiter J, et al. Diagnosis and treat-
ment of acute extremity compartment syndrome. Lancet. 2015;386:1299–310.
13. Joos D, Kadakia A. Compartment syndrome. In: Miller M, Sanders T, editors. Presentation,
imaging and treatment of common musculoeskeletal conditions. Elsevier; 2012. p. 576–9.
14. Long B, Koyfman A, Gottlieb M. Evaluation and management of acute compartment syn-
drome in the emergency department. J Emerg Med. 2019;56(4):386–97.
15. Tillinghast C, Gary J. Compartment syndrome of the lower extremity. In: Mauffrey C, Hak D,
16. Duckworth A, Court-Brown C, McQueen M. Pressure measurement: surrogate of ischaemia.
In: Mauffrey C, Hak D, Martin III M, editors. Compartment syndrome. Springer; 2020.
p. 35–50.
17. Oni O, Fenton A, Iqbal S, Gregg P. Prognostic indicators in tibial shaft fractures: serum creati-
nine kinase activity. J Orthop Trauma. 1989;3(4):345–7.
18. Shadgan B, Menon M, O’Brien P, Reid W. Diagnostic techniques in acute compartment syn-
drome of the leg. J Orthop Trauma. 2008;22(8):581–7.
19. Azar F. Traumatic disorders. In: Azar F, Beaty J, Canale T, editors. Campbell’s operative ortho-
paedics. Memphis: Elsevier; 2017. p. 2405–11.
20. Hatz B, Frima H, Sommer C. Selective fasciotomy for acute traumatic lower leg compartment
syndrome: is it feasible? Arch Orthop Trauma Surg. 2019 agosto;139:1755–62.
21. Bodansky D, Doorgakant A, Alsousou J, Iqbal H, Fischer B, Scicluna G, et al. Acute com-
partment syndrome: do guidelines for diagnosis and management make a difference? Injury.
2018;49:1699–702.
22. Middleton S, Clasper J. Compartment syndrome of the foot: implications for military sur-
geons. J R Army Med Corps. 2010;4(156):241–4.
23. Thakur N, McDonnell M, Got C, Arcand N, Spratt K, DiGiovanni C. Injury patterns causing
isolated foot compartment syndrome. J Bone Joint Surg Am. 2012;11(94):1030–5.
24. Park Y, Choi W, Choi G, Kim H. Role of antiplatelet/anticoagulant medications and blood-
clotting tests in prediction of traumatic foot compartment syndrome. Foot Ankle Int.
2018;6(39):725–30.
25. Santi M, Botte M. Volkman’s isquemic contracture of the foot and ankle: evaluation and treat-
ment of established deformity. Foot Ankle Int. 1995;16(6):368–77.
26. Michelson J. Isolated compartment syndrome of the calcaneal compartment secondary to min-
imal incision surgery. Foot Ankle Int. 1995;16(3):162–3.
27. Pisan M, Klaue K. Compartment syndrome of the foot. Eur J Foot Ankle Surg. 1994;1:29–36.
28. Myerson M. Management of compartment syndromes of the foot. Clin Orthop.
1991;271:239–48.
29. Dodd A, Le I. Foot compartment syndrome: diagnosis and management. J Am Acad Orthop
Surg. 2013;21:657–64.
30. Cortina J, Amat C, Selga J, Corona P. Isolated medial foot compartment syndrome after ankle
sprain. Foot Ankle Surg. 2014;20(1):e1–2.
31. Bayer J, Davies A, Darrah C, Shepstone L, Patel A. Calcaneal compartment syndrome after
tibial fractures. Foot Ankle Int. 2001;22(2):120–2.
32. Sharma H, Rana B, Naik M. Bipedal compartment syndrome following bilateral intra-articular
calcaneal fractures. Foot Ankle Surg. 2004;10:93–6.
33. Noorpuri B, Shahane S, Getty C. Acute compartment syndrome following revisional arthro-
plasty of the forefoot: the dangers of ankle-block. Foot Ankle Int. 2001;21(8):680–2.
34. Batra S, McMurtrie A, Sinha A, Griffin S. Recurrent compartment syndrome of foot following
a calcaneal fracture. Foot Ankle Surg. 2007;13:154–6.
35. Middleton D, Johnson J, Davies J. Exertional compartment syndrome of bilateral feet: a case
report. Foot Ankle Int. 1995;16(2):95–6.
36. Myerson M, Berger B. Isolated medial compartment syndrome of the foot: a case report. Foot
Ankle Int. 1996;17(3):183–5.
37. Barshes N, Pisimisis G, Kougias P. Compartment syndrome of the foot associated with a
delayed presentation of acute limb ischemia. J Vasc Surg. 2016 Mar;63(3):819–22.
38. Straus W. Structure and function as seen in the foot. By Frederic Wood Jones. Am J Phys
Anthropol. 1944;3:211–3.
39. Guyton G, Shearman C, Saltzman C. The compartments of the foot revisited: rethinking the
validity of cadaver infusion experiments. J Bone Joint Surg Br. 2001;83(2):245–9.
40. Myerson M. Experimental decompression of the fascial compartments of the foot: the basis for
fasciotomy in acute compartment syndromes. Foot Ankle. 1988;8(6):308–14.
41. Manoli A, Weber T. Fasciotomy of the foot: an anatomical study with special reference to
release of the calcaneal compartment. Foot Ankle. 1990;10(4):267–75.
42. Manoli A, Fakhouri A, Weber T. Concurrent compartment syndromes of the foot and leg. Foot
Ankle. 1993;14(6):339–42.
43. Ling Z, Kumar V. The myofascial compartments of the foot. A cadaver study. J Bone Joint
Surg (Br). 2008;90:1114–8.
44. Reach J, Amrami K, Felmlee J, Stanley DW, Alcorn J, Turner N. The anatomic compartments
of the foot: a 3-tesla magnetic resonance imaging study with clinical correlates for needle pres-
sure testing. Foot Ankle Int. 2006;28(5):201–8.
45. Fakhouri A, Manoli A. Acute foot compartment syndromes. J Orthop Trauma. 1992;6(2):223–8.
46. Myerson M. Diagnosis and treatment of compartment syndrome of the foot. Orthopedics.
1990;13:711–7.
47. Raza H, Mahapatra A. Acute compartment syndrome in orthopedics: causes, diagnosis, and
management. Adv Orthop. 2015;2015:543412.
48. Johnstone A, Ball D. Determining ischaemic thresholds through our understanding of cel-
lular metabolism. In: Mauffrey C, Hak D, Martin III MP, editors. Compartment syndrome.
Switzerland: Springer; 2020. p. 25–34.
49. Manoli A. Compartment syndrome of the foot. Current concepts. Foot Ankle. 1990;10:340–4.
50. Whitesides T, Haney T, Morimoto K, Harada H. Tissue pressure measurements as a determi-
nant for the need of fasciotomy. Clin Orthop Relat Res. 1975;113:43–51.
51. Finnoff J, Henning P, Cederholm S, Hollman J, Smith J, Turner N. Accuracy of medial
foot compartment pressure testing: a comparison of two techniques. Foot Ankle Int.
2010;31(11):1001–5.
52. Daniels M, Reichman J, Brezis M. Mannitol treatment for acute compartment syndrome.
Nephron. 1998;79:492–3.
53. Better O, Zinman C, Reis N. Hypertonic mannitol ameliorates intracompartmental tamponade
in model compartment syndrome in the dog. Nephron. 1991;58:344–6.
54. Ojike N, Roberts C, Giannoudis P. Foot compartment syndrome: a systematic review of the
literature. Acta Orthop Belg. 2009;75(5):573–80.
55. John B. Murphy. JAMA: the journal of the American Medical Association Myositis. 1914;15.
56. Bourne R, Rorabeck C. Compartment syndromes of the lower leg. Clin Orthop.
1989;240:97–105.
57. Mittelmeier T, Machler G, Lob G, Mutschler W, Bauer G, Vogl T. Compartment syndrome of
the foot after intrarticular calcaneal fracture. Clin Orthop. 1991;269:241–8.
58. Perry M, Manoli A. Foot compartment syndrome. Orthop Clin North Am. 2001;32(1):103–11.
Index
A diagnosis, 1145–1147
Abductor digiti minimi aponeurosis, 191 distal region, 1145
Abductor splint, 150, 151 Dresden instruments, 1152
Absorbable suture materials, 95 eccentric contracture, 1146
Accessory bones of the foot, 1335 elongated gastrosoleus complexes, 1150
Acetabulum pedis, 116, 117, 137, 138, 1258 entrapment of the sural nerve, 1150
Achilles-calcaneal-plantar system, 21 etiology, 1142
Achilles-calcanean-plant system, 898 exclusion criteria, 1148
Achilles contracture, 318 fibers converge, 1144
Achilles end injuries, 1148 functional threshold, 1151
Achilles lengthening gastrosoleus complex, 1143
cerebral palsy, 874 genetic factors, 1143
decision factors, 885, 886 high tensile loads, 1141
deep gastrocnemius-soleus recession, incidence, 1142
882, 883 inclusion criteria, 1148
distal gastrocnemius tenotomy, 880–882 inflammatory response and reparative
equinus, 874 processes, 1155
gastrocnemius-soleus complex, 873 isokinetic tests, 1150
gastrocnemius-soleus recession, 878–880 Kuwada classification, 1157
indications, 874, 875 local infiltrations with corticoids, 1143
proximal gastrocnemius medial region, 1145
tenotomy, 883–885 medical check-ups, 1148
surgical techniques, 875, 876 metallic anchors, 1150
TAL, 876–878 Myerson classification, 1157
Achilles tendon, 1145 non-contact mechanism, 1145
Achilles tendon lengthening, 119, 1252 orthopedic and surgical treatment, 1154
Achilles tendon ruptures (ATR), 1148 passive dorsiflexion, 1152
activities of daily living or sports, 1154 pathology, 1142
ankle in maximum plantar flexion, 1148 posterior enhancements, 1149
antithrombotic prophylaxis with oral posterior tibial artery, 1144
anticoagulants, 1151 pre-insertional region, 1142
classification, 1157 proximal approach, 1150
complications, 1149, 1165 proximal region, 1145
conservative treatment, 1148, 1154 risk factors, 1143
© The Editor(s) (if applicable) and The Author(s), under exclusive license to 1385
Springer Nature Switzerland AG 2022
https://doi.org/10.1007/978-3-030-95738-4
1386 Index
Achilles tendon ruptures (ATR) (cont.) low or medium impact injury

shortening for elongated tendons, 1160 mechanism, 1173
surgical repairs, 1147 manual stress radiography in external
surgical treatment, 1149, 1154 rotation, 1179
sutures retrieved through proximal nuclear magnetic resonance, 1176
approach, 1153 osteosynthesis systems, 1185
tendinopathic tendons, 1143 patient positioning, 1184–1185
treatment protocol, 1148 perimalleolar hematoma, 1173
treatments, 1147, 1157 posterior malleolar fragment, 1182
V-Y flap, 1160 posterior syndesmosis, 1172
Active muscular control, 6 posterior tibial vasculonervous
Active plantar flexion, 1156 bundle, 1188
Acute Achilles tendon rupture, 1142, posterolateral approach, 1187
1146, 1147 posterolateral corner of the tibial
Acute compartment syndrome, 348, 1235, plafond, 1181
1368, 1369 posteromedial access, 1188
Acute osteochondral fractures, 1078 postoperative protocol, 1205
Advanced Vital Trauma, 338 pronation-abduction, 1171
Allograft reconstruction, 1164 pronation-external rotation, 1171
Allograft transfers, 1041–1042 radiographic interpretation, 1178
American orthopaedic foot and ankle society radiography under body weight
(AOFAS), 1119 loading, 1179
Amputation, 216, 223, 269–272 supination-adduction, 1170
Aneurysmal bonce cyst (ABC), 77 supination-external rotation, 1171
Angiosomes, 91 suprasyndesmal fractures, 1172
Angular alignment assessment, 120 surgical approach, 1186
Ankle arthroplasty, 739–742 tibio-peroneal mortise, 1169
Ankle dorsiflexor, 6 tibio-peroneal syndesmosis, 1170
Ankle entrapment syndrome tibiotalar contact surface, 1179–1180
defined, 1049 tomographic classifications, 1181
Ankle foot orthosis, 326 type 44-B or trans-syndesmal
Ankle fusion, 732–734, 736, 738, 739 fractures, 1172
Ankle instability, 551, 1056–1060, 1062 Ankle plantarflexion-knee extension
Ankle or malleolar fractures couple, 20
anatomical point of view, 1169 Ankle rocker, 7
ankle region, 1186 Anterior calcaneal tuberosity, 1297
anterior-posterior projection, 1179 Anterior distal tibial angle (ADTA), 707, 708
bullas or superficial or deep Anterior pilon fracture, 1219
abrasions, 1177 Anterior tibial tendon transfer, 154
capsulo-ligamentary structures, 1169 Anterograde Medullary pinning, 1345
complications, 1206 Anterograde Perforations and
computed axial tomography, 1176 Microfractures, 1080
decision making, 1178 Anterolateral ankle impingement, 39
diagnostic methodology, 1174 Antero-posterior (AP) view, 362
distal tibio-fibular relationship, 1175 Anticipated leg length discrepancy, 226
flexor retinaculum and posterior tibial AO-Orthopaedic Trauma Association
tendon sheath, 1189 classification, 1171
forefoot in external rotation, 1179 ArthroBroström, 1060
high-energy injury with joint Arthrodesis, 55, 175
dislocation, 1177 Arthrofibrosis, 1056
infection rates (deep infection) in Arthroscopic access through two ventral and
patients, 1207 dorsal anterolateral portals, 1279
instrumentation, 1185 Arthroscopic ankle drainage, 773, 774
kinetics, 1172 Arthroscopic ATFL repair, 1061
lesional complexity, 1171 Arthroscopic surgery, 1078
Index 1387
Arthroscopic treatment of ankle Bone surgery, 54

instability, 1059 Bone transport technique, 85
Arthroscopic vision of an anterior talofibular Brachymetapodia, 284–286
ligament (ATFL) rupture, 1060 Brachymetatarsia
Artificial prostheses, 21 acute and gradual correction, 288
Art of Limb Alignment, 226 anatomy, 276
Associated congenital osseous anomalies, 215 brachymetapodia, 284–286
ATiFL, 1054 conservative management, 279
Auto decompression, 1373 diagnosis, 277, 278
Autologous chondrocyte implantation external fixation, 287–289
(ACI), 1100 external fixator, 282, 283
Autologous Osteochondral Graft for the fourth metatarsal, 277
treatment of osteochondral talar idiopathic causes, 276
lesion, 1083 lengthening recommendations, 285
Autologous osteochondral grafting, 1083 metatarsal length, 275
Avascular necrosis (AVN), 440–442 post-operative protocol, 285, 287
Avascular necrosis of the navicular, 1299 simple radiographic method, 278
Avulsed scaphoid fracture, 1295 surgical planning/treatment, 279–282, 284
Avulsion fibular fracture of Wagstaffe- unilateral or bilateral, 275
LeFort, 1171 with Iliac crest autograft, 280, 282
Bunionette deformity
clinical symptoms and signs, 520, 521
B conservative management, 524
Ballerina fracture, 1343 deformity correction power, 531, 533
Barouk´s procedure, 329 diaphyseal fifth metatarsal
Bartoniceck III posterior pilon fracture, 1220 osteotomies, 527–530
Bean-shaped/bunioned foot, 139 distal fifth metatarsal osteotomies,
Below-knee amputation 526, 527
causes, 821 epidemiology, 519
clinical evaluation, 821, 822 factors, 520, 521
conditions for, 822 intractable plantar keratosis, 531
factors, 822 minimally invasive surgery, 530, 531
life expectancy, 821 postoperative/Barouk shoe, 526
preoperative requirements, 822 proximal fifth metatarsal osteotomy, 530
transtibial amputation surgical treatment, 524, 525
Chopart’s amputation, 827–829 Taylor’s bunion, 519
fishmouth, 823–826 type I deformity, 522
guillotine, 823, 824 type II deformity, 523
hindfoot amputation, 826, 827 type III deformity, 523
Pirogoff, Boyd, modified type IV deformity, 523
Pirogoff, 829–833 Butler’s technique, 301
tarsometatarsal amputation, 835–838
tennis ball stump, 825–827
toes, 837–840 C
transmetatarsal amputation, 833–835 Calcaneal Fracture-Dislocations, 1245–1247
types, 822 Calcaneal tuberosity, 1288
Body fractures, 1275–1278, 1282 Calcaneocuboid arthrodesis
Body Weight Support, 1076 anatomy and biomechanics, 654, 655
Bone avulsions, 1292 indications, 655
Bone defects, 1295 lateral column lengthening, 656
Bone entrapment syndrome, 1050, 1051 results, 657, 658
Bone marrow cell transplantation surgical technique, 655, 656
(BMDCT), 1100 Calcaneo-cuboid-cuneiform osteotomy
Bone marrow Edema, 1077 technique, 191
Bone Marrow Stimulation, 1079 Calcaneocuboid joint, 1244
1388 Index
Calcaneonavicular (CN) coalition, 195, 196 wound healing, 1250

Calcaneus fractures Calcaneus osteotomy, 574–576
anatomic features, 1230 Cavovarus deformity with peroneal tendon
anatomic joint reduction, 1237 tears, 1043
AO/OTA classification, 1234 Cavovarus foot
axial and lateral projections of the anatomy, 165, 166, 168
hindfoot, 1232 diagnosis, 168–170
axial impaction force, 1231 etiology, 165
calcaneal shape and implant non-operative management, 170
positioning, 1242 surgical management, 170, 171
calcaneus supplements, 1242 arthrodesis, 175
classification, 1234, 1251 concurrent equinus, 173
classification system, 1234 dynamic or fixed supination, 173
congruity of the subtalar joint, 1239 forefoot pronation flexible or rigid, 171
contraindications to open reduction and gradual deformity correction, 175
internal fixation, 1235 hindfoot varus flexible or rigid, 172
direct manipulation of the tuberosity intraarticular and tibial deformity, 174
fragment, 1238 midfoot wedge resections, 175
dislocation approach, 1246 postoperative protocol, 175, 176
displaced calcaneus fractures, 1232 toe deformities, 174
displaced tuberosity to the sustentacular Cavus, 118
fragment, 1237 Cavus foot deformity
dry subtalar arthroscopy, 1241 approach to correction, 572, 573
emergency procedures, 1235–1236 calcaneus osteotomy, 574–576
fracture-dislocations, 1232 examination of, 570–572
hematoma, 1231 forefoot equinus correction of, 584, 585
imminent incarceration of the soft midfoot osteotomy-arthrodesis, 578–583
tissue, 1236 plantar fascia release, 573, 574
inadequate reduction or fixation, 1251 tendon transfers, 575, 577
indications for surgical treatment, 1234 triple arthrodesis, 585, 586, 589, 590
internal fixation of facture- Cedell fractures, 1279
dislocations, 1247 Cellular imbalance, 947–948
intra-articular, 1229 Centre of rotation and angulation
intra-articular fracture, 1232 (CORA), 752–755
“joint depression type” fractures, 1234 Charcot-Marie-Tooth (CMT) disease, 911
medial facet, 1230 Charcot Marie Tooth neuropathy, 321, 322
nonoperative treatment, 1235 Charcot’s neuroarthropathy (CN)
pathomechanics, 1230–1231 Achilles lengthening, 998
percutaneous reduction and screw amputation, 1005
fixation, 1237 arthrodesis-joint fusion, 999–1001,
polytraumatized patients, 1236 1003, 1005
postoperative care and rehabilitation, classification, 992–994
1249–1250 complications, 1005
skin incision, 1238 definition, 989
subtalar joint, 1230 diagnosis, 994–996
surgical techniques, 1229 exostectomy-bony prominence resection,
sustentaculum and reduction, 1239 999, 1000
sustentaculum tali and at the history, 989
tuberosity, 1230 physiopathology, 990, 991
time to surgery, 1236 prevalence, 990
tuberosity reduction and restoration of the treatment
medial wall, 1239 conservative treatment, 996, 997
12-point fracture scale, 1234 goal, 996
Index 1389
surgical treatment, 997, 998 percutaneous tenotomy of the Achilles

Chevron-Austin osteotomy, 390 tendon, 149, 150
Chevron technique, 391, 392 procedure, 146–148
Child’s torsional profile, 120 recurrence, 152–154
Chondral lesions x Osteochondral subtalar kinematics, 138
lesions, 1076 syndromic clubfoot, 155
Chondroblastoma, 76, 77 transcription factors PITX1-TBX4, 136
Chondrocyte Autologous Implant (ACI), treatment, 140
1086–1088 two-handed manipulation technique,
Chondrocyte autologous implant for the 140, 142–145
treatment of extensive Coleman test, 332
osteochondral lesions, 1087 Collateral ligaments (CL), 474–476
Chondrogenesis by Autologous Columnar stabilization in multiple or complex
Matrix, 1089 fractures with soft tissue
Chondrosarcomas, 84 involvement, 1348
Chopart joint injury, 1285–1287, 1289, 1292 Comminuted fractures, 1304
Chopart’s amputation, 827–829 Comminuted scaphoid fracture, 1297
Chopart’s joint, 1294 Common peroneal nerve, 1010, 1011
Chronic Achilles tendon ruptures, 1154–1158, Compartment syndrome of leg
1160, 1161 anterior intermuscular septum, 1373
Chronic hyperextension, 475 arterial line pressure monitor, 1371
Chronic regional pain syndrome, 120 circulatory alteration, 1368
Chronic rupture Achilles tendon clinical examination, 1371
ruptures (ATR) complications, 1367, 1377
with percutaneous technique, 1162 CPK, 1372
Cierny-Mader classification, 778 diagnosis, 1367, 1370–1372
Claw deformity, 1389 incidence, 1368
Claw toe, 482 indicators, 1371
Claw toe and hallux correction, 1380 intracompartmental pressure, 1368
Claw toes, 1377, 1380, 1388 legal defense of the medical
Clinical Gait Analysis, 4 personnel, 1368
Closed distal tibia fracture, 1325 lymphatic and arterial system, 1368
Clubfoot, 328–330 medial approach, 1374
abductor splint, 150, 151 monitoring methods, 1371
articular facets, 137 mubarak and hargens technique,
CASP gene family, 136 1373–1375
classification, 139 near infrared spectroscopy, 1371
collagen family, 136 necrosis of the tissues, 1368
complex clubfoot, 154 technological advances, 1370
corrected feet and long-term tibia-peroneal fractures, 1373
follow-up, 153 treatment, 1372
diagnosis, 134, 135 Compartment syndrome of the foot (CSF),
etiology, 135, 136 1380, 1382–1384, 1386–1390
functional anatomy, 137 Complementary imaging evaluation, 1134
genetics, 136 Complex clubfoot, 154
histological and imaging studies, 134 Complex regional pain syndrome (CRPS),
HOX gene family, 136 757, 1127
HOXD13, 136 Computed Axial Tomography (CT),
hypoplasia or vascular alterations, 135 1308–1309
kinematic coupling, 138, 139 Computed tomography or MRI of muscle
materials, 145, 147 atrophy and fatty degeneration in
normal anatomy, 137 rotator cuff pathology, 1157
one-handed technique, 144–146 Concurrent calcaneal osteotomy, 171
1390 Index
Congenital and developmental hip description, 945

subluxations, 118 diagnosis, 948–950
Congenital deformities, 119 etiology - pathophysiology, 946–948
Congenital fibular deficiency. See Fibular infected plantar neuropathic ulcers,
hemimelia (FH) 952, 953
Congenital talipes equinovarus. See Clubfoot non-Infected plantar neuropathic ulcers,
Consolidated remodeling osteotomy and 950, 952
metatarsal parabola, 1342 prevalence, 946
Consolidation delays or formal nonunions, 349 Diabetic neuropathy, 946, 1021
Corticosteroids, 731 Diaphyseal and distal fractures of the 5th
Cotton osteotomy, 549 metatarsal, 1343
C-reactive protein (CRP), 781 Diaphyseal fracture of the first
Crushing, 1289 metatarsal, 1340
Cuboid approach, 1298 Diaphyseal fractures of the 5th
Cuboid approach and visualization, with metatarsal, 1343
ostesynthesis with perimetral Diffuse ankle osteoarthritis
plate, 1298 anatomy
Cuneiform osteochondrosis, 210 bony elements, 728
Cuneometatarsal joint damage, 1348 ligaments, 729
Curly toes, 294 conservative management, 730, 731
bilaterality, 295 diagnosis, 730
Butler procedure, 296, 297 etiology, 727
conservative management, 295 range of motion, 729, 730
definitive surgical treatment, 295 rotational axis, 729
externally rotation, 294 surgical treatment
fixed flexion deformity, 295 ankle arthroplasty, 739–742
incidence of, 294 ankle fusion, 732–734, 736, 738, 739
mild or dynamic forms, 296 distraction arthroplasty, 731, 732
severity of, 295 fusion vs. arthroplasty, 742–744
strapping / taping method, 295 Diparesia, 316
symptom, 295 Direct lateral approach, 1243
with a V to Y skinplasty, 296 Distal gastrocnemius tenotomy, 880–882
Distal interphalangeal (DIP) joint deformity
flexible DIP flexion deformity, 482
D flexion PIP joint (PIP) flexible, 482
Davey technique, 1375–1376 flexion rigid PIP, 483, 484
De Cuveland’s disease, 210 MP dorsal flexion deformity, 485–487
Deep gastrocnemius-soleus recession, rigid DIP flexion deformity, 482
882, 883 Distal metatarsal osteotomy, 60
Deep soft tissue and bone infections, 1250 Distal tibia fracture with medial
Degenerative” theory, 1143 malleolus, 1326
Degree of deformity in the frontal plane, 385 Distal tibia fractures
Degree of joint surface inclination anatomy, 338
(DMAA), 386 conservative treatment, 339, 340
Degree of pronation of the medial column, 386 diagnosis, 338, 339
Deltoid reconstruction, 551 etiology, 338
Developmental deformities, 119 orthopedic treatment, 341
Developmental equinocavovarus foot pathophysiology, 338
deformity, 119 post reduction handling, 342, 343
Diabetes mellitus (DM), 945 rehabilitation, 343
Diabetic foot syndrome surgical management, 343–347
classification, 945 treatment, 346–348
definition, 945 yesotomy, 342
Index 1391
Distal tibio-fibular syndesmosis, 1183 Evident lisfranc injuries, 1305

Distraction arthroplasty, 731, 732 Ewing sarcoma, 85
Distraction osteogenesis (DO) Exostectomy, 57, 58
classic bone transport, 807, 808 Extensile lateral approach, 1243–1245
corticotomy, 807 Extensor digitorum brevis (EDB), 473
gradual distraction, 807 Extensor digitorum longus (EDL), 471, 472
Ilizarov method, 806 Extensor hallucis brevis (EHB), 376
motorized endomedullary nail, 812, 813 Extensor hallucis longus (EHL), 376
shortening-lengthening, 810 Extensor hood, 472
transport phase, 807 External fixation, 1329
Distraction wedge osteotomy, 191 External rotation stress maneuver under
Dorsal ligaments of the metatarsal tarsal fluoroscopy, 1183
joint, 1301 Extracorporeal shock waves (ESW), 895
Dorsal talo-navicular ligaments, 1288
Double/triple arthrodesis, 550
Dresden surgical technique, 1151 F
Dynamic electromyography, 17 Fasciotomies in the foot, 1387
Fasciotomy, 1374, 1390
Fasciotomy by anterolateral approach, 1375
E Fibular hemimelia (FH)
Elective surgical wounds bilateral vs. unilaterla cases, 215
incisions, 94 classification, 216, 218–225
iNPWT, 97, 99 clinical assessment, 225
location of incision, 93, 94 clinical manifestations, 215
suture materials, 95 external fixation, 241
suture removal, 99 formulaic method, 216
suturing technique, 95, 96 nonsurgical treatment, 265, 266
wound and scar care management, 99, 100 outcomes, 269–271
wound dressing, 97 phenotype, 216
Emergency fasciotomy, 348 post-surgical care, 268, 269
Enchondromas, 77, 78 principles of treatment, 229–232, 236
Endochondral ossification process, 199 radiographic assessment, 225–236
Endocrinopathies, 1125 surgical technique
Endomedullary fixation with Kirschner Paley Type 1, lengthening for, 237,
wires, 1344 239–242, 244, 245, 247
Endoscopic approach for diagnosis and Paley Type 2, lengthening plus ankle
treatment of posterior ankle realignment, 246
pathology, 1115, 1116 Paley Type 3, lengthening plus
Entrapment of ankle soft tissues, 1054 SUPERankle reconstruction,
Epiphysiodesis, 220, 226, 230, 270, 307, 308 247–249, 255–257, 261, 262, 265
Equine foot, 327 Fifth metatarsal nonunion
Equinus, 318, 874 or refracture, 1360
Equinus-cavo-varus 5th metatarsal-phalangeal (MTP-5) angle, 523
conservative management, 327, 328 Fifth metatarsal resections, 525
surgicalmanagement, 331, 332 Fifth metatarsal stress fracture, 1361
Equinus-cavus-varus, 318, 319 First metatarsal fracture, 1336
deformity, 319 First metatarsophalangeal joint (MTPJ), 412
Equinus-plano-valgus, 320, 321 arthrodesis, 969
conservative management, 327 arthroplasty, 970
surgical management, 330, 331 articular preservation, 968, 969
Erythrocyte sedimentation rate (ESR), Fishmouth technique, 823–826
781, 782 Fixation with plates, 1345–1347
Evans osteotomy, 330, 331 Flatfoot, 118, 121
1392 Index
Flexible flatfoot interosseous membrane route, 912,

anatomy, 183 914–918, 920
clinical characteristics, 182 medial incision, 935, 936
diagnosis navicular transfer, 926–938
conservative treatment, 190 peroneal tendon injury, 925–931
history, 184 Foot-CORA method, 123, 124
imaging, 185, 186 Forefoot driven hindfoot deformity
physical examination, 184, 185 alignment view, 678, 680
etiology, 182 conservative treatment, 681
follow-up, 191 braces, 682
indications, 191 physical therapy, 681
lateral column lengthening, 191 shoe modifications, 682
pathophysiology, 182 conventional imaging, 677–679
postoperative protocol, 193 definition, 674
surgical treatment, 191 forefoot-driven hindfoot valgus, 675
Flexor digitorum brevis (FDB), 473 forefoot-driven hindfoot varus, 674
Flexor digitorum longus (FDL), 472, 1161 functional testing, 676, 677
Flexor digitorum longus (FDL) tenotomy, 299 inspection, 675
Flexor digitorum longus (FDL) transfers, MRI and computed tomography, 680, 681
1040–1041 palpation, 675, 676
Flexor hallicus longus (FHL), 1040–1041 surgical treatment
Flexor hallucis longus (FHL) transfer, 850 forefoot-driven hindfoot
Flexor hallucis longus tendon (FHL), valgus, 684–689
375, 918–923 forefoot-driven hindfoot
Flexor hallucis longus tendon transfer, 1163 varus, 682–684
Flexor tenotomies, 1389 Forefoot rocker, 9
Focal dome osteotomy, 248 Forefoot varus/supination, 549
Foot and ankle biomechanics Formulaic method, 216
biological phenomena, 4 Fracture of the fifth metatarsal tuberosity
gait study, 13–16 (zone 1), 1355
human gait, 4–10 Fracture of the metatarsal bones, 1333, 1335,
intrinsic and extrinsic function, 3 1336, 1340, 1344, 1347, 1350,
kinematic and kinetic recordings, 16–21 1354, 1359
mechanical functioning, 10–13 Fracture pattern, 1216
practical applications, 21 Fractures of the head, 1277–1278
resources, 21 Fractures of the medial malleolus, 1180,
Foot and ankle offset (FAO), 571 1196–1198
Foot and ankle tendon transfers Fractures of the medial plantar
anamnesis and physical examination, tuberosity, 1248
906, 907 Fractures of the posterior malleolus,
characteristics, 906 1181–1183, 1198–1201
fixation, 907–909 Fracture with comminution of all metaphyseal
imaging tests, 909, 910 pillars, 1220–1223
patient’s expectations, 906 Freiberg’s disease, 205–209, 212
posterior tibial tendon, 909–913 Functional failure, 6
principles, 905 “Functional” procurvatum deformity, 122
requirements, 906
spastic/flaccid paralysis, 905
surgical technique G
chronic Achilles rupture, 923, 924 Gait analysis, 3
EHL, 930, 933, 934, 939 Ganglions, 81
FHL, 918–923 GAPNOT protocol, 1148
Girdlestone-Taylor surgical technique, Gastrocnemius-soleus recession, 878–880
936–938, 940, 941 Gastroc-release, 898–900
Index 1393
Gastroc-soleus complex, 185 stiffness, 384

Giant cell tumor (GCT) of bone, 75 TMT arthrodesis, 399–401
Girdlestone-Taylor (GT) tendon, 485 Hammer and claw toes
Gradual deformity correction, 175 characterization, 297
Graft reconstruction, 1163–1164 complications, 299
Gravity stress radiography, 1179 postoperative flexor tenotomies, 298
Ground reaction force vector (GRF), 6 preoperative, 298
treatment, 297, 299
Hammertoes, 470, 477, 482
H Hammock ligament, 1289
Hallux metatarsophalangeal (MTP) joint, 375 Haraguchi’s classification, 1181
Hallux rigidus Hawkins’ sign, 1275
anatomy and radiological findings, 414, 415 Heel bisector method, 161, 162
conservative treatment, 416, 417 Heel rocker, 18
diagnosis, 415, 416 Heim/Cotton or “hook test”, 1183
etiology Hemiparesis, 317
functional hallux limitus, 412 Hemostasis, 92
structural factor, 412–414 High energy injuries, 1306, 1310
joint preserving procedures High energy malleolar fractures, 1174
dorsal cheilectomy, 418 High energy trauma fractures of the
metatarsal osteotomies, 418–420 metatarsals, 1348
phalangeal osteotomy, 420 High-volume image guided injections
joint sacrificing techniques (HVIGI), 864
metatarsophalangeal Hindfoot arthrodesis, 1043
arthrodesis, 423–425 Hindfoot arthrodesis procedures, 191
metatarsophalangeal Hindfoot valgus deformity, 546, 547
arthroplasty, 420–422 Hoke’s technique, 877
metatarsophalangeal Homologous Osteochondral Graft (Allograft),
hemiarthroplasty, 422 1084, 1085
polyvinyl alcohol implant, 422, 423 Human gait, 3–10
resection and interposition Human Walking, 4
arthroplasty, 425 Hyaluronic acid (HA), 863, 864
Hallux valgus (HV) Hypertrophic or keloid scar, 108
anatomy, 374–376 Hypertrophic scar, 106
conservative treatment, 384
diagnostic imaging, 375, 379–383
history, 378 I
physical examination, 378 Iatromechanics, 4
physiopathology, 376–378 Ilizarov method, 806
surgical complications, 402–404 Imaging
surgical treatment computed tomography, 34–36
decision making, 382, 383, 385–388 fluoroscopic techniques, 27
diaphyseal osteotomies, 395, 396 gravity stress view projections, 27
distal extracapsular, 392–395 magnetic resonance imaging, 37–41
distal intracapsular, 390–392 radiography, 25–28
exostectomy, 389, 390 Single Photon Emission Computed
metatarsophalangeal arthrodesis, Tomography-Computed
400, 401 Tomography, 36, 37
objectives, 385 stress projections, 27
phalanx osteotomy, 400–402 tomosynthesis, 28, 29
postoperative dressing, 402 ultrasound, 29–33
proximal osteotomies, 397–399 Implant removal combined with subtalar
skeletal alignment, 387 arthrolysis and tenolysis of the
soft tissue technique, 390 peroneal tendons, 1250
1394 Index
Incisional negative pressure wound therapy Joint reduction, 1217

(iNPWT), 97, 98 Juvenile arthritis, 212
Incisional negative pressure wound therapy
(NPWT), 98
Induced membrane technique, 812, 814, 816 K
Infant cerebral palsy (ICP), 316–318 Kager’s fat, 1163
Inferior calcaneonavicular (ICN) Keloid scar, 107
ligament, 541 Kinematic gait measurements, 4
Infrapatellar approach, 1325 Kite technique, 139
Infrasyndesmal fractures of the fibula, 1190 Köhler disease, 204, 205
Insertional Achilles tendinopathy Krackow technique, 1158
conservative treatment, 847 Kump’s hump, 356
corticosteroids infiltration, 848
debridement and Achilles reinsertion, 849
endoscopic and minimally invasive L
techniques, 848, 849 Lapidus technique, 399–401
epidemiological data, 845 Lateral column lengthening (LCL), 547–549
FHL transfer, 850 Lateral condylectomy, 525
measurement, 846 Lateral ligament of lisfranc or Liverpool
overweight and hindfoot deformities, 845 ligament, 1302
pathology, 845, 846 Lateral plantar fascia, 191
physical therapy, 847 Lauge Hansen classification, 1170
postoperative care, 851 Ledderhose disease, 81
pump bump, 846 Left foot central polidactily, 303
surgical technique, 849 Lesser toes
surgical treatment, 848 anatomy, 471
SWT, 847 complications, 490–492
Insertional tear of the peroneus brevis, 1029 correction options, 481
Insulin-like Growth Factor 1 (IGF-1), 1078 diagnosis, 476–478
Interdigital nerves, 1020, 1021 DIP joint deformity (see Distal
Interosseous ligament, 137 interphalangeal (DIP) joint
Interosseous (IO) muscles, 472–474 deformity)
Interosseous route (IO), 910 etiology, 470, 471
Interosseous talocalcaneal ligament, 137 extrinsic musculature
Interphalangeal (IP) joint, 471 EDL, 471, 472
Intraarticular and tibial deformity, 174 FDL, 472
Intraarticular compromise of the fracture, 1338 5th toe deformity, 490
Intraarticular fracture, 1338 intrinsic musculature
Intracompartmental pressure, surgical collateral ligaments, 474–476
decompression, 1385 EDB, 473
Intractable plantar keratosis (IPK), 443 FDB, 473
Intramedullary canal, 1359 interosseous muscles, 472–474
Intramedullary screw fixation, 1355 lumbrical muscles, 473
Intraosseous lipomas, 80 plantar plate (PP), 474
Inverted flaps (turndown), 1159 minimally invasive surgery
Irrigation, 90 dorsal MP joint, 487, 488
Iselin’s disease, 209, 210 postoperative bandage, 485
Isolated fractures of the sustentaculum tali, 1231 rigid and flexible DIP flexion
Isolated peroneus longus tears, 1030 deformity, 487
rigid and flexible PIP flexion
deformity, 487
J non-surgical treatment, 479–481
Joint Cartilage Replacement, 1082, 1083, pathophysiology, 471
1085, 1086 PIP arthrodesis, resorbable
Joint instability and repeated traumas, 1077 pin, 488–490
Index 1395
treatment lesions, 1299

functionality of, 479 Lisfranc lesions
gait alteration, 479 diagnostic protocol, 1310
pathology, 479 Lisfranc occult lesions, 1303
Lesser toes deformities Loaded radiographs, 1307
curly toes, 294 Localized osteoarthritis of the
bilaterality, 295 ankle (LOA)
Butler procedure, 296, 297 clinical analysis, 702–705
conservative management, 295 complications, 724
definitive surgical treatment, 295 distraction arthroplasty, 695
externally rotation, 294 etiology and pathophysiology, 696–702
fixed flexion deformity, 295 mechanical analysis
incidence of, 294 alignment of the foot, 710
mild or dynamic forms, 296 mechanical situations, 705
severity of, 295 neutral ankles, 706
strapping / taping method, 295 subtalar joint, 709, 710
symptom, 295 symmetry of ankle joint, 708, 709
with a V to Y skinplasty, 296 talar anterior/posterior subluxation,
hammer and claw toes 707, 708
characterization, 297 talar tilt, 708
complications, 299 varus/valgus ankles, 706, 707
postoperative flexor tenotomies, 298 prevalence, 696
preoperative, 298 published results, 722
treatment, 297, 299 surgical treatment
macrodactyly, 308 anterior/posterior mechanical overload
bone and soft tissue debulking, 310 of the ankle, 721–724
etiology, 306 lateral mechanical ankle
incidence, 306 overload, 711–717
indications, 308 medial ankle mechanical
management, 307 overload, 717–721
postop clinical image, 311 Longitudinal medial arch, 159
postop x-ray, 312 Long oblique osteotomy, 1341
preop planning, 309 Lower extremities, teleradiography, 348
preop x-ray, 310 Lower limbs, 4–5
primary and secondary, 306 causes of, 1009
overlapping toe, 300, 301 clinical complaint, 1009
polydactyly, 302 common peroneal nerve,
classification, 302, 303 1010, 1011
diagnosis, 303 deep peroneal nerve, 1011–1014
etiology, 302 diabetic neuropathy, 1021
imaging evaluation, 304 differential diagnoses, 1009
incidence, 302 electromyographic study, 1009
left foot central polidactily, 303 interdigital nerves, 1020, 1021
management, 304, 305 lateral plantar nerve-baxter nerve,
pathophysiology, 302 1018, 1019
zone of polarizing activity, 302 medial digital nerve of the
Ligament injuries, 1292 hallux, 1020
Ligamentoplasty, 1058 medial plantar nerve, 1019, 1020
Limb length discrepancy, 220 saphenous nerve, 1014, 1015
Lipoma, 82 solear arch syndrome, 1011
Lisfranc-Chopart joint injuries, 1292 superficial peroneal nerve,
Lisfranc joint 1012, 1014
intraoperative postoperative yawning sural nerve, 1015
fluoroscopy, 1314 tibial nerve, 1015–1017
Lisfranc joint injury, 1302 with stable hip, knee, and ankle, 229
1396 Index
M proximal osteotomies, 457, 458

Macrodactyly, 308 second rocker (non-propulsive
bone and soft tissue debulking, 310 metatarsalgia), 456
etiology, 306 third rocker (propulsive metatarsalgia),
incidence, 306 458, 459
indications, 308 triple Weil osteotomy, 459–461
management, 307 third rocker/propulsive phase, 447, 448
postop clinical image, 311 Metatarsophalangeal capsulotomy, 59
postop x-ray, 312 Metatarso-phalangeal (MTP) joint, 297, 470,
preop planning, 309 471, 961
preop x-ray, 310 Metatarsus adductus, 386
primary and secondary, 306 anatomy, 160
Magnetic Resonance Imaging (MRI), 1309 anteroposterior (AP) radiographs, 160, 161
Maisonneuve injury, 1173 clinical diagnosis, 160, 161
Mallet toe. See Distal interphalangeal (DIP) etiology, 159
joint deformity incidence, 159
Malunion and pseudoarthrosis, 1299 non-operative management, 162, 163
Malunion of the first metatarsal, 1339–1340 plantar and posterior photographs, 160
Masquelet” technique, 812, 814, 816 surgical management, 163, 164
Materials and fixation methods, 1356 Micro-fractures at the bottom of the
Matles test, 1146 osteochondral talar lesion, 1081
Medial approach, 1337 Microinstability of the ankle, 1062–1063
Medial displacement calcaneal osteotomy Microinstability or ankle instability, 1062
(MDCO), 546, 547 Midfoot/forefoot abduction
Medial oblique (MO) view, 521 deformity, 547–549
Medial or posterior malleolus fracture, 1180 Midfoot injuries
Medial pilon fracture, 1218–1219 Lisfranc joint injury, 1286, 1287, 1292,
Medial Plantar Approach, 1248 1296, 1299
Meggitt-Wagner System, 947 Midfoot inversion, 1353
Mercedes-Benz sign, 364 Midfoot wedge resections, 175
Mesenchymal stem cells, 1088, 1089 Minimally invasive and endoscopic
Metallic implants, 1090 procedures, 1163
Metaphyseal filling with bone graft, 1217 Minimally Invasive Techniques: Percutaneous
Metastatic disease, 86 and Mini-open, 1150–1153
Metatarsal epiphysis, 275 Mini-open techniques, 1150
Metatarsal fractures, 1333, 1335, 1336, 1340, Mini open technique using autologous
1344, 1346, 1349, 1353, 1356, 1360 hamstring tendons, 1164
Metatarsalgia Modified Dresden technique, 1150
conservative treatment, 455, 456 Modified Jones procedure, 174
first rocker, 447 Molecular diagnostics methods, 788, 789
management, 463, 465, 466 Morton’s neuroma
mechanical disturbance, 446 anatomy, 496–500
physical exploration, 449–453 conservative treatment
radiological examination, 451, 453–455 hyaluronic acid, 507
second rocker, non propulsive, 447, 448 improvements, 508
surgical treatment infiltrations, 506, 507
cervico-cephalic Weil, 459–461 orthotics, 506
distal osteotomies, 458 shock waves, 508
gastrocnemius lengthening, 456, 457 diagnosis
goal of, 456 clinical presentation, 500–502
iatrogenic (mixed metatarsalgia), imaging study, 502–504
462, 464 differential diagnosis, 504
mini invasive metatarsal osteotomies, epidemiology, 496
462, 463 erythema nodosum, 513
Index 1397
failure rate, 512 Neck fractures, 1264–1275

pathological anatomy, 505, 506 long-term functional outcomes, 1280
revision surgery, 511, 513, 514 Negative pressure wound therapy
surgical treatment (NPWT), 97, 98
benefit, 508 Neisseria gonorrohoeae, 770
dorsal longitudinal approach, 505, Neurogenic flatfoot, 196
509, 510 Neurologic foot
endoscopic decompression, 509 Charcot marie tooth neuropathy, 321, 322
metatarsal osteotomy, 509 clubfoot, 328–330
neurectomy, 508 equine, 327
plantar approach, 509–511 equinus, 318
postoperative management, 512 equinus-cavo-varus
surgical resection, 508 conservative management, 327, 328
Motor disorder, 316 surgical management, 331, 332
Motorized endomedullary nail, 812, 813 equinus-cavus-varus, 318, 319
Motorized instruments, 45–47 :deformity, 319
Mulder’s sign or click, 501, 502 deformity, 319
Müller Weiss disease (MWD) equinus-plano-valgus, 320, 321
clinical examination, 626 equinus-plano-valgus
diagnosis, 626 conservative management, 327
epidemiology, 618–620 surgical management, 330, 331
imaging studies, 626, 627 infant cerebral palsy, 316–318
pathomechanics, 620–625 muscular dystrophies, 324, 325
treatment neuromuscular diseases, 316
arthrodesis, 629–631 spinal dysraphia, 322–324
conservative treatment, 628, 629 Neuromuscular diseases, 316
joint preservation osteotomies/ Newton’s laws, 3
surgery, 631–635 Newton’s third law, 15
surgical, 629 Non-absorbable materials, 95
Multiple drilling in the talar osteochondral Non-ambulatory children foot
lesion, 1080 deformities, 317
Multiple Hereditary Exostosis (MHE), 78 Non-comminuted anterior pillar, 1222
Multiple metatarsal fracture, 1381 Non-comminuted medial pillar, 1222
Multiple metatarsal involvement, 1353 Non-comminuted posterior pillar, 1222
Multiple reconstructions with autografts, 1164 Non-displaced type 2 fractures, 1134
Multiplier app, 226 Non-insertional Achilles tendinopathy
Muscle imbalance, 119 anatomy, 859, 860
Muscular dystrophies, 324, 325 clinical diagnosis, 861, 862
Muscular interstitium, 1368 clinical presentation, 861
Musculoskeletal tumors conservative management, 862–864
anatomy, 72 history, 860
biopsy, 74 incidence, 861
clinical presentation, 72, 73 instrumental diagnosis, 862
epidemiology, 71, 72 surgical management, 864–866
imaging, 73, 74 Non-union or refracture, 1359
principles of treatment, 75 Nutcracker effect, 624
Musculo-tendinous junction, 860 Nutritional and hormonal replacement, 1128
N O
Navicular fractures, 1290 Occult Unstable, 1312
Naviculo-cuneal and calcaneocuboid OCL Algorithm, 1093
joint, 1384 One-handed technique, 144–146
Naviculocuneiform joint, 1132 Open AT gap debridement, 1158
1398 Index
Open AT repair using the Krackow anatomy and biomechanics, 639

technique, 1158 biomechanics, 642
Open midfoot and forefoot fracture due to block grafting, 642
high energy trauma, 1352 conservative treatment, 641
Open reduction and internal fixation of the history, 640
fracture with plates, 1347 image evaluation, 640
Open repair, 1154 internal fixation, 645–647
Open surgical drainage, 775 intervention, 641
Open surgical techniques, 1115 post-operative protocol, 641
Open tenorrhaphy, 1149 results, 648
Open vs. minimally invasive surgery surgical management, 641
advantages, 56 surgical technique, 642–646
anatomy technical considerations, 647, 648
approach angle, 49 talonavicular joint
approach path, 49, 51 anatomy and biomechanics, 648, 649
incision, 48, 49 approach for, 650
bone clinical, 649
healing disorders, 66 image evaluation, 649
secondary displacement of immobilization, 654
osteotomies, 65, 66 internal fixation, 650
disadvantages, 56 Muller-Weiss disease, 650
intraoperative preparation, 51, 52 results, 651, 652
motorized instruments, 45–47 surgical procedures, 649
percutaneous surgical technique, 57 technical considerations, 650–652
preoperative anatomy, 51 treatment complications, 653
radiological control instruments, 47 tarso-metatarsal arthrosis
soft tissues anatomy and biomechanics, 659
cutaneous, 62, 63 conservative treatment, 661
deep infection, 65 physical examination, 659–661
deep vein thrombosis, 65 radiographic exams, 659–661
edema, 64 surgical treatment, 661–667
joint stiffness, 64 Osteoarticular deformities, 947
neurovascular lesions, 63 Osteochondral ankle injuries, 1078
tendinous, 63 Osteochondral Autologous Graft, 1082,
surgical planning, 57 1084, 1086
surgical technique Osteochondral lesions of the distal tibia, 1090
bandaging, 61 Osteochondral lesions of the talus, 1069–1072,
distal metatarsal osteotomy, 60 1074, 1075, 1077, 1078, 1082,
exostectomy, 57, 58 1084, 1086, 1088, 1090, 1092,
metatarsophalangeal capsulotomy, 59 1094, 1098, 1100
proximal phalanx, 61 Osteochondral Talus Injury in the Immature
surgical treatments, 44 Skeleton, 1094
Orthopedic Treatment, 1336 Osteochondritis dissecans, 1100
Orthoses, 731 Osteochondromas, 78
Osteoarthritis, 1226 Osteochondrosis
Osteoarthrosis Cuneiform disease, 210
calcaneocuboid joint De Cuveland’s disease, 210
anatomy and biomechanics, 654, 655 diagnosis, 201, 202
indications, 655 1st metatarsal
lateral column lengthening, 656 base of, 211
results, 657, 658 head of, 211
surgical technique, 655, 656 Freiberg’s disease, 205–209
subtalar joint Iselin’s disease, 209, 210
Index 1399
Köhler disease, 204, 205 Peritalar subluxation/dislocation, 550

multiple local factors, 200 Peroneal artery, 90
regulation mechanisms, 200 Peroneal tendon tears, 1033
sesamoid, 211 classification systems, 1035
Sever’s disease, 202–204 conservative treatment, 1027, 1035
specialized growth cartilage, 199 debridement and repair, 1036
Thiemann’s disease, 212 distal tenodesis or transfer, 1038
Osteodesis, 1298 examination findings, 1031
Osteosarcoma (OS), 84 MRI, 1032, 1033
Osteosynthesis, 349, 1339 operative technique of peroneus
Osteosynthesis material, 1315 brevis, 1037
Osteosynthesis of fractures, 1295 pathophysiologic and pathoanatomic
Osteosynthesis of the calcaneus, 1390 patterns of tears, 1028
Os trigonum syndrome, 1113, 1118 pathophysiology, 1028
Overlapping toe, 300, 301 peroneus brevis and peroneus longus, 1036
plain film radiography, 1032
retromalleolar groove or retinaculum, 1037
P soft tissue irritation, 1036
Painful edema, 1384 tendons with small reconstructable
Pain with resisted eversion, 1031 tears, 1036
Palpation of the GAP, 1146 tendoscopy, 1035
Pan-arthrodesis, 983 ultrasound, 1033
Parabolic arch, 275 undiseased cadaver tendon, 1036
Para patellar approach, 1327 with lateral ankle pain, 1027
Paresthesia, 1371 Peroneal tendon tears on MRI, 1034
Particulate juvenile cartilage, 1090 Peroneus brevis, 1028, 1029, 1162
Particulate Juvenile Joint Cartilage, 1089 Peroneus brevis and peroneus longus
Passive hallux motion, 1115 tears, 1042
Pathological scar, 106–108 Peroneus brevis tears, 1028
Pediatric diaphyseal tibia Peroneus brevis to longus tenodesis, 1037
anatomy, 338 Peroneus brevis transfer, 1162
conservative treatment, 339, 340 Peroneus longus tear, 1030
diagnosis, 338, 339 Peroneus longus tendon, 1030
etiology, 338 Pes cavus, 697
orthopedic treatment, 341 Peyronie’s disease, 81
pathophysiology, 338 Physical therapy, 1249
post reduction handling, 342, 343 Pirani score, 140
rehabilitation, 343 Pirogoff amputation, 826
surgical management, 343–347 Planovalgus deformities, 1031
yesotomy, 342 Plantar fasciitis (PF)
Pediatric foot deformity anatomy, 890
biomechanics principles, 115–118 clinical presentation - diagnosis, 892, 893
clinical assessment principles, 118–126 definition, 889
management principles, 126–131 epidemiology, 890–892
Penetrating trauma, 1370 gastrocnemius release, 898–900
Percutaneous and arthroscopically-assisted imaging study and complements, 894
technique, 1059 non-surgical treatment, 894–896
Percutaneous repair, 1154 pathomechanics, 892, 893
Percutaneous tenotomy of the Achilles tendon, plantar fasciotomy, 896–898
149, 150 surgical treatment, 896
Peripheral arterial disease, 946 Plantar fibromatosis, 81
Peritalar instability, 700 Plantar-medial soft tissue release (PMR), 129
Peritalar stability, 699 Plasma rich in growth factors, 1078
1400 Index
Plastic surgeon, 105, 106 Posterolateral posterior approach, 1221

Platelet-derived Growth Factor (PDGF), 1078 Postoperative protocol in process
Platelet-rich plasma (PRP), 731 fractures, 1280
Plate-rich plasma (PRP), 895 Postoperative rehabilitation for peroneal
Plating tibial fractures, 1327–1329 tendon reconstruction, 1044
Poikilothermy, 1371 Post reduction handling, 342, 343
Poland’s hump, 356 Primary subtalar fusion, 1248
Polydactyly, 302 Procalcitonin (PCT), 766, 782
classification, 302, 303 Process fractures, 1278
diagnosis, 303 Procurvatum/recurvatum
etiology, 302 deformity, 122
imaging evaluation, 304 Progressive cavovarus foot
incidence, 302 deformities, 128
left foot central polidactily, 303 Progressive collapsing foot deformity
management, 304, 305 (PCFD)
pathophysiology, 302 anatomy, 540, 541, 558, 559
zone of polarizing activity, 302 ankle instability, 551
Polymerase chain reaction (PCR), 789 conservative management, 559
Polyvinyl alcohol (PVA), 422, 423 conservative treatment, 545, 546
Ponseti method, 140, 152 diagnosis
Ponseti technique, 139, 143 clinical examination, 541, 542
Posterior ankle arthroscopy, 1116, 1119 clinical staging, 543–545
Posterior ankle endoscopy, 1116 radiographs, 542–544
Posterior ankle impingement (PAI), etiology, 540
1111–1114 flexor tendon transfer, 552
athletes during season, 1118 gastrocnemius recession/Achilles tendon
avulsion of the posterior talo-fibular lengthening, 552
ligament, 1112 hindfoot valgus deformity, 546, 547
computed tomography, 1114 midfoot/forefoot abduction
corticoid injections, 1118 deformity, 547–549
diagnosis, 1114 pathophysiology, 540, 558
diagnosis and treatment, 1119 peritalar subluxation/dislocation, 550
endoscopic management, 1119 spring ligament reconstruction, 552
4.0-mm aggressive soft-tissue surgical management
shaver, 1117 calcaneonavicular and tibiospring
hindfoot conventional endoscopic components, 561
portals, 1116 FiberTape®, 561–565
imaging assessment, 1113 index procedure, 566
magnetic resonance imaging, 1114 Internal Brace System (Arthrex®),
nuclear medicine bone scintigraphy, 1114 561, 562
open and arthroscopic debridement, 1119 isolated spring ligament injury, 560
physical examination, 1114 medial ligament
posterior ankle debridement, 1117 reconstruction, 563–565
treatment, 1115 spring ligament repair, 560, 561
treatment to surgery, 1118 Swivelock®, 561, 563
Posterior ankle syndrome, 1115 surgical plan, 546
Posterior pilon fracture, 1219–1220 tarsometatarsal joint fusion, 549
Posterior tibial artery, 90 treatment complication, 553, 554
Posterior tibialis tendon (PTT), 906 Prosthetic-mediated reconstruction, 216
Posterior tibial tendon (PTT), 577, 909–913 Proton density (PD) sequences, 38
Posterior tibial tendon (PTT) dysfunction Proximal articular fractures, 1348
(PTTD), 976 Proximal 5th metatarsal fracture, 1348, 1352
Index 1401
Proximal gastrocnemius tenotomy, 883–885 arthrodesis, 979, 980

Proximal phalanx, 61 osteoarticular, 979
Pseudodorsiflexion, 7 clinical presentation, 959, 964–966
Push-up test, 168 complications
risk factors, 982
total arthroplasty, 982
Q TTC, 983
Quadratus plantaris, 1387 connective tissue diseases–
Quatrimalleolar fracture, 1201, 1202 mesenchymopathies, 964
conservative treatment, 967
diagnosis, 963, 964
R DMARDs, 960
Radiographs with monopodal loading, 1308 first metatarsophalangeal joint
Radiological control instruments, 47 arthrodesis, 969
Reconstruction for concomitant tears of arthroplasty, 970
peroneus brevis and longus, articular preservation, 968, 969
1039–1040 forefoot, 961–963, 968
Reconstruction of the superior peroneal hindfoot
retinaculum, 1039 joints, 976–979
Reconstruction with grafts, 1163 soft tissues, 975, 976
Recurrent clubfoot deformity images, 966, 967
anterior tibia closing wedge lesser metatarsals, joint reconstruction,
osteotomy, 598 973, 974
extensor tendons, 611, 613 lesser metatarsals, resection, 971–973
flexion contracture, 614, 615 lesser toes, 974, 975
nitroglycerin paste, 615 midfoot, rearfoot and ankle, 961, 962
patient evaluation, 596–598 mild to moderate deformities, 980, 981
Ponseti treatment, 595, 596 prevalence, 959
posterior and anterior tibial tendons, 614 severe deformities, 981
talectomy, 603–605, 607, 608, 611, 614 surgical treatment, 967, 968
triple arthrodesis, 600–603 symptoms, 960
Recurvatum gait, 17 tarsometatarsal joint, 970, 971
Reduction and Fixation of Osteochondral tenosynovitis, 960
Fragments, 1078 Rigid deformity, 550
Reduction and synthesis of diaphyseal Rigid flatfoot
fractures of the metatarsal with calcaneonavicular coalition, 195, 196
retrograde intramedullary neurogenic flatfoot, 196
pinning ., 1344 talocalcaneal coalition, 194, 195
Reflex sympathetic dystrophy syndrome, 1127 Rotational deformity, 750
Regenerative Cell Therapy, 1086–1090 Rotational instability of the ankle, 1063–1064
Rehabilitation, 343, 1165 Rüedi and Allgöwer’s principles, 1217
Repaired cartilage, 1092–1100 Ryerson’s technique, 585
Repair techniques, 1062
Retrocalcaneal bursitis, 975
Retrograde drilling with radiographic S
control, 1082 Sanders type II joint depression, 1239
Retrograde Medullary pinning, 1344–1345 Sanders type III (and IV) fractures, 1240
Reverdin-Isham, 391 Sanders type IV fractures, 1238
Rheumatic diseases, 1127 Sangeorzan classification, 1291
Rheumatoid arthritis (RA), 477 Saphenous nerve, 1014, 1015
Rheumatoid foot Sarcomas, 84
ankle, 963 Sarmiento’s protocol, 1322
1402 Index
Selective fasciotomies, 1376 Soft tissue injuries, 1298

Septic ankle arthritis (SAA) Soft tissue necrosis-wound dehiscence, 1206
antibiotic treatment, 772, 773 Soft tissue sarcomas, 82
arthroscopic ankle drainage, 773, 774 Soft tissue surgery, 53
blood tests, 766 Solear arch syndrome, 1011
clinical outcomes, 775, 776 Spasticity, 317
clinical presentation, 764, 765 Spinal dysraphia, 322–324
diagnostic tools, 766, 767 Spring’s ligament, 1289
differential diagnoses, 770, 771 Squeeze test, 1146, 1147
imaging, 770 Stable occult, 1311
morbidity and mortality, 764 Staphylococcus aureus, 772
open surgical drainage, 775 Static and progressive deformities, 119
pathophysiology, 764 Stem cell therapy, 1088
postoperative rehabilitation protocol, 775 Stimulation of osteochondral talus repair, 1089
serial joint aspiration, 773 STIR sequence (short tau inversion
synovial fluid aspiration and recovery), 38
analysis, 767–770 Strayer’s technique, 330
Sesamoidectomy, 1137 Stress fracture of the metatarsals, 1335
Sesamoiditis Stress fractures (SF)
anatomy, 429, 430 analgesic and anti-inflammatory
circulation, 431, 432 medication, 1132
clinical presentation, 432, 433 analgesic drugs, 1129
definition, 432 anamnesis, 1125
differential diagnosis, 434–436 athletic unpreparedness, 1125
imaging, 434 bone formation and resorption, 1123
pathology, 432 catabolism and bone metabolism, 1123
treatment, 436 classification, 1128
acute and stress fracture, 439, 440 classification according to magnetic
AVN, 440–442 resonance imaging, 1126
bone edema, 440–442 classification of stress fractures according
capsular ligament injuries, 437–439 to their prognosis, 1128
complications of, 443, 444 concept and pathophysiology, 1123
infections, 440 elderly people with sarcopenia, 1125
IPK, 443 ethiopathogenesis, 1124–1125
metatarso-sesamoid arthritis, 441 in athletes, 1135
Sesamoid osteochondrosis, 211 injury mechanism, 1135
Sesamoid stress fractures, 1136, 1137 laboratory evaluation, 1127
Sever’s disease, 202–204 magnetic nuclear resonance, 1127
Shock vessels, 90 magnetic resonance imaging, 1126
Shock wave therapy (SWT), 847 musculoskeletal complaints, 1125
Shoe modifications, 731 non-gradual increase in mechanical
Shortening-lengthening, 810 demand on bone tissue, 1124
Shortening osteotomy realignment distal tibia of the anterior (cervical) region of the
(SHORDT) procedure, 231, 238 calcaneus, 1133
Silferskiold test, 168 of the calcaneus, 1131
Silfverskiold test, 122 of the metatarsals, 1135
Silfverskiöld test, 193, 318, 874 of the navicular, 1132
Silfverskjöld test, 893 of the talus, 1130
Sinus tarsi approach, –, 1237, 1243 orthopedic care service, 1125
Skin integrity, 121 osteoclastic activity, 1124
Soft tissue entrapment, 1052–1056 physical demand, 1128
Soft tissue entrapment as a consequence of an physical examination, 1126
ankle fracture, 1055–1056 prevention and management, 1129
Index 1403
primary and relapse prevention, 1129 approach for, 650

radiographic evaluation, 1126, 1131 clinical, 649
risk factors, 1124 image evaluation, 649
RNM, 1136 internal fixation, 650
tomographic classification, 1132 Muller-Weiss disease, 650
treatment of overloaded bone lesions, 1128 results, 651, 652
weight bearing radiographs, 1126 surgical procedures, 649
Stress fractures of the cuboid, 1134, 1135 technical considerations, 650–652
Stress fractures of the talus, 1129, 1131 treatment complications, 653
Stress radiographs (abduction test), 1308 Talus dislocation, 1282
Subcapital fractures, 1347 Talus fractures
Subchondral cystic lesions, 1076 clinical findings, 1261
Subcutaneous ( SC) route, 910 forced ankle dorsiflexion, 1259
Subluxation, 118 high energy mechanism, 1259
Subtalar joint, 142 morphology, 1257
Subtalar joint arthrodesis, 550 physiopathogenesis, 1259, 1261
Subtalar joint complex, 117 posterolateral tubercle, 1261
Subtalar motion, 121 radiographic study, 1262
Subungual exostosis, 79 talar irrigation, 1258
SUPERankle procedure, 271 Talus osteochondral lesions
Superior medial calcaneonavicular ankle radiographs, 1070, 1073
(SMCN), 541 ankle radiography, 1095
Superior peroneal retinaculum bone marrow stimulation, 1100
reconstruction, 1039 cartilage injury with bone lesion, 1073
Supramalleolar osteotomy, 174 chronic ankle instability, 1070
Supramalleolar osteotomy (SMOT), 707, 708, classification, 1072
713, 714 dorsal joint surface of the talus, 1075
Supramalleolar rotational dome fibrillation and fissures, 1073
osteotomy, 248 foot posture during the static and dynamic
Suprapatellar approach, 1326 support, 1070
Suprasyndesmal lesions, 1193–1195 hypersignal of cartilage at MRI, 1073
Sural nerve, 1015 imaging modality, 1070
Sural nerve branches, 1043 magnetic resonance imaging, 1071–1073,
Surgical or non-surgical (e.g., Ponseti) 1084, 1097
technique, 126 non-surgical treatment modalities, 1077
Sustentacular approach, 1247–1248 osteochondral fragment, 1079
Swing flexion, 18 patient’s age, 1075
Syme amputation, 827 prognosis, 1074
Symptomatic non-anatomic healing, 1281 retrograde perforation, 1100
Synchondrosis of the os trigonum, 1116 surgical treatment, 1078, 1098
Syndromic clubfoot, 155 tibiotalar alignment, 1070
Synovial fluid aspiration, 767–770 treatment, 1077, 1096
Synovial sarcoma, 82 Talus reimplantation, 1282
Tarsal coalition, 183, 215, 220, 221, 226
Tarsometatarsal amputation, 835, 836
T Tarsometatarsal (TMT) arthrodesis, 399–401
Talar fractures, 1257 Tarsometatarsal arthrodesis (TMT)
Talar tilt, 708 techniques, 383
Talocalcaneal (TC) coalition, 194, 195 Tarso-metatarsal arthrosis
Talocalcaneal joint, 137 anatomy and biomechanics, 659
Talocalcaneonavicular joint, 137 conservative treatment, 661
Talonavicular (TN) joint physical examination, 659–661
anatomy and biomechanics, 648, 649 radiographic exams, 659–661
1404 Index
Tarsometatarsal instability, 386 Tibial overload injury, 1127

Tarsometatarsal joint, 970, 971 Tibial pilon fracture
Tarsometatarsal joint disorders, 1299–1302, anterior approach, 1221
1304–1306, 1310, 1313 anteromedial approach, 1221
Tarsometatarsal joint fusion, 549 arthroscopic assistance, 1223
Taylor maps, 90 classification, 1212, 1213
Taylor’s bunion, 519 clinical evaluation, 1214
Tears of the peroneus brevis, 1033 complications, 1225
Tears of the peroneus longus, 1033 conservative management, 1215
Tendinopathies of the Achilles tendon, 1145 definitive fracture management,
Tendo-Achilles Lengthening (TAL), 876–878 1216–1218
Tendon advancement with V-Y flap, 1159 distal fibula, 1214
Tendon defect, 1159 emergency external fixation, 1216
Tendon mobilization and end-to-end suturing, external fixation, 1224
1158–1159 fracture with compromise and impaction of
Tendon transfer and interphalangeal the medial column, 1218
arthrodesis of the hallux, 1379 GOLD for the acute management, 1216
Tendon transfers, 1161–1163 great metaphyseal comminution, 1221
Tenodesis, 1037–1039 hybrid or monoplanar medial
Tenodesis of the peroneus brevis, 1038 fixation, 1224
Tenosynovial giant cell tumors, 80, 81 joint and metaphyseal comminution and
Terminal tendon, 472 displacement, 1212
Testing ankle stability, 1070 joint involvement, 1211
Tetraparesis, 316 lesional mechanism, 1211
Thiemann’s disease, 212 metaphyseal and diaphyseal tibial
Thompson test, 1147 zones, 1213
Thompson’s test, 1146 open fibula synthesis and circular external
Tibia and talus neck osteophyte, 1052 fixation, 1225
Tibial chronic osteomyelitis percutaneous techniques, 1223
blood cultures, 783 pronation-dorsiflexion fracture, 1212
bone biopsy, 783, 784 sensitive and motor neurological
bone cultures, 784–788 evaluation, 1214
bone stabilization, 796 stabilization of the medial column, 1218
classification, 777, 778 surgical treatment, 1226
CRP, 781 tobacco patient, 1224
definition, 776 treatment concepts, 1212
diagnosis, 779, 780 Tibial posttraumatic deformity
diagnostic tools, 782 anatomy, 750, 751
eradication of the infection, 794 complications, 755, 757, 760
ESR, 781, 782 conservative management, 752
etiology, 776–779 diagnosis, 750–752
imaging, 789–792 etiology and pathophysiology, 750
laboratory studies incidence, 749
WBC, 780 limitations, 749
local antibiotherapy, 795 malunion, 749
microbiology, 779 posttraumatic malalignment, 749
molecular microbiology diagnostic surgical management, 752–758
methods, 788, 789 Tibial segmental defects
pathophysiology, 779 bone reconstruction, 806
systemic antibiotherapy, 794, 795 comparative results, 816–818
treatment, 793, 794 definition, 806
Tibial diaphysis fractures, 337 distraction osteogenesis
Tibial nerve, 1015–1017 classic bone transport, 807, 808
Index 1405
corticotomy, 807 pathophysiology

gradual distraction, 807 juvenile Tillaux, 357–359
Ilizarov method, 806 triplanar fracture, 359–362
motorized endomedullary nail, physiology and physeal anatomy, 354–358
812, 813 treatment, 365–368
shortening-lengthening, 810 Translational deformity, 750
transport phase, 807 Transmetatarsal amputation, 833–835
etiology, 805, 806 Transtibial amputation
induced membrane technique, 812, Chopart’s amputation, 827–829
814, 816 fishmouth, 823–826
structural allograft, 816 guillotine, 823, 824
vascularized fibular graft, 816, 817 hindfoot amputation, 826, 827
Tibial shaft fractures Pirogoff, Boyd, modified
anatomy, 1320 Pirogoff, 829–833
bimodal distribution, 1319 tarsometatarsal amputation, 835–838
compartment syndrome associated, 1329 tennis ball stump, 825–827
complications, 1329 toes, 837–840
diagnosis, 1321–1322 transmetatarsal amputation, 833–835
diagnostic approach, 1322 Trapping by the lower fascicle of the ATiFL,
etiology, 1319–1320 1053–1054
functional outcomes, 1330 Trapping due to the presence of pathological
history of present illness, 1321 soft tissue after ankle sprain,
infection rates, 1330 1054–1055
mechanism of action, 1320 Traumatic wounds, 100, 101
minimally invasive plating, 1328 Triceps suralis, 1144
non-operative treatment, 1324 Triple C osteotomy, 191, 192
operative treatment, 1323 Tuberosity avulsion fractures, 1236
physical examination, 1321 Two-handed manipulation technique,
preoperative planning, 1323 140, 142–145
reamed intramedullary nailing, 1325 Type (1A) “Stable hidden”: negative
reamed locked intramedullary nailing, 1324 radiographic stress, 1305
semi-extended position, 1325 Type (1B) “Unstable hidden” positive
soft tissue conditions, 1321 radiographic stress, 1305
torsional patterns, 1320 Type 1 Hidden lesions, 1305
Tibiocalcaneal (TC) arthrodesis, 596 Type 44-A or infrasindesmal fractures, 1171
Tibio-fibular ligament anterior-inferior
(LTFAI), 1183
Tibio-fibular ligament interosseous U
(LTFI), 1183 “U” capsulotomy, 209
Tibio-fibular ligament posterior-inferior Ultrasonography, 1126
(LTFPI), 1183 Unicameral bone cyst (UBC), 79
Tibio-talo-calcaneal arthrodesis (TTC), 983 Unstable trans-syndesmal fractures, 1179
Tillaux-Chaput tubercle, 1190
Torg I fractures, 1355
Torg II and III fractures, 1353 V
Torg III fifth metatarsal stress fractures, 1360 Varus/valgus ankles, 706–708
Torsional profile analysis, 120 Vascular endothelial growth factor, 200
Total ankle arthroplasty (TAA), 982 Vascularized fibular graft, 816, 817
Transindesmal fractures of the fibula, Vascular” theory, 1143
1192, 1193 VAS pain score, 1042
Transitional fractures Visual analog pain scales, 120
complications, 368 Visual gait analysis, 21, 120
diagnosis, 362–365 Vitamin D, 1125
1406 Index
W Wound healing process, 91

Wagstaffe tubercle, 1190 factors, 92, 93
Weightbearing computerized tomography scan phases, 92
(WBCT), 571
Weil technique, 301
Wound dehiscence Y
classification, 102 Yesotomy, 342
deep dehiscences, 104, 105
definition, 102
infection, 104 Z
prevention, 103 Z-Lenghthening” procedure, 877
risk factors, 102, 103 Zone 2 and zone 3 fractures, 1354
superficial dehiscences, 104 Zwipp’s classification, 1290
Wound healing problems, 1250

2022 Book FootAndAnkleDisorders

Uploaded by

Copyright:

Available Formats

2022 Book FootAndAnkleDisorders

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

2022 Book FootAndAnkleDisorders

Uploaded by

Copyright:

Available Formats

Foot and Ankle

Foot and Ankle Disorders

ISBN 978-3-030-95737-7 ISBN 978-3-030-95738-4 (eBook)

On so many levels, it is an extraordinary pleasure to review this book. Foot and

It is incredibly well illustrated, and the thoughtful approach to supramalleolar oste-

Santiago, RM - Santiago, Chile Emilio Wagner Hitschfeld

Part I Basic Science and General Considerations

Part II Pediatric Orthopaedics and Traumatology

Part III Adult Orthopaedics: Forefoot

Part IV Adult Orthopaedics: Midfoot, Rearfoot and Ankle

Part V Adult Orthopaedics: Tibial Reconstruction

Part VI Adult Orthopaedics: Tendinopathy, Soft Tissue Pathology

Part VII Adult Sports Lesions and Traumatology

Mario Abarca Hospital Sótero del Río, Santiago, Chile

Maryse Bouchard The Hospital for Sick Children, Division of Orthopaedic

Valeria Lopez Instituto de Ortopedia y Traumatología Dr. Jaime Slullitel, Rosario,

Pablo Schaufele Muñoz Universidad de Concepción, Concepción, Chile

Florencio Pablo Segura Universidad Nacional de Córdoba, Nuevo Hospital San

Pablo Wagner Hitschfeld Orthopedic Surgery Department, Clínica Alemana de

Manuel Monteagudo and Pilar Martínez de Albornoz

1 Introduction and History

Biomechanics is the study of mechanical engineering, specifically Newton’s laws,

© The Author(s), under exclusive license to Springer Nature 3

limbs is described in terms of a series of events that occur repeatedly, constituting

Stance phase Swing phase

Double Double Single Double

Fig. 2 First rocker (“heel

Fig. 4 Second rocker

Fig. 5 Third rocker

Fig. 6 Posterior view of a

3 Mechanical Functioning of the Ankle and Foot

Fig. 7 If the heel is inside

establishment of the pathogenesis in a particular case difficult. On the other hand,

Fig. 8 Patient with

5 Kinematic and Kinetic Recordings of the Hip, Knee,

Fig. 9 Kinematics of the

Fig. 10 Knee joint

mechanism, the action of the popliteus muscle/tendon, for unlocking. If during

Fig. 11 Kinematics of the

Fig. 12 Patient under

© The Author(s), under exclusive license to Springer Nature 25

Fig. 1 Comparative ankle weight-bearing radiographs in AP and lateral projections

Stress projection: These can be active or passive, demonstrating indirect evidence of

Fig. 4 Comparative weight-bearing radiograph of both ankles. Dysfunctional osteopenia.

Ultrasound plays a key role in the diagnosis and management of musculoskeletal

As an example, dynamic ultrasound can elucidate peroneal subluxation not evi-

DER CAB MTT HALL

DER CAB MTT HALL

Fig. 11 Morton’s neuroma

Fig. 12 Fine needle

Fig. 13 Panoramic view

5 Computed Tomography (CT)

Computed tomography is accomplished by multiple parallel images through an

Fig. 15 Computed tomography with VRT cinematic rendering reconstructions of a trimalleolar

(weight-bearing CT scans). This modality better demonstrates the true orientation

6 SPECT-CT (Single Photon Emission Computed

SPECT is based on the detection of gamma rays emitted by a radiopharmaceutical

also in infections. Historically, the contribution of bone scintigraphy to the diag-

7 Magnetic Resonance Imaging (MRI)

Magnetic resonance imaging has revolutionized musculoskeletal imaging, offering

Santiago, RM - Santiago, Chile Emilio Wagner Hitschfeld

Part I Basic Science and General Considerations

Part II Pediatric Orthopaedics and Traumatology

Part III Adult Orthopaedics: Forefoot

Part IV Adult Orthopaedics: Midfoot, Rearfoot and Ankle

Part V Adult Orthopaedics: Tibial Reconstruction

Part VI Adult Orthopaedics: Tendinopathy, Soft Tissue Pathology

Part VII Adult Sports Lesions and Traumatology

1 Introduction and History

3 Mechanical Functioning of the Ankle and Foot

5 Kinematic and Kinetic Recordings of the Hip, Knee,

5 Computed Tomography (CT)

6 SPECT-CT (Single Photon Emission Computed

7 Magnetic Resonance Imaging (MRI)

2.3 Radiological Control Instruments

4 Differences Between Open and Minimally

4.2.2 Preparation of the Surgical Field

4.3 Types of Surgical Techniques

4.3.1 Soft Tissue Surgery

4.4 Advantages and Disadvantages

5 Surgery for the Beginner in MIS

5.2 Percutaneous Surgical Technique Recommended

5.6 Distal Metatarsal Osteotomy

5.7 Osteotomy of the Base of the Proximal Phalanx

6.2.1 Secondary Displacement of Osteotomies

8 Common Types of Tumors

8.1 Giant Cell Tumor (GCT) of Bone

8.3 Aneurysmal Bone Cyst (ABC)

8.7 Unicameral Bone Cyst (UBC)

8.9 Tenosynovial Giant Cell Tumor

8.13 Soft Tissue Sarcoma