Md Abid Hossain Mollah

MBBS, FCPS (Paediatrics), Diploma in Medical Education (UK), FACP (USA), FRCP (Edinburgh, UK)

Ex-Professor & Head, Department of Paediatrics

Dhaka Medical College, Dhaka, Bangladesh
Professor & Head, Department of Paediatrics
Ibrahim Medical College & BIRDEM General Hospital
Dhaka, Bangladesh

Nazmun Nahar
MBBS, FCPS (Paediatrics), FRCP (Edinburgh, UK)

Ex-Professor & Head, Department of Paediatrics

Dhaka Medical College, Dhaka, Bangladesh
Professor of Paediatrics & Director General
BIRDEM, Dhaka, Bangladesh

April 2018
© All rights reserved by the Authors.
Copyright Registration No. 12031-CORP, dated 26th August, 2010

No part of this book may be reproduced, stored in a retrieval system or transmitted in any form or by any means, electronic,
mechanical, photocopying, recording or otherwise without prior permission of the authors.
Send inquiries to: Dr. Md. Abid Hossain Mollah, E-mail: [email protected]

First Edition: March 2010

Revised Second Print: November 2010
Second Edition: August 2012
Revised Second Print: September 2013
Reprint: November 2014
Third Edition: April 2015
Revised Third Edition: January 2016
Second Print: January 2017
Forth Edition: April 2018

Published by
Syeda Amena Meher
Century Estate Apartments
Moghbazar, Dhaka, Bangladesh

Illustrations & Sketch

Dr. Nabila Tabassum

Cover & Typesetting

De-Graph Systems
Sheikh Mahtab Ahmed

Printing
Dhaka

Dhaka

Price: Taka 850.00

US$ 28.00

International Standard Book Number (ISBN): 978-984-33-0987-7

Note:
Medical knowledge is constantly changing. Standard safety precautions must be followed, but as new research and clinical
experience broaden our knowledge, changes in treatment and drug therapy may become necessary or appropriate. Readers are
advised to check the most current product information provided by the manufacturer of each drug to be administered to verify the
recommended dose, the method and duration of administration, and contraindications. It is the responsibility of the practitioners,
relying on experience and practical knowledge from dealing the patients, to determine dosages and the best treatment for each
individual patient. None of the authors assumes any liability for any injury and or damage to persons or property arising from this
publication.
Contributors
Prof. ARM Luthful Kabir Dr. Ahmed Murtaza Chowdhury Dr. Tajul Islam A Bari
MBBS, FCPS (Paediatrics) MBBS, FCPS (Paediatrics)
Professor of Paediatrics Ex-Associate Professor Consultant
Ad-Din Women Medical College Department of Paediatric Infectious Diseases Division
Moghbazar, Dhaka, Bangladesh Haematology & Oncology ICDDR,B Mohakhali, Dhaka-1212
Mymensingh Medical College
Prof. Shakil Ahmed Mymensingh, Bangladesh Dr Azizur Rahman
MBBS, FCPS (Paediatrics), MD (Paediatrics) MBBS, MD (Cheast)
Professor of Paediatrics Dr Zohora Jameela Khan Associate Professor
Shaheed Suhrawardy Medical College MBBS, MD (Haematology & Oncology) Respiratory Medicine
and Hospital Associate Professor Faculty of Medicine, Dhaka University
Dhaka, Bangladesh Paediatric Haematology & Oncology
Dhaka Medical College Hospital Dr Tanvir Ahmed
Dr Sadeka Chowdhury Moni Dhaka, Bangladesh
MBBS, FCPS (Paediatrics) Assistant Professor
Assistant Professor Dr. Shegufta Rahman Department of Burn & Plastic Surgery
Department of Neonatology, BSMMU MBBS, DCH, FCPS (Paediatrics) Dhaka Medical College Hospital
Resident Physician Dhaka, Bangladesh
Dr. Dipa Saha Department of Neonatology
MBBS, FCPS (Paediatrics) National University Hospital Dr M Munirul Islam
Assistant Professor of Paediatrics Singapore
Bashundhora Ad-Din Medical College Scientist
Hospital, Dhaka, Bangladesh Dr. Abu Syeed (Shimul) Nutrition and Clinical Services Division
MBBS, FCPS (Paediatrics) & Senior Consultant Physician
Dr. Mehdi Pervez Junior consultant Dhaka Hospital, ICDDR,B
MBBS (DMC), FCPS Part I (Paediatrics) Department of Paediatrics Dhaka, Bangladesh
Assistant Registrar Mughda Medical College Hospital
Department of Paediatrics Dhaka, Bangladesh Dr Md Iqbal Hossain
Sher-e-Bangla Medical College Hospital MBBS, DCH, PhD (USA)
Barisal, Bangladesh Senior Scientist & Head
Dr Nasrin Islam
MBBS, FCPS (Paediatrics)
Child Malnutrition UNIT
Dr. Nazmun Nahar Shampa Dhaka Hospital, NCSD, ICDDR,B
Registrar
DCH, MCPS, FCPS (Paediatrics)
Department of Paediatrics
Junior Consultant Mohammad Jobayer Chisti
BIRDEM General Hospital-2
Dohar Upazila Health Complex Shegun Bagicha, Dhaka, Bangladesh
Dhaka, Bangladesh Senior Scientist & Head
Clinical Research, Hospitals & Clinical
Dr. Tasnima Ahmed
Dr. Jillur Rahman Siddiki MBBS, FCPS (Paediatrics)
Lead, ICU, Dhaka Hospital, NCSD
MBBS, MCPS, FCPS (Paediatrics)
Registrar ICDDR,B
OSD, DGHS Department of Paediatrics
BIRDEM General Hospital-2 Dr Shareen Khan
Dr Nabila Tabassum MBBS, FCPS (Paediatrics)
Shegun Bagicha, Dhaka, Bangladesh
MBBS, FCPS Part I (Paediatrics) Registrar
Trainee Department of Paediatrics
Department of Paediatrics BIRDEM General Hospital-2
Dhaka Medical College Hospital Shegun Bagicha, Dhaka, Bangladesh
Dhaka, Bangladesh
TOMORROW IS TOO LATE

We are guilty of many errors and many faults.

But our worst crime is abandoning the children,
Neglecting the fountain of life,
Many of the things we need can wait,
The child cannot.
Right now is the time his bones are being formed,
His blood is being made and his sense are being developed
To him we cannot answer ‘tomorrow’ .
His name is ‘today’.

Gabriela Mistral
Nobel Laureate (Chile, 1889 - 1957)
Dedicated to our

Parents
Teachers
Families
Children
Foreword

I am very happy to see the book “Step on to Paediatrics” published in

March 2010. I congratulate both the authors and the contributors for
accomplishing such a comprehensive work.

It was my long felt desire and perhaps of the undergraduate medical

students, to get such a book on paediatrics, so as to strengthen themselves
with core information on common child health problems of the country.
$QGWKLVLVLPSRUWDQWDVDIWHUJUDGXDWLRQWKHVHVWXGHQWVZLOOEHWKH¿UVW
hand health care providers for the vast majority of sick children of the
country.

The beauty of this book is the comprehensive problem based discussions

on common child health problems. Moreover, the essential elements in
diagnosis and treatment are also highlighted considering the socioeconomic status of the people.

Each and every chapter of the book is enriched with a good number of photographs and sketches. Problems
that are discussed in this book are so close to real life situation that readers will never feel bored and will
not be overburdened with theoretical details. Important information are presented in boxes and tables. The
book is also written in a clear and lucid language.

This book will be very helpful to enrich the medical students as well as the graduates and to minimize
the existing gap in their knowledge in Paediatrics. Although the book is written mainly for the medical
XQGHUJUDGXDWHVWKHSRVWJUDGXDWHVVWXGHQWVDQGVHQLRUQXUVHVZLOODOVREHEHQH¿WWHG

I hope, this book will act as medical student’s armour during their formative and summative assessment.

May this book be a handy companion to all those who love and work for children.

National Professor M R Khan

Dhaka, March 2010
Preface to forth edition
It is indeed a great privilege for us to introduce to you the 4th edition of ‘Step on to Paediatrics’ which is a
substantial revision and reorganization, based on recent updates in medical advancement, latest text books
and the suggestions kindly provided by our beloved students and teachers of Paediatrics. In this edition,
we have tried to incorporate a brief pathogenesis of all the diseases to have a better understanding of
pathology, to rationalize the investigations as well as treatment. In addition, new topics such as, child
with polyuria, haematuria, burn injury, foreign body aspiration, SDG goals etc. are included. The different
aspects of the diseases are made easier to understand with the aid of a bunch of new X-Rays, sketches and
patient photographs. The key points of the diseases are highlighted in boxes and tables as always.

We would like to appreciate all the contributors, who worked very hard to accomplish this herculean task. We
are indebted to our beloved students, colleagues, teachers and faculties of Paediatrics of all Medical Colleges
& Institutions of Bangladesh for their overall supports and thoughtful feedbacks on how to improve the
quality of this book. We, would like to mention the names of Prof Md Ruhol Amin, Ex-Prof of Paediatrics,
Dhaka Shishu hospital, Prof M Karim Khan, Prof of Paediatrics, CBMCB, Mymensingh, Prof Ranjit R Roy,
Prof of Paediatric Nephrology, BSMMU for their continuous inquiry & suggestions. We must appreciate
the contribution of the respected contributors, colleagues of department of Paediatrics, BIRDEM for their
constant supports. It will be unfare, if we do not acknowledge Prof Ashraful Hoque, Prof Abdul Hanif Tablu,
Pediatric surgeons of DHMC, Prof Kamal Ahmed, Dr Masud, Assistant Prof of Ped Surgery, BIRDEM for
supplying with different academic pictures.

Our sincere appreciation will always remain to Sheikh Mahtab Ahmad, who despite his many limitations,
made the edition as furnished as possible.

We hope that the 4th edition of Step on to Paediatrics will create interest of our beloved students on Paediatrics
and this will facilitate their learning on child health & wellbeing as well as their sickness.

Md Abid Hossain Mollah

Nazmun Nahar
Dhaka, April 2018
Preface to revised third edition
It is indeed a great pleasure for us to present the revised version of the third edition. In this revision, we have tried to
provide recent data pertaining to childhood morbidity & mortality, recent EPI schdule of Bangladesh and updates on case
management from the latest edition of text books and journals. Moreover, we also changed some clinical photographs
given previously with the better ones and added few new pictures and sketches.
We cannot thank enough our respected teachers, colleagues and beloved students for their continued belief in our
endeavour. In the revision process, we would like offer our special thanks to Dr Abu Sayeed Chowdhury, Dr Nazmun
Nahar Shampa, Registrars of Paediatrics, Dhaka Medical College Hospital who through their very keen ovservation
compiled all the necessary updates for this revision. We would also like to acknowledge the support from Dr Amit Shome
and Dr Sumon Shahriar Morshed, Assistant Registrars of Paediatrics, Dhaka Medical College Hospital.
Finally, we would like to thank our family members for their relentless moral support, positive understanding and
unprecedented patience which paved the smooth completion of this revision.

Md Abid Hossain Mollah

Nazmun Nahar
Dhaka, January 2016

Preface to the third edition

The publication of the 3rd edition of Step on to Paediatrics is the assembly of evidence based updates of common childhood
problems of Bangladesh. This edition represents a substantial revision,reorganization and expansion of already existing
and few new chapters. The changes are made in accordance with the criticism, suggestions and wishes expressed by our
teachers, students and several other readers. We tried to prepare this edition more reader friendly, easily understandable
with lucid and easy language. Most of the texts are enhanced with a large number of photographs and X-Rays, taken
mostly from our patients. A fair number of sketches, illustrations and algorithm are arranged in such a way that students
clearly understand the pathophysiological basis of the disease and can explain the clinical features & consequences,
rationalize investigations, interpret laboratory reports and optimize principles of management. The cardinal points are
highlighted in coloured boxes & tables so the readers will have a scope of quick review before examination. At the end of
each chapter, there are substantial number of self-assessment questions for the readers.
We would like to appreciate all the contributors who have been an outstanding and insightful partner to the editors and
DFFRPSOLVKHGWKLVFRPSOH[SURGXFWLRQVPRRWKO\DQGHI¿FLHQWO\
We are indebted to our beloved students, teachers, colleagues and faculties of Paediatrics of all Medical Colleges of
Bangladesh as well as colleagues of BSMMU, BICH, BIRDEM, ICMH, ICH for their overall supports and providing
thoughtful feedbacks on how to improve the quality of the book! However, we must remember Dr Sadeka Chowdhury
Moni, Assistant Professor of Neonatology, BSMMU and Dr Abu Sayeed Chowdhury, Registrar of Paediatrics, DMCH who
went through all the trouble to check the details of the manuscript several times.
Our sincere appreciation will always remain to Sheikh Mahtab Ahmad, who despite his many limitations, made the
publication as furnished as possible.
We are privileged to have compiled this 3rd edition and are enthusiastic about all that it offers to our readers. We hope that
WKH\ZLOO¿QGWKLVHGLWLRQDXQLTXHO\YDOXDEOHHGXFDWLRQDOUHVRXUFHDQGDQ\VXJJHVWLRQVRUFRPPHQWVDUHDOZD\VZHOFRPH
Finally, we would like to acknowledge the patience and moral supports given by our family members.

Md Abid Hossain Mollah

Nazmun Nahar
Dhaka, April 2015
Preface to the second edition
We are really amazed to see the overwhelming acceptance of Steps on to Paediatrics by both the
undergraduate and post graduate medical students, residents, paediatricians and teachers, and this is the real
inspiration to edit the book. We do express our gratitude to them for their support.
The new edition attempts to provide the essential information that the students, doctors always think
imperative to address the common childhood illnesses. In addition to a substantial expansion and
reorganization of the chapters, the 2nd edition also has additions of new problems like birth injuries,
vomiting including blood vomiting, common surgical problems of children, croup, myopathy, Turner
V\QGURPHDQGEDVLFVRIÀXLGHOHFWURO\WHVDQGDFLGEDVHKRPHRVWDVLV$OOWKHGLVFXVVLRQVDUHHQULFKHGZLWK
many tables, algorithms, photographs and sketches so that the readers can have better understanding of the
clinico-pathological basis of the problem, can rationalize and interpret investigations and can optimize the
treatment. The cardinal features of the diseases are highlighted in coloured boxes and at the end of each
chapter, there are questions for self-assessment of the students.
We do humbly acknowledge the support and encouragement by the faculty of Paediatrics of all medical
colleges of Bangladesh, BSMMU, BICH, BIRDEM and ICMH. We do particularly express our thanks to
Prof. Tahmina Begum, Prof. M Karim Khan, Dr. Narayan Saha, Dr. Bikash Majumder, Dr. Chandan Kumar
Saha, Dr. A K M Amirul Morshed Khasru, Dr. Md Saiful Islam, Dr. Zohirul Alam Chowdhury, Dr. Kazi
Selim Anwar, Dr. Mesbah Uddin Ahmed, Dr. Md Golam Sadik Mamun, Dr. A S M Hasibul Hasan, Dr.
Sanjoy Kumar Das, Dr. Abu Sadat M Saleh, Dr. Janifa Akter for their valuable contributions.
To accomplish this edition, we also have had informal assistance from the faculty members, students and
doctors of the department of Paediatrics, Dhaka Medical College & Hospital. Our sincere appreciation
always remains for them.
We, gratefully acknowledge the publications and books from where information has been taken. At the end
of each chapter, reference list has been cited. However, if any have been left out through oversight, we offer
our sincere apologies.
The untiring efforts of the friends of Ahsania e solutions is especially appreciated to make the publication
as perfect as possible.
Last and certainly not the least, we especially wish to thank our families for their patience and moral
support without which this edition would not have been possible.
We hope that the 2nd edition will stimulate the students and serve their purpose.

Md Abid Hossain Mollah

Nazmun Nahar
Dhaka, August ‘2012
Preface to the first edition
Truly, not much careful attention was exercised on child health/paediatrics while planning the curriculum of
our current undergraduate medical science. More undesirably, paediatrics is being pondered by the medical
curriculum board merely as a branch of medicine since long, in strict sense. Contrarily, it demands huge
importance & due attention, since more than one-third (37%) of our total population comprises of children
and their health care associated responsibilities would often be conveyed to shoulder of our fresh medical
graduates, passing out every year successfully.
In fact, the very question posed by several undergraduate students frequently– “Which book on Paediatrics
should we go through?”, remains the true inspiration for writing up this book on Paediatrics, just to contribute
a modest effort to strengthen students' knowledge on child health so that they can contribute to child care
successfully. In this book, we have tried to highlight the most common child health problems, if not all,
matching with the undergraduate paediatric curriculum so that students can face formative and summative
assessments, successfully.
Discussions are made essentially on symptoms rather than a formal review of disease entities as symptoms
provide a major clue to the underlying disease particularly in Paediatrics. Starting with the cardinal
PDQLIHVWDWLRQVFRPPRQGLIIHUHQWLDOGLDJQRVLVDUHOLVWHGRXWVSHFL¿FDOO\IROORZHGE\WKHLUDHWLRSDWKRJHQHVLV
clinico-epidemiological features, establishing the diagnosis and detailed treatment plan. In order to ensure
better understanding of individual clinical problem a good number of patient’s photographs & essential
sketches have also been incorporated. Moreover, at the end of each chapter, a number of short answer
questions (SAQ) and multiple choice questions (MCQ) are given pertaining to that chapter for self evaluation
of the students. These will certainly build up their knowledge and understanding and help them to avoid
dependency on note books.
Alike others, several formal and informal assistance were sought in editing various chapters of this book
from many faculties and house staffs of the department of Paediatrics at the Dhaka and Mymensingh Medical
Colleges and we do express our gratefulness for their contribution.
The untiring efforts of Sheikh Mahtab Ahmed and Atikur Rahman is specially appreciated for secretarial
assistance and desk top publishing.
Finally, special thanks go to our family members for their long-standing patience, positive understanding and
active moral support in completing this book successfully without which this effort would have been futile.
We would, however, look forward optimistically to see if it serves the need of our undergraduate students and
WKXVEHEHQH¿FLDOWRRXUEXGGLQJGRFWRUVVLJQL¿FDQWO\

Md Abid Hossain Mollah

Nazmun Nahar
Dhaka, March 2010
Contents
Chapter 01: The Child . . . . . . . . . . . . . . . . . . . . . . . . 1

Chapter 02: Child Health Scenario . . . . . . . . . . . . . . . . . . . 3

Chapter 03: Examination of A Child: Crucial to Remember . . . . . . . . . . . 7

Chapter 04: Growth and Development . . . . . . . . . . . . . . . . . . 8

Chapter 05: Infant and Young Child Feeding (IYCF) . . . . . . . . . . . . 16

Chapter 06: Integrated Management of Childhood Illness [IMCI] . . . . . . . . 21

Chapter 07: Childhood Immunization and Vaccine Preventable Diseases . . . . . . 27

Chapter 08: Newborn and Common Neonatal Problems . . . . . . . . . . . 47

Chapter 09: Nutritional Disorders . . . . . . . . . . . . . . . . . . . 72

Chapter 10: Cough and or Difficult Breathing . . . . . . . . . . . . . . 89

Chapter 11: Diarrhoea . . . . . . . . . . . . . . . . . . . . . . . 105

Chapter 12: Vomiting . . . . . . . . . . . . . . . . . . . . . . . 113

Chapter 13: Abdominal Pain . . . . . . . . . . . . . . . . . . . . . 116

Chapter 14: Constipation . . . . . . . . . . . . . . . . . . . . . . 119

Chapter 15: Sore Throat & Difficulty in Swallowing . . . . . . . . . . . . 121

Chapter 16: Undue Exhaustion to Normal Activities . . . . . . . . . . . . 123

Chapter 17: Joint Pain and Swelling . . . . . . . . . . . . . . . . . . 137

Chapter 18: Fever and Rash . . . . . . . . . . . . . . . . . . . . . 145

Chapter 19: Prolonged High Fever . . . . . . . . . . . . . . . . . . 153

Chapter 20: Jaundice . . . . . . . . . . . . . . . . . . . . . . . 163

Chapter 21: Blood Vomiting . . . . . . . . . . . . . . . . . . . . . 170

Chapter 22: Lymph node enlargement . . . . . . . . . . . . . . . . . 174

Chapter 23: Pallor or Anaemia . . . . . . . . . . . . . . . . . . . 179

Chapter 24: Pallor, Bleeding and Fever . . . . . . . . . . . . . . . . 195

Chapter 25: Bruising and Bleeding . . . . . . . . . . . . . . . . . . 198

Chapter 26: Puffy Face and Scanty Urine . . . . . . . . . . . . . . . . 206

Chapter 27: Smoky/Red urine . . . . . . . . . . . . . . . . . . . . 217

Chapter 28: Dysuria . . . . . . . . . . . . . . . . . . . . . . . 221

Chapter 29: Excessive urine output (polyuria) . . . . . . . . . . . . . . . 225

Chapter 30: Sudden Paralysis of limbs . . . . . . . . . . . . . . . . . 231

Chapter 31: Convulsion . . . . . . . . . . . . . . . . . . . . . . 238

Chapter 32: Developmental Delay . . . . . . . . . . . . . . . . . . . 253

Chapter 33: Abnormal Behavour . . . . . . . . . . . . . . . . . . . 261

Chapter 34: Short Stature . . . . . . . . . . . . . . . . . . . . . 265

Chapter 35: Difficulties in Movement and Posture . . . . . . . . . . . . . 270

Chapter 36: Accidents and Emergencies . . . . . . . . . . . . . . . . 277

Chapter 37: Parasitic Infestations . . . . . . . . . . . . . . . . . . . 290

Chapter 38: Common Surgical Problems of Children . . . . . . . . . . . 296

Chapter 39: Fluid, Electrolytes and Acid-Base Homeostasis . . . . . . . . . 312

Chapter 40: Instruments & Procedures in Paediatrics . . . . . . . . . . . 321

Chapter 41: Model OSPE for Practice . . . . . . . . . . . . . . . . 329

Annexure . . . . . . . . . . . . . . . . . . . . . . . . . . 335

Index . . . . . . . . . . . . . . . . . . . . . . . . . . 358
 01
The Child
Children are the future asset and hope of a nation. They Characteristics of a child
are the foundation of a stable nation. $FKLOGLVQRWDPLQLDGXOW+LVKHUERG\SK\VLRORJ\
Who is a child?
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The United Nations
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Convention on the
maturity passing through different stages of life.
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means every human
being below the age XX Intrauterine period
of eighteen years TT (PEU\R)HUWLOL]DWLRQWRZHHNV

unless under the law TT )RHWXVZHHNVWRELUWK

DSSOLFDEOHWRWKH XX Perinatal period

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attained earlier.” XX 1HRQDWHV%LUWKWRZHHNVRIDJH

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 2 Step on to Paediatrics

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References
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Press.
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SELF ASSESSMENT
Short answer questions [SAQ]
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 02
Child Health Scenario
Global Scenario- - - - - - - - - - - - - - 3
Bangladesh Scenario- - - - - - - - - - - - - 3

GLOBAL SCENARIO
(YHU\\HDUDERXWPLOOLRQFKLOGUHQEHORZ\HDUVGLHWKURXJKRXWWKHZRUOG7KHPDMRUFDXVHVRIWKHVH
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Where most under 5 deaths occur

Child health scenario

Source:
Bangladesh scenario
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3
 4 Step on to Paediatrics

The major causes of under 5 child deaths in

Bangladesh
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and neonatal mortality rates
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including birth asphyxia 11%
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to developed world %'+6 Neonatal sepsis
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FKDOOHQJHLQWKHKHDOWKVHFWRU 10%

LVXQDFFHSWDEO\ high neonatal Congenital anomalies

5%
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diseases
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Injuries 6%
Development Goal 4 (MDG
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child mortality 1% 9% 2%

Goal
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 6 Step on to Paediatrics

References
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 03
Examination of A Child:
Crucial to Remember
Tips - - - - - - - - - - - - - - - - 7

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Examination of a child

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 04
Growth and Development
Growth - - - - - - - - - - - - - - - 8
Development - - - - - - - - - - - - - - 11
Milestones of development - - - - - - - - - - - - 12

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 Step on to Paediatrics 9

Postnatal growth curves for general somatie, brain, lymphoid

and reproduction systems (Tanner, 1962)
Measuring length/height

200% A. Recumbent or Supine length

180
For children who are±
Size attained (% of total postnatal growth)

Lymphoid
160 XX /HVVWKDQ\HDUVRIDJH
140 XX Unable to stand or¿QGVGLI¿FXOWLHVLQVWDQGLQJ
120 Procedure
100%
Instrument: InfantometerD¿UPPHDVXULQJERDUGZLWK
Brain and head
80
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60

atie
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General som

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20
Reproductive
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Birth 2 4 6 8 10 12 14 16 18 20
Age (years)

Normal growth velocity during childhood

Infantometer

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 year
st
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nd year FP\HDU XX /D\WKHFKLOGRQKLVEDFNRQWKHERDUG2QHSHUVRQ
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Growth spurt

Courtesy: Dr Maliha Alam

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in boys than that of girls.

ASSESSMENT OF GROWTH
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XX 3K\VLFDOJURZWKi.e.anthropometry
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height in children <5 years.
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XX

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 10 Step on to Paediatrics

B. Standing height Measurement of Body Weight

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sides
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the lower margins of the
orbits will remain in the Measurement of Occipito-Frontal
same plane with the tragi (Frankfort plane). The
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Instrument: Non-stretchable measuring tape
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tape.
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glabellas and superior
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i.e.100 cm by 4th year and 3 times (150 cm) by 14th year. OHYHORQHDFKVLGHDQGSRVWHULRUO\DWWKHOHYHORIH[WHUQDO
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 Step on to Paediatrics 11

Average OFC of a child

At 3 At 6 At 1 At 2
At Birth

Source: Internet
months months year years
(cm)
(cm) (cm) (cm) (cm)
  44  49

Measuring skinfold thickness by Harpenden Calipers

Measurement of Mid Upper Arm
Circumference (MUAC)
Instrument: Shakir’s tape Assessment of reproductive growth
,WLVPHDVXUHGLQFKLOGUHQEHWZHHQDJHVPRQWKVWR L $VVHVVRIWHVWLFXODUYROXPHE\orchidometer.
years for PDVVVFUHHQLQJ of nutritional status.

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Orchidometer showing variable size of balls with numbers

Procedure corresponding to normal testicular volume at different ages

It is measured at a point approximately midway between

LL $VVHVVPHQWRIJURZWK GHYHORSPHQWRIGLIIHUHQWVH[
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organs HJSHQLVEUHDVWSXELFDQGD[LOODU\KDLUHWFat
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the tissue. It is RUJDQVRIDQ\FKLOGFDQEHHYDOXDWHGXVLQJWKLVFKDUW

traditionally
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side while the arm
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&DOFXODWLRQ:HLJKW NJ +HLJKW P
XX 0HDVXUHPHQWRIWULFHSV VXEVFDSXODUVNLQIROG Early childhood development
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Harpenden Calipers
 12 Step on to Paediatrics

DEVELOPMENT 7KHUHIRUHDSSURSULDWHFDUHDVZHOODVSURSHUVWLPXOL
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Birth 3 months 3-5 years 14 years

100 billion cells

Synapses: 50 trillion 1000 trillion 100 trillion

Number of synapses Reduction of
increasing unnecessary synapses

Principles of Development
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Milestones of development

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 Step on to Paediatrics 13

Domains of Development
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gone and laughs toys
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XX $WPRQWKVZLWKURXQG hand to other out of sight herself Milestones of development
EDFN XX Palmar grasp is attained XX

XX $WPRQWKVZLWK XX

VWUDLJKWEDFN
6 - 8 months
 14 Step on to Paediatrics

Age Specific Normal Milestones of Development

)LQHPRWRU  Social, emotional,
group
6SHHFKODQJXDJH KHDULQJ
Age

Gross motor Vision behavior, self help/

autonomy
XX Crawls XX 3LQFHUJULS XX Says bi syllable words HJ%DED XX 3OD\VSHHNDERR
XX Stands holding furniture 'DGD0DPD XX :DYHVE\HE\H
Says one word
9 - 10 months

XX

with meaning

XX :DONLQJ XX 7KURZVREMHFWV XX 6D\VZRUGVZLWKPHDQLQJRWKHU XX 'ULQNVIURPFXS

XX unsteadily XX Turns pages of a WKDQ GDGD  PDPD
XX broad ERRN XX Responds to
12 months

XX gaits own name by

XX hands turning when
FDOOHGIURP
XX apart
behind

XX :DONVDORQH XX 6FULEEOHVZLWK XX 6D\VZRUGV XX $VNVIRUWKLQJVE\

XX steadily pen pointing
15 - 18 months

XX :DONVEDFNZDUGV XX Builds a tower of XX 3RLQWVWRERG\SDUWVRQUHTXHVW XX +ROGVVSRRQDQG

FXEHV XX %HJLQVWRMRLQZRUGVWRJHWKHU gets food to
18 - 20 months

mouth
Milestones of development

Adapted from Module on Early Childhood Development for Undergraduate Medical Students, Teachers Guide
Courtesy: Late Professor SM Shahnawaz Bin Tabib
 Step on to Paediatrics 15

References
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 .KDQ055DKPDQ0((VVHQFHRI3HGLDWULFVthHG(OVHYLHU&KDSWHU*URZWKDQG'HYHORSPHQWS
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 %DQJODGHVK6KLVKX$FDGHP\'KDND0RGXOHVRQ(DUO\&KLOGKRRG'HYHORSPHQWIRU8QGHUJUDGXDWH0HGLFDO6WXGHQWV
(/&'3URMHFW

SELF ASSESSMENT
Short answer questions [SAQ]
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Infant and Young Child Feeding (IYCF)
Breast feeding - - - - - - - - - - - - - - 16
Complementary feeding - - - - - - - - - - - - 18

$SSURSULDWHIHHGLQJSURJUDPPHLVHVVHQWLDOWRSURYLGH LQLWLDWHGZLWKLQ¿UVWKRXURIELUWK7KHUHLVDOVRSXEOLVKHG
optimum nutrition and to ensure optimum growth and HYLGHQFHWKDWXQGHU¿YHPRUWDOLW\UDWHFRXOGEHUHGXFHG
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XX Promotion of early initiation of breast feeding
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XX (QVXULQJH[FOXVLYHEUHDVWIHHGLQJIRU¿UVWPRQWKV
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BREAST FEEDING
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VWUDWHJ\DVEUHDVWPLONFRQWDLQVDOOWKHHQHUJ\DQG
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It is estimated that about PLOOLRQQHZERUQGHDWKVFRXOG
EHDYHUWHGJOREDOO\LIEUHDVWIHHGLQJZRXOGKDYHEHHQ
16
 Step on to Paediatrics 17

Colostrum: Anti-infective Components Proper positioning Good attachment

XX Immunoglobulins HJ6HFUHWRU\,J$,J*,J0 XX The body is fully
XX Cellular elements HJ:KLWHEORRGFHOOV TT 7KHEDE\¶VFKLQLV
supported
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TT 7KHEDE\¶VPRXWKLV
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mother
of &DQGC4 open widely
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XX
body
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TT 0RUHDUHRODLVVHHQ
XX
opposite to the
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nipple

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XX 7KHEDE\WDNHVVORZGHHSVXFNOHVIROORZHGE\
a visible or audible swallow
XX 6RPHWLPHVWKHEDE\SDXVHVIRUDIHZVHFRQGV
DOORZLQJWKHGXFWVWR¿OOXSZLWKPLONDJDLQ
XX 7KHEDE\¶VFKHHNVUHPDLQURXQGHGGXULQJWKH
feed
XX :KHQVDWLV¿HGEDE\XVXDOO\UHOHDVHVWKHEUHDVW
spontaneously
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XX $EDE\PD\VXFNTXLFNO\DOOWKHWLPHZLWKRXW
swallowing
XX 7KHFKHHNVPD\EHµGUDZQLQ¶LQGLFDWLQJWKDW
Exclusive Breast Feeding (EBF) PLONLVQRWÀRZLQJZHOO
,WPHDQV±
XX $QLQIDQWUHFHLYHVRQO\EUHDVWPLONIURPKLVor her mother or Prelacteal Feeding and the Hazards
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XX 1RRWKHUOLTXLGVor solids are given not even a drop of water
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 18 Step on to Paediatrics

How to ensure successful Breast Feeding?

XX %XLOGFRQ¿GHQFHRIWKH
mother about her ability
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XX (QVXUHSULYDF\RI
mother
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the mother
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to the mother during
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breast feeding UHDFKHGZKHQEUHDVWPLONDORQHLVLQDGHTXDWHWRPHHW
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It means giving the baby other foods in addition to breast
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as they ideally
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Ideal complementary food chart Courtesy: ICMH, UPHCP, Bangladesh

 Step on to Paediatrics 19

Properties of Complementary Foods

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l l l l l

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l l l l

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l l

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l

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l

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l l

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ing
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fe
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m
co
h
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d
oul
sh
g
din
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s t
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Complimentary feeding schedule 9-11 completed months 12-24 completed months

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6-8 completed months
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 20 Step on to Paediatrics

References
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 &OLQLFDOJXLGHOLQHVRQ,QIDQWDQG<RXQJChild Feeding (,<&) *2%¶

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Integrated Management of
Childhood Illness [IMCI]
What is IMCI - - - - - - - - - - - - - - 21
Rationale & Components - - - - - - - - - - - - 21
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 22 Step on to Paediatrics

I. Assessment of the sick child

Zero day upto 2 months 2 months upto 5 years

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Case Management at Higher Centre

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 24 Step on to Paediatrics

Cardinal Features of Certain

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 Step on to Paediatrics 25

Summary of Stepwise Case Management

IMCI case management at a glance for IMCI case management at a glance for
children from 0 day up to 2 months children from age 2 months up to 5 years

Steps of case management in IMCI

 26 Step on to Paediatrics

References
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 07
Childhood Immunization and
Vaccine Preventable Diseases
Immunization: The basics- - - - - - - - - - - - 27
EPI - - - - - - - - - - - - - - - - 28
Vaccine preventable diseases
¼¼ Tuberculosis - - - - - - - - - - - - - - 29
¼¼ Measles- - - - - - - - - - - - - - 37
¼¼ Mumps- - - - - - - - - - - - - - - 38
¼¼ Chickenpox - - - - - - - - - - - - - - 39
¼¼ Tetanus - - - - - - - - - - - - - - 40
¼¼ Pertussis - - - - - - - - - - - - - - 42
¼¼ Diphtheria - - - - - - - - - - - - - - 43

IMMUNIZATION: THE BASICS

Vaccine Adverse Events Following
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and to provide immunity against one or several diseases. ,WLVDPHGLFDOLQFLGHQWWKDWWDNHVSODFHDIWHU
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 28 Step on to Paediatrics

National immunization coverage (July 2016 revision) $QRWKHUREMHFWLYHRI(3,LVWRSUHYHQWGHDWKVRIPRWKHUV

as well as their newborn babies from tetanus. This is
Full vaccination coverage <1 year of age 
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N.B. If 5 doses of TT are completed, no TT is required
Source: EPI fact sheet, Bangladesh,
WHO.SEARO/FGL/IVD. 31 August 2016 during pregnancy.

Congenital Rubella Syndrome

EPI SCHEDULE IN BANGLADESH &56  Measles-Rubella (MR)
vaccination campaign ’2013-14
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EPI schedule, Reviewed in 2017 Courtesy: Dr Tajul Islam A Bari

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 Step on to Paediatrics 29

TUBERCULOSIS 7KHEDFLOOLDUHWKHQGUDLQHGWKURXJKO\PSKDWLFVWR
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Organism (Hilar lymphadenopathy)7KH*KRQIRFXVDQGKLODU
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Source: Internet
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 30 Step on to Paediatrics

Photographs of different types of extra-pulmonary TB

Tubercular lymphadenitis Lupus vulgaris (skin TB) Gibbus in spinal TB

Courtesy: Dr Iffat Ara Shamshad

Courtesy: Prof Sayeeda Anwar

Source: Internet
Cold abscess, paravertebral TB dactylitis with skin TB TB of elbow and wrist joint
Tuberculosis

Pleural effusion Pericardial effusion

 Step on to Paediatrics 31

Tuberculoma of brain X-Ray wrist joint showing erosion of lower end of radius

Paravertebral abscess & destruction of vertebral bodies

Pott's disease

Clinical Manifestations
Symptom Criteriae suggestive of Pulmonary TB
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Tuberculosis

National Guideline for Tuberculosis in Children. 2nd edition; March 2016

NB: If any one of the above symptom criteria in a child <15 years, in close contact with a known bacteriologically
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 32 Step on to Paediatrics

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Diagnosis
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TT )HDWXUHVRISUHVVXUHHIIHFWVHJFROODSVH

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Right hilar lymphadenopathy AP view Right hilar lymphadenopathy, Lateral view

 Step on to Paediatrics 33

XX

XX

Paratracheal lymphadenopathy Patchy opacity

Middle lobe consolidation Miliary mottling

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 34 Step on to Paediatrics

Causes of False Negative and Sites of Extra-pulmonary TB and relevant

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histopathology
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 Step on to Paediatrics 35

Specialty of childhood TB
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Aspects Childhood TB
XX &ORVHFRQWDFWZLWKVSXWXPSRVLWLYHDGXOWFDVHV
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XX 2YHUFURZGLQJ
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no haemoptysis

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investigations XX $)%SRVLWLYLW\UDWH
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 36 Step on to Paediatrics

Treatment Indications of corticosteroid in TB

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 Step on to Paediatrics 37

MEASLES
Organism: Rubeola virus,DQ51$YLUXV
Transmission: Inhalation of air borne droplets
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Pathogenesis
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 38 Step on to Paediatrics

Complications XX Cough remedy l :DUPZDWHU 7XOVLOHDIMXLFH

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 Step on to Paediatrics 39

Complications Pathogenesis
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 40 Step on to Paediatrics

Complications TETANUS
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 Step on to Paediatrics 41

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 42 Step on to Paediatrics

PERTUSSIS Complications
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 Step on to Paediatrics 43

XX $PSLFLOOLQ PJNJGD\ KRXUO\IRU Clinical Manifestations

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surrounded by minimal erythema
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 44 Step on to Paediatrics

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 Step on to Paediatrics 45

References
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 08
Newborn and Common Neonatal Problems
Characteristics healthy term newborn - - - - - - - - - - 47
Newborn care - - - - - - - - - - - - - - 49
Common neonatal problems
¼¼ Low Birth Weight - - - - - - - - - - - - - 50
¼¼ Post maturity/Post term- - - - - - - - - - - - 52
¼¼ Perinatal asphyxia - - - - - - - - - - - - - 53
¼¼ Respiratory Distress Syndrome - - - - - - - - - - 58
¼¼ Transient tachypnoea of newborn (TTN): Wet lungs - - - - - - - 59
¼¼ Neonatal sepsis - - - - - - - - - - - - - 60
¼¼ Neonatal jaundice - - - - - - - - - - - - - 62
¼¼ Neonatal convulsions - - - - - - - - - - - - 66
¼¼ Birth injuries- - - - - - - - - - - - - - 68

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 48 Step on to Paediatrics

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2000
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 Step on to Paediatrics 51

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 52 Step on to Paediatrics

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 54 Step on to Paediatrics

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immediately after birth may be either in primary ENCEPHALOPATHY (HIE)
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Ischaemic Encephalopathy (HIE)+RZHYHURWKHU K\SR[LDDVZHOODVGXHWRLPSDLUHGFHUHEUDOEORRGÀRZ
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QHXURORJLFV\QGURPHLVUHODWHGWRWKHH[WHQWRIEUDLQLQMXU\
DQGLVFODVVL¿HGLQWRVWDJHV±
Brain
+\SR[LF Kidney
,VFKDHPLF $FXWHNLGQH\ +\SHUDOHUWLUULWDEOHZLWKGLODWHGSXSLOVDQG
(QFHSKDORSDWK\ LQMXU\ +,(, VWURQJPRURUHIOH[0XVFOHWRQHQRUPDO
6\PSWRPVXVXDOO\SHUVLVWIRUKRXUV
Heart
Gut &RQYXOVLRQOHWKDUJ\ZHDNPRURUHIOH[
+\SR[LF +,(,,
1HFURWL]LQJ PLOGK\SRWRQLDDQGFRQVWULFWHGSXSLOV
FDUGLRP\RSDWK\
Perinatal HQWHURFROLWLV

Asphyxia &RPDWRVHIODFFLGPXVFOHVDEVHQWSULPLWLYH
+,(,,, UHIOH[HVGLPLQLVKHGRUDEVHQWVSRQWDQHRXV
Lungs PRYHPHQWDQGXQHTXDOSXSLOV
Adrenal pulmonary
+DHPRUUKDJH KDHPRUUKDJH Ref: Sarnat ‘1976
33+1
Liver Management
+HSDWRFHOOXODU
QHFURVLV
$(IIHFWLYHUHVXVFLWDWLRQDWELUWKWKHFRUQHUVWRQHRI
management
%3RVW5HVXVFLWDWLRQFDUH
Clinical Manifestations
XX 7KHDVSK\[LDWHGEDE\SUHVHQWVZLWK± Resuscitation: Preparation
TT 1RUHVSLUDWLRQQRFU\

TT $EVHQWRUZHDNUHVSLUDWRU\HIIRUWV
XX 3HUVRQ$WOHDVWRQHSHUVRQWUDLQHGLQQHZERUQ
UHVXVFLWDWLRQ
TT Gasping respiration with long pauses in between
XX :DUPHQYLURQPHQW%\FORVLQJZLQGRZV
respirations
PLQLPL]LQJGUDXJKWVSUHZDUPLQJWRZHOVKHDG
TT &RQYXOVLRQV +,(
FRYHULQJIRUWKHEDE\KHDWHUUDGLDQWZDUPHU
TT 3DOHFRORXU
XX 5HVXVFLWDWLRQVXUIDFH$UUDQJHÀDW ¿UPVXUIDFH
(asphyxia XX 5HVXVFLWDWLRQHTXLSPHQWV
SDOOLGD
Post maturity, Perinatal asphyxia

TT 6HOILQÀDWLQJEDJZLWKFRUUHFWVL]HGPDVN
TT %UDG\FDUGLD
TT 2[\JHQVRXUFH
EHDWV
TT Pulse-oxymeter with probe
PLQ
TT ,QWXEDWLRQHTXLSPHQWV/DU\QJRVFRSHVZLWK
TT Less tissue

perfusion VWUDLJKWEODGHVHQGRWUDFKHDOWXEHV
TT 'UXJV$GUHQDOLQH(1:10,000)1DOR[RQH
FDSLOODU\
UH¿OOWLPH! '$1D&O
VHF TT 2WKHUV

TT 0XVFXODU l 6WHWKRVFRSH l 8PELOLFDOYHQRXVFDWKHWHU

hypotonia
TT Features of

DFXWHNLGQH\ An asphyxiated baby (vacant stare)

LQMXU\e.g
oliguria
 Step on to Paediatrics 55

A. Resuscitation at birth B. Post-Resuscitation management

,WLVDVHWRILQWHUYHQWLRQVUHTXLUHGDWWKHWLPHRIELUWKWRVXSSRUW XX Maintain body temperature PHQWLRQHGHDUOLHU
HVWDEOLVKLQJEUHDWKLQJDQGFLUFXODWLRQ7KHLQWHUYHQWLRQVVXSSRUW
WRDFKLHYHQRUPDOWUDQVLWLRQUDWKHUWKDQLPSRVLQJDQDOWHUQDWH XX Support respiration E\±
SURFHVV TT 6XSSOHPHQWDO2E\QDVDOFDQXOD /PLQ 
KHDGER[ /PLQ 
TT 0HFKDQLFDOYHQWLODWLRQ

XX Maintain adequate hydration, electrolyte,

calcium and glucose homeostasis by
TT ,QIXVLRQRIDSSURSULDWH,9ÀXLGZLWK

UHVWULFWLRQRIWRWDOGDLO\DOORZDQFH

XX Regular monitoring of
TT Respiratory status: Respiratory rate
l

lCyanosis l 5K\WKP SDWWHUQ

TT &LUFXODWRU\VWDWXV

l+HDUWUDWH l BP CRT l

TT 5HQDOIXQFWLRQDOVWDWXV

lUrine volume 6FUHDWLQLQH

l

TT &DSLOODU\EORRGJOXFRVHVWDWXV

TT $UWHULDOEORRGJDV $%* DQDO\VLVZKHQ

needed
XX 7UHDWPHQWRIVSHFL¿FVLWXDWLRQV
TT ,IVKRFN(CRT>3 sec, low volume pulse, low

Steps of Resuscitation at a glance BP):

,QIXVH1RUPDO6DOLQHEROXVPONJRYHU
min
7KHNH\SRLQWVDUH Give 'RSDPLQH'REXWDPLQH—JPNJPLQ
XX Keep the baby warm by TT ,IFRQYXOVLRQ&RQWURODVSHUSURWRFRO 3DJH

TT ,PPHGLDWHGU\LQJDQGZUDSSLQJWKHEDE\LQFOXGLQJKHDG TT ,IVHSVLV3DUHQWHUDOEURDGVSHFWUXPDQWLELRWLFV

with a dry warm towel

TT 3URYLGLQJDURRPKHDWHULIDYDLODEOH Prognosis
XX 2YHUDOOPRUWDOLW\$PRQJWKHVXUYLYRXUV
XX Open and maintain airway by PD\GHYHORSWKHIROORZLQJQHXUR
TT .HHSLQJWKHEDE\LQQHXWUDODLUZD\SRVLWLRQ QHLWKHURYHU GHYHORSPHQWDOVHTXHODH
H[WHQVLRQQRUK\SHUÀH[LRQRIQHFN TT Cerebral palsy  Cranial nerve palsy


Post maturity, Perinatal asphyxia

TT &KLQOLIW MDZWKUXVW TT (SLOHSV\6HL]XUHGLVRUGHUV ,QWHOOHFWXDO


TT 3ODFLQJDUROORIWRZHO FP XQGHUEDE\¶VVKRXOGHUV disability

TT &OHDULQJWKHDLUZD\E\JHQWOHVXFWLRQ TT 'HDIQHVV9LVXDOSUREOHPV 0LFURFHSKDO\


XX Support breathing by
TT Stimulating the baby HJUXEELQJWKHEDFNJHQWO\VODSSLQJ

RUÀLFNLQJWKHVROHVRIWKHIHHW
TT Positive pressure ventilation using EDJDQGPDVNwith or

ZLWKRXW(QGRWUDFKHDOWXEH

XX Maintain oxygenation and circulation by

TT &KHVWFRPSUHVVLRQDQGFRRUGLQDWHGSRVLWLYHSUHVVXUH

ventilation
TT 0HFKDQLFDOYHQWLODWLRQ
 56 Step on to Paediatrics

The Steps of Resuscitation (WHO 2005)

Hypoxic ischaemic encephalopathy

,IDIWHUPLQXWHVRIUHVXVFLWDWLRQWKHEDE\LVQRWEUHDWKLQJDQGSXOVHLVDEVHQWVWRSDOOHIIRUWVDQG
FRXQVHOSDUHQWVWKDWWKHEDE\KDVH[SLUHG
 Step on to Paediatrics 57

ACTION PLAN Respiratory distress in newborn

Helping Babies Breathe :KHQHYHUDQHRQDWHSUHVHQWVZLWKUHVSLUDWRU\GLVWUHVVWKH
Prepare for birth IROORZLQJFRQGLWLRQVVKRXOGEHFRQVLGHUHG±
Birth
XX Respiratory distress XX 'LDSKUDJPDWLF
V\QGURPH 5'6 KHUQLDHYHQWUDWLRQRI
XX Perinatal asphyxia diaphragm
XX 7UDQVLHQWWDFK\SQRHD XX Persistent pulmonary
RIQHZERUQ 771 hypertension
,IPHFRQLXPFOHDUDLUZD\ XX 0HFRQLXPDVSLUDWLRQ XX Congenital heart
Dry throughly syndrome GLVHDVHVKHDUWIDLOXUH
Crying Crying 1RWFU\LQJ

SM
XX Congenital pneumonia XX Pulmonary hypoplasia

The Golden Minute

XX Spontaneous orFRQJDQRPDO\RI
pneumothorax UHVSWUDFW

In this section RDS and TTN will be discussed.

Clear airway
Stimulate
Breathing?

Keep warm Not breathing

Breathing well
Check Cut cord
breathing RESPIRATORY DISTRESS
SYNDROME (RDS): HYALINE
MEMBRANE DISEASE
5'6 DOVRNQRZQDVK\DOLQHPHPEUDQHGLVHDVH LV
Cut cord 60 sec GH¿QHGDVUHVSLUDWRU\GLI¿FXOW\VWDUWLQJVKRUWO\DIWHUELUWK
Breathing Ventilate FRPPRQO\DPRQJSUHWHUPLQIDQWVDQGLVGXHWRGH¿FLHQF\
of Surfactant.
Not breathing
Call for help Risk factors
Monitor XX Prematurity
with mother XX ,QIDQWRIGLDEHWLFPRWKHU
XX )(DUO\FRUGFOXPSLQJ

Breathing Improve ventilate XX +\SRWKHUPLD

XX &DHVDUHDQVHFWLRQ
Not breathing
Heart rate
XX Birth depression
XX 2WKHUVHJER\V!JLUOVndWZLQJHQHWLFSUHGLVSRVLWLRQ
*Prepare for birth Timer

Gloves
Pathogenesis
Normal 1RUPDOO\VXUIDFWDQW UHOHDVHGE\W\SHSQHXPRF\WHV
Cloths DSSHDUVLQIRHWXVE\ZHHNVRIJHVWDWLRQEXW
Slow DGHTXDWHDPRXQWVDUHQRWVHFUHWHGXQWLOZHHNVRI
Not Continue ventilation
Ventilation JHVWDWLRQ UHGXFHVVXUIDFHWHQVLRQLQWKHDOYHROLVRWKDW
bag-mask breathing Advanced care WKH\FDQLQÀDWH,Q5'6VXUIDFWDQWGH¿FLHQF\UHVXOWV
Ties Head LQFROODSVHRIDOYHROL7KLVFDXVHVUHGXFHGDLUHQWU\
Scissors covering
LQDOYHROLLPSDLUPHQWLQJDVH[FKDQJHK\SR[LD 
Stethoscope Suction Timer
device (clock, watch) K\SHUFDUELDDFLGRVLVDQG¿QDOO\UHVSLUDWRU\GLVWUHVVDQG
respiratory failure.
Adapted from: American Academy of Pediatrics. Helping
Babies Breathe, Learner Workbook; 2010
 58 Step on to Paediatrics

Investigations
Prematurity XX ;5D\&KHVW
5HGXFHGVXUIDFWDQWV\QWKHVLVVWRUDJHDQGUHOHDVH VKRZV±

'HFUHDVHGDOYHRODUVXUIDFWDQW TT Ground glass

,QFUHDVHGDOYHRODUVXIDFHWHQVLRQ DSSHDUDQFH

$WHOHFWDVLV
TT $LU
8QHYHQSHUIXVLRQ+\SRYHQWLODWLRQ EURQFKRJUDP

Hypoxemia + CO2 retention

TT Complete
$FLGRVLV white out
lungs e.g.
Pulmonary loss of
YDVRFRQVWULFWLRQ ,QFUHDVHG
diffusion
GHPDUFDWLRQ
Pulmonary hypoperfusion gradiant visualization
of heart Ground glass appearance with air bronchogram

Epithelial damage Endothelial damage borders

TT 3QHXPRWKRUD[ SQHXPRPHGLDVWLQXP LQFDVHRI
DVVRFLDWHGDLUOHDN 
3DOVPDOHDN )LEULQQHFURWLFFHOOV
into alveoli K\DOLQHPHPEUDQH
XX Blood
TT &%&3%)1RQVSHFL¿F

Pathophysiology of RDS, Adopted from Robbins pathology, 8th ed. TT &535DLVHGLIDVVRFLDWHGLQIHFWLRQ

TT $UWHULDOEORRGJDV $%* $OWHUHGe.g. DFLGRVLV

TT 6HUXPHOHFWURO\WHV0D\KDYHG\VHOHFWURO\WDHPLD

Normal
Collapsed
alveoli
alveoli Management
A. Supportive
.HHSWKHEDE\ZDUPHJNHHSLQJXQGHUUDGLDQW
Source: Internet

TT

ZDUPHUFRYHULQJWKHEDE\ZLWKZDUPFORWKHV
TT .HHSWKHEDE\132DQGSXWRQDSSURSULDWH,9ÀXLG
'$XSWRstKRXUVWKHQ'H[WURVHLQ
1D&O
TT Respiratory support HJ&OHDULQJDLUZD\JLYLQJ2
Clinical Manifestations /PLQ WKURXJKKHDGER[
XX 5HVSLUDWRU\GLVWUHVVZLWKLQst hour of birth in a preterm
EDE\DVPDQLIHVWHGE\±
TT )DVWEUHDWKLQJ !EUHDWKVPLQ

TT Flaring of alae nasi

Helping babies breathe

TT 6WHUQDO LQWHUFRVWDOUHWUDFWLRQFKHVWLQGUDZLQJ
TT Grunting

XX Cyanosis
XX 0DQLIHVWDWLRQVRIUHGXFHGDLUHQWU\LQWROXQJVe.g.
SDXFLW\RIFKHVWPRYHPHQWIHHEOHEUHDWKVRXQGV
XX )DOOLQJ2[\JHQVDWXUDWLRQ 632 O2 supplementation through Head box

Diagnosis ³³ If baby does not improve and develop severe

'LDJQRVLVLVEDVHGRQFOLQLFDOSUHVHQWDWLRQDQGVXSSRUWV EUHDWKLQJGLI¿FXOW\ZLWKIDOOLQJ632WKHQ
from relevant investigations NHHSWKHEDE\RQnCPAPDQGLIUHTXLUHGRQ
mechanical ventilator
 Step on to Paediatrics 59

Aetiology: 8QNQRZQ
Pathophysiology
TTN results from delayed absorption RIÀXLGIURPIRHWDO
DOYHROLZKLFKOHDGVWRDOYHRODUK\SRYHQWLODWLRQZLWKD
variable severity of respiratory distress and the related
FRQVHTXHQFHV

Clinical Manifestations
Respiratory support with CPAP XX 0LOGWRPRGHUDWHUHVSLUDWRU\GLVWUHVVDVPDQLIHVWHGE\±
TT 7DFK\SQRHD &KHVWUHWUDFWLRQV Cyanosis
 

TT Flaring of alae nasi *UXQWLQJ RFFDVLRQDO

Investigations
XX ;5D\FKHVW6KRZVSURPLQHQWYDVFXODUPDUNLQJVÀXLG
LQWKHLQWHUOREDU¿VVXUHRYHUDHUDWLRQÀDWGLDSKUDJP
XX &%&&531RQVSHFL¿F
Courtesy: Dr. Farzana Sharmeen

Newborn in mechanical ventilation

XX 5HJXODUEHGVLGHPRQLWRULQJRI±
TT Respiratory status HJF\DQRVLVUHVSLUDWRU\UDWH

UK\WKP SDWWHUQDLUHQWU\632
TT &LUFXODWRU\VWDWXVHJ&57KHDUWUDWH%3

TT Body temperature

TT &DSLOODU\JOXFRVHVWDWXV

XX $UWHULDOEORRGJDV $%* DQDO\VLVZKHQLQGLFDWHG

XX ,IVHSVLV,9$QWLELRWLFVe.g. Ampicillin plus Gentamicin

%6SHFL¿F
XX $GPLQLVWHUSurfactant 'RVHPONJ'LYLGHLQWR Respiratory distress syndrome
DOLTXRWV DQGLQWURGXFHWKURXJK(7WXEH'XULQJWKLV Treatment
SURFHVVNHHSWKHEDE\HLWKHURQ&3$3RURQYHQWLODWRU XX 0DLQO\VXSSRUWLYHe.g.
TT .HHSWKHEDE\ZDUP

TT 2 LQKDODWLRQ/PLQ E\QDVDOFDQXOD /PLQ


by head box
TRANSIENT TACHYPNOEA OF TT 132DQGLQIXVLRQRIDSSURSULDWH,9ÀXLG

NEWBORN (TTN): WET LUNGS TT $QWLELRWLFV±XVXDOO\QRWUHTXLUHG

7UDQVLHQWWDFK\SQRHDRIQHZERUQ 771 LVDUHODWLYHO\

PLOGVHOIOLPLWHGSXOPRQDU\GLVRUGHUXVXDOO\QRWHG
Prognosis
DPRQJEDELHVZKRDUHERUQDWQHDUWHUP *RRGZLWKXQHYHQWIXOUHFRYHU\E\KRXUV
 60 Step on to Paediatrics

NEONATAL SEPSIS (NS)

6HSVLVLVRQHRIWKHOHDGLQJFDXVHRIQHRQDWDOPRUELGLW\DQG
PRUWDOLW\,WLVGH¿QHGDVSUHVHQFHRIPLFURRUJDQLVPVWKHLU
SUROLIHUDWLRQZLWKSURGXFWLRQRIWR[LQVLQWKHEORRG%DVHGRQWKH
WLPHRIDFTXLVLWLRQRILQIHFWLRQQHRQDWDOVHSVLVLVGLYLGHGDV±
XX Early onset sepsis (EONS):6HSVLVWKDWLVDFTXLUHGEHIRUHRU
GXULQJELUWKDQGPDQLIHVWHGZLWKLQ¿UVWKRXUVRIELUWK
XX Late onset sepsis (LONS):6HSVLVWKDWLVDFTXLUHGDIWHU
GHOLYHU\ LQWKHQXUVHU\RULQWKHFRPPXQLW\ PDQLIHVWHG
XVXDOO\DIWHUKRXUVRIELUWK

Aetiology
Common Organisms
EONS LONS
Lethargic baby
TT *URXS%6WUHSWRFRFFXV XX Staphylococcus aureus
TT Escherichia coli XX Coagulase-Ve Staph.
,,6SHFL¿FDQGUHODWHGWRWKHLQYROYHPHQWRI
TT H. Influenzae XX Klebsiella pneumoniae
VSHFL¿FERG\V\VWHPV
TT .OHEVLHOODVS XX Pseudomonas aeruginosa
TT Listeria XX $FLQHWREDFWHU Candida sp. Systems Clinical features
monocytogenes XX (QWHUREDFWHU Serratia XX Central ,UULWDELOLW\IXOOIRQWDQHOOHVHL]XUH
nervous YDFDQWVWDUHKLJKSLWFKHGFU\
Risk Factors system QHFNUHWUDFWLRQK\SRWRQLD
XX 3UHPDWXULW\ ZHHNV *UXQWLQJDSQRHDLUUHJXODU
/RZELUWKZHLJKW JUDPV 
XX Respiratory
XX
EUHDWKLQJIDVWEUHDWKLQJVHYHUH
system
XX )HEULOHLOOQHVVRIPRWKHUZLWKHYLGHQFHRIEDFWHULDOLQIHFWLRQ FKHVWLQGUDZLQJorF\DQRVLV
ZLWKLQZHHNVRIGHOLYHU\
%UDG\FDUGLDRUWDFK\FDUGLD
XX )RXOVPHOOLQJDQGRUPHFRQLXPVWDLQHGOLTXRU XX Cardio-
IHDWXUHVRIVKRFNHJK\SRWHQVLRQ
XX 5XSWXUHRIDPQLRWLFPHPEUDQH!KRXUV YDVFXODU
poor perfusion (prolonged
XX 6LQJOHXQFOHDQor!VWHULOHYDJLQDOH[DPLQDWLRQ V GXULQJ system
FDSLOODU\UHILOOLQJWLPH!VHF 
labour
XX 3URORQJHGODERXU VXPRIGXUDWLRQRIst nd stage of labour 3HULXPELOLFDOUHGQHVVRUIRXO
Transient tachypnoea of the newborn

!KRXUV XX 6NLQ VPHOOLQJXPELOLFDOGLVFKDUJH

XX 3HULQDWDODVSK\[LD $3*$5VFRUHDWPLQXWH FKDQJHV PXOWLSOHSXVWXOHVPRWWOLQJ
XX 0HFKDQLFDOYHQWLODWLRQ VFOHUHPD
XX ,QYDVLYHSURFHGXUHV XX +DHPDWR $QDHPLDMDXQGLFHEOHHGLQJe.g.
XX 3RRUK\JLHQHSRRUFRUGFDUH ORJLFDO SHWHFKLDHSXUSXUD
XX %RWWOHIHHGLQJSUHODFWHDOIHHGV
$.,PDQLIHVWHGDVROLJXULDRU
XX .LGQH\V
Clinical Manifestations anuria.
I. 1RQVSHFL¿FLQPRVWFDVHV 9RPLWLQJDEGRPLQDOGLVWHQVLRQ
XX GIT
KHSDWRVSOHQRPHJDO\MDXQGLFH
XX 1RWIHHGLQJZHOOUHIXVDO XX 3RRUFU\
WRVXFN XX 0RYHPHQWRQO\
XX /HVVDOHUWOHVVDFWLYH when stimulated or no Diagnosis
XX +\SRor hyperthermia movement at all
%DVHGRQFOLQLFDOVXVSLFLRQVXJJHVWLYH&)DQG
XX /HWKDUJ\SRRUPXVFOH XX 3ULPLWLYH5HÀH[HV±
VXSSRUWLYH¿QGLQJVIURPUHOHYDQWLQYHVWLJDWLRQV
WRQHOHVVPRYHPHQW 'LPinished or$EVHQW
 Step on to Paediatrics 61

Investigations
XX CBC with PBF
TT 7& '&RI:%&,QFUHDVHRUGHFUHDVH
TT +E0D\EHGHFUHDVHG

TT 3ODWHOHWV0D\EHGHFUHDVHG

TT 3%)6KRZVWR[LFJUDQXOHVRUEDQGIRUPRI

neutrophil
XX Blood
TT 6HSVLV6FUHHQLQJ

7RWDOOHXFRF\WHFRXQW FPP
$EVROXWHQHXWURSKLO FPPIRUWHUP
Sepsis screening

FRXQW FPPIRUSUHWHUP
Immature to total
!
QHXWURSKLO ,7 UDWLR
&UHDFWLYHSURWHLQ &53  Positive
0LFUR(65 !PPLQst hour
+DSWRJORELQ 3RVLWLYH !PJGO

TT 3URFDOFLWRQLQ5DLVHG
TT &XOWXUH VHQVLWLYLW\0D\UHYHDOWKHRUJDQLVP
TT &6)VWXG\(YLGHQFHRIPHQLQJLWLV± Pneumoperitoneum (Drooping Lily sign)
l +D]\CSF 3OHQW\RI:%&
l /RZJOXFRVH
l

l Raised CSF pressure 5DLVHGSURWHLQHWF

l XX Ultrasonogram of brain or others as individualized

Courtesy: Prof. Shahida Akhter, Dr, Baki, BIRDEM

CSF profile of healthy term neonates

Parameters Result

$SSHDUDQFH Clear

&HOOFRXQW :%& PP301

3URWHLQ PJGO  5DQJH

*OXFRVH PJGO  5DQJH

XX 8ULQHVWXG\ 50(&6 (YLGHQFHRI87,e.g.

SUHVHQFHRISXVFHOOV5%&DOEXPLQXULDJURZWKRI
EDFWHULDDQGDQWLELRWLFVHQVLWLYLW\
XX ;5D\&KHVW7RORRNIRUDQ\HYLGHQFHRISQHXPRQLD
XX ;5D\DEGRPHQ(YLGHQFHRI1(&e.g.
Neonatal sepsis

TT Pneumatosis intestinalis

TT Gas in portal vein

TT 3QHXPRSHULWRQLXP VXEGLDSKUDJPDWLFJDV DVRFFXUV

Pneumatosis intestinalis
in perforation of gut
 62 Step on to Paediatrics

Treatment C. Follow up (during hospital staying)

XX +RVSLWDOL]HWKHEDE\ TT Vital signs HJKHDUWUDWHUHVSLUDWRU\UDWH%3DQG
$6SHFL¿F 6HOHFWWKHUHFRPPHQGHGDQWLELRWLFV temperature
TT 3ULPLWLYHUHÀH[HVHJVXFNLQJURRWLQJPRURDQGRWKHUV
 line
st
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nd line &HIWD]LGLPH$PLNDFLQ PRWWOLQJHWF
TT $QWHULRUIRQWDQHOOHe.g. any bulging or fullness
0HURSHQHP&LSURIOR[DFLQ TT $EGRPHQHJDQ\GLVWHQWLRQSUHVHQFHRIERZHOVRXQG
9DQFRP\FLQ&HIHSLPH
rd line passage of urine and stool
&ODULWKURP\FLQ1HWLOPLFLQ
5HVHUYH TT $Q\XQWRZDUGHYHQWVHJFRQYXOVLRQDSQRHDF\DQRVLV
,PLSHQHP3LSHUDFLOOLQ
HWF
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Interventions addressing newborn complications and
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sickness '2014
meningitis 0HURSHQHP$PLNDFLQ
XX &KORUKH[LGLQHDSSOLFDWLRQDVSDUWRIURXWLQH(1&
N.B. Antibiotics are given parenterally and may be
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changed according to culture & sensitivity report.
XX $QWHQDWDOFRUWLFRVWHURLG $&6 HJ%HWDPHWKDVRQH
Empirical use of reserve antibiotics should be avoided.
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promote lungs maturation
Diagnosis Duration XX .DQJDURR0RWKHU&DUH .0& IRUWKHUPDOSURWHFWLRQ
XX 5LVNIDFWRUSRVLWLYHLH FOLQLFDOO\ZHOO RISUHWHUPORZELUWKZHLJKWQHZERUQV
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XX 5LVNIDFWRUSRVLWLYHVFUHHQSRVLWLYH
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XX &OLQLFDOO\VHSVLV VFUHHQQHJDWLYH GD\V
XX &OLQLFDOO\VHSVLVVFUHHQSRVLWLYH
GD\V
FXOWXUHQHJDWLYH
XX %ORRGFXOWXUHSRVLWLYHEXWQRPHQLQJLWLV GD\V NEONATAL JAUNDICE
XX 0HQLQJLWLV ZLWKRUZLWKRXWSRVLWLYH
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B. Supportive
XX Hypothermia:UDSSLQJWKHEDE\ZLWKZDUPWRZHO
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XX Hypoglycaemia,QWUDYHQRXV'$#PONJ
stat
XX Nutrition: Breast feeding
TT ,IVXFNLQJLVQRWVDWLVIDFWRU\WKHQQDVRJDVWULF

RURJDVWULFIHHGLQJZLWKH[SUHVVHGEUHDVWPLON
TT ,IEDE\FDQQRWWROHUDWHRUDOQDVRJDVWULFIHHGLQJ

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Neonatal sepsis

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XX 2WKHUVXSSRUWLYHRSWLRQVe.g.
TT ,9LPPXQRJOREXOLQ FRQWDLQV,J* DOVR,J0 Newborn with jaundice extending to palms & soles
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Aetiology Pathogenesis
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hematopoiesis decompensation
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 64 Step on to Paediatrics

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 Step on to Paediatrics 65

But if S bilirubin is raised at a level when treatment What is the mechanism of action?
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end
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 66 Step on to Paediatrics

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 Step on to Paediatrics 67

Algorithm for Control of Neonatal Convulsion

Phenobarbitone IV Wean anti-epileptic
20 mg/kg over 20 drug slowly when
minutes Convulsion stops
(slowly@
1mg/kg/min) Convulsion continues
Investigation for
NB. Check & correct specific cause
hypoglycaemia or depending upon
clinical feature Consider other
hypocalcaemla if present antiepileptic drug

Convulsion continues
Convulsion continues
Repeat
Phenobarbitone
Consider
10 mg/kg/dose.
*Midazolum
If Convulsion continues Pyridoxine
repeat Lidocaine
Phenobarbitone Folinic acid
10 mg/kg/dose
Total
40mg/kg
Start Fosphenytoin
30 mg/kg/dose (IV)
diluted in Normal saline
Convulsion continues slowly@ 1mg/kg/min Convulsion continues

*Midazolam: Initial bolus 0.2 mg/kg then 0.05 – 2 mg/kg/hour in drip. Increase every 15 minute upto 2 mg/kg/hour if no response

Treatment of babies with maternatal antenatal illnesses

Management of babies delivered from mothers with specific antenatal diseases

Maternal diseases
Management to be given to baby
during pregnancy
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Common Birth Injuries

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 Step on to Paediatrics 69

Common Birth Injuries and their cardinal features

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 70 Step on to Paediatrics

Common Birth Injuries and their cardinal features

XX 7KHFKDUDFWHULVWLFSRVLWLRQLQ'XFKHQQH(UE VSDOV\OLNHWKDWRIwaiters tip

hand. 7KLVFRQVLVWVRI±
TT $GGXFWLRQDWWKHVKRXOGHU

TT Internal rotation of the upper arm

TT Pronation of the forearm

TT 2XWZDUGGLUHFWLRQRIWKHSDOPRIWKHKDQG

XX ,QDGGLWLRQSDWLHQWZLOOKDYHDV\PPHWULF0RURUHÀH[DEVHQWELFHSVMHUNEXW
hand grasp is usually present

Management
XX 5HOD[DWLRQRIWKHSDUDO\]HGPXVFOHVMXVWRSSRVLWHWRWKHSDWKRORJLFDOSRVLWLRQ
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pillow beside head
Brachial plexus injuries e.g. Duchenne- XX 3K\VLRWKHUDS\PLOGHOHFWULFDOVWLPXODWLRQQHXURSODVW\
Erb's palsy, Klumpke's palsy.

XX ,QIDQWGRHVQRWPRYHWKHDUPIUHHO\RQWKHDIIHFWHGVLGH
XX Crepitus and bony irregularity may be palpated
Source: Internet

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Common birth injuries

XX 6SRQWDQHRXVPRYHPHQWRIWKHDIIHFWHGOLPELVDEVHQW
Source: Internet

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 Step on to Paediatrics 71

References
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SELF ASSESSMENT
Short answer questions [SAQ)
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 09
Nutritional Disorders
Protein energy malnutrition (PEM) - - - - - - - - - - 72
Acute malnutrition
¼¼ Moderate acute malnutrition (MAM) - - - - - - - - - 74
¼¼ Severe acute malnutrition (SAM)- - - - - - - - - - 74
Vitamin deficiency disorders
¼¼ Xerophthalmia - - - - - - - - - - - - - 79
¼¼ Scurvy- - - - - - - - - - - - - - - 80
¼¼ Rickets - - - - - - - - - - - - - - - 81
Childhood obesity - - - - - - - - - - - - - 85

,QDGHYHORSLQJFRXQWU\OLNH%DQJODGHVKPDQ\ Aetiology & Risk factors

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Risk Factors

FRPSOHPHQWDU\IHHGLQJIDXOW\SUHSDUDWLRQRIIRRGV 
XX Protein energy malnutrition (3(0 O/RZFDORULHIRRG )RRGGH¿FLHQWLQSURWHLQ
O

XX 9LWDPLQDQGRWKHUPLFURQXWULHQWGH¿FLHQFLHV O Fat and minerals

XX 1XWULWLRQDODQDHPLDHJLURQGH¿FLHQF\ XX &ORVHO\VSDFHGSUHJQDQFLHV
anaemia XX /DFNRIWHQGHUORYH FDUH
XX ,RGLQHGH¿FLHQF\GLVRUGHUVe.g. hypothyroidism XX +HOPLQWKLDVLV
XX 0HQWDORUSK\VLFDOKDQGLFDSRURWKHUFRQFRPLWDQW
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Weight-for-age
PROTEIN ENERGY Without oedema With oedema
(% of median*)
MALNUTRITION (PEM)  Under nourished .ZDVKLRUNRU
,WLVDSDWKRORJLFDOFRQGLWLRQRFFXUULQJPRVW 0DUDVPLF
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Weight-for-age
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(% of median*)
VWDWXVRIXQGHUFKLOGUHQLQ%DQJODGHVKDUH±
 Normal
PEM

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st
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nd

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72

* Median is the 50th percentile value of CDC chart.

 Step on to Paediatrics 73

&KDUW &KDUW

How to Calculate Z Score

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PEM
 74 Step on to Paediatrics

ACUTE MALNUTRITION SEVERE ACUTE MALNUTRITION

(SAM)
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features given below VXFKDV 6$0LVFKDUDFWHUL]HGE\WKHSUHVHQFHRIVHYHUHZDVWLQJ
D 08$&PPDQGRU HJORZZHLJKWIRUKHLJKW :+=±6'08$&
PP DQGRUELSHGDORHGHPD+HUHQRGLVWLQFWLRQLV
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IROORZV±
XX 0RGHUDWH$FXWH0DOQXWULWLRQ 0$0 DQG
XX 6HYHUH$FXWH0DOQXWULWLRQ 6$0
Revised Diagnostic Criteria for SAM

Parameters Normal MAM SAM A. Children between 6-60 months :+2¶

XX 08$&PP • WR  Indicators Measure Cut-off
•± ± Severe wasting :HLJKWIRUKHLJKW ±6'
XX :+=6' ±WR±6'
6' 6'
0LGXSSHUDUP
XX Bipedal oedema $EVHQW $EVHQW Present Severe wasting PP
FLUFXPIHUHQFH 08$&
MAM: Moderate Acute Malnutrition; SAM: Severe Acute Malnutrition
WHZ: Weight for Height Z score; MUAC: Mild upper arm circumference Bilateral oedema &OLQLFDOVLJQ Present

&KLOGUHQZLWKVHYHUHDFXWHPDOQXWULWLRQPD\DGGLWLRQDOO\ 1 = Based on WHO standard; 2,3 = independent indicators of SAM

have bipedal oedema B. Children <6 months

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XX :HLJKWIRUKHLJKW= XX Visible wasting

VFRUH :+= ±6' XX Bipedal oedema

MODERATE ACUTE MALNUTRITION

(MAM) Clinical Features of SAM
(.ZDVKLRUNRU 0DUDVPXV
Management XX 6NLQFKDQJHV QXWULWLRQDOGHUPDWRVHV
7RVWRSSURJUHVVLRQIURP0$0WRZDUGV6$0DQGKHOSWR
TT )ODN\SDLQWGHUPDWRVLV TT 0RVDLFGHUPDWRVLV
EULQJWKHQXWULWLRQDOVWDWXVEDFNWRQRUPDOIRUDJHDQGVH[
TT Crazy pavement TT 'HSLJPHQWDWLRQ
0DQDJHPHQWFRPSULVHV± dermatosis TT ,QGROHQWVRUHV XOFHUV
XX &RXQVHOLQJWKHSDUHQWVFDUHJLYHUVRQKHDOWK\IHHGLQJ TT 5HWLFXODUSLJPHQWDWLRQ TT 6XSHULPSRVHGLQIHFWLRQ
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TT +RPHPDGHIRRGZLWKDJRRGSURSRUWLRQIURP
Severe acute malnutrition

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TT ([WUDPHDOWRSURYLGHDGGLWLRQDO!NFDONJGD\

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TT )RUWL¿HGVWDSOHIRRGZLWKPLFURQXWULHQWSRZHU

XX 'HZRUPLQJVKRXOGEHGRQHDWOHDVWPRQWKO\
XX 7UHDWPHQWRIDQ\DVVRFLDWHGLQIHFWLRQV
XX 3URPRWLRQRIIRRG RWKHUK\JLHQHWRSUHYHQWIXUWKHU
LQIHFWLRQ Shiny skin due to oedema (Seen in kwashiorkor)
 Step on to Paediatrics 75

Crazy pavement dermatosis with sores (Seen in kwashiorkor) Baggy pant appearance (seen in marusmus)

Salient Features: Marasmus

& Kwashiorkor
Clinical features Marasmus Kwashiorkor

:HOODOHUW Rounded and

XX )DFH
ZL]HQHGIDFH oedematous
XX Visible severe
2EYLRXV Less obvious
wasting
Flaky paint dermatosis with hypo and hyper pigmentations XX 2HGHPD $EVHQW Present
(Seen in kwashiorkor)
XX 6NLQFKDQJHV /HVVIUHTXHQW Present
XX +DLUFKDQJH $EVHQW Present
XX 0HQWDOFKDQJH Sometimes Usually present
XX $SSHWLWH Good Poor
XX +HSDWRPHJDO\ $EVHQW Present

Complications
Flaky paint dermatosis with hypo and hyper pigmentations
(seen in kwashiorkor) XX ,QIHFWLRQERWKRYHUW KLGGHQHJ7%
XX 'HK\GUDWLRQ G\VHOHFWURO\WDHPLD
XX +\SRJO\FDHPLD
XX +\SRWKHUPLD
XX $QDHPLD
XX &RQJHVWLYHFDUGLDFIDLOXUH
Bleeding
Management of SAM

XX

XX ;HURSKWKDOPLD EOLQGQHVV
XX Sudden infant death syndrome

Severe wasting of periorbital and other facial muscles

 76 Step on to Paediatrics

Diagnosis Time-frame for Management of SAM

9LUWXDOO\FOLQLFDO+RZHYHULQYHVWLJDWLRQVVKRXOGEHGRQH Rehabilitation
WRDVVHVVWKHELRFKHPLFDOVWDWXVDQGWRVFUHHQLQIHFWLRQ Stabilization Phase
Steps Phase
Days 1-7
7KHVHDUH± Weeks 2-6
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Investigations Results
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TT ,QIHFWLRQ feeding
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Prepare for
Management
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1. Stabilization phase
General Principles of 10 Steps
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WKLVSKDVH±
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XX Feeding is started TT *LYHPORIJOXFRVHRUDOO\1*WXEHRUPO

NJRIJOXFRVH,9
TT 6WDUW FRQWLQXHKRXUO\IHHGGD\DQGQLJKW
2. Rehabilitation phase
Step 2: 7UHDW3UHYHQW+\SRWKHUPLD
This phase is signaled by return of appetite and
$[LOODU\ƒ&RUƒ)5HFWDOƒ)RUƒ&
GLVDSSHDUDQFHRIPRVWDOORIWKHRHGHPD,WXVXDOO\WDNHV
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XX :DUPWKHFKLOG
SKDVH'XULQJWKLVSKDVH±
TT &ORWKHWKHFKLOGLQFOXGLQJWKHKHDGFRYHUZLWKD
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XX ,QWHQVLYHIHHGLQJLVVWDUWHGEXWVORZO\WRUHFRYHUWKH TT 3XWWKHFKLOGRQPRWKHU¶VEDUHFKHVWIRUVNLQWRVNLQ
lost weight
Management of SAM

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XX The mother orFDUHJLYHUVDUHWUDLQHGKRZWR NHHSDZD\
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XX 3UHSDUDWLRQVDUHPDGHIRUGLVFKDUJHRIWKHFKLOG XX $YRLG
prolonged
exposure for
examination
SURFHGXUH
 Step on to Paediatrics 77

Step 3:7UHDW3UHYHQW'HK\GUDWLRQ Step 6:&RUUHFW0LFURQXWULHQWGH¿FLHQFLHV

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is rehydrated
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and heart failure
XX ,IFKLOGLVEUHDVWIHGHQFRXUDJHPRWKHUWRFRQWLQXH
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TT )ROLFDFLGPJ WDE RQGD\WKHQPJGD\
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TT =LQF PJWVI PJNJGD\
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TT &RSSHUPJNJGD\ LIDYDLODEOH
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lost in urine or stools Step 7: Start Feeding Cautiously
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the following manner.
TT .PPRONJGD\ HDFKPOFRQWDLQVPPRO 
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tube feeding
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XX IV nutrition should never
TT Prepare food without salt
be given NG tube feeding
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XX :LWKEURDGVSHFWUXPDQWLELRWLFV± should be given
TT 2UDO$PR[LFLOOLQ PJNJ KRXUO\IRUGD\VRU XX 7RWDOÀXLGLQWDNHVKRXOGEH”PONJGD\EXW
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XX ,QVHYHUHO\LOOSDWLHQWV± HQFRXUDJHG
Management of SAM

TT ,9,0$PSLFLOOLQ PJNJ KRXUO\  Step 8:$FKLHYH&DWFKXSGrowth

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XX $ERXWZHHNDIWHUDGPLVVLRQZKHQDSSHWLWHKDV
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 78 Step on to Paediatrics

XX :HLJKWJDLQVKRXOGEHPRQLWRUHGWRDVVHVVUHVSRQVH± Treatment of Associated Conditions

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 82 Step on to Paediatrics

Investigations
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Treatment
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References
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 92 Step on to Paediatrics

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Conditions presenting with stridor Pathogenesis

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 Step on to Paediatrics 101

Diagnosis ACUTE EPIGLOTTITIS

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Treatment Clinical Manifestations

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References
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Self assessment
 11
Diarrhoea
Acute watery diarrhoea
¼¼ Rota virus - - - - - - - - - - - - - - 105
¼¼ V Cholerae- - - - - - - - - - - - - - 106
Persistent diarrhoea- - - - - - - - - - - - - 108
Dysentery- - - - - - - - - - - - - - 110

Diarrhoeal diseases are the leading cause of malnutrition ROTA VIRUS

and the second leading cause of deaths of children under
5 years of age. Each year about 10% under 5 children die XX Route of entry in the gut: Oral
from diarrhoea. XX ,QFXEDWLRQ3HULRGGD\V
:+2GH¿QHGGLDUUKRHDDVWKHIUHTXHQWSDVVDJHRIORRVH Pathogenesis
VWRROV'XULQJGLDUUKRHDLPSRUWDQWFOLQLFRSDWKRORJLFDO After entry, the virus infects, kills and destroy the mature
FRQVHTXHQFHVRFFXU7KHVHDUH± DEVRUSWLYHHQWHURF\WHV7KHGDPDJHGFHOOVDVZHOODV
XX Increased loss of water and electrolytes (e.g. WKHLUDIIHFWHGYLOOLDUHUDSLGO\UHSODFHGE\LPPDWXUHQRQ
Na+, K+ and HCO3 )LQWKHOLTXLGVWRROVOHDGLQJWR DEVRUSWLYHFU\SWOLNHFHOOV having no brush border and no
dehydration and dyselectrolytaemia brush border enzymes e.g. disaccaridase (lactase).
XX Loss of greater quantity of zinc in the loose stool
ZKLFKGHOD\VUHFRYHU\RISDWLHQWVIURPWKHGLVHDVH Ingestion of Rota virus particles
and make the child vulnerable to suffer afterwards
XX Weight loss due to decreased intake of food,
,QIHFWLRQRIDEVRUSWLYH Stimulation of enteric
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intestinal villus cells nervous system
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Types %OXQWLQJRIWLSFHOORIYLOOLRI
XX Acute watery diarrhoea intestine
XX Persistent diarrhoea
XX Dysentery ĻDEVRUSWLRQ ĻEUHDNGRZQRI
RIÀXLGDQG disaccharide
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DVVRFLDWHGYRPLWLQJDQGORZJUDGHIHYHU Osmotic diarrhea
Organisms
XX Rota virus, V. cholerae 01, 0139 $VDUHVXOWWKHUHLV±
XX Enterotoxigenic E.coli, Enteropathogenic E. coli, XX /HVVDEVRUSWLRQRIÀXLG HOHFWURO\WHVe.g. Na+, K+,
Enteroadherent E.coli, Campylobacter jejuni HCO± and their loss in stool which gives rise to
XX Cryptosporidium (dehydration, dyselectrolytaemia)
Of all these microbes, rota virus and V cholerae commonly XX Decreased breakdown of disaccaride/lactose and their
affect the gut of the children and will be discussed in this excretion in stool, which results in (Osmotic diarrhoea)
105

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 106 Step on to Paediatrics

V CHOLERAE TT Stool characteristics e.g.consistency e.g. watery,

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XX ,QFXEDWLRQSHULRG)HZKRXUVWRGD\VXVXDOO\ A B
days

Mechanism of cholera

Coutesy: Dr. Iqbal, Scientist, ICDDRB

V. CholeraeDFFXPXODWHVLQWKHJXW SURGXFHWR[LQV
D
7R[LQ$ELQGVWR*3URWHLQFRXSOHGUHFHSWRU C

Persistent stimulation of Adenylyl cyclase

2YHUSURGXFWLRQRIF$03 Appearances of stool in diarrhoea caused by A. Cholera,

B. ETEC, C. Shigella and D. Rota virus

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TT Diarrhoea/diarrhoeal deaths in the family or
,QFUHDVHGSXUJLQJRIZDWHU HOHFWURO\WHV neighbourhood
II. Physical examinationSDUWLFXODUO\WRDVVHVVIRU±
Pathogenesis 7R[LQPHGLDWHG TT Signs of dehydration
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toxins bind to a regulatory sub unit of adenyl cyclase in TT Signs of severe malnutrition
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lumen of small gut.

Clinical manifestations
XX Lethargy/unconscious
XX 0LOGGLDUUKRHDLQPRVWFDVHV+RZHYHULQ
XX Sunken eyes
ofcases diarrhoea is severe (Severe cholera) where there XX Unable to drink orGULQNVSRRUO\
LVVXGGHQRQVHWRIPDVVLYHIUHTXHQWZDWHU\VWRROV XX 6NLQSLQFKJRHVEDFNYHU\VORZO\ •VHF
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RIRQVHWWUHPHQGRXVORVVRIÀXLG HOHFWURO\WHVUHVXOWV 7KHQWKHFKLOGZLOOEHFDWHJRUL]HGDVSevere dehydration
LQ± and will be managed as Plan C.
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How to assess a child with diarrhoea ?

Whenever, a child is brought to you with diarrhoea, then
Acute diarrhoea

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TT Duration of diarrhoea
Unconsciousness & sunken eyes of a severely dehydrated child
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 Step on to Paediatrics 107

Irritable child Sunken eye

Investigations
XX 6WRRO50(1R5%&3XVFHOOVPDFURSKDVH
Skin pinch goes back to normal very slowly XX Stool for V. cholerae:
XX 6WRRO&67RVHHWKHJURZWKRIDQ\RUJDQLVP
XX ,I•RIWKHIROORZLQJVLJQVDUHSUHVHQW± XX %ORRGIRU&%&3%)/RZ+EFKDQJHVLQ:%&
XX S Electrolytes: Low Na+, K+, Cl±, HCO3±
XX Restless, irritable XX 2WKHUVHJ6&UHDWLQLQH;5D\DEGRPHQ LILQGLFDWHG
XX Drinks eagerly, thirsty
XX Sunken eyes
XX 6NLQSLQFKJRHVEDFNVORZO\
Treatment
7KHessential elements ofWUHDWPHQWDUH±
7KHFKLOGZLOOEHFDWHJRUL]HGDVsome dehydration and XX Antibiotics, when
will be managed as plan B.
XX Rehydration
diarrhoea is due to
XX Continued feeding
If the child has not enough signs to classify some or severe V cholerae or other
XX Zinc bacteriae
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and will be managed as plan A.

A. Rehydration
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Plan C
•RIWKHIROORZLQJVLJQV± XX &KRLFHRIÀXLGCholera saline, Ringer's lactate
TT Lethargy/ XX If not available: Dextrose in Normal Saline or Normal Saline
unconsciousness TT 1HYHUXVH'H[WURVHLQ$TXD '$

TT Sunken eyes XX $PRXQWRIÀXLGPONJ

Severe
TT Unable to drink or
dehydration
XX Route of rehydration: Intravenous
GULQNVSRRUO\ XX Duration of rehydration: 3 hours (<1 year), 6 hours (>1 year)
TT 6NLQSLQFKJRHVEDFNWR TT During rehydration, foods other than breast milk should be withheld

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0RQLWRULQJ
Acute diarrhoea

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XX ,IVLJQVRIVRPHGHK\GUDWLRQ'LVFRQWLQXH,9ÀXLGDQGJLYH256IRUKRXUVDVLQ3ODQ%
XX If no signs of dehydration: Advise mother to give ORS after each loose stool as in Plan A
 108 Step on to Paediatrics

•RIWKHIROORZLQJVLJQV± Plan B
TT Restless, irritable XX &KRLFHRIÀXLG2UDOUHK\GUDWLRQVROXWLRQ 256 
TT Sunken eyes XX $PRXQWRIÀXLGPONJ
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TT Drinks eagerly, thirsty XX Route of rehydration: Oral
dehydration
TT 6NLQSLQFKJRHVEDFNWR XX 'XUDWLRQRIUHK\GUDWLRQKRXUV
normal slowly TT During rehydration, foods other than breast milk should be withheld

Monitoring
XX 5HDVVHVVFKLOG VK\GUDWLRQVWDWXVDIWHUKRXUVRIRUDOUHK\GUDWLRQDQGGHFLGHDFFRUGLQJO\±
XX If no signs of dehydration: Advise mother to give ORS after each loose stool as in Plan A
XX If signs of some dehydration: Rehydrate with 256IRUDQRWKHUKRXUVDVLQ3ODQ%
XX ,IVLJQVRIVHYHUHGHK\GUDWLRQSUHVHQW5HK\GUDWHZLWK,9ÀXLGDVLQ3ODQ&

Plan A
XX&KRLFHRIÀXLGOral rehydration solution
TT Others HJFKLUDSDQLFRRNHGULFHZDWHU\RJXUW
XX Not enough signs to
classify as some or No $PRXQWRIÀXLGDIWHUHDFKVWRRO
severe dehydration dehydration XX /HVVWKDQ\HDUVPO
XX \HDUVDQGDERYHPO
Avoid: Very sweet tea, VRIWGULQNV VZHHWHQHGIUXLWGULQNV

$IWHUUHK\GUDWLRQDGYLFHPRWKHU±
XX 7RFRQWLQXHWUHDWPHQWDWKRPH Advice mother to encourage the child to eat at least 6
XX 7RFRQWLQXHIHHGLQJDWKRPH WLPHVDGD\ZLWKDQH[WUDPHDOGDLO\IRUZHHNVDIWHU
XX &RPHIRUURXWLQHIROORZXSLQGD\VDQG cessation of diarrhoea.
XX When to return immediately
D. Antibiotics
,IWKHEDE\± XX Rota diarrhoea: Antibiotic not indicated
XX 'ULQNVSRRUO\or unable to drink or breastfeed XX &KROHUDDQ\RQHRIWKHIROORZLQJ±
XX Becomes sicker TT 7HWUDF\FOLQHPJNJKRXUO\IRUGD\V

XX 'HYHORSVIHYHUor TT Azithromycin, 10 mg/kg/day OD for 5 days

XX %ORRGDSSHDUVLQVWRRO TT &LSURÀR[DFLQPJNJGD\KRXUO\IRUGD\V

TT &RWULPR[D]ROH703PJNJGD\KUO\IRU

days
B. Zinc supplementation
Age Dose Duration
Persistent diarrhoea, dysentery

< 6 months 10 mg/day GD\V

•PRQWKV PJGD\ GD\V

C. Feeding, to be continued PERSISTENT DIARRHOEA (PD)

Age Foods Diarrhoea, that begins acutely (with or without blood) and
0RQWKV XX Breast feeding ODVWVIRUGD\Vor PRUHZLWKQR!LQWHUYHQLQJGD\V
ZLWKRXWGLDUUKRHD,QGHYHORSLQJFRXQWULHVRIDOO
XX Breast feeding FKLOGKRRGGLDUUKRHDEHFRPHSHUVLVWHQWDQGFRQWULEXWHWR
XX )UHVKO\SUHSDUHGHQHUJ\GHQVH DERXWѿWRòRIDOOGLDUUKRHDUHODWHGGHDWKV
!0RQWKV
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O mashed banana fresh fruit juice etc.

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 Step on to Paediatrics 109

Types Investigations
XX Non-severe PD: PD, not associated with dehydration TT 6WRRO50(IRU*LDUGLD&6S+UHGXFLQJ
DQGFDQEHPDQDJHGDWKRPHZLWKVSHFLDOGLHWVH[WUD substance, neutral fat
ÀXLGV TT CBC, RBS, S electrolytes, S albumin
XX Severe PD: PD, when associated with signs of TT 8ULQH50(DQG&6
GHK\GUDWLRQDQGXVXDOO\UHTXLUHVKRVSLWDOL]DWLRQ TT 'XRGHQDOÀXLGIRUDHURELF DQDHURELFFXOWXUH
Risk factors
A. Host factors Treatment
TT <RXQJDJHPRQWK I. Non-Severe PD 7UHDWPHQWDWKRPH
TT Low birth weight (LBW) baby Objective:,PSURYHGLDUUKRHDE\GLHWDU\PDQLSXODWLRQ
TT 0DOQXWULWLRQ 7RGRWKDWGLHWVDUHUHFRPPHQGHGIRUFKLOGUHQ!
TT )DXOW\IHHGLQJSUDFWLFHe.g. lack of breast feeding months. Initially Diet 1 is started and is evaluated after
TT Recent introduction or feeding of cows milk GD\V,IQRLPSURYHPHQWLQUHODWLRQWRHLWKHUVWRRO
TT ,QMXGLFLRXVXVHRIDQWLELRWLF DQWLPRWLOLW\GUXJV IUHTXHQF\or weight gain, then Diet1 changed to Diet
TT ,PSDLUHGLPPXQHIXQFWLRQ 2IRUDQRWKHUGD\V0RVWFDVHVDUHLPSURYHGZLWK
TT Systemic infections HJ87,SQHXPRQLDRUDOWKUXVK this intervention. But if not, then the cases should be
TT +LVWRU\RISUHYLRXV3' UHIHUUHGIRUIXUWKHUHYDOXDWLRQ7KHRWKHURSWLRQVOLNH
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B. Environmental factors
TT Living in highly contaminated environment and their Diet 1:
LOOHIIHFWVRQ*,PRFURHFRORJ\ Starch based, reduced milk (low lactose) diet 7KLV
TT if Enteroadherent E. coli, was the causative organism GLHWLVFRPSRVHGRI±
of recent acute diarrhea TT )XOOIDWGULHGPLONZKROHOLTXLGPLONPO
Organisms TT Rice: 15 gm Vegetable oil: 3.5 gm


XX E. coli (enteroadherent)  Aeromonas TT Cane sugar: 3 gm :DWHUPO



XX Klebsiella  Cryptosporidium
XX Campylobacter  Giardia lamblia Diet 2:
Reduced starch based, No milk diet
Pathogenesis
7KLVGLHWLVFRPSRVHGRI±
1RWZHOOXQGHUVWRRG+RZHYHULWLVVDLGWKDWSHUVLVWHQW
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

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 

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Treatment of diarrhoea by rehydration

II. Severe PD 7UHDWPHQWDW+RVSLWDO
SHUPHDELOLW\RIWKHERZHOWRDEQRUPDOGLHWDU\or microbial
DQWLJHQV7KHVHYHULW\RIWKHVHFKDQJHVLVJUHDWHULQ It includes–
younger children due to their delayed intestinal mucosal XX Rehydration as outlined in acute diarrhoea
maturation. XX 'LHWDU\PDQLSXODWLRQDQGWKHUHFRPPHQGHGVSHFLDO
GLHWV 'LHW 'LHW DUH±
Diagnosis TT Low lactose diet0DGHIURPIXOOIDWPLONULFH

%\FOLQLFDODVVHVVPHQWDQGVXSSRUWVIURPLQYHVWLJDWLRQV vegetable oil, cane sugar and water

TT Lactose free diet0DGHIURPZKROHHJJFRRNHG

Clinical assessment chicken, rice, vegetable oil, glucose and water

XX $VVHVVPHQWRIWKHFDVHNHHSLQJLQPLQGWKHULVNIDFWRUV XX $GGLWLRQDOPDQDJHPHQWLQFOXGHV±
XX Check evidence of any TT 7UHDWPHQWRIQRQLQWHVWLQDOLQIHFWLRQif present. e.g.

TT Dehydration
Pneumonia, Sepsis, UTI, Oral thrush, Otitis media,
TT 1RQLQWHVWLQDOLQIHFWLRQVHJSQHXPRQLDVHSVLV TT 7UHDWPHQWRILQWHVWLQDOLQIHFWLRQV e.g. Amoebiasis/

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TT 0DOQXWULWLRQPLFURQXWULHQWGH¿FLHQF\
for 10 days
 110 Step on to Paediatrics

TT 6XSSOHPHQWDWLRQRIPLFURQXWULHQW YLWDPLQVe.g. Complications

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XX Electrolyte imbalance
XX *URZWK
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Dietary manipulation (According to age)
metabolic acidosis, *XLOODLQ±%DUUp6\QGURPH
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XX Paralytic ileus In addition, dysentery can
Encourage breast feeding Milk based diet (low lactose diet) XX Acute renal failure/ OHDGWR±
Not improved Not improved Haemolytic uraemic XX 5HFWDOSURODSVH
Low lactose diet (yoghurt) Lactose free preparation syndrome XX Convulsions
(rice based diet)
Not improved
Not improved
Lactose Free diet
(Soya based diet) Chicken based diet Diagnosis
%DVHGRQWKHFOLQLFDOIHDWXUHVDQGVXSSRUWVIURPUHOHYDQW
Stool electrolyte & osmolarity investigations.

Secretary diarrhoea Osmotic diarrhoea Investigations

Bacterial overgrowth Pregestimil XX Stool for 7RORRNIRU5%&SXVFHOOV 
Not improved 50( PDFURSKDJH
Antimicrobial agent Total perenteral nutrition
7RJURZWKHFDXVDWLYHRUJDQLVPDQG
XX Stool for C/S
WKHLUGUXJVHQVLWLYLW\SDWWHUQ
XX Blood for 7RDVVHVVDQDHPLDQHXWURSKLOLF
&%&3%) leukocytosis
DYSENTERY XX Serum 7RFKHFNK\SRNDODHPLD
Electrolytes K\SRQDWUDHPLDDFLGRVLV
'\VHQWU\LVDQRWKHUW\SHRIGLDUUKRHDZKHUHSDWLHQWSDVVHV XX Arterial blood
IUHTXHQWORRVHVWRROVDORQJZLWKEORRG 0HWDEROLFacidosis
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Organisms 7RHYDOXDWHFRPSOLFDWLRQVDVLWPD\
XX S creatinine
TT Shigella spp, Salmonella spp be raised in acute renal failure/HUS
TT Enteroinvasive E.Coli, Enterohaemorrhagic E.Coli
Treatment of severe persistent diarrhoea

TT Campylobacter spp. Treatment

XX Antibiotics
Pathogenesis TT &LSURÀR[DFLQPJNJGD\KRXUO\IRUGD\V

After entering in the gut, the organisms invade into the gut TT 3LYPHFLOOLQDPPJNJGD\KRXUO\IRUGD\V

ZDOOFDXVHVXOFHUDWLRQ EOHHGLQJZLWKPDQLIHVWDWLRQVRI TT Nalidixic acid, 50 mg/kg/day 6 hourly for 5 days

SDLQFUDPSDQGEORRG\GLDUUKRHD XX Diet: Usual family diet

Clinical manifestations
XX Rehydration: Plan A, B or&LIUHTXLUHG
XX Loose stool, containing blood
XX =LQFVXSSOHPHQWDWLRQDVRXWOLQHGEHIRUH
XX )HYHUDEGRPLQDOFUDPSWHQHVPXV
XX 2WKHUVHJ3DUDFHWDPROIRUIHYHUDQWLVSDVPRGLFIRU
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XX Pallor
 Step on to Paediatrics 111

References
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Multiple choice questions [MCQ] Treatment of diarrhoea by rehydration

 $FKLOGLVVDLGWRVXIIHUIURPVHYHUHGHK\GUDWLRQLIKHKDV±
___ a) lethargy ___ b) sunken eyes ___ c) increased thirst
BBBG VORZUHWXUQRIVNLQSLQFKBBBH GHSUHVVHGDQWHULRUIRQWDQHOOH
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 112 Step on to Paediatrics

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 12
Vomiting
Vomiting
¼¼ The Red flag signs - - - - - - - - - - - - 114

:KHQHYHUDFKLOGSUHVHQWVZLWKYRPLWLQJRQHVKRXOG¿UVW Patho-physiological consequences

FRQVLGHUWKHVLWHRISDWKRORJ\LVLQJDVWURLQWHVWLQDO a) Metabolic
KHSDWRELOLDU\V\VWHPSDQFUHDVOLNH± TT )OXLGORVVe.g. dehydration, shock
XX Acute gastritis/ TT HCl loss in vomitus HJDONDORVLVK\SRFKORUDHPLD
*DVWURHQWHULWLV TT Na+, K+ loss in vomitus HJK\SRQDWUDHPLD
XX $FXWHKHSDWLWLV
K\SRNDODHPLD
XX Acute
b) Nutritional
DSSHQGLFLWLV
XX Acute
TT )DLOXUHWRWKULYHGXHWRORVVRIFDORULHVDQGQXWULHQWV
SDQFUHDWLWLV c) Others
XX )RRG TT 2HVRSKDJLWLVGXHWRH[SRVXUHRIORZHUHQGRI
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XX Intestinal TT 3QHXPRQLDGXHWRDVSLUDWLRQRIYRPLWXV
obstruction TT 0DOORU\:HLVVWHDUDWWKHOHVVHUFXUYHRI
XX Acute JDVWURHVRSKDJHDOMXQFWLRQGXHWRIRUFHIXOYRPLWLQJ
cholecystitis,
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LQGXFHYRPLWLQJ± XX )UHTXHQF\RIYRPLWLQJ
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XX Renal diseases HJS\HORQHSKULWLVFKURQLFNLGQH\ XX &RORXU FRQWHQWe.g. blood in vomitus
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XX CNS diseases e.g. meningitis, brain tumor, XX $EGRPLQDOSDLQDQGVLWHRISDLQ
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XX Endocrine disorders e.g. diabetic ketoacidosis, SDVVHG
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XX Cyclic vomiting syndrome XX )HYHUSUHVHQWor not
XX Inborn errors of metabolism XX Pain in ear or VRUHWKURDWSUHVHQWor not
7KHFDXVHVRIYRPLWLQJDPRQJNeonatesDUHTXLHW
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XX State of consciousness e.g. alert, drowsy
XX State of hydration e.g. general condition, sunken eyes,
XX *DVWURHVRSKDJHDOUHÀX[GLVHDVHV
VNLQSLQFKWKLUVW
XX Duodenal atresia XX Haemodynamic status HJSXOVH%3SXOVHSUHVVXUH
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XX Intestinal obstruction XX $Q\IHDWXUHVVXJJHVWLQJXQGHUO\LQJSDWKRORJ\e.g.
XX Congenital malrotation of gut TT $EGRPHQ'LVWHQVLRQWHQGHUQHVV DEVHQWERZHO
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TT -DXQGLFH3UHVHQWDEVHQW
 114 Step on to Paediatrics

TT &161HFNULJLGLW\FRQYXOVLRQSXSLOV Investigations
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XX S. bilirubin, 6*37DONDOLQHSKRVSKDWDVHFUHDWLQLQH
XX 6HOHFWURO\WHVDUWHULDOEORRGJDV $%*
D/D based on characteristics of vomitus XX Others HJ6HUXPXULQDU\DP\ODVHOLSDVHUDQGRP
Site of blood sugar
Materials Diagnoses
patholology XX 8ULQH50(&6JOXFRVHNHWRQHV
XX ;5D\DEGRPHQLQHUHFWSRVWXUH
Undigested 2HVRSKDJHDO
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IRRGSDUWLFOHV stricture, achalasia
XX &RQWUDVW;5D\RIXSSHU*,
Small bowel XX &7VFDQRIDEGRPHQEUDLQ
Digested obstruction e.g. 0HWDEROLFVFUHHQLQJHJEORRGS+DPPRQLDODFWDWH
'LVWDOWRDPSXOOD XX
food, milk malrotation,
of Vater
curds Prolonged vomiting
due to any cause

Bile: green/ Stomach

Pyloric stenosis
yellow $WS\ORUXV  THE RED FLAG SIGNS

Blood: red Lesion above 5XSWXUH

XX Altered sensorium (cause or effect)
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dehydration
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XX 7UHDWPHQWRIWKHXQGHUO\LQJFDXVH
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 Step on to Paediatrics 115

References
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Self assessment
 13
Abdominal Pain
Abdominal Pain - - - - - - - - - - - - - 116

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may be acute or chronic and recurrent in nature.Causes Acute abdominal pain Recurrent abdominal pain
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TT $FXWHDSSHQGLFLWLV XX Helminthiasis
disorders contribute only about 10% of cases. On the other
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hand, recurrent abdominalSDLQ DWOHDVWRQHHSLVRGHRI
TT Intestinal obstruction XX Cholelithiasis
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to interfere with routine functioning) are mostly functional
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TT Acute cholecystitis disease
of cases.
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TT %DVDOSQHXPRQLD XX

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Cardinal features of conditions commonly causing recurrent abdominal pain

Diseases Characteristics features Investigations Treatment

XX $EGRPLQDOSDLQGLVWHQVLRQ XX Albendazole 0HEHQGD]ROH
Helminthiasis TT 6WRRO50(±WRVHH
EORDWLQJJDVPDODEVRUSWLRQ XX Healthy measures HJSHUVRQDO
(discussed in ova and egg
growth failure, intestinal hygiene, hand washing, use of
FKDSWHU TT &%&ZLWK3%)
obstruction sanitary latrine, etc.
XX 3DLQOHVVSHUUHFWDOEOHHGLQJ
0HFNHO¶V TT 0HFNHOVFDQZLWK7F
brick colour/currant jelly stool XX Surgery
diverticulum SUHWHFKQHWDWHLVRWRSH
XX Intestinal obstruction, vomiting
XX 3URWRQSXPSLQKLELWRU+
TT (QGRVFRS\RIXSSHU
XX %XUQLQJHSLJDVWULFSDLQZRUVH blocker
*,7
3HSWLFXOFHU on awaking or before meal XX 7UHDWPHQWRIH. Pylori
TT Urea breath test
disease XX Pain relieved with antacid, ZLWKSURWRQSXPSLQKLELWRU
TT Detection of Abti H.
vomiting, haemorrhage Clarithromycin, Amoxicillin for
S\ORLDQWLERG\LQVHUXP
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XX Prednisolone
Abdominal pain

XX $EGRPLQDOSDLQQDXVHD TT ;5D\RIDEGRPHQ XX Sulfasalazine

,QÀDPPDWRU\
YRPLWLQJGLDUUKRHDSHUUHFWDO TT 86*RIDEGRPHQ XX $]DWKLRSULQH
bowel disease
bleeding, tenesmus, urgency TT &RORQRVFRS\ XX 0RQRFORQDODQWLERG\
XX Surgery
116
 Step on to Paediatrics 117

Cardinal features of conditions commonly causing acute abdominal pain

Diseases Clinical features Investigations Treatment

$FXWHDSSHQGLFLWLV

XX $EGRPLQDOSDLQYRPLWLQJ TT &%&1HXWURSKLOLF XX NPO, nasogastric

XX 0F%XUQH\¶VSRLQWWHQGHUQHVV leukocytosis 1* 6XFWLRQ
XX Rebound tenderness, Rovsing sign TT 86*RIDEGRPHQ:DOO XX ,9ÀXLG
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TT XX

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XX 3UR[LPDOREVWUXFWLRQIUHTXHQWELOLRXV XX 1321*6XFWLRQ
obstruction

emesis, little or no abdominal distension. ;5D\DEGRPHQ0XOWLSOH

Intestinal

TT
XX ,9ÀXLG
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XX Antibiotic
XX 'LVWDOREVWUXFWLRQPRGHUDWHor marked TT 86*RIDEGRPHQ
abdominal distension, vomiting
XX Surgery

XX $EGRPLQDOSDLQ9RPLWLQJ
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XX +LJKIHYHUZLWKFKLOOV ULJRU
Urine C/S Antibiotics
Acute

TT
XX 7HQGHUQHVVDWUHQDODQJOH TT CBC, &533%) XX Antibiotics as
XX In newborn: Poor feeding, irritability, sensitive to C/S
TT 86*RIDEGRPHQ
jaundice, weight loss

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LQIHFWHGSDQFUHDWLF
umbilicus TT 5%6KLJK
necrosis
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Abdominal pain
 118 Step on to Paediatrics

References
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 14
Constipation
Constipation - - - - - - - - - - - - - - 119

&RQVWLSDWLRQLVDJURZLQJSUREOHPDPRQJFKLOGUHQLQRXU XX Dietary history HJORZ¿EHUGLHWFKDQJHRIGLHWIURP

VRFLHW\ZLWKFKDQJLQJIRRGKDELWVDQGOLPLWHGSK\VLFDO breast milk to cow’s milk
activity. XX )DPLO\KLVWRU\RIFRQVWLSDWLRQHJSDUHQWDOKDELW
'H¿QLWLRQ3DVVDJHRIKDUGVWRROZLWKGLI¿FXOW\LQHYHU\
XX )RUFHIXOSRWW\WUDLQLQJ
3rd day.
:KHQHYHUDQ\FKLOGZLWKWKHSUREOHPLVEURXJKWWKH Physical Examination
following causes should be considered.
XX $SSHDUDQFH,IFRDUVHIDFLHVORZKDLUOLQHSURWUXGHG
tongue FRQJHQLWDOK\SRWK\URLGLVP
Aetiology XX Abdomen: If distended (+LUVFKVSUXQJGLVHDVH
XX 3HULDQDOUHJLRQ&KHFNLQJIRUSUHVHQFHRIDQDO¿VVXUHV
Non organic (functional) Organic XX Back: Checking for meningocele/myelomeningocele
TT Anatomic e.g.
XX Digital rectal examination
XX ,GLRSDWKLF TT ,QFUHDVHGWRQHRIDQDOVSKLQFWHU(+LUVFKVSUXQJ
anal stenosis, Anal
XX Change in diet: not enough ¿VVXUH disease)
¿EUHULFKIUXLWVYHJHWDEOHV TT 3UHVHQFHRIH[SORVLYHORRVHVWRRORQZLWKGUDZDORI
TT Abnormal
or ÀXLGLQFKLOG¶VGLHW H[DPLQLQJ¿QJHU(+LUVFKVSUXQJGLVHDVH
musculature e.g.
XX Stool withhelding, Down syndrome XX 0XVFOHWRQH+\SRWRQLD K\SRWK\URLGLVP
because the child is afraid Down syndrome), K\SHUWRQLF (meningocele/
TT Intestinal nerve
RISDLQIXOGHIHFDWLRQ myelomeningocele)
abnormality e.g.
or doesn’t want to take
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disease
Complications
uncomfortable using XX $QDO¿VVXUH 5HFWDOSURODSVH (QFRSDUHVLV
SXEOLFWRLOHWV
TT Hormonal disorder
HJK\SRWK\URLGLVP
XX Change in routine e.g.
TT Drugs e.g. Diagnosis
travel, hot weather or
stress Phenytoin, %DVHGRQFODVVLFFOLQLFDOIHDWXUHVDQGVXSSRUWVIURP
anticholinergics, anti relevant investigations.
XX )RUFHIXOSRWW\WUDLQLQJ
GHSUHVVDQWV
XX )DPLO\KLVWRU\ TT Psychiatric disorder Investigations Results
XX Cow’s milk allergy: e.g. anorexia
consuming too much milk 7RORRNIRUHYLGHQFHRIERZHO
nervosa 3ODLQ;5D\RI
daily obstruction HJSUHVHQFHRIPXOWLSOH
TT Acute febrile illness abdomen
DLUIOXLGOHYHOV
3UHVHQFHRIQRUPDOO\GLODWHGSUR[LPDO
Approach Barium enema
to a patient with constipation colon and a smaller calibre constricted
;5D\RIODUJH
Constipation

distal colon as seen in +LUVFKVSUXQJ

History gut
disease
XX +LVWRU\RIGHOD\HGSDVVDJHRIPHFRQLXPe.g.
+LUVFKVSUXQJGLVHDVH High 76+ ORZ)7 level indicate
Serum 76+)7
XX +LVWRU\RISURORQJHGMDXQGLFHLQWKHQHRQDWDOSHULRG FRQJHQLWDOK\SRWK\URLGLVP
HJFRQJHQLWDOK\SRWK\URLGLVP 3UHVHQFHRIH[WUDFRS\RIFKURPRVRPH
XX 3DLQIXOSDVVDJHRIVWRROHJDQDO¿VVXUH .DU\RW\SLQJ
RQDVVHHQLQDown syndrome
XX +LVWRU\RISDVVDJHRIVWRROLQLQDSSURSULDWHSODFHV e.g.
119

HQFRSUHVLV
 120 Step on to Paediatrics

Treatment TT Drugs
³³ Osmotic laxative (lactulose)

A. Supportive ³³ %XONIRUPLQJOD[DWLYHV ,VSDJKXODKXVN

TT &RXQVHOLQJUHJDUGLQJWKHFRQVHTXHQFHVRI ³³ 6WRROVRIWHQHUV OLTXLGSDUDI¿Q

FRQVWLSDWLRQDQGWKHLPSRUWDQFHRIUHJXODUERZHO TT Others
habbit ³³ *O\FHULQHVXSRVLWRU\
TT (QFRXUDJHLQWDNHRIPRUHÀXLGLQWDNHRI¿EHUULFK ³³ (QHPDVLPSOH[
diet e.g. vegetables, fruits
³³ 0DQXDOHYDFXDWLRQXQGHU*$
TT $YRLGH[FHVVLYHFRQVXPSWLRQRIPLONFHUHDOVPHDW
mashed foods %6SHFL¿F
TT 7RLOHWWUDLQLQJ5HJXODUWRLOHWVLWWLQJIRUPLQXWHV
7UHDWPHQWRIWKHXQGHUO\LQJFDXVHLIDQ\
twice a day after meal
TT 3URPRWHSK\VLFDODFWLYLW\

References
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 15
Sore Throat & Difficulty in Swallowing
Viral pharyngitis - - - - - - - - - - - - - 121
Acute bacterial pharyngotonsillitis- - - - - - - - - - 121

6RUHQHVVLQWKURDWLVDFRPPRQSUHVHQWDWLRQRIWKURDW ACUTE BACTERIAL

LQIHFWLRQDQGLVRQHRIWKHPDMRUFDXVHRIKHDOWKFDUH PHARYNGOTONSILLITIS
seeking in children.
7KHFRPPRQFDXVHVRIVRUHWKURDWDUH± Organisms: *URXS$EHWDKDHPRO\WLF6WUHSWRFRFFLLV
WKHSUHGRPLQDQWRUJDQLVP2WKHURUJDQLVPVDUHStaph.
XX 9LUDOSKDU\QJLWLV aureus, gram-negative organism and Mycoplasma.
XX $FXWHEDFWHULDOSKDU\QJRWRQVLOOLWLV
Clinical Manifestations
XX 'LSKWKHULD XX Sudden onset of
XX Infectious mononucleosis high fever
XX 6HYHUHSDLQLQ
,QWKLVVHFWLRQYLUDOSKDU\QJLWLVDFXWHEDFWHULDO throat
SKDU\QJRWRQVLOOLWLVZLOOEHGLVFXVVHG
XX 'LI¿FXOW\LQ
deglutition
XX Refusal to feed
XX Drooling of saliva

VIRAL PHARYNGITIS
,QÀDPHGWRQVLOVZLWKSXVLQWKHFU\SWV
Organisms: Adenovirus, Coxsackie virus, EBV, Herpes
simplex virus. Cough is characteristically absent
,QDGGLWLRQKHDGDFKHYRPLWLQJDQGDEGRPLQDOSDLQPD\
Clinical Manifestations EHSUHVHQW

Pharyngitis & pharyngotonsillitis

XX Sore throat
XX Runny nose, red eye
Physical examination
XX 7KURDWLVVHHQUHGDQGFRQJHVWHG
XX Hoarseness, cough
XX 7RQVLOVDUHHQODUJHGDQGSXVSRLQWVLQWKHFU\SWV(white
XX Low grade fever
SDWFK
XX 7KURDWH[DPLQDWLRQ
XX $QWHULRUFHUYLFDOO\PSKQRGHVDUHHQODUJHGDQGWHQGHU
may reveal redness of
IDXFHV WRQVLOEXWQR Other causes of white patches over tonsil
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XX )DXFLDOGLSKWKHULD XX Oral thrush
XX Infectious XX Scarlet fever
mononucleosis XX 0RQLOLDVLV
Treatment: Supportive
XX Analgesic HJSDUDFHWDPRO XX Vincent angina:$FXWH SDLQIXOLQIHFWLRQRIWKHWRRWK
XX Saline water gurgling PDUJLQV JXPFDXVHGE\V\PELRLFRUJDQLVP%DFLOOXV
XX Lemon tea to soothe the throat IXVLIRUPLV %RUUHOLDYLQFHQW
XX )HHGLQJDVXVXDOVRIWOHVVVSLF\
121
 122 Step on to Paediatrics

Complications Treatment
7KHIROORZLQJFRPSOLFDWLRQVPD\RFFXULIWKHFDVHVRI
$6SHFL¿F(LWKHURIWKHIROORZLQJ
DFXWHVWUHSWRFRFFDOSKDU\QJRWRQVLOOLWLVDUHQRWDGHTXDWHO\ XX Penicillin
WUHDWHG± TT 3KHQR[\PHWK\OSHQLFLOOLQPJNJGD\KRXUO\IRU
XX Acute rheumatic fever 10 days or
XX $FXWHJORPHUXORQHSKULWLV TT %HQ]DWKLQHSHQLFLOOLQXQLWGHHS,0 NJ 

DQGXQLW !NJ VLQJOHGRVH

Diagnosis
XX (U\WKURP\FLQPJNJGD\LQGLYLGHGGRVHV LQ
%DVHGRQFOLQLFDOIHDWXUHV UHOHYDQWLQYHVWLJDWLRQV FDVHVRISHQLFLOOLQK\SHUVHQVLWLYLW\ IRUGD\V
Investigations XX &HISRGR[LPHSUR[HWLOPJNJGD\WZLFHGDLO\IRU
days
Investigations Results XX Azithromycin 10 mg/kg/day for 5 days
TT CBC 3RO\PRUSKRQXFOHDUOHXNRF\WRVLV B. Supportive
TT ASO titre Raised
XX $QDOJHVLFDQWLS\UHWLF
XX Warm saline gurgling
TT Culture of throat 0D\EHSRVLWLYHIRUbeta XX )HHGLQJ$VXVXDOEHWWHUWRFKRRVHZLWKFKLOG¶VGHVLUH
swab haemolytic streptococcus and conditions

References
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___ d) infectious mononucleosis ___ e) moniliasis
 16
Undue Exhaustion to Normal Activities
Congenital heart diseases
¼¼ Ventricular septal defect - - - - - - - - - - - 123
¼¼ Atrial septal defect - - - - - - - - - - - - 125
¼¼ Patent ductus arteriosus - - - - - - - - - - - 126
¼¼ Tetralogy of Fallot - - - - - - - - - - - - 127
Heart failure - - - - - - - - - - - - - - - 131
Infective endocarditis - - - - - - - - - - - - - 132

Undue exhaustion of a child to normal activities &ODVVL¿FDWLRQ

(effort intolerance), shortness of breath and %URDGO\EDVHGRQWKHSUHVHQFHor absence of cyanosis in the
SDOSLWDWLRQZLWKIDLOXUHWRWKULYHDUHWKHXVXDO affected child.
SUHVHQWDWLRQVRIXQGHUO\LQJKHDUWGLVHDVHV
Cyanotic CHD Acyanotic CHD
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FDXVLQJFKURQLFK\SR[DHPLDe.g. thalassaemia major, XX 7HWUDORJ\RI)DOORW 72) XX With left to right shunts
chronic lung diseases, neuromuscular disorders may XX 7UDQVSRVLWLRQRIJUHDW TT 9HQWULFXODUVHSWDOGHIHFW

also give rise to undue exhaustion. DUWHULHV 7*$ (VSD)

TT $WULDOVHSWDOGHIHFW $6'
Heart diseases among children are mostly congenital, XX 7RWDODQRPDORXV
LQFRQWUDVWWRDGXOWVZKRXVXDOO\VXIIHUIURPDFTXLUHG SXOPRQDU\YHQRXV TT Patent ductus arteriosus

heart diseases like coronary heart diseases, rheumatic GUDLQDJH 7$39'  (PDA)
valvular heart diseases etc. XX Persistent truncus XX Without shunt
arteriosus TT Coarctation of aorta
,QWKLVFKDSWHUZHZLOOGLVFXVVWKHFRPPRQ XX 7ULFXVSLGDWUHVLD TT Pulmonary stenosis
congenital heart diseases, heart failure and infective XX Ebstein anomaly TT Aortic stenosis
endocarditis.

Congenital heart diseases

Congenital heart diseases (CHD)
VENTRICULAR SEPTAL DEFECT (VSD)
Prevalence:SHUOLYHELUWKV
7KHFRPPRQHVWFRQJHQLWDOKHDUWGLVHDVH7KHGHIHFWRFFXUV
Aetiology
DWDQ\SRLQWRQWKHLQWHUYHQWULFXODUVHSWXPPRVWO\LQLWV
XX Unknown, mostly
membranousSDUW  DQGWKHUHPDLQLQJLQWKHmuscular
XX Chromosomal anomalies e.g. Down syndrome,
SDUW,WFDQRFFXUDVDQLVRODWHGGHIHFWor along with other
7XUQHUV\QGURPH1RRQDQV\QGURPH
cardiac defect HJ72).
XX Antenatal illnesses of mothers, e.g. diabetes
mellitus, rubella infection, radiation, smoking, etc.
96'LVFODVVL¿HGDFFRUGLQJWRLW¶VVL]HDV±
Small < 5 mm
0RGHUDWH PP
Large > 10 mm VSD
123
 124 Step on to Paediatrics

Haemodynamics Precordium
During ventricular systole oxygenated blood shunts from
the left ventricle XX ,QVSHFWLRQ+\SHUG\QDPLFPD\EHEXOJHG
to right ventricle XX 3DOSDWLRQ
(left to right shunt) TT $SH[EHDWLVVKLIWHGWROHIW GXHWRFDUGLRPHJDO\ 

through VSD and is thrusting

and adds with TT /HIWSDUDVWHUQDOKHDYHPD\EHSUHVHQW

the deoxygenated TT 7KULOOPD\EHSUHVHQWLQWULFXVSLGDUHD UHODWHGWR

EORRGSUHVHQW grading of murmur)

there, coming TT 3 SXOPRQDU\FRPSRQHQWRInd heart sound) may

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from right atrium. EHSDOSDEOHLQSXOPRQDU\DUHDZKHQDVVRFLDWHG
7KLVH[FHVVEORRG ZLWKSXOPRQDU\K\SHUWHQVLRQ
WKHQSDVVWRWKH XX Auscultation
TT 1stDQGndKHDUWVRXQGVDUHDXGLEOHLQDOODUHDV
SXOPRQDU\YDVFXODU
bed through TT $KDUVKSDQV\VWROLFPXUPXU JUDGH EHVWKHDUG

SXOPRQDU\WUXQN7KHF\FOHFRQWLQXHVDJDLQDQGDJDLQ at lower left sternal border at the 3rdth th

:LWKFRQWLQXHGH[SRVXUHRIWKHSXOPRQDU\YDVFXODUEHG LQWHUFRVWDOVSDFHV7KHPXUPXUPD\UDGLDWHWRWKH
WRWKHVHKLJKEORRGÀRZSDWLHQWGHYHORSVSXOPRQDU\ right lower sternal border. Intensity varies based
K\SHUWHQVLRQSXOPRQDU\RHGHPDDQGODWHUSXOPRQDU\ RQWKHVL]HRIWKH96'DQGSXOPRQDU\YDVFXODU
resistance
vascular obstructive disease, resulting in right to left shunt
(Eisenmenger syndrome)7KLVUHYHUVDORIVKXQWGLUHFWLRQ
UHVXOWVLQDSSHDUDQFHRIcyanosis.
Diagnosis
Clinical Manifestation Based on the clinical features and relevant investigations.
Small defect Investigations
XX 3DWLHQWVXVXDOO\UHPDLQDV\PSWRPDWLFZLWKQRUPDO XX &KHVW;5D\
JURZWKDQGGHYHORSPHQW TT Cardiomegaly (cardiothoracic ratio > 60%)
XX ,QFLGHQWDOGHWHFWLRQRIDSDQV\VWROLFPXUPXUDWOHIWrd TT Increased

DQGthLQWHUFRVWDOVSDFHV SXOPRQDU\
Large defect vascular

Source: Internet
markings
TT CXR may
XX '\VSQRHDDWUHVWor on exertion
be normal
XX 3RRUIHHGLQJLQWHUUXSWHGIHHGLQJ
in small
XX Poor weight gain (failure to thrive) defects
XX Easy fatigability XX (&*
XX 3URIXVHSHUVSLUDWLRQ GLDSKRUHVLV e.g. head sweating TT Normal

XX 5HFXUUHQWUHVSLUDWRU\WUDFWLQIHFWLRQV in small
XX Cyanosis is usually absent defect
Ventricular septal defect

TT Left

ventricular
General physical examination K\SHUWURSK\ Cardiomegaly
XX $SSHDUDQFH6LFNORRNLQJRIWHQPDOQRXULVKHG in large VSD
XX 5HVSLUDWRU\UDWH,QFUHDVHG TT %LYHQWULFXODUK\SHUWURSK\ZKHQDVVRFLDWHGZLWK

XX 3XOVHUDWH,QFUHDVHG9ROXPH*RRG SXOPRQDU\K\SHUWHQVLRQ
XX %ORRGSUHVVXUH1RUPDO TT P waves may be notched or SHDNHG

XX -XJXODUYHQRXVSUHVVXUH0D\EHUDLVHGLQ&&) XX (FKRFDUGLRJUDPZLWKFRORU'RSSOHULVGLDJQRVWLF,W
XX 3HGDORHGHPD$EVHQWEXWPD\EHSUHVHQWLQKHDUW VKRZVORFDWLRQDQGVL]HRIWKHGHIHFW GLUHFWLRQRI
failure EORRGÀRZ
 Step on to Paediatrics 125

Treatment ATRIAL SEPTAL DEFECT (ASD)

&RXQVHOWKHSDUHQWVDERXWWKHGLVHDVHLWVFRPSOLFDWLRQV
$WULDOVHSWDOGHIHFWLVDQDEQRUPDOFRPPXQLFDWLRQ
DQGSURJQRVLV
EHWZHHQWKHDWULDGXHWRDGHIHFWLQWKHLQWHUDWULDOVHSWXP

Medical Types of ASD

Small defects Ostium secundum 60%
Parents should be reassured of the relatively benign nature 2VWLXPSULPXP 30%
of the lesion, and the child should be encouraged to live Sinus venosus 10%
DQRUPDOOLIHZLWKQRUHVWULFWLRQVRQSK\VLFDODFWLYLW\
6SRQWDQHRXVFORVXUH  GXULQJst year of life Haemodynamics
Moderate to Large defects In ASD there is shunting of oxygenated blood from the
7KHJRDOVRIWUHDWPHQWDUHWR± left to the right atrium where it is added to the usual
venous return (volume overload)7KHEORRGWKHQSDVVHV
XX (QVXUHDGHTXDWHJURZWKRIWKHSDWLHQW
to the right ventricle and
XX 3UHYHQWGHYHORSPHQWRIEisenmenger syndrome
SXPSHGWRWKHOXQJV
XX Prevent infective endocarditis
XX 7RFRQWUROFRQJHVWLYHFDUGLDFIDLOXUH $VWKHSUHVVXUH
difference between
A. Supportive WKHDWULDLVORZWKH
TT Nutrition: High calorie diet (add fat and sugar) to amount of blood shunting
HQVXUHDGHTXDWHZHLJKWJDLQ through the defect is not

Source: Internet
TT )UXVHPLGH PJNJGD\ LQGLYLGHGGRVHV as high as that of other
TT Afterload reducing agents: ACE inhibitors KLJKSUHVVXUHJUDGLHQW
³³ (QDODSULO PJNJGD\ RQFHor twice daily
e.g. VSD. As a result, the
³³ &DSWRSULO PJNJGRVH KRXUO\ SXOPRQDU\FLUFXODWLRQ
TT 'LJR[LQ —JNJGD\ PD\EHLQGLFDWHGLI SXOPRQDU\DUWHU\
diuresis and afterload reduction do not relieve SUHVVXUHDVZHOODVSXOPRQDU\YDVFXODUUHVLVWDQFHUHPDLQV
V\PSWRPVRIKHDUWIDLOXUHDGHTXDWHO\ normal throughout the childhood although, it may begin to
increase in adulthood and may eventually result in reversal
B. Surgical repair
of the shunt and clinical cyanosis.
Indications:3DWLHQWVZLWK±
TT Cardiomegaly Clinical Manifestations
TT Poor growth Vary with the size of defect.
TT Poor exercise tolerance or XX 6PDOOGHIHFW$V\PSWRPDWLFDQGLVXVXDOO\GLDJQRVHG
TT 2WKHUFOLQLFDODEQRUPDOLWLHVZKRKDYHDVLJQL¿FDQW GXULQJDURXWLQHKHDOWKFKHFNXS
VKXQW ! XX /DUJHGHIHFW6\PSWRPDWLF SDWLHQWVSUHVHQWZLWK±
Time of surgery$WDJHPRQWKV,QPRVWFHQWHUV TT Exercise intolerance

surgery is done before 1 year. As a result, Eisenmenger TT Easy fatigability

V\QGURPHKDVEHHQYLUWXDOO\HOLPLQDWHG7KHVXUJLFDO TT ,QFUHDVHGSHUVSLUDWLRQ

PRUWDOLW\UDWHLV(Current Ped Dx & Rx 23rd Ed’2016) TT Poor weight gain (failure to thrive)

TT 5HFXUUHQWUHVSLUDWRU\WUDFWLQIHFWLRQV
Contra-indication
Atrial septal defect

XX 6HYHUHSXOPRQDU\REVWUXFWLYHYDVFXODUGLVHDVHQRQ General Physical Examination

UHVSRQVLYHWRSXOPRQDU\YDVRGLODWRUV XX $SSHDUDQFH8VXDOO\QRUPDO
XX Pulses: Normal
XX 5HVSLUDWRU\UDWH1RUPDO
XX :HLJKW KHLJKW$JHDSSURSULDWH
 126 Step on to Paediatrics

Precordium PATENT (PERSISTENT) DUCTUS

ARTERIOSUS (PDA)
XX ,QVSHFWLRQ+HDUWXVXDOO\K\SHUDFWLYH
XX 3DOSDWLRQ PDA is the Persistence of the normal foetal vessel (ductus
TT $SH[EHDWPD\EHVKLIWHGWROHIW
venosus) joining the Aorta to the Pulmonary artery. It
TT 3PD\EHSDOSDEOH
accounts for 10% of all congenital heart diseases and
TT /HIWSDUDVWHUQDOKHDYHPD\EHSUHVHQW
IRXQGPRUHDPRQJSUHWHUPLQIDQWVZHLJKLQJJUDP
XX Auscultation
TT S1 is normal Haemodynamics
TT 6LVZLGHO\VSOLWWHGDQG¿[HG DWSXOPRQDU\DUHD During ventricular
TT Added sound. An ejection systolic murmur (grade systole,
,,,, EHVWKHDUGDWWKHXSSHUOHIWVWHUQDOHGJH oxygenated blood
LQSXOPRQDU\DUHD 7KLVLVFDXVHGE\LQFUHDVHG ÀRZVIURPDRUWD
ÀRZDFFURVVWKHSXOPRQDU\YDOYHQRWGXHWRÀRZ WRWKHSXOPRQDU\
accross ASD trunk through
WKLVSDWHQWGXFWXV
Diagnosis because of high

Source: Internet
Based on the clinical features and relevant investigations. SUHVVXUHJUDGLHQW
7KLVEORRGLVWKHQ
Investigations Results added with the
XX Normal size heart or Cardiomegaly deoxygenated
XX 'LODWHGPDLQSXOPRQDU\DUWHU\ blood in
TT Chest SXOPRQDU\WUXQN
)XOO3XOPRQDU\FRQXV 
;5D\ coming from
shows
XX ,QFUHDVHGSXOPRQDU\YDVFXODU
markings due to increased right ventricle. As a result of this added volume, there
SXOPRQDU\EORRGÀRZ LVSXOPRQDU\FRQJHVWLRQSXOPRQDU\K\SHUWHQVLRQDQG
XOWLPDWHO\SXOPRQDU\YDVFXODUREVWUXFWLYHGLVHDVHDQG
XX 5LJKWD[LVGHYLDWLRQ
TT (&*VKRZV reversal of shunt (Eisenmengar syndrome).
XX 565SDWWHUQLQ9
XX 'LODWHGULJKWDWULXP 59 Clinical Manifestations
TT Echo shows XX $QDWRPLFORFDWLRQ VL]HRI$6'
Vary with the size of defect.
XX 6PDOOGHIHFWPD\EHDV\PSWRPDWLF
&RORXU)ORZ'RSSOHU&RQ¿UPWKHGLDJQRVLVE\
GHPRQVWUDWLQJDOHIWWRULJKWVKXQWDFFURVVWKHGHIHFW
XX 0RGHUDWHWRODUJHGHIHFWJHQHUDOO\UHVXOWVLQ±

Treatment XX Poor feeding

XX &RXQVHOSDUHQWVDERXW$6'LWVWUHDWPHQW SURJQRVLV
XX Poor weight gain (failure to thrive)
XX ,QWROHUDQFHWRSK\VLFDODFWLYLWLHV
A. Medical management is aimed to reduce volume
XX Profuse sweating with crying and feeding
RYHUORDGDQGWRSUHYHQW&&)E\±
XX 5HFXUUHQWUHVSLUDWRU\WUDFWLQIHFWLRQV
)UXVHPLGH PJNJ 'LJR[LQ
Patent ductus arteriosus

TT

B. Surgical closure of the defect. It is generally

UHFRPPHQGHGIRUV\PSWRPDWLFFKLOGUHQZLWKDODUJH
General Physical Examination
defect and associated right heart dilatation XX $SSHDUDQFH1RUPDOor GLVWUHVVHG0D\EHZDVWHG
C. Device closure QRQRSHUDWLYH GXULQJFDUGLDF XX 5HVSLUDWRU\UDWH7DFK\SQRHD
cathterization XX Pulses: +LJKYROXPHDQGFROODSVLQJwithZLGHSXOVH
SUHVVXUH due to diastolic runoff through the ductus
Prognosis
*RRG3XOPRQDU\K\SHUWHQVLRQ5HYHUVDORIVKXQWDQG
,QIHFWLYHHQGRFDUGLWLVDUHXQFRPPRQ6SRQWDQHRXV
FORVXUHRFFXUVLQ$6'RIPPLQGLDPHWHU
 Step on to Paediatrics 127

Precordium B. Surgical repair:%\RQH\HDUDJHIRUSDWLHQWVZLWK

VLJQL¿FDQWOHIWWRULJKWVKXQW
XX ,QVSHFWLRQ+\SHUG\QDPLF C. Device closure:&DQVDIHO\EHGRQHIRUV\PSWRPDWLF
XX 3DOSDWLRQ 3'$FDVHV :HLJKWNJ ZLWKQRUPDO3$SUHVVXUH
TT $SH[EHDWLVVKLIWHGWROHIWKHDYLQJLQFKDUDFWHU

TT $WKULOOPD\EHSDOSDEOHDWOHIWnd ICS Prognosis: 6SRQWDQHRXVFORVXUHPD\RFFXUZLWKLQ

XX Auscultation \HDURIDJH$IWHU\HDUVSRQWDQHRXVFORVXUHLVUDUH
TT S1: Normal ,QIHFWLYHHQGRFDUGLWLVLVDSRWHQWLDOFRPSOLFDWLRQ
TT 62IWHQREVFXUHGE\WKHPXUPXU

TT Added sound : Continuous machinery murmur

SUHVHQWDWOHIWnd ICS near the sternum (maximal

TETRALOGY OF FALLOT (TOF)
DWPLGFODYLFXODUOLQH LVWKHFODVVLF¿QGLQJ
>(WLHQQH/$)DOORW@
Diagnosis Commonest congenital cyanotic cardiac lesion, accounts
Based on the clinical features and relevant investigations. for 10% of all congenital heart diseases.
Pathology: )RXUFRPSRQHQWV±
Investigations Results
XX 2EVWUXFWLRQWRULJKWYHQWULFXODURXWÀRZWUDFW
If shunt small,&;5DSSHDUV1RUPDO SXOPRQDU\LQIXQGLEXODUVWHQRVLV
If shunt is large XX 9HQWULFXODUVHSWDOGHIHFW 96'
XX Left atrial and LV enlargement
XX 2YHUULGLQJRI$RUWD RYHU96'
TT &KHVW;5D\ XX Prominence of aorta and main XX 5LJKWYHQWULFXODUK\SHUWURSK\
SXOPRQDU\DUWHU\
XX ,QFUHDVHGSXOPRQDU\YDVFXODU
:KHQDGGLWLRQDOO\$6'LVSUHVHQWDORQJZLWKWKHVH
markings
defects, it is called 3HQWDORJ\RI)DOORW
XX Normal, in small shunt
XX LVH, in large shunt Haemodynamics
TT (&* XX %LYHQWULFXODUK\SHUWURSK\in 2ZLQJWRULJKWYHQWULFXODURXWÀRZREVWUXFWLRQGXULQJ
pulmonary hypertension ventricular systole
XX RVH in pulmonary VODisease deoxygenated blood
of right ventricle
TT (FKR XX 9LVXDOL]HWKHGXFWXVDQGFRQ¿UPWKH
shunts through VSD
cardiogram direction and degree of shunting
to left ventricle, mix
with oxygenated
Treatment blood there and then
&RXQVHOWKHSDUHQWVDERXWWKHGLVHDVHWUHDWPHQWRSWLRQV this mixed blood
Source: Internet
DQGSURJQRVLV SDVVHVWKURXJKWKH
A. Medical aorta to different
SDUWVRIWKHERG\
Patent ductus arteriosus
7RIDFLOLWDWHFORVXUHRI3'$E\DQ\RIWKHIROORZLQJGUXJV
ZKHQJLYHQZLWKLQKRXUVRIDJH 7KHUHIRUHWKHQHW
SDWKRORJLFDOHIIHFWV
XX Indomethacin: IV slowly over 30 minutes in the
of these events are±
IROORZLQJGRVDJH±
TT 1stGRVHPJNJ

TT ndGRVHPJNJ KRXUVDIWHUst dose if

XX 3HUVLVWHQWO\OHVVEORRGLQSXOPRQDU\FLUFXODWLRQ
3'$SHUVLVWV ROLJDHPLFOXQJ¿HOGV
TT 3rdGRVHPJNJ KRXUVDIWHUnd dose if
XX Persistently low O saturation of blood in systemic
3'$SHUVLVWV circulation FKURQLFK\SR[DHPLD F\DQRVLV 
XX Ibuprofen*LYHQRUDOO\
XX Polycythaemia GXHWRFKURQLFK\SR[DHPLD
TT Day 1: 10 mg/kg 'D\PJNJ Day 3:5 mg/kg
XX *URZWKIDLOXUHGXHWRFKURQLFK\SR[DHPLD
 128 Step on to Paediatrics

Clinical Manifestations Sometimes,

&OLQLFDO¿QGLQJVDUHYDULDEOHDQGPDLQO\GHSHQGVRQWKH because of
GHJUHHRIULJKWYHQWULFXODURXWÀRZREVWUXFWLRQ VXGGHQG\VSQRHD
the affected child
XX Cyanosis
TT Patients with mild obstruction are minimally
DGRSWVVTXDWWLQJ
SRVLWLRQ till
cyanotic or even acyanotic SLQN72)
TT 7KRVHZLWKPD[LPDOREVWUXFWLRQDUHGHHSO\F\DQRVHG
G\VSQRHD
LPSURYHVDQG
since birth
TT 0RVWKDYHSURJUHVVLYHF\DQRVLVE\PRQWKVRIDJH
then the child
UHVXPHVSK\VLFDO
activity.
6TXDWWLQJLV
of diagnostic
VLJQL¿FDQFHDQG
LVKLJKO\W\SLFDO
of infants with
A TOF child in squatting position
72)
6TXDWWLQJFDXVHVLQFUHDVHGUHVLVWDQFHLQPeripheral
Clubbing and Blue tongue (central cyanosis)
Systemic blood vessels. 7KLVUDLVHVOHIWYHQWULFXODU
SUHVVXUHDERYHWKDWRIULJKWYHQWULFOHZKLFKGHFUHDVHV
XX 3DUR[\VPDOK\SHUF\DQRWLFDWWDFNV +\SR[LFVSHOOVEOXH ULJKWWROHIWVKXQWDFURVVWKH96'%ORRGWKXVÀRZV
VSHOOV7HWVSHOOV WKURXJKWKHVWHQRVHGSXOPRQDU\LQIXQGLEXOXP7KLV
7KLVLVWKHKDOOPDUNRIVHYHUH72)DQGXVXDOO\RFFXUV XOWLPDWHO\LPSURYHVSXOPRQDU\FLUFXODWLRQEHWWHU
GXULQJ¿UVW\HDUVRIOLIHPRVWFRPPRQO\E\PRQWKV R[\JHQDWLRQDQGUHOLHYHVWKHFKLOGIURPG\VSQRHDDQG
RIDJH7KHDWWDFNVDUHDVVRFLDWHGZLWKIXUWKHUUHGXFWLRQ HSLVRGHVRIF\DQRWLFVSHOOV
RIDQDOUHDG\FRPSURPL]HGSXOPRQDU\EORRGÀRZ PRUH XX )DLOXUHWRWKULYH QRWJDLQLQJZHLJKWDQGKHLJKW
VHYHUHV\VWHPLFK\SR[LDDQGPHWDEROLFDFLGRVLV6SHOOV
RFFXUPRVWIUHTXHQWO\LQWKHPRUQLQJRQDZDNHQLQJor General Physical Examination
DIWHUHSLVRGHVRIYLJRURXVFU\ XX $SSHDUDQFH&\DQRVLV VNLQOLSVDQGPXFRXV
membranes inside the mouth and nose looks blue)
&\DQRWLFVSHOOVSUHFLSLWDWLQJIDFWRUVDUH± XX Conjunctiva: Congested
XX Exertion XX 6OHHSOHVVQHVV
XX 8SVHWLQJGXHWRDQ\ XX Irritation to the baby
cause XX Vigorous crying

&\DQRWLFVSHOOVDUHFKDUDFWHUL]HGE\±

XX 6XGGHQRQVHWRIG\VSQRHD6RPHWLPHVJDVSLQJ
UHVSLUDWLRQDQGV\QFRSH
Conjunctival congestion
XX 6XGGHQGHHSHQLQJRIF\DQRVLV
XX )LQJHUVDQG
XX Alterations in consciousness, from irritability to
V\QFRSH6RPHWLPHVFRQYXOVLRQVDQGKHPLSDUHVLV toes: Clubbing
XX Pulse and
Tetralogy of fallot

XX 7HPSRUDU\GLVDSSHDUDQFHor decrease in the intensity

RIWKHV\VWROLFPXUPXUDWSXOPRQDU\DUHD EORRGSUHVVXUH
Normal
XX 0HWDEROLFacidosis
XX Oedema: Absent
XX $QWKURSRPHWU\
(DV\IDWLJDELOLW\DQGG\VSQRHDRQH[HUWLRQ7KHDIIHFWHG Stunting
child tires easily (easy fatigability)DQGEHJLQVSDQWLQJ
ZLWKDQ\IRUPRIH[HUWLRQ G\VSQRHDRQH[HUWLRQ  &OXEELQJRI¿QJHUV
 Step on to Paediatrics 129

Precordium XX ;5D\FKHVW
TT Heart

XX ,QVSHFWLRQ0D\EHEXOJHGGXHWRULJKWYHQWULFXODU ³³ Size: Not enlarged

K\SHUWURSK\(RVH) ³³ 6KDSH%RRWVKDSHG FRHXUHQVDERW GXHWR

XX 3DOSDWLRQ FRQFDYLW\DWSXOPRQDU\FRQXV(because of low

TT $SH[EHDWLVWDSSLQJLQFKDUDFWHUQRWVKLIWHG SUHVVXUHRISXOPRQDU\DUWHU\ DQGXSWXUQLQJRI
TT 3LVQRWSDOSDEOH FDUGLDFDSH[ GXHWROLIWLQJXSRIFDUGLDFDSH[E\WKH
TT /HIWSDUDVWHUQDOKHDYHPD\EHSUHVHQW K\SHUWURSKLHGULJKWYHQWULFOH
TT $V\VWROLFWKULOOPD\EHIHOWDWOHIWXSSHU 2OLJDHPLFOXQJV¿HOG Concavity at pulmonary area
LQWHUFRVWDOVVSDFHV
XX Auscultation
TT S1 is normal R6LVORXG VLQJOH
TT Added sound: A loud ejection systolic murmur

LVKHDUGDWSXOPRQDU\DUHD RULJLQDWLQJIURP
WKHWXUEXOHQFHDWULJKWYHQWULFXODURXWÀRZWUDFW
obstruction)

Lifting of apex
Complications
XX +\SHUF\DQRWLFVSHOOV
XX 6HYHUHSRO\F\WKDHPLD
XX Cerebral abscess as
%RRWVKDSHGKHDUWDQGROLJDHPLFOXQJV¿HOGV
deoxygenated blood
enters the systemic TT/XQJ¿HOGV/RRNEODFNGXHWRGHFUHDVHGSXOPRQDU\
circulation and brain, vascularity (oligaemia)
E\SDVVLQJOXQJVZLWKRXW XX (&*59+DQGULJKWD[LVGHYLDWLRQ
clearing the germs by XX (FKRFDUGLRJUDSK\&RQ¿UPVWKHGLDJQRVLV
SXOPRQDU\VFDYHQJHU
cells Treatment
XX &HUHEUDOWKURPER XX &RXQVHOWKHSDUHQWVDERXWWKHGLVHDVHWUHDWPHQWRSWLRQV
embolism and stroke DQGSURJQRVLV
XX Infective endocarditis Cerebral abscess in a child with TOF
XX Delayed growth,
A. Medical
GHYHORSPHQWDQGSXEHUW\
XX Neonates with severe cyanosis is treated with IV infusion
of Prostaglandin E1 ȝJNJPLQ,9 WRNHHSWKH
XX Others:
TT +\SHUXULFDHPLD
GXFWXVDUWHULRVXVRSHQSDWHQWDQGWKHUHE\WRLPSURYH
JRXW
SXOPRQDU\FLUFXODWLRQDQGLVOLIHVDYLQJ
TT Relative IDA
XX 7UHDWPHQWRIF\DQRWLFVSHOOV LQKRVSLWDO
TT %OHHGLQJGLVRUGHUVFRDJXORSDWK\

XX 3ODFHWKHLQIDQWLQDNQHHFKHVWSRVLWLRQ ROGHUFKLOGUHQ
+HDUWIDLOXUHLVXQFRPPRQLQFODVVLFDO72)
XVXDOO\VTXDWVSRQWDQHRXVO\DQGGRQRWGHYHORS
Diagnosis F\DQRWLFVSHOOV
XX *LYH2/PLQWKURXJKIDFHPDVNKHDGER[
Based on the clinical features and relevant
investigations.
XX (VWDEOLVKDFDOPHQYLURQPHQWE\LVRODWLQJWKHSDWLHQW
,IWKHVSHOOSHUVLVWVJLYHWKHIROORZLQJ
Investigations
Tetralogy of fallot

XX ,QWUDYHQRXVÀXLGV 10 ml/kg bolus normal saline

XX &RPSOHWHEORRGFRXQWV IROORZHGE\PDLQWHQDQFHÀXLGV
TT Haemoglobin and haematocrit values are usually XX Morphine:PJNJ6&IRUNHHSLQJWKHFKLOG
HOHYDWHGZKLFKLVSURSRUWLRQDOWRWKHGHJUHHRI calm and for muscle relaxation
cyanosis XX NaHCO3:P(TNJ,9WRFRUUHFWacidosis
TT 7& '&RI:%&3ODWHOHWFRXQWV1RUPDO XX Propranolol: 0.1 mg/kg IV which relaxes the
TT 3%)VKRZVPLFURF\WLFK\SRFKURPLFDQDHPLD
LQIXQGLEXODUPXVFOHDQGWKHUHE\UHGXFHVVSDVP
 130 Step on to Paediatrics

B. Surgical repair
,IWKHVHPHDVXUHVGRQRWFRQWUROWKHVSHOOWKHQDUUDQJH XX Total correction:7KHWUHDWPHQWRIFKRLFHFDQEHGRQH
to trancfer the child to CCU. DVHDUO\DVPRQWKRIDJH HOHFWLYHO\LQEHWZHHQ
XX Phenylephrine (alfa agonist):7RUDLVHV\VWHPLF months of age)
%3DVZHOODVV\VWHPLFYDVFXODUUHVLVWDQFH7KLVZLOO XX Palliative surgery (Blalock Taussig Shunt)
UHGXFHULJKWWROHIWVKXQWDQGXOWLPDWHO\SURPRWH 7KLVLVGRQH RSA - Right subclavian artery
RSA
SXOPRQDU\EORRGÀRZ RPA - Right pulmonary artery
between Shunt
TT Phenylephrine:—JNJEROXV,0or SC.
Subclavian artery
IROORZHGE\ȝJNJPLQ,9LQIXVLRQWLWUDWHG
(systemic) and
DFFRUGLQJWRKHDUWUDWHDQGEORRGSUHVVXUH
SXOPRQDU\DUWHU\
,IWKHSUHFHGLQJVWHSVGRQRWUHOLHYHWKHVSHOORULI SXOPRQDU\ RPA
WKHLQIDQWLVUDSLGO\GHWHULRUDWLQJLQWXEDWLRQDQG circulation)
YHQWLODWRU\VXSSRUWVKRXOGEHJLYHQ to increase

Source: Internet
circulation to the
XX 7UHDWPHQWDWKRPH OXQJV7KLVZLOO
TT 3URSUDQROROPJNJGD\RUDOO\WREHFRQWLQXHG
LPSURYHWLVVXH
WRSUHYHQWF\DQRWLFVSHOOV oxygenation, BT shunt

TT )OXLG 1XWULWLRQ relieves cyanosis and allow the child to grow good
³³ Provide high calorie diets to ensure growth
HQRXJKWRGRFRPSOHWHVXUJLFDOUHSDLU7KLVSURFHGXUHLV
³³ 6XSSOHPHQW,URQPJNJGD\HOHPHQWDOLURQ
UHVHUYHIRU72)ZLWKDVVRFLDWHGFRPRUELGLWLHVHJRWKHU
RUDOO\WRSURPRWHPDWXUDWLRQRI5%& congenital anomalies or SUHPDWXULW\
³³ 6XSSOHPHQW9LWDPLQV PLQHUDOV
Prophylaxis for infective endocarditis: Recommended.
XX &RXQVHOSDUHQWVWRSD\VSHFLDODWWHQWLRQWRÀXLGLQWDNH
VRDVWRSUHYHQWGHK\GUDWLRQKDHPRFRQFHQWUDWLRQDQG Prognosis
thereby to reduce thromboembolism. Dehydration of
7KHORQJWHUPRXWFRPHRIWUHDWPHQWRI72)GHSHQGV
DQ\FKLOGZLWK72)VKRXOGEHUHIHUUHGLPPHGLDWHO\IRU
SULPDULO\RQWKHVL]HDQGDQDWRP\RIWKHSXOPRQDU\
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arteries.

Clinico-pathological differences between TOF and VSD

Traits TOF VSD
Direction of shunt XX Right to left XX Left to right
XX Single, mostly but may be associated
Nature of defect XX 0XOWLSOH
with other defects
XX 0RUHEORRGLQWRSXOPRQDU\FLUFXODWLRQ
Status of XX Less entry of blood from right ventricle to
SXOPRQDU\FLUFXODWLRQ
XX +LJKFKDQFHRIGHYHORSLQJSXOPRQDU\
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circulation XX /RZSXOPRQDU\SUHVVXUH
untreated cases
Cyanosis XX Present XX Absent
0RVWO\H[WUDSXOPRQDU\DQGDUHUHODWHGWR XX Pulmonary congestion and recurrent
XX +\SHUYLVFRVLW\RIEORRGWKURPERHPEROLVPVWURNH SQHXPRQLD
&RPSOLFDWLRQV XX Direct entry of venous blood to systemic circulation XX &DUGLDFRYHUORDG±&&)
Tetralogy of fallot

E\SDVVLQJOXQJVPD\OHDGWREUDLQDEVFHVV XX 7XUEXOHQFHDQGLQIHFWLYHHQGRFDUGLWLV
XX Heart failure (uncommon)
XX %RRWVKDSHGKHDUW XX Cardiomegaly
&KHVW;5D\ XX 'HSUHVVLRQDWSXOPRQDU\FRQXV XX Normal or SURPLQHQWSXOPRQDU\FRQXV
¿QGLQJV
XX 2OLJDHPLFOXQJ¿HOGV XX 3URPLQHQWSXOPRQDU\YDVFXODUPDUNLQJV
 Step on to Paediatrics 131

HEART FAILURE (HF) B. Chest examination

XX Cardiomegaly
,WLVDFOLQLFDOVLWXDWLRQZKHUHKHDUWIDLOVWRSXPSEORRGWR XX Wheeze
XX *DOORSUK\WKP
meet the circulatory or metabolic needs of the body. XX %DVDOFUHSLWDWLRQ
XX 0XUPXUV
Aetiology
C. Other features
Congenital 96'7*$7$39'3'$
Heart diseases Coarctation of Aorta (CoA) XX 7HQGHUKHSDWRPHJDO\
Cardiac causes

TT Valvular heart diseases XX 3RVLWLYHKHSDWRMXJXODUUHÀX[

e.g.mitral, aortic etc.
TT Infective endocarditis
$FTXLUHG Diagnosis
TT +\SHUWHQVLYHKHDUW
Heart diseases
diseases e.g. acute %DVHGRQFOLQLFDOIHDWXUHV VXSSRUWVIURPWKHUHOHYDQW
JORPHUXORQHSKULWLV investigations.
TT Viral myocarditis etc.
Investigations
1RQFDUGLDF

TT )OXLGRYHUORDG TT Severe anaemia XX ;5D\&KHVW

causes

TT 6HSWLFDHPLD TT Beriberi (wet) XX Cardiomegaly (Increased cardiothoracic ratio, the

TT $VSK\[LDO TT 7K\URWR[LFRVLV ratio between
FDUGLRP\RSDWK\
the maximum
diameters of chest
,VFKDHPLFKHDUWGLVHDVHDQGFDUGLRP\RSDWKLHVDUHOHVV KHDUW
common causes of heart failure in children.

Pathogenesis Normal ratio

Source: Internet
TT Newborn: 60%
:KHQKHDUWIDLOVWRSXPSRXWLWVEORRGLWGDPVHLWKHULQ TT Children: 55%
SXOPRQDU\or in systemic circulations or both.
TT Adult: 50%

Cardiothoracic Ratio > 60%

Features of pulmonary Features of systemic
overload (LHF) overload (RHF) TTPulmonary vascular congestion
TT 5HVSLUDWRU\GLVWUHVV XX (&*1RWGLDJQRVWLFEXWFDQVD\WKHSULPDU\KHDUW
XX 8SSHUDEGRPLQDOSDLQ
TT Cough with frothy defects
XX 'HSHQGHQWRHGHPD
VSXWXP XX (FKRFDUGLRJUDSK\'HPRQVWUDWHVWUXFWXUDOSDWKRORJ\
XX 7HQGHUKHSDWRPHJDO\
TT 7DFK\SQRHD XX &%&+EPD\EHORZLI+)LVUHODWHGWRVHYHUHDQDHPLD
XX 5DLVHG-93
TT %DVDOFUHSLWDWLRQV
Treatment
XX &RXQVHOLQJSDUHQWVDERXWWKHSUREOHP
Clinical Manifestations XX *HQHUDOPHDVXUHV
XX ,QIDQWV1RQVSHFL¿Fe.g. irritability, excessive TT 'HFXELWXV8SULJKWSRVLWLRQ

VZHDWLQJSRRUIHHGLQJ GLI¿FXOWIHHGLQJUHVSLUDWRU\ TT O LQKDODWLRQ+XPLGL¿HGR[\JHQE\KHDGER[


distress PDVNQDVDOSURQJV
XX Older children: (IIRUWLQWROHUDQFHG\VSQRHDRQ TT %HGUHVW UHVWULFWLRQRISK\VLFDODFWLYLWLHV
H[HUWLRQH[FHVVLYHVZHDWLQJFRXJKDEGRPLQDOSDLQ TT 0DLQWHQDQFHRIERG\WHPSHUDWXUH

A. General examination TT )HHGLQJBreast feeding or nasogastric tube feeding

of foods rich in calory and low in sodium

XX 7DFK\SQRHD XX 3URORQJHGFDSLOODU\ XX &RQWURORIÀXLGRYHUORDGE\
XX 7DFK\FDUGLD UH¿OOLQJWLPH
Heart failure

TT )OXLGUHVWULFWLRQ%\
XX &ROGSHULSKHULHV XX 'HSHQGHQWRHGHPD
TT Salt restriction: Avoid table salt and salt rich foods
XX :HDNWKUHDG\SXOVH XX 5DLVHG-93
TT Diuretics HJ)UXVHPLGH7KLD]LGHRU.+VSDULQJ
XX /RZEORRGSUHVVXUH XX Cyanosis, may be
diuretics
 132 Step on to Paediatrics

XX $XJPHQWDWLRQRIP\RFDUGLDOFRQWUDFWLOLW\E\LQRWURSLF Pathogenesis
agents e.g.
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TT &DUGLDFJO\FRVLGHV 'LJR[LQ 7RWDOGLJLWDOL]DWLRQ
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GRVHPJNJ
QHWZRUNRISODWHOHWVDQG¿EULQRQWKHHQGRFDUGLDOVXUIDFH
TT 6\PSDWKRPLPHWLFDPLQHVe.g. 'RSDPLQH
6XEVHTXHQWO\WKLVLVFRORQL]HGE\PLFURRUJDQLVPVDQG
Dobutamine
IRUPVYHJHWDWLRQV7KHVHYHJHWDWLRQVPD\VRPHWLPHV
TT 3KRVSKRGLHVWHUDVHLQKLELWRUVHJ%LS\ULGLQHV
become large enough to cause obstruction in blood
$PULQRQHDQG0LOULQRQH
circulation within heart or may break away as emboli
XX Afterload reducing agents: ACE inhibitors e.g.
DQGGHSRVLWLQGLIIHUHQWRUJDQV6RPHWLPHVWKHUHPD\EH
&DSWRSULO(QDODSULOLVJLYHQWRUHGXFHWKHLPSHGDQFHWR
left ventricular ejection. manifestation of immune mediated vasculitis.
XX &RUUHFWLRQRIXQGHUO\LQJFDXVHVDQGSUHFLSLWDWLQJ
factors Clinical Manifestations
XX +LVWRU\RI±
TT +HDUWGLVHDVHVLQPDMRULW\RISDWLHQWV
TT 6XUJLFDOSURFHGXUHe.g. cardiac surgery, tooth

INFECTIVE ENDOCARDITIS (IE) extraction, tonsilectomy

TT Long continued fever with chills and night sweat

It is one of the most serious of all infections and is TT 1RQVSHFL¿FPDQLIHVWDWLRQVe.g. malaise, anorexia,

characterized by colonization or invasion of the heart weight loss, cough, shortness of breath, headache,
valves or the endocardium by a microbial agent, leading to P\DOJLDVMRLQWSDLQ
formation of bulky, friable vegetation laden with
RUJDQLVP7KHYHJHWDWLRQVDUHFRPSRVHGRI¿EULQ
A. General Features
XX $SSHDUDQFH6LFNORRNLQJSDOH
LQÀDPPDWRU\FHOOVDQGPLFURRUJDQLVPV
XX %RG\WHPSHUDWXUH5DLVHGLQRISDWLHQWV
Clinical Types XX Heart rate: Increased
XX 5HVSLUDWRU\UDWH0D\EHLQFUHDVHG
Types Natural history Prognosis XX 2HGHPD0D\SUHVHQWLIDVVRFLDWHG&&)
Acute Produce destructive
High
By virulent infections usually to a
mortality
B. Cutaneous manifestations
organism SUHYLRXVO\QRUPDOKHDUWYDOYH
Subacute Low
XX )RXQGRQWKHSDOSHEUDOFRQMXQFWLYD
Less destructive infection Petechiae
By low mortality, buccal or SDODWDOPXFRVD
SDUWLFXODUO\RQGHIRUPHG
virulent good 6SOLQWHU
valves XX Dark red linear lesions in the nail beds
organism recovery haemorrhages

Risk Factors XX 6PDOOUHGWRSXUSOHWHQGHUQRGXOHV

Osler's nodes
IRXQGLQSXOSRI¿QJHUVVROHVRIWKH
XX &RQJHQLWDOKHDUWGLVHDVHSDUWLFXODUO\WKRVHFUHDWLQJ
IHHWWKHQDUDQGK\SRWKHQDUHPLQHQFHV
high velocity jet streams HJVPDOO96'3'$RU72)
XX Valvular defects e.g. valvular stenosis -DQHZD\ XX Nontender haemorrhagic maculae on
XX $UWL¿FLDOYDOYHVDQGYDVFXODUJUDIWV lesions WKHSDOPVDQGVROHV
XX Normal heart with indwelling vascular catheter
Clubbing XX )LQJHUVDQGWRHV
XX ,PPXQRGH¿FLHQF\e.g. +,9WKHUDSHXWLFLPPXQH
VXSSUHVVLRQ'0,9GUXJXVHUV XX 5HWLQDOKDHPRUUKDJHVZLWKSDOH
5RWK VVSRWV
centers
Organisms
Heart failure

XX StreptococciYLULGDQV  &XWDQHRXVOHVLRQVUHSUHVHQWYDVFXOLWLVSURGXFHGE\

XX Staphylococcus aureus (25-30%) FLUFXODWLQJDQWLJHQDQWLERG\FRPSOH[HV
XX Fungal agents (5%)
 Step on to Paediatrics 133

Source: Internet
Splinter haemorrhage Osler's node Roth spot Janeway lesion

C. Systemic Manifestations Complications

XX &KDQJHLQDSUHH[LVWLQJPXUPXUor XX 0\RFDUGLDOLQIDUFWLRQSHULFDUGLWLVFDUGLDF
GHYHORSPHQWRIDQHZPXUPXU arrhythmia
CVS XX 7DFK\FDUGLD XX &DUGLDFYDOYXODULQVXI¿FLHQF\
XX )HDWXUHVRIFRQJHVWLYHFDUGLDFIDLOXUH XX Congestive heart failure
XX Embolic stroke XX Sinus of Valsalva aneurysm
CNS XX ,QWUDFHUHEUDOKDHPRUUKDJHDQGPXOWLSOH XX Aortic root or myocardial abscesses
microabscesses XX Arterial emboli, infarcts, mycotic aneurysms
XX Arthritis, myositis
-RLQWV XX Arthritis
XX *ORPHUXORQHSKULWLVacute renal failure
XX )ODQNSDLQDQGKDHPDWXULDGXHWRUHQDO Stroke syndromes
Renal
XX

emboli XX 0HVHQWHULForVSOHQLFDEVFHVVor infarct

XX 6SOHQRPHJDO\DQGOHIWXSSHUTXDGUDQWSDLQ
6SOHHQ
LQVSOHQLFHPEROL

Investigations
Investigations Results
$QDHPLDSUHVHQWLQRISDWLHQWVDQGLVXVXDOO\QRUPRF\WLFDQG
TT &RPSOHWHEORRGFRXQWV
QRUPRFKURPLF/HXNRF\WRVLVQRWHGLQRISDWLHQWV
TT $FXWHSKDVHUHDFWDQWV (65CRP) Raised
XX ,WVKRXOGEHGRQHLQDOOSDWLHQWVZKRKDYHDSDWKRORJLFKHDUWPXUPXUDKLVWRU\
of heart disease or SUHYLRXVHQGRFDUGLWLV
XX VHSDUDWHVDPSOLQJV POHDFK ZLWKLQKRXUVVKRXOGEHREWDLQHGIURP
TT Blood culture GLIIHUHQWSHULSKHUDOVLWHV
XX Cultures should be grown aerobically and anaerobically for at least 1 week
XX ,IQRJURZWKLVREVHUYHGE\KRXUVRILQFXEDWLRQPRUHEORRGFXOWXUHV
should be obtained
TT (FKRFDUGLRJUDSK\ 7\SLFDOILQGLQJVLQFOXGHYHJHWDWLRQVDEVFHVVDQGYDOYXODULQVXIILFLHQF\
TT Urinalysis 0D\UHYHDOSURWHLQXULD  and/orPLFURVFRSLFKDHPDWXULD 
TT Immune assays ,QFUHDVHG,JFLUFXODWLQJLPPXQHFRPSOH[HVDQGUKHXPDWRLGIDFWRU
6FUDSLQJIURPFXWDQHRXVOHVLRQXULQHV\QRYLDOIOXLGDEVFHVV&6) LQSUHVHQFH
&XOWXUHRIRWKHUVSHFLPHQ
Heart failure

TT
of meningitis)

Diagnosis
Based on Revised Duke Clinical Diagnostic Criteriae.
 134 Step on to Paediatrics

Revised Duke Clinical Diagnostic Criteriae for Infective Endocarditis

Major Criteriae Minor Criteriae
XX 3UHGLVSRVLQJKHDUWFRQGLWLRQV
TT 3RVLWLYHEORRGFXOWXUHV  XX )HYHU
VHSDUDWHFXOWXUHVIRUDXVXDO XX (PEROLFYDVFXODUVLJQVHJDUWHULDOHPEROLVPVHSWLFSXOPRQDU\HPEROLVPP\FRWLF
SDWKRJHQor PRUHIRUOHVV DQHXU\VPLQWUDFUDQLDOKDHPRUUKDJHFRQMXQFWLYDOSHWHFKLDH-DQHZD\OHVLRQV
W\SLFDOSDWKRJHQV DQG XX ,PPXQHFRPSOH[SKHQRPHQDHJJORPHUXORQHSKULWLVDUWKULWLVUKHXPDWRLGIDFWRU
TT Evidence of endocarditis on 2VOHUQRGHV5RWKVSRWV
HFKRFDUGLRJUDSK\ XX $VLQJOHSRVLWLYHEORRGFXOWXUHor serologic evidence of infection, and
TT Intracardiac mass on a valve (FKRFDUGLRJUDSKLFVLJQVQRWPHHWLQJWKHPDMRUFULWHULD
or other site XX Presence of newly diagnosed clubbing
TT 5HJXUJLWDQWÀRZQHDUD XX 6SOHQRPHJDO\
SURVWKHVLV XX 6SOLQWHUKHPRUUKDJHVDQGSHWHFKLDH
TT $EVFHVVSDUWLDOGHKLVFHQFH XX A high erythrocyte sedimentation rate
RISURVWKHWLFYDOYHVor XX $KLJK&UHDFWLYHSURWHLQOHYHO
TT 1HZYDOYHUHJXUJLWDQWÀRZ XX 7KHSUHVHQFHRIFHQWUDOQRQIHHGLQJOLQHVSHULSKHUDOOLQHVDQGSUHVHQFHRI
PLFURVFRSLFKHPDWXULD

'H¿QLWHGLDJQRVLV2 major criteriae or 1 major + 3 minor criteria or 5 minor criteria

Possible diagnosis: 1 major + 1 minor criteria or 3 minor criteria

Adapted from Kliegman RM, Stanton BF, Geme III JWS, Schor NF, Behrman RE. Editors. Nelson
Textbook of Pediatrics, 20th Edition. New Delhi: Elsevier; 2016

Treatment Organisms Regimen, Dose and Route Duration

Antibiotics should be started &3HQLFLOOLQ* XNJGD\ ,9
immediately, once a diagnosis of IE is hourly
PDGH7KHGRVHGXUDWLRQDQGURXWHRI ZHHNV
or
administration of antibiotics should be Ceftriaxone (100mg/kg/day) IV once daily
decided jointly with cardiologist and or
microbiologist. 6WUHSYLULGDQV
&HIWULD[RQH*HQWDPLFLQ PJNJGD\,9
XX (PSLULFWKHUDS\ZLWK9DQFRP\FLQ DQG6WUHSERYLV ZHHNV
,0VLQJOHor in 3 divided doses)
SOXV*HQWDPLFLQIRUZHHNV
SHULRGLVWKHPRVWFRPPRQUHJLPHQ or
IRUSDWLHQWVZLWKRXWDSURVWKHWLF
valve and when there is a high risk 9DQFRP\FLQ PJNJGD\ ,9KRXUO\
ZHHNV
of S aureus, Enterococcus, or S IRUSHQLFLOOLQ FHIWULD[RQHDOOHUJLFSDWLHQWV
viridans infection
6WDSK\ORFRFFXV
Infective endocarditis

XX 7KHUDS\FDQEHWDLORUHGZLWK ZHHNV
(Oxacillin Nafcillin or R[DFLOOLQ PJNJGD\,9
DSSURSULDWHDQWLELRWLFVRQFHWKH
VXVFHSWLEOH KRXUO\“*HQWDPLFLQ
SDWKRJHQ VHQVLWLYLWLHVDUHGH¿QHG
strain)
&HID]ROLQH PJNJGD\ ,9KRXUO\
6 weeks
3HQLFLOOLQDOOHUJLF“*HQWDPLFLQ
6WDSK\ORFRFFXV
(Oxacillin
6 weeks
Resistant Vancomycin
Strain)
 Step on to Paediatrics 135

Prophylaxis Highest risk group people for prophylaxis of IE

2QO\WKHKLJKULVNSDWLHQWVOLVWHGEHORZUHTXLUHDQWLELRWLF XX 5HFLSLHQWVRISURVWKHWLFYDOYHor SURVWKHWLFPDWHULDO
SURSK\OD[LVEHIRUH± XX 3DWLHQWVZLWK±
TT Previous endocarditis
XX 'HQWDOSURFHGXUHVLQYROYLQJPDQLSXODWLRQRIJLQJLYDO
TT Congenital heart diseases (CHD) e.g.
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³³ Palliated cyanotic CHD
oral mucosa
³³ Completely repaired CHD with prosthesis/device
XX 3URFHGXUHVLQYROYLQJUHVSLUDWRU\WUDFWor infected skin
or musculoskeletal tissue during 1st 6 months postprocedure
³³ CHD with residual defects bordered by the
XX ,(SURSK\OD[LVLVQRWUHFRPPHQGHGIRU*HQLWRXULQDU\
RU*,WUDFWSURFHGXUHVERG\SLHUFLQJRUWDWWRRLQJ prosthetic material
XX &DUGLDFWUDQVSODQWZLWKYDOYXORSDWK\
Antibiotic prophylaxis options include the following
Regimen: Single dose
Situations Drug Route 30 to 60 min before
procedure
&DQWDNHRUDOO\ QRWDOOHUJLFWR
Amoxicillin Oral 50 mg/kg
Penicillins or $PSLFLOOLQ
$PSLFLOOLQor PJNJ,0or IV
Unable to take oral medication Parenteral
Cefazolin or Ceftriaxone PJNJ,0or IV
&HSKDOH[LQ ‚or 50 mg/kg
Can take orally but allergic to
Clindamycin or Oral PJNJ
Penicillins or $PSLFLOOLQ
Azithromycin or Clarithromycin 15 mg/kg
Allergic to Penicillins or $PSLFLOOLQ Cefazolin or &HIWULD[RQH‚or PJNJ,0or IV
Parenteral
and unable to take oral medication Clindamycin PJNJ,0or IV

* Or other first or second generation Cephalosporin in equivalent dose † Cephalosporin should not be used in a
child with history of anaphylaxis, angioedema or urticaria with Penicillin or Ampicillin

References
 -RQH31HWDO&DUGLRYDVFXODUGLVHDVHV,QCurrent Ped Diagnosis and treatment 23rd Ed’2016 : 550-610.
'DQLHO%HUQVWHLQ&RQJHQLWDO+HDUW'LVHDVH,Q.OLHJPDQ506WDQWRQ%)*HPH,,,-:66FKRU1)%HKUPDQ5((GLWRUV
1HOVRQ7H[WERRNRI3HGLDWULFVth(GLWLRQ1HZ'HOKL(OVHYLHU
Infective endocarditis

 .LWFKQHU'-&DUGLRYDVFXODU'LVHDVHV,Q)RUIDU $UQHLO¶V7H[W%RRNRI3HGLDWULFVthHG/RQGRQ
 *HZLW]0+:RROI3.&DUGLDF(PHUJHQFLHV7H[WERRNRI3HGLDWULF(PHUJHQF\0HGLFLQHthHG3KLODGHOSKLD/LSSLQFRWW
:LOOLDPV :LONLQV
 6RQGKHLPHU-0&DUGLRYDVFXODU'LVHDVHV,Q&XUUHQW(VVHQWLDOV3HGLDWULFVstHG86$0F*UDZ+LOO
 3UHYHQWLRQRI,QIHFWLYH(QGRFDUGLWLV*XLGHOLQHVIURPWKH$PHULFDQ+HDUW$VVRFLDWLRQ&LUFXODWLRQ
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$YDLODEOHIURPKWWSHPHGLFLQHPHGVFDSHFRPDUWLFOH
 .KDQ055DKPDQ0((VVHQFHRI3HGLDWULFVthHG(OVHYLHU&KS&96S
 136 Step on to Paediatrics

SELF ASSESSMENT
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 17
Joint Pain and Swelling
Acute rheumatic fever (ARF)- - - - - - - - - - - 137
Juvenile idiopathic arthritis (JIA) - - - - - - - - - - 140

:KHQHYHUDFKLOGSUHVHQWVZLWKSDLQIXOVZROOHQMRLQW ACUTE RHEUMATIC FEVER (ARF)

tenderness and limitation of movements, the following
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XX -XYHQLOHLGLRSDWKLFDUWKULWLV HQWHURSDWKLF XURJHQLWDO OHDGWRGHYHORSPHQWRIUKHXPDWLFKHDUWGLVHDVHV
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truely in the joints, usually occurs at night and get relieved by SKDU\QJLWLVDUHQRORQJHUSUHVHQW . However, in about
JHQWOHPDVVDJH7KHVHDUHSUREDEO\UHODWHGWRoveruse of limbs RQHWKLUGRIFDVHVKLVWRU\RISKDU\QJLWLVDUHDEVHQW
or growing pain or QRQVSHFL¿FOLPEVSDLQ and should not be 7KHGLVHDVHLVLPPXQHPHGLDWHGDQGLVUHODWHGWR
confused with arthritis. immunogenic cross reactivityEHWZHHQVWUHSWRFRFFDO
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Sometimes, atients with 7KDODVVDHPLDPDMRUPD\SUHVHQWZLWK
carbohydrate etc) and tissues of heart, joints and
SDLQLQMRLQWVDQGOLPEV
brain.
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GLVFXVVHGLQWKLVFKDSWHU

Group A Streptococcal pharyngitis

6HQVLWL]DWLRQRI%O\PSKRF\WHV IRUPDWLRQRIDQWL6WUHSWRFRFFDODQWLERG\

Antibodies cross react with tissue antigens

,QÀDPPDWLRQ Acute rheumatic fever

Heart -RLQW CNS Skin

7UDQVLHQWDUWKULWLVDUWKUDOJLD Sydenham’s chorea • Subcutaneous nodule

• Erythema marginatum

0\RFDUGLXP Endocardium Pericardium

Aschoff nodule (QGRFDUGLWLVHVSRIOHIWVLGHGYDOYHV %UHDG EXWWHUSHULFDUGLWLV

137

Pathophysiology of ARF (adopted from Robbin's & Cotran's pathology '2010)

 138 Step on to Paediatrics

Clinical Manifestations JonesLQSURSRVHGDJXLGHOLQH UHYLVHGLQ IRU

$JH&KLOGUHQEHWZHHQ\HDUVRIDJHKDYHKLJKULVNRI diagnosis and to limit over diagnosis of acute rheumatic
VWUHSWRFRFFDOSKDU\QJLWLVDQGDFXWHUKHXPDWLFIHYHU IHYHU7KH-RQHV&ULWHULDDVUHYLVHGE\WKH$PHULFDQ
+HDUW$VVRFLDWLRQ LQ LVQRZXVHGIRUGLDJQRVLVRI
As there is no clinical or ODERUDWRU\¿QGLQJV the initial attack of acute rheumatic fever and recurrent
SDWKRJQRPRQLFIRUDFXWHUKHXPDWLFIHYHUT. Duckett attacks.

Evidence of antecedent group A

Major criteriae Minor criteriae
streptococcal (GAS) infection
XX Clinical features e.g. XX 0LFURELRORJLFDO3RVLWLYHWKURDW
TT 0LJUDWRU\SRO\DUWKULWLV TT Arthralgia
swab culture or UDSLGVWUHSWRFRFFDO
TT Pancarditis TT )HYHU antigen test
TT Sydenham's chorea XX Laboratory features, e.g. or
TT Subcutaneous nodules TT (OHYDWHGDFXWHSKDVHUHDFWDQWVe.g. ESR, CRP XX Serological: Elevated or increasing
TT Erythema marginatum TT 3URORQJHG35LQWHUYDO VWUHSWRFRFFDODQWLERG\WLWHU±ASO

TT Low-Risk populations:,QFLGHQFH”SHUVFKRRODJHFKLOGUHQSHU\HDUor DOODJHUKHXPDWLFKHDUWGLVHDVH

SUHYDOHQFHRI”SHUWKRXVDQGSRSXODWLRQV
TT Moderate/High Risk populations:7KRVHZLWKKLJKHULQFLGHQFHor SUHYDOHQFHUDWHV

XX Initial attack:PDMRUPDQLIHVWDWLRQVor 1 major and B. Carditis (pancarditis)

PLQRUPDQLIHVWDWLRQVSOXVHYLGHQFHRIUHFHQW*$6 TT 2FFXUVLQRIFDVHV
infection TT It involves all the 3 layers of heart i.e. endocardium,
XX Recurrent attack: PDMRUor PDMRUDQGPLQRUor 3 myocardium or SHULFDUGLXP
minor manifestations WKHODWWHURQO\LQWKH0RGHUDWH
+LJK5LVNSRSXODWLRQ SOXVHYLGHQFHRIUHFHQW*$6 Features of Pancarditis
infection
XX (QGRFDUGLWLV0XUPXUVGXHWRYDOYXODULQYROYHPHQW
Exception: In the following 3 circumstances, the
XX 0\RFDUGLWLV7DFK\FDUGLDFRQGXFWLRQGHIHFW
GLDJQRVLVRI$5)FDQEHPDGHZLWKRXWVWULFWDGKHUHQFHWR
cardiomegaly
WKH-RQHVFULWHULD XX 3HULFDUGLWLV3HULFDUGLDOUXE HIIXVLRQ
XX Chorea occurs as the only major manifestation
XX Indolent carditis is the only manifestation and $VSHU5HYLVHG-RQHVFULWHULD¶± Subclinical carditis
XX 5HFXUUHQWUKHXPDWLFIHYHULQKLJKULVNSRSXODWLRQV GH¿QHGDVFDUGLWLVLGHQWL¿HGE\HFKRFDUGLRJUDPZLWKRXW
A. Migratory polyarthritis clinical evidence i.e. murmur) LVDOVRDFFHSWHGDVPDMRU
TT 2FFXUVLQDERXWRISDWLHQWVRI$5) criteria.
TT 7\SLFDOO\large joints e.g. knees, ankles, wrists and Commonly, mitral valves are involved. Sometimes along
elbows are involved with with mitral valves, aortic valves may be involved. But
SDLQDQGOLPLWDWLRQRI
isolated aortic or ULJKWVLGHGYDOYXODULQYROYHPHQWLV
movements
uncommon.
TT Affected joints are
swollen, red, hot and Common murmurs are–
Acute rheumatic fever

H[TXLVLWHO\WHQGHU$
VHYHUHO\LQÀDPHGMRLQW XX +LJKSLWFKHGKRORV\VWROLFPXUPXUUDGLDWLQJWRD[LOOD
can become normal because of mitral regurgitation
ZLWKLQGD\VHYHQ XX $SLFDOPLGGLDVWROLFPXUPXUGXHWRUHODWLYHPLWUDO
Swollen knee joints
without treatment stenosis
TT $GUDPDWLFUHVSRQVHWRRUDODVSLULQLVFKDUDFWHULVWLF XX +LJKSLWFKHGGHFUHVFHQGRGLDVWROLFPXUPXUGXHWR
NB: Monoarthritis and involvement of spines, small DRUWLFLQVXI¿FLHQF\
joints of hands and feet and hip joints are uncommon
in rheumatic fever. Rheumatic arthritis is typically not 6RPHWLPHVFDUGLWLVUHVXOWVLQFDUGLRPHJDO\DQG&&)ZLWK
deforming. SXOPRQDU\DQGV\VWHPLFFRQJHVWLRQ
 Step on to Paediatrics 139

C. Sydenham’s chorea Complication

TT 2FFXUVLQDERXWRISDWLHQWV Rheumatic valvular diseases e.g. mitral (stenosis,
TT &KDUDFWHULVWLFPRYHPHQWVDUH± regurgitation), aortic (stenosis, regurgitation) and
³³ 0LONPDLGVJULS
involvement of other valves.
³³ 6SRRQLQJDQGSURQDWLRQRIKDQGVZKHQSDWLHQW¶V

arms are extended Diagnosis

³³ :RUPLDQGDUWLQJPRYHPHQWVRIWKHWRQJXHXSRQ
,WLVEDVLFDOO\&ULWHULDHEDVHGZLWKVXSSRUWVIURPWKH
SURWUXVLRQ following relevant investigations.
³³ Deterioration of handwriting

Investigations
XX &RPSOHWHEORRGFRXQWVDQG3%)+E QRUPDO 7&
'& OHXNRF\WRVLV 3%)1RUPDO
XX $FXWHSKDVHUHDFWDQWV (65CRP): Raised
XX &KHVW;5D\1RUPDOor may have cardiomegaly in

Source: Internet
case of carditis
XX (&*)HDWXUHVRIstGHJUHHKHDUWEORFN SURORQJHG35
interval)

Sydenhams chorea

TT Associated features are  emotional lability

 incoordination SRRUVFKRROSHUIRUPDQFHDQG

IDFLDOJULPDFLQJ7KHVHDUHH[DFHUEDWHGE\VWUHVV

DQGGLVDSSHDUVZLWKVOHHS

D. Subcutaneous nodules
7KHVHDUH¿UP
QRQWHQGHUQRGXOHV
SUHVHQWDORQJ
the extensor
Source: Internet

surfaces of
tendons near bony
SURPLQHQFHV7KHUH
XX (FKRFDUGLRJUDSK\7RGHWHFWHYLGHQFHRIFDUGLWLV
including changes in valve rings
is a correlation Subcutaneous nodules
between the
XX 7KURDWVZDEIRU&60D\UHYHDOJURXS$‰KDHPRO\WLF
VWUHSWRFRFFL
SUHVHQFHRIWKHVHQRGXOHVDQGUKHXPDWLFKHDUWGLVHDVHV
Treatment
E. Erythema marginatum (Rare) XX &RXQVHOSDUHQWVDERXWWKHGLVHDVHLWVFRPSOLFDWLRQV 
TT (U\WKHPDWRXVPDFXODUUDVKZKLFKDUHVHUSLJLQRXV LPSRUWDQFHRIVWULFWDGKHUHQFHWR3HQLFLOOLQSURSK\OD[LV
ZLWKSDOH XX 6XSSRUWLYH%HGUHVW
centers and TT Immobilization of affected joints

DUHQRQ
Acute rheumatic fever

TT Close monitoring to note any features of carditis

SUXULWLF XX Antibiotics
TT Occurs
Source: Internet

TT $VLQJOH,0LQMHFWLRQRI%HQ]DWKLQH3HQLFLOOLQ
SULPDULO\RYHU
XQLWIRUNJDQGXQLWIRU!
WKHWUXQN 
kg) is the drug of choice or
extremities
TT Phenoxymethyl Penicillin (50 mg/kg/day PO 6
but not on
the face and Erythema marginatum hourly) for 10 days or
TT (U\WKURP\FLQ PJNJGD\32KRXUO\ IRU
accentuated
by warming the skin days
 140 Step on to Paediatrics

XX $QWLLQÀDPPDWRU\GUXJV$VSLULQDQGVWHURLGVDQGWKHUHFRPPHQGDWLRQVDUH±
$QWLLQÀDPPDWRU\
Category Dose & duration
Agents
Patients with
TT PJNJGD\LQGLYLGHGGRVHVIRUGD\VIROORZHGE\PJ
XX Polyarthritis
$VSLULQ NJGD\LQGLYLGHGGRVHVIRUZHHNV PJNJGD\IRUDQRWKHU
XX Isolated carditis without ZHHNV
cardiomegaly or &&)
TT PJNJGD\LQGLYLGHGGRVHVIRUZHHNVIROORZHGE\PJNJ
GD\IRUZHHNVDQGWKHQWDSHULQJRIWKHGRVHE\PJKRXUV
Patients with carditis and
Prednisolone HYHU\GD\V
cardiomegaly or &&) TT :KHQSUHGQLVRQHLVWDSHUHGDVSLULQVKRXOGEHVWDUWHGDWPJNJ
GD\LQGLYLGHGGRVHVIRUZNWRSUHYHQWUHERXQGRILQÀDPPDWLRQ

N.B. Digoxin may be used in heart failure of acute rheumatic carditis if needed. But with caution as it may precipitate
arrhythmia.
XX Treatment of Sydenham’s chorea Duration of penicillin prophylaxis
TT 3KHQREDUELWDO PJHYHU\KRXU32 LVWKHGUXJRI
Duration after last
choice Category
attack
,ISKHQREDUELWDOLVLQHIIHFWLYHDQ\RIWKHIROORZLQJGUXJV 5 years orXQWLO\HDUV
should be initiated TT Rheumatic fever
of age whichever is
without carditis
XX +DORSHULGRO PJNJKRXU32LQGLYLGHGGRVHV  longer
XX &KORUSURPD]LQH PJNJHYHU\KRXUO\32  TT Rheumatic fever with
XX $QWLLQÀDPPDWRU\DJHQWVDUHXVXDOO\QRWLQGLFDWHG 10 years orXQWLO
carditis but no residual
XX 'XUDWLRQRIWUHDWPHQWGHSHQGVRQWKHUHVSRQVHDose is years of age whichever
heart disease i.e. no
LQFUHDVHGXQWLOGHVLUHGUHVSRQVHLVDFKLHYHGDQGWKHQWDSHUHG is longer
valvular disease
gradually
TT Rheumatic fever with 10 years orXQWLO
Prevention carditis and residual years of age, whichever
%RWKLQLWLDODQGVXEVHTXHQWDWWDFNVRI$5)FDQEHSUHYHQWHG heart disease i.e. is longer.
SHUVLVWHQWYDOYXODU
WKURXJK3HQLFLOOLQSURSK\OD[LV Sometimes lifelong
disease
XX 3UHYHQWLRQRILQLWLDODWWDFN 3ULPDU\SUHYHQWLRQ 
Phenoxymethyl Penicillin or erythromycin orally for 10 days
LQDQ\FDVHRIVWUHSWRFRFFDOVRUHWKURDW
XX 3UHYHQWLRQRIVXEVHTXHQWDWWDFNV 6HFRQGDU\SUHYHQWLRQ 
Penicillin or other drugs according to the following
VFKHGXOH± JUVENILE IDIOPATHIC ARTHRITIS

Drug Dose Route (Synonyms: JRA, JCA) It is the most common

chronic rheumatic illness of children.
PLOOLRQXQLWVIRUSDWLHQWV!
TT Benzathine
NJXQLWVIRU ,0 Aetiology
Acute rheumatic fever

Penicillin
SDWLHQWVNJHYHU\ZHHNO\ Unknown, but it is thought to be a multifactorial
PJEG ZHLJKW!NJ JHQHWLFDOO\SUHGLVSRVHGDXWRLPPXQHGLVRUGHU
TT Penicillin V Oral
PJEG ZHLJKWNJ LQÀXHQFHGE\HQYLURQPHQWDOIDFWRUVDQGLQIHFWLRQ

PJEG ZHLJKW!NJ Pathogenesis

TT Erythromycin Oral
PJEG ZHLJKWNJ
7KHQHWSDWKRORJLFDOHIIHFWLQ-,$LVFKURQLFV\QRYLDO
TT Sulfadiazine/ LQÀDPPDWLRQ,QLWLDOO\WKHV\QRYLDOPHPEUDQH
0.5 gram once daily Oral
6XO¿VR[D]ROH LVLQ¿OWUDWHGZLWKPDQ\LQÀDPPDWRU\FHOOVHJ
O\PSKRF\WHVSODVPDFHOOVDQGPDFURSKDJHVDQG
 Step on to Paediatrics 141

the membrane become swollen and congested (synovitis). 6\VWHPLFDUWKULWLV  

6XEVHTXHQWO\WKHLQÀDPPDWRU\SURFHVVH[SDQGVDQGJLYH $ORQJZLWKMRLQWPDQLIHVWDWLRQVLWKDVSURPLQHQW
ULVHWRYLOORXVK\SHUWURSK\ K\SHUSODVLDRIV\QRYLXPDQG H[WUDDUWLFXODUV\VWHPLFPDQLIHVWDWLRQVe.g. non
VHFUHWLRQRIV\QRYLDOÀXLGLQMRLQWV HIIXVLRQ ,QÀDPPDWRU\ UHPLWWHQWIHYHUUDVKO\PSKDGHQRSDWK\VHURVLWLVDQG
JUDQXODWLRQWLVVXH SDQQXV GHYHORSVDQGWKDWVSUHDGVXQGHU KHSDWRVSOHQRPHJDO\
WKHDUWLFXODUFDUWLODJHFDXVHVSURJUHVVLYHHURVLRQRIWKH
5. (QWKHVLWLVUHODWHGDUWKULWLV  
DUWLFXODUFDUWLODJHDQGWKHDGMDFHQWERQHV)LQDOO\WKHUHLV
¿EURVLVDQGDQN\ORVLVRIWKHDIIHFWHGMRLQWVOLPLWDWLRQRI ,QÀDPPDWLRQDW•RIWKHHQWKHVHV VLWHRILQVHUWLRQ
PRYHPHQWDQGDWURSK\RISHULDUWLFXODUPXVFOHV of tendons, ligaments orIDVFLDLQWRERQHV 7KH
FRPPRQVLWHVRILQÀDPPDWLRQDUHDWLQVHUWLRQRI
Diagnostic Criteriae SODQWHUIDVFLDDQGDWWKHLQVHUWLRQVRIWHQGR$FKLOOHV
$OOWKUHHRIWKHIROORZLQJPXVWEHPHW± into calcaneum.
3VRULDWLFDUWKULWLV 
XX $UWKULWLVSHUVLVWLQJIRU•ZHHNV
XX Onset of arthritis before 16 years of age $UWKULWLV SVRULDVLVorDUWKULWLVDQGDWOHDVWRIWKH
XX Exclusion of other causes of arthritis IROORZLQJ±
O Dactylitis

O Nail
$UWKULWLVLVGH¿QHGDV±
SLWWLQJDQG
XX Swelling or
onycholysis
effusion, or

Source: Internet
O H/O
XX •RIWKH
Psoriasis
following
VLJQV± in a 1st
TT Limitation
degree
Pitting of nails
of range of relative
motion 8QGLIIHUHQWLDWHG
TT 7HQGHUQHVV
&RYHUVRYHUDOOGH¿QLWLRQVRI-,$EXWGRQRWIXO¿OO
or Pain on
Swollen knee joints with periarticular wasting DQ\VSHFL¿FFDWHJRU\
motion
TT ,QFUHDVHGWHPSHUDWXUH
Clinical manifestations

&ODVVL¿FDWLRQ $OWKRXJKYDULDEOHWKHXVXDOSUHVHQWDWLRQVDUH±
%DVHGRQWKHQXPEHURIMRLQWVDIIHFWHGGXULQJWKH¿UVW
XX 3HUVLVWHQWSDLQ VZHOOLQJRIMRLQWVERWKVPDOODQG
PRQWKVRIWKHGLVHDVHDQGWKHSUHVHQFHRIH[WUDDUWLFXODU large
PDQLIHVWDWLRQVFDWHJRULHVRI-,$DUHVHHQDPRQJFKLOGUHQ
XX /LPSLQJor refusal to walk or trying not to use the
affected joints (guarding of joints)
2OLJRDUWKULWLV  XX Involvent of PIP joints of hands gives rise to
$UWKULWLVDIIHFWVMRLQWVGXULQJWKH 6 months of
st FKDUDFWHULVWLFVSLQGLOHVKDSHGDSSHDUDQFH
GLVHDVH7ZRVXEFDWHJRULHVDUHUHFRJQL]HG±
TT 3HUVLVWHQWROLJRDUWKULWLVDIIHFWLQJ”MRLQWVWKURXJKRXW
the disease course
TT ([WHQGHGROLJRDUWKULWLVDIIHFWLQJ!MRLQWVDIWHUWKHst
6 months of disease
3RO\DUWKULWLV5KHXPDWRLGIDFWRUQHJDWLYH 
$IIHFWV•MRLQWVGXULQJWKHstPRQWKVRIGLVHDVH0D\
be symmetric or asymmetric; Affects small and large
MRLQWVFHUYLFDOVSLQHWHPSRURPDQGLEXODUMRLQW
3RO\DUWKULWLV5KHXPDWRLGIDFWRUSRVLWLYH 
$IIHFWV•MRLQWVGXULQJWKHst 6 months of disease. Proximal interphalangeal (PIP) joints with deformity (spindle shaped)
JIA

$JJUHVVLYHV\PPHWULFSRO\DUWKULWLV
 142 Step on to Paediatrics

XX 6RPHWLPHVG\VIXQFWLRQQRWHGLQXSSHUOLPEVQHFN
(torticollis)
XX -RLQWVWLIIQHVVIROORZLQJVOHHSLQJUHVWor decreased
activity (as morning stiffness)
XX Presence of rheumatoid nodules on the extensor
VXUIDFHRIHOERZ RYHU$FKLOOHVWHQGRQV
XX 1RQVSHFL¿FV\PSWRPVVXFKDVOHWKDUJ\
KLJKIHYHUSRRUDSSHWLWHorLUULWDELOLW\VOHHS
disturbances
XX Presence of evanescent rash
XX 2FFDVLRQDOO\IHDWXUHVRIH[WUDDUWLFXODU
manifestations HJSHULFDUGLWLVVHURVLWLV
RUJDQRPHJDO\XYHLWLVPD\EHSUHVHQW Evanescent rash on the inner aspects of knee joints
Courtesy: Dr. Anindita Bose

Characteristics of arthritis in acute Diagnosis

rheumatic fever and rheumatoid arthritis %DVHGRQFOLQLFDOIHDWXUHV VXSSRUWVIURPUHOHYDQW
investigations.
Acute
Parameters Rheumatoid arthritis
Rheumatic fever
Large joints.
Involvement of Investigations
VSLQHVVPDOO XX Blood
7\SHVRIMRLQWV %RWKODUJH VPDOO
joints of hands
involved joints
and feet and Investigations Results
KLSMRLQWVDUH +E ORZ 7& 
uncommon '& QHXWURSKLOLF
TT &RPSOHWHEORRG
Symmetry of counts
Asymmetrical Usually symmetrical OHXNRF\WRVLV SODWHOHWV
involvement
(thrombocytosis)
Acute onset and Insidious onset and
Onset of TT 3%) 1RQVSHFLILF
lasts for shorter arthritis remains for a
arthritis
SHULRG longer duration TT $FXWHSKDVHUHDFWDQWV
Raised
0LJUDWRU\ $UWKULWLV MRLQW (ESR, CRP, ferritin)
SRO\DUWKULWLVZLWK V\PSWRPVDUHPRUH TT $QWL1XFOHDU 3RVLWLYHLQRI
Characteristics H[TXLVLWHSDLQ marked early in the Antibody (ANA) SDWLHQWV
of arthritis WHQGHUQHVV morning (morning
0RQRDUWKULWLV stiffness) or after a TT 5KHXPDWRLG)DFWRU 2QO\SDWLHQWVDUH
unusual SHULRGRIUHVW 5) SRVLWLYH
5HVSRQVHWR +LJKO\VSHFLILF
Dramatic Not such $QWLF\FOLF
DVSLULQ TT
serological marker
FLWUXOOLQDWHGSHSWLGH
Chance of 7\SLFDOO\QRQ for early diagnosis of
High $QWL&&3 DQWLERG\
deformity deforming disease Rheumatoid arthritis
6RUHWKURDW 0D\UHYHDOSURWHLQXULD
Preceding
ZHHNVSULRUWRWKH Absent  DQGRU
history TT Urinalysis
RQVHWRIMRLQWSDLQ PLFURVFRSLFKDHPDWXULD
Heart (carditis/ 
Involvement Uveitis,
valvular lesions),
of other O\PSKDGHQRSDWK\
Basal ganglia
organs KHSDWRVSOHQRPHJDO\
JIA

(chorea)
 Step on to Paediatrics 143

XX Radiology & Imaging XX 'LVHDVHPRGLI\LQJDQWLUKHXPDWLFGUXJV '0$5'V ±

7KHVHGUXJVKLQGHUWKHSURJUHVVLRQRIGLVHDVHDQG
Investigations Results VHOHFWHGIRUDQ\IRUPRIDUWKULWLVUHVSRQGHGQRWE\
0D\VKRZVRIWWLVVXHVZHOOLQJ NSAID. 7KHGUXJVLQFOXGH±
TT 0HWKRWUH[DWH2UDOor S/C (dose:10 mg/m/week)
SHULDUWLFXODURVWHRSRURVLV
TT Sulfasalazine /HÀXQDPLGH
TT ;5D\RI SHULRVWLWLVVXEFKRQGUDOERQ\
affected joints erosion, loss of cartilage, XX Corticosteroid: Used as an adjunct when severe
QDUURZLQJRIMRLQWVSDFH KDQGLFDSSLQJIURPSDLQorDVEULGJLQJWKHUDS\±
TT Systemic steroid HJ3UHGQLVRORQH0HWK\O
RVWHRSHQLD
SUHGQLVRORQH
TT 8OWUDVRQRJUDSK\
0D\LGHQWLI\MRLQWHIIXVLRQ TT ,QWUDDUWLFXODUVWHURLGHJ7ULDPFLQRORQH
of affected joints
hexacetonide
TT 05,RIWKH 0RUHVHQVLWLYHWKDQ;5D\WR XX Biological agents
affected joints detect early changes TT 7RFLOL]XPDE(WDQHUFHSW ,QÀL[LPDE

TT Adalimumab $EDWDFHSW Rituximab

XX 6\QRYLDOÀXLGDQDO\VLV V\QRYLDOELRSV\
TT Anakinra
XX $UWKURVFRS\DUWKURJUDSK\
XX Others
TT 6OLWODPSH[DPLQDWLRQRIWKHH\HVWRDVVHVVXYHLWLV Treatment algorithm
TT 8ULQH50(WRH[FOXGHSLE e.g. haematuria,
for JIA at a glance
SURWHLQXULD All subtypes of JIA

Complications ZHHNV

XX -RLQWFRQWUDFWXUHV XX *ORPHUXORQHSKULWLV 67(3 16$,'“,QWUDDUWLFXODU7+$

XX Anaemia XX Chronic anterior uveitis
XX Pericarditis XX *URZWKGLVWXUEDQFH
XX 0\RFDUGLWLV XX Amyloidosis Oligo Poly 62-,$ Others

Treatment 67(3 '0$5' '0$5' '0$5' '0$5'

7UHDWPHQWRI-,$LVPXOWLGLVFLSOLQDU\LQYROYLQJ
SDHGLDWULFLDQUKHXPDWRORJLVWSK\VLRWKHUDSLVWDQG 67(3 Biological Biological
agent agent
RSKWKDOPRORJLVW7UHDWPHQWRSWLRQVDVZHOODVGXUDWLRQRI
WUHDWPHQWYDU\DPRQJGLIIHUHQWVXEW\SHV IURPSDWLHQWWR * THA - Triamcinolone hexacetodide, ** SOJIA - Systemic onset JIA

SDWLHQW
All subtypes of JIA
7UHDWPHQWVKRXOGEHVWDUWHGZLWKNSAID and unless
adversity noted, the drug should be continued for at least Rule
WRZHHNVWRDOORZVXI¿FLHQWWLPHWRDVVHVVFOLQLFDO If no good If no good
response response Add or switch
UHVSRQVH 67(3 67(3
Cmplication WR67(3
Sometimes, along with 16$,'RWKHURSWLRQVDUHDGGHG
GHSHQGLQJRQWKHUHVSRQVHWRGUXJVW\SHVRIDUWKULWLV B. Physiotherapy
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A. Drugs VWUHQJWKDQGSURWHFWVMRLQWLQWHJULW\
XX 16$,'V&RPPRQO\XVHGDUH±
TT 1DSUR[HQ PJNJGD\32ELGPD[JPGD\ 
Follow up
XX 7RVHHLPSURYHPHQWLQDFWLYLWLHVRIGDLO\OLIHDQGHDUO\
or
TT ,EXSURIHQ PJNJGD\32WLGPD[JPGD\ 
GHWHFWLRQRIFRPSOLFDWLRQVe.g. joint contractures,
muscle wasting etc.
or
TT 0HOR[LFDP PJNJGD\32RQFHGDLO\PD[
XX 3HULRGLFVOLWODPSRSKWKDOPRORJLFH[DPLQDWLRQVWR
PRQLWRUIRUDV\PSWRPDWLFXYHLWLV
15 mg/day)
JIA
 144 Step on to Paediatrics

References
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___ a) arthralgia ___ b) fever ___ c) Sydenham’s chorea
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 18
Fever and Rash
Dengue syndrome - - - - - - - - - - - - - 145
Chikungunya fever - - - - - - - - - - - - - 149

:KHQDFKLOGSUHVHQWVZLWKIHYHUDQGUDVKWKH DENGUE SYNDROME

following conditions should be considered as the
SRVVLEOHGLIIHUHQWLDOGLDJQRVHV± 'HQJXHLVWKHPRVWFRPPRQDQGLPSRUWDQWDUWKURSRGERUQHYLUDO
DUERYLUDO LOOQHVVLQKXPDQV,WLVWUDQVPLWWHGE\PRVTXLWRHVRI
XX 0HDVOHV XX &KLFNHQSR[ WKHJHQXV$HGHVZKLFKDUHZLGHO\GLVWULEXWHGLQVXEWURSLFDODQG
XX Dengue syndrome XX 0HQLQJRFRFFDO WURSLFDODUHDVRIWKHZRUOG7KHLQFLGHQFHRIGHQJXHKDVLQFUHDVHG
XX Rubella infection GUDPDWLFDOO\LQUHFHQW\HDUVDQGHVWLPDWHGWKDWRIWKH
XX Exanthem subitum XX 7\SKXV ZRUOG¶VSRSXODWLRQDWULVNIRUWKHGLVHDVH
+69  ,GLRSDWKLF Organism:'HQJXHYLUXVVHURW\SHV±'HQ'HQ'HQ'HQ
XX

XX Scarlet fever WKURPERF\WRSHQLF

XX Kawasaki disease SXUSXUD ,73
XX )LIWKGLVHDVH XX Henoch Schönlein Pathogenesis
XX Chikungunya SXUSXUD +63 Dengue infection

Of the different causes, dengue syndrome e.g. Antibody formation

dengue fever, dengue haemorrhagic fever and
Reinfection
dengue shock syndrome and Chikungunya are
highlighted in this section.
$XJPHQDWLRQRIYLUXVPXOWLSOLFDWLRQ

Increased vascular 5HGXFHGSODWHOHWV

SHUPHDELOLW\
&RDJXORSDWK\
Plasma leakage
Disseminated intravascula
+\SRYROHPLD Coagulation

Shock Severe bleeding

Death Dengue syndrome

Spectrum of Dengue Syndrome
Dengue fever (DF) Dengue hemorrhagic fever (DHF)
Dengue Shock syndrome

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+ + '+) +
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features High dengue
dengue virus/ manifestation High dengue dengue virus/
+ ,J0WLWUH
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body (YLGHQFHRISODVPDOHDNDJH • the body
145

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 146 Step on to Paediatrics

A. Dengue fever (DF) SHUPHDELOLW\PDQLIHVWHGE\RQHor more of the

IROORZLQJ±
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Suspected dengue: &RQWLQXHGIHYHUIRUGD\V$1' XX •ULVHLQKDHPDWRFULWIRUDJHDQGVH[
7ZRorPRUHRIWKHIROORZLQJIHDWXUHV± XX •GURSLQKDHPDWRFULWIROORZLQJWUHDWPHQWZLWK
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XX Severe headache, rash XX 3OHXUDOHIIXVLRQDVFLWHVK\SRSURWHLQHPLD
XX 5HWURRUELWDOSDLQ
XX 6HYHUHP\DOJLDDUWKUDOJLDEDFNSDLQ
XX 1DXVHDYRPLWLQJDEGRPLQDOSDLQ
XX Haemorrhagic manifestation
XX /HXNRSHQLD
XX 7KURPERF\WRSHQLD
XX 5DLVLQJ+FW  Typical rash in dengue fever

AND
TT +LJKLQGH[RIVXVSLFLRQEDVHGRQSHULRGSRSXODWLRQ
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AND
TT Absence of convincing evidence of any other febrile

illness.
XX Probable dengue:6XVSHFWHGGHQJXHZLWKVXSSRWLYH
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XX &RQ¿UPHGGHQJXH Probable dengue with one of the
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XX Isolation of dengue virus

XX Detection of dengue virus or Ag in tissue, serum or
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XX Suspected DHF
TT )HDWXUHVRIGHQJXHIHYHU ') DWWKHLQLWLDOVWDJH

AND
TT (YLGHQFHRI•RIWKHIROORZLQJhaemorrhagic

PDQLIHVWDWLRQV±

XX 3RVLWLYHWRXUQLTXHWWHVW
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XX Bleeding from injection sites XX Probable DHF

XX Haematemesis, PHODHQDKDHPDWXULDSHUYDJLQDO 6XVSHFWHGGHQJXH+DHPRUUKDJLF)HYHU '+) ZLWK
bleeding VHURORJLFDOHYLGHQFH GHQJXH,J0WLWUH•
XX 7KURPERF\WRSHQLD SODWHOHWFRXQW”FPP XX &RQ¿UPHG'+)

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XX (YLGHQFHRISODVPDOHDNDJHGXHWRLQFUHDVHGFDSLOODU\ dengue antigen in tissue, serum or&6)
 Step on to Paediatrics 147

Dengue Shock Syndrome (DSS) 7KHPDMRUSDWKRSK\VLRORJLFDEQRUPDOLWLHVRI'+)DQG

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XX ,QFUHDVHGYDVFXODUSHUPHDELOLW\
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XX 7KURPERF\WRSHQLD
of the features of PP+J
circulatory failure XX 5DSLGZHDNSXOVH 7KHFXWRIISRLQWEHWZHHQGHQJXHIHYHUDQGdengue shock
given alongside. XX Cold clammy skin V\QGURPHLVWKHHYLGHQFHRISODVPDOHDNDJH which will
XX Profound shock LQYDULDEO\EHSUHVHQWLQWKHODWHUEXWDEVHQWLQWKHIRUPHU

Severity grading of Dengue Shock Syndrome

Dengue
Grade Clinical Features Laboratory Features
Syndrome
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') )HDWXUHVDVSHUFDVHGHILQLWLRQ FPP FKDQJHLQ
haematocrit
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from nose orJXPSHWHFKLDHorSXUSXUDWDUU\VWRRO
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III
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fluid leakage
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'+) '66 IV
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Clinical Course at A Glance

Dengue Syndrome:
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'+)'66
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'+), '+),, '+),,, '+),9

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Diagnosis XX &%&7RWDOOHXNRF\WHFRXQW UHGXFHG SODWHOHWFRXQW

(reduced) and haematocrit (raised)
Dengue syndrome

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XX %ORRGIRU16 1RQ6WUXFWXUDOSURWHLQRIGHQJXH 
investigations
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Investigations QHJDWLYHRQth day of illness
XX 'HQJXHDQWLERGLHV ,J* ,J0 3RVLWLYHDIWHUGD\V
1RDSSUHFLDEOHFKDQJHLVVHHQLQWKHODERUDWRU\WHVWV
XX &KHVW;5D\ULJKWODWHUDOGHFXELWXVYLHZor
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should be done before 3 days, if not otherwise indicated
XX 8OWUDVRQRJUDSK\RIFKHVW DEGRPHQ7RGHWHFWSOHXUDO
effusion or ascitis
e.g. unusual haemorrhage
 148 Step on to Paediatrics

XX Serum DOEXPLQ0D\EHUHGXFHG TT (YLGHQFHRISOHXUDOHIIXVLRQor ascites

XX 3URWKURPELQWLPH0D\EHHOHYDWHG TT ,QWDNHRXWSXWFKDUW
XX 6HUXPHOHFWURO\WHV0D\EHDOWHUHG TT Platelet count and haematocrit, twice daily
XX 2WKHUV03WRH[FOXGHPDODULDLQPDODULDHQGHPLF]RQH
Treatment
Serial leukocyte counts, haematocrit level and
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SODWHOHWFRXQWDUHYHU\LPSRUWDQWIRUSURJQRVWLF
SXUSRVH/HXNRF\WHFRXQWKDVDYHU\LPSRUWDQW Crystalloids
SURJQRVWLFJXLGHLQHDUO\SKDVHRIGHQJXHLQIHFWLRQ '' 5% dextrose in isotonic normal saline
/HXNRSHQLDFHOOVFPPLQGLFDWHVWKDWZLWKLQ '' 5% dextrose in half strength normal saline
WKHQH[WKRXUVWKHSDWLHQWZLOOKDYHVXEVLGHQFH '' 5% dextrose in Ringer's lactate solution
defervescence of fever and he will be entering the
Colloids
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'' 3ODVPDH[SDQGHUe.g. Haemaccel
Treatment '' Plasma

A. Dengue Fever
6XSSRUWLYHPDQDJHPHQWDWKRPH±
XX Rest Fluid (volume) Replacement Algorithm
XX $QWLS\UHWLFV2QO\3DUDFHWDPRO
XX )OXLG0RUHLQFOXGLQJORS DHF I & II
XX )RRGV8VXDOIDPLO\GLHW $IHEULOH&ULWLFDOSKDVH
XX Investigations:
TT &%&+E:%&SODWHOHWFRXQWVDQGKDHPDWRFULW
‡5HVW‡&KHFNSODWHOHW +&7‡,9ÀXLG
XX 5HIHUUDONQRZOHGJHWRSDUHQWV,IDQ\RIWKHIROORZLQJ
VLJQVQRWHGWKHQWKHFKLOGVKRXOGEHWDNHQWRKRVSLWDO± Initiate IV crystalloid
Dose:1.5 ml/kg/hr for 6 hours
XX $EGRPLQDOSDLQ XX Bleeding in the skin/
XX Passage of black tarry nose/gums 3 ml/kg/hr for 6 hours
stool XX Excessive sweating
5 ml/kg/hr for 6 hours
B. DHF and DSS
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Assessment (Clinical & Laboratory)
&KHFN NHHSUHFRUGVRI±
If improved If not improved
XX 0DLQWHQDQFHRI± 7KHUDWHRI,9ÀXLGVKRXOG )XUWKHUDVVHVVPHQW
TT &LUFXODWRU\YROXPH
be gradually reduced from VKRXOGIROORZ
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TT Blood osmolality
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Haemodynamic status HJSXOVH%3SXOVHSUHVVXUH
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TT Evidence of bleeding
 Step on to Paediatrics 149

DHF III & IV Shock

XX 8QGHWHFWDEOHSXOVHDQGEORRGSUHVVXUH
‡8QVWDEOHYLWDOVLJQV
‡8ULQHRXWSXWIDOOV DON’Ts in Dengue
• Signs of shock XX *LYHDVSLULQor NSAID
XX *LYHDQWLELRWLF
‡,PPHGLDWHUDSLGYROXPHUHSODFHPHQWZLWK,9FU\VWDOORLG XX *LYHVWHURLG
WKHUDS\#PONJKURYHUKRXUV
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XX Change the rate of infusion
XX *LYHWUDQVIXVLRQXQOHVVLQGLFDWHG
XX ,QVHUW1*WXEHWRGHWHUPLQHFRQFHDOHGEOHHGLQJ
,PSURYHPHQW 1R,PSURYHPHQW
:KHQWRVWRSÀXLG
,9WKHUDS\E\ &KHFNIRU$%&6  FRUUHFW
XX 6LJQVRIFHVVDWLRQRISODVPDOHDNDJH
FU\VWDOORLG  XX 6WDEOH%3SXOVH SHULSKHUDOSHUIXVLRQ
successivly XX )DOORI+DHPDWRFULWWRZDUGVQRUPDOLQWKHSUHVHQFHRI
reduceing hourly Haemotorit Haemotorit JRRGSXOVHYROXPH
IURP Rises )DOOV XX 1RIHYHUIRUKRXUVZLWKRXWDQWLS\UHWLFV
PONJKU XX Restoration of bowel and abdominal function
IV colloid Blood
'H[WUDQ  transfusion
XX ,PSURYLQJXULQHRXWSXW
)XUWKHU or Plasma (10 ml/kg/
10 ml/kg/hr as hr) even if
Criterie for Discharging Patients
,PSURYHPHQW
,9EROXV UHSHDW Haematocrit
XX $EVHQFHRIIHYHUIRUDWOHDVWKRXUV
if necessary) is still >35% XX 0LQLPXPGD\VDIWHUUHFRYHU\IURPVKRFN
Discontinue IV
WKHUDS\DIWHU
XX Presence of signs of recovery e.g.
KRXUV ,PSURYHPHQW TT Stable Vital signs

TT 1RUPDOWHPSHUDWXUHZLWKRXW3DUDFHWDPRO

,97KHUDS\E\FU\VWDOORLG TT No evidence of bleeding

A = Acidisis (ABG)
B = Bleeding (Hct) VXFFHVVLYHO\UHGXFHLQJ TT 5HWXUQRIDSSHWLWH

C = Calcium & Electrolyte KRXUO\IURP TT *RRGXULQHRXWSXW

S = Sugar ((blood sugar) PONJKUDQGFRQWLQXH
TT Stable haematocrit
LWXSWRKRXUV
TT 3ODWHOHWFRXQW•FPP

* Improvement
XX Haematocrit falls
XX 3XOVHUDWHDQGEORRGSUHVVXUHVWDEOH
XX 8ULQHRXWSXWULVHV
** No improvement CHIKUNGUNYA FEVER (CF)
XX +DHPDWRFULWSXOVHUDWHULVHV
XX 3XOVHSUHVVXUHIDOOVEHORZPP+J &KLNXQJXQ\DIHYHULVDPRVTXLWRWUDQVPLWWHGYLUDO
XX 8ULQHRXWSXWIDOOV illness, emerging as a global threat because of its highly
*** Unstable vital signs GHELOLWDWLQJQDWXUHDQGXQSUHFHGHQWHGPDJQLWXGHRILWV
XX Signs of shock VSUHDG
XX 8ULQHRXWSXWIDOOV Organism: Chikungunya virus (CHIKV), an RNA virus,
Dengue syndrome

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Signs of circulatory failure
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XX Restlessness
XX +\SRWHQVLRQ Incubation period:GD\V XVXDOO\GD\V
XX 5DSLGZHDNWKUHDG\SXOVH
Pathogenesis
XX 1DUURZSXOVHSUHVVXUH ”PP+J
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XX Cold clammy skin
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XX &DSLOODU\UH¿OOWLPH!VHFRQGV
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7KHYLUXVSULPDULO\WDUJHWVWKH¿EUREODVWV of muscles, joints, TT 'HWHFWLRQRIYLUXVVSHFL¿F,J0DQWLERG\LQD

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of onset of fever
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TT $IROGULVHRI,J*DQWLERG\LQVDPSOHV
endothelium of many organs,
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GD\VRIIHYHU
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onset of clinical disease without &)VKRXOGEHVXVSHFWHGZKHQDSHUVRQGHYHORSV
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DFXWHSKDVHRI&+,.9LQIHFWLRQ Chikungunya arthrities 7KHFDVHVDUHFDWHJRUL]HGDV±
W\SLFDOO\UHVROYHVE\GD\V XX Possible case:0HHWLQJRQO\FOLQLFDOFULWHULD
XX Probable case:0HHWLQJERWKFOLQLFDODQG
HSLGHPLRORJLFDOFULWHULDH
XX &RQ¿UPHGFDVH0HHWLQJWKHODERUDWRU\FULWHULD
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How to identify CHIK infection ?

Clinical criteriae
XX $FXWHRQVHWRIIHYHU!ƒ)
XX 6HYHUHDUWKUDOJLDDUWKULWLVQRWH[SODLQHGE\RWKHU
Skin rash Skin rash medical condition
Epidemiological criteria
Clinical manifestation XX Residing orKDYLQJYLVLWHGHSLGHPLFDUHDV
XX +DYLQJUHSRUWHGWUDQVPLVVLRQZLWKLQGD\VSULRU
Rare in adult but
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children Differential Diagnoses
TT )HYHU XX Stomatitis
TT 3KRWRSKRELD XX 'HQJXHIHYHU ')  Reactive arthritis
TT Arthritis/ XX Oral ulcers
TT 5HWURRUELWDOSDLQ XX Serum sickness  Rickettsial disease
arthralgia
TT Vomiting +RZHYHULWPRVWFORVHO\UHVHPEOHV')7KHUHIRUH
XX Exfoliative TT Diarrhea
TT Backache dermatitis DQ\SDWLHQWZLWKVXVSHFWHG&+.IHYHUVKRXOGEH
TT 0HQWDOFRQIXVLRQ
TT Headache XX Photosensitivity PDQDJHGDV')XQWLOH[FOXGHG
TT Signs of meningeal
TT Rash XX +\SHUSLJPHQWDWLRQ irritation Clinico-pathological differences between
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Complications
XX Bleeding  +\SRWHQVLRQ VKRFN Characteristics Chikungunya DF
TT )HYHU !) +++ ++
Diagnosis
TT Arthralgia/ arthritis +++ ±
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+ (after
 ZLWKLQ
Investigations TT Rash
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6 days of
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Chikungunya fever

XX

(raised) TT 0\DOJLD + ++
XX 6*37 HOHYDWHG TT Haemorrhage ± ++
XX 6SHFL¿FLQYHVWLJDWLRQV DWOHDVWRQHRIWKHIROORZLQJLQWKH TT Shock ± +
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TT Virus isolation by cell culture
TT /\PSKRSHQLD +++ ++
TT 'HWHFWLRQRIYLUDO51$E\UHDOWLPH 57±3&5 ZLWKLQ
TT 7KURPERF\WRSHQLD + +++
days of onset of illness TT Haemoconcentration ± +++
 Step on to Paediatrics 151

Management XX Bleeding manifestations

TT 0LOG PRGHUDWHFDVHV+RPHPDQDJHPHQW XX Altered sensorium
TT 6HYHUHFDVHV0DQDJHPHQWLQKRVSLWDO XX 3HUVLVWHQWMRLQWSDLQGLVDEOLQJDUWKULWLVHYHQDIWHU
days of treatment
Home management
XX &RQVXPHSOHQW\RIOLTXLGVHJSODLQZDWHU256DQG Hospital management
fruit juice and homemade normal diet XX 5HK\GUDWLRQZLWKDSSURSULDWHFU\VWDOORLGVDIWHU
XX 7DNHSDUDFHWDPROLIMRLQWSDLQAvoid NSAID assessing dehydration
XX Rest at home and refrain from exertion
XX &ROGFRPSUHVVLRQVRYHUWKHMRLQWVWRUHOLHYHIURPSDLQ
XX 7HSLGVSRQJLQJZLWKZDUPZDWHU :DUPZDWHUEDWK
XX $QWLELRWLFVLIVHFRQGDU\LQIHFWLRQLVVXVSHFWHG
XX 0RQLWRU8ULQHRXWSXWSXOVH%3orDQ\EOHHGLQJVSRW
XX 0RQLWRU±
TT 9LWDOVLJQVHJSXOVH%3UHVSLUDWLRQWHPSHUDWXUH
Criteriae for Hospitalization
TT Any evidence of bleeding
XX 8QVWDEOHKHPRG\QDPLFVWDWXV /RZ%3UDLVHG&57 TT )HDWXUHVRIFDUGLWLVPHQLQJRHQFHSKDOLWLV
XX Oliguria
XX Steroid has no role in acute stage
XX 3DWLHQWVDJHPRQWKV

D/D of Fever and Rash (except DF, Chickenpox, CHIKungunya

Diseases & Aetiology Characteristics of rash
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 152 Step on to Paediatrics

References
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 19
Prolonged High Fever
Enteric fever - - - - - - - - - - - - - - 153
Malaria - - - - - - - - - - - - - - - 155
Kala-azar - - - - - - - - - - - - - - 158

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ZLWKVHYHUHSURVWUDWLRQGHVSLWHJHWWLQJWKH¿UVWOLQH Bacteraemia, which coincides with the onset of
management. In such situation the following clinical V\PSWRPVDQGPDUNVWKHHQGRILQFXEDWLRQSHULRG
conditions should be considered
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XX Enteric fever diseases e.g. -,$SLE XX Fever: 3URORQJHGKLJKJUDGHIHYHULVWKHPDLQ
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XX 0DOLJQDQF\e.g. XX Liver abscess or XX Abdominal symptoms:9RPLWLQJ  GLDUUKRHD
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ENTERIC FEVER myalgia
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condition children usually suffers from fever for more than OHWKDUJLFDQGDEGRPLQDOV\PSWRPVLQFUHDVHLQVHYHULW\
GD\VZLWKVLJQL¿FDQWVLFNQHVVDQGSURVWUDWLRQ Vomiting and meningism PD\EHSURPLQHQWLQLQIDQWVDQG
young children in this stage.
Organisms: Salmonella typhi, S. paratyphi A, B, C
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Incubation period:GD\V
XX +LJKERG\WHPSHUDWXUH XX 6SOHQRPHJDO\
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contaminated foods orGULQNV7KHRUJDQLVPVDIWHU XX +HSDWRPHJDO\ XX 5RVHVSRWV
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 154 Step on to Paediatrics

Complications TT In younger children leukocytosis is common and

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Central nervous
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system 1:160 or7+LVFRQVLGHUHGVLJQL¿FDQWLIFOLQLFDO
meningitis, ventriculitis
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vascular system
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system EURQFKRSOHXUDOILVWXOD XX &RXQVHOSDUHQWVDERXWWKHQDWXUDOKLVWRU\RIWKHGLVHDVH
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TT Azithromycin 10 mg/kg stat on D1, followed by
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 Step on to Paediatrics 155

MALARIA Clinical Manifestations

9DU\DFFRUGLQJWRVSHFLHVVWUDLQDQGKRVWLPPXQLW\
0DODULDLVDPDMRUSDUDVLWLFSUREOHPWKURXJKRXWWKHZRUOGDV
ZHOODVLQ%DQJODGHVK7KHGLVHDVHNLOOVDPLOOLRQRIFKLOGUHQ Infant:5HFXUUHQWERXWVRIIHYHULUULWDELOLW\SRRU
worldwide each year and they are mostly due to Plasmodium IHHGLQJYRPLWLQJMDXQGLFHDQGVSOHQRPHJDO\
falciparum. Older Children:)HYHUPD\EHF\FOLF HYHU\
,Q%DQJODGHVKDSSUR[LPDWHO\RIWKHWRWDOSRSXODWLRQDUH hours for all but P. malariae infection, in which it
DWULVNRIPDODULD0DMRULW\RIPDODULDFDVHVDUHUHSRUWHGIURP RFFXUVHYHU\KRXUV or irregular (most commonly
the following 13 districts. in P. falciparum infection).
XX 7KHFODVVLFDOcold stage IHHOLQJRIFKLOOV ULJRU 
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Khagrachari,
endemic XX 6RPHWLPHVSDWLHQWVZLWKP. falciparum infection
Bandarban
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TT Change of behaviour, convulsion and
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Cox’s Bazar
endemic unconsciousness (cerebral malaria)
TT &ROGVNLQSURIRXQGZHDNQHVVDQGVHYHUH
Hobigonj,
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Kurigram,
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Low 0RXODYLED]DU
TT Intravascular haemolysis, haemoglobinuria and
endemic 0\PHQVLQJK
renal failure (black water fever)
Netrokona, TT 5HVSLUDWRU\GLVWUHVVdue to acute pulmonary
6KHUSXU6\OKHWDQG6XQDPJRQM&KLWWDJRQJ oedema or acute respiratory distress syndrome
(acidotic breathing)
Organism: Plasmodium (P. falciparum, P. vivax, P. ovale and TT 6HYHUHSURVWUDWLRQi.e. extreme generalized

P. malariae) ZHDNQHVVVRWKHSDWLHQWFDQQRWZDONVWDQGRU
Vector: )HPDOHDQRSKHOHVPRVTXLWR sit without assistance and in small child failure
to feed
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vivax, P. ovale: GD\VDQGP. malariaeGD\V  TT Oliguria or acute renal failure POKRXURU

Transmission:7KURXJK± POKRXUV
TT Other features e.g. confusion or drowsiness,
XX %LWHRIIHPDOHDQRSKHOHVPRVTXLWR
XX Blood transfusion jaundice, severe anaemia (haematocrit <15%,
Hb% <5 gm/dl)
XX 5DUHO\DIIHFWIRHWXVWKURXJKSODFHQWD
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backache, myalgia and fatigue.
Pathogenesis XX &OLQLFDOH[DPLQDWLRQPD\UHYHDOKHSDWRPHJDO\
6\PSWRPVRIPDODULDUHVXOWVZKHQHU\WKURF\WHVRIWKHKRVWV and/orVSOHQRPHJDO\
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distinguishing it from viral infections.
$SDUWIURPLQYDVLRQRI5%&DQGFRQVHTXHQWKLJKIHYHUWKH
SDUDVLWL]HG5%& P. falciparum) also causes microvascular
blockade and anoxic damageRIGLIIHUHQWRUJDQVSDUWLFXODUO\ Diagnosis
brain (cerebral malaria), kidney (acute tubular necrosis), %DVLFDOO\FOLQLFDO7KHSRVVLELOLW\RIPDODULDLVKLJK
OXQJV SXOPRQDU\RHGHPD JXW algid malaria) etc. In if a febrile child comes from any high risk area for
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 156 Step on to Paediatrics

Investigations I. Falciparum malaria (FM)

XX %ORRGVOLGHH[DPLQDWLRQ WKLFN WKLQ¿OP IRU
GHWHFWLRQRISODVPRGLDLQEORRGVPHDU a. Uncomplicated malaria (UM)
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and
Absence of convincing evidence of any other febrile

Courtesy: Dr Rasheda Samad

illness
and
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season)
and
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P. falciparum in Blood Slide Examination (BSE)
or
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XX ,&7IRUPDODULD 5DSLG'LDJQRVWLF7HVW5'7 6LPLODU
diagnostic accuracy like that of blood slide examination
for P. falciparum b. Severe malaria (SM)
)HYHURUKLVWRU\RIIHYHUZLWKLQODVWKRXUV
and
Courtesy: Dr Rasheda Samad

One or more of the clinical or laboratory features of

VHYHULW\ &OIHDUXUHVMXVWGLVFXVVHGLQSUHYLRXVSDJH

Laboratory findings of severe

Falciparum malaria
XX +\SHUSDUDVLWDHPLD !or—/
XX +\SRJO\FDHPLD PPRO/orPJGO
XX Severe normocytic anaemia (Hb <5 gm/dl, PCV <15%)
XX )OXLGDQGHOHFWURO\WHGLVWXUEDQFH K\SRQDWUDHPLD
XX &RPSOHWHEORRGFRXQWV+E ORZ 7&'& XX Haemoglobinuria
OHXNRF\WRVLV SODWHOHWFRXQW ORZ UHWLFXORF\WHFRXQW XX 0HWDEROLFDFLGRVLV SODVPDELFDUERQDWHPPRO/
KLJK DQG¿QGLQJVUHODWHGWRWKHVHYHULW\RIKDHPRO\VLV XX +\SHUODFWDWDHPLD !PPRO/
XX 5HQDOLPSDLUPHQW VHUXPFUHDWLQLQH!—PRO/
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II. Vivax malaria (VM)

Malaria Chemoprophylaxis
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and
before travel to endemic zone, continued during the
Absence of convincing evidence of any other febrile illness VWD\DQGIRUZHHNVDIWHUUHWXUQLQJ
and
'UXJVXVHGIRUFKHPRSURSK\OD[LV
+LJKLQGH[RIVXVSLFLRQEDVHGRQWLPHSODFHDQGSHUVRQ
and O &KORURTXLQHSOXV3URJXDQLOor O0DÀRTXLQH
'LDJQRVLVLVFRQ¿UPHGE\SUHVHQFHRIDVH[XDOIRUPRI or O Doxycycline
Malaria

P. vivax in Blood Slide Examination (BSE) or 5DSLG NB: Doxycycline should be given for 1 day before
'LDJQRVWLF7HVW 5'7 YHIRU3YLYD[ travel.
 Step on to Paediatrics 157

TREATMENT OF MALARIA
FALCIPARUM MALARIA
B. Severe Falciparum Malaria
A. Uncomplicated Falciparum XX 5HIHUXUJHQWO\WRWKHKRVSLWDOZLWKSUHUHIHUUDO
Malaria (UM) treatment.
A. First line treatment I. Pre-referral Treatment
No of 5- 15- 25- >35 ,04XLQLQH PJVDOWNJVWDW,0±KDOIGRVHLQHDFK
Drug Day Time
dose <15 kg <25 kg <35 kg kg
thigh) or $UWHVXQDWHUHFWDOFDSVXOHPJNJ
1st 0 hour 1  3 
Artemether + Lumefantrine

D1 II. Hospital Treatment

nd KRXU 1  3 
combination (ACT)

XX IV Artesunate PJNJVWDWIROORZHGE\PJNJ
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th 36 hour 1  3  XQWLOSDWLHQWFDQWROHUDWHRUDODQWLPDODULDO
or
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D3
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6th 60 hour 1  3 
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or
B. Alternative therapy XX ,04XLQLQHWRWKHDQWHULRUWKLJK GLOXWHGLQVWHULOH
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or
III. Follow on Treatment
XX 4XLQLQHGD\V'R[\F\FOLQH PJGD\ GD\V
or 2QFHSDWLHQWWROHUDWHVRUDOWKHUDS\LWLVHVVHQWLDO
XX 4XLQLQHGD\V&OLQGDP\FLQ PJNJWZLFHGDLO\  WRFRQWLQXHDQGFRPSOHWHWKHWUHDWPHQWOLNHWKDWRI
GD\V XQFRPSOLFDWHGIDOFLSDUXPPDODULD
or
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XX 2WKHU:+2UHFRPPHQGHG$&7e.g. $UWHVXQDWH
0HÀRTXLQH$UWHVXQDWH$PRGLDTXLQH IV. Gametocytocidal drug
XX 7HWUDF\FOLQHDQG'R[\F\FOLQHDUHFRQWUDLQGLFDWHGLQ $WWKHHQGRIWUHDWPHQW±
FKLOGUHQ\HDUVROGDQGSUHJQDQW ODFWDWLQJPRWKHU XX 3ULPDTXLQH PJNJ 6LQJOHGRVHVKRXOGEHJLYHQ
1RWUHFRPPHQGHGIRU\HDUVRIDJHDQGLQSUHJQDQF\

VIVAX MALARIA
,6SHFL¿F$QWLPDODULDO II. Supportive
XX &KORURTXLQHPJNJRQ'D\ 
XX *LYH3DUDFHWDPRO WHSLGVSRQJLQJ III. Treatment of
and 5 mg/kg on Day3 Plus for fever Complications
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TT )OXLG HOHFWURO\WHLPEDODQFH
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anaemia
Malaria
 158 Step on to Paediatrics

KALA-AZAR (KA) well as the reticular cells are markedly increased and
SDFNHGZLWKDPDVWLJRWHV6LPLODUO\LQOLYHU.XSIIHUFHOOV
.DODD]DU are increased in size and number, giving rise to gross
(Black sickness) KHSDWRVSOHQPHJDO\ %RQHPDUURZWXUQVK\SHUSODVWLFDQG
or visceral SDUDVLWL]HGPDFURSKDJHVUHSODFHLWVQRUPDOKDHPRSRLHWLF
leishmaniasis is a WLVVXH,QNDODD]DUWKHUHLVPDUNHGVXSSUHVVLRQRIWKH
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7KH*RYHUQPHQW
of Bangladesh The Net clinical effects are–
declared the XX +HSDWRVSOHQPHJDO\ /\PSKDGHQRSDWK\
GLVHDVHUHSRUWDEOH XX 3DQF\WRSHQLD )HYHU  Weight loss
VLQFH
Clinical Manifestations
Pabna, Sirajgonj, XX 9DULDEOH7KHGLVHDVHPD\EHDV\PSWRPDWLF
5DMVKDKL'LQDMSXU
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Natore, Naogaon, XX )HYHU(in a case who reside/travel in an endemic areas)
7KDNXUJDRQ TT Commonly: Long standing intermittent with a
0\PHQVLQJK
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7DQJDLO-DPDOSXU TT Sometimes
DQG*D]LSXU Kala-azar endemic districts in Bangladesh
³³ *UDGXDORQVHWRIORZJUDGHIHYHUZLWKPDODLVHor

³³ Very acute high grade remittent associated with

Aetio-pathogenesis SURVWUDWLRQDQGIHDWXUHVRIWR[DHPLD
Agent: Leishmania donovani (India, Bangladesh) XX $SSHWLWHLVXVXDOO\JRRGZLWKQRUPDOGLJHVWLYH
functions
Host: Humans
XX (SLVWD[LVDQGEOHHGLQJIURPJXPPD\EHSUHVHQW
Vector: 6DQGÀ\ Phlebotomus argentipes) XX *UDGXDOEODFNHQLQJRIVNLQ %ODFNVLFNQHVVor.DOD
azar)
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VKHGVGDPSSODFHV UXUDODUHDV %XWLQXUEDQDUHDVWKH\ Physical Examination
breed in cracks and crevices of human dwellings, between XX $SSHDUDQFH
bricks holes. Sick,
wasted,
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cachectic.
XX %LWHRIVDQGÀ\2QO\IHPDOHVELWHPDLQO\GXULQJ Patients
nocturnal feeding are usually
XX 2WKHUSRVVLEOHZD\VRIWUDQVPLVVLRQDUHWKURXJK± mentally
TT Blood transfusion  Placenta clear and
TT Inoculation from cultures in the laboratory alert
Gross splenomegaly in Kala-azar
Peak seasonal incidence XX Pallor: Usually
7KUHHPRQWKVDIWHUWKHRQVHWRIUDLQ $XJXVWWR2FWREHU  moderate to severe
,QFXEDWLRQSHULRG
XX -DXQGLFH0D\EHSUHVHQW
XX 2HGHPD0D\EHSUHVHQW
5DQJHVIURPGD\VWR\HDUVEXWXVXDOO\PRQWKV XX /\PSKDGHQRSDWK\8VXDOO\DEVHQW
XX Skin: Dry, rough earthy grey colour
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$IWHULQRFXODWLRQE\VDQGÀLHVWKHSURPDVWLJRWHV XX 0DUNHGVSOHQRPHJDO\DQGKHSDWRPHJDO\ VSOHHQVL]H!
Kala-azar

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PDFURSKDJHVGLVVHPLQDWHWRDOOSDUWVRIWKHERG\EXW In terminal stage, there may be severe anaemia, heart
PRUHVRWRVSOHHQOLYHUDQGERQHPDUURZ7KHYDVFXODU IDLOXUHMDXQGLFHRHGHPDDVFLWHVVHSWLFDHPLDDQG
VSDFHVRIVSOHHQDUHGLODWHGDQGHQJRUJHGZLWKEORRGDV bleeding manifestations.
 Step on to Paediatrics 159

Differential Diagnoses TT 'HWHFWLRQRISURPDVWLJRWHVLQWKHFXOWXUHRI

DVSLUDWHV 1RY\0DFQHDO1LFROOHPHGLD
0DODULDOHXNDHPLDW\SKRLGWXEHUFXORVLVDQGO\PSKRPD
TT 'HWHFWLRQRI'1$RISDUDVLWHE\PCR
Complications
&DVH'H¿QLWLRQV
XX Secondary bacterial infection HJSQHXPRQLD Kala-azar (KA)
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XX Haemorrhage  Cancrum oris XX 5HVLGLQJWUDYHOLQJLQNDODD]DUHQGHPLFDUHDV
XX 3RVW.DODD]DU'HUPDO/HLVKPDQLDVLV PKDL) XX $Q\RQHRIWKHIROORZLQJV\PSWRPVDQGVLJQV
O6SOHQRPHJDO\O Weight loss O Anaemia
Diagnosis XX $QGSRVLWLYHµUNWHVW
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Treatment
Investigations
Recommended drugs, dose and duration, based on
XX &RPSOHWHEORRGFRXQWV+E UHGXFHGWRJPGO 7&
National guidelines.
OHXNRSHQLD '& UHODWLYHLQFUHDVHRIO\PSKRF\WHV
PRGHUDWHLQFUHDVHLQPRQRF\WHVDEVHQFHRIHRVLQRSKLOV 
SODWHOHWV WKURPERF\WRSHQLD (65 KLJK 1st line Drugs
XX Serum albumin: (low), Serum globulin XX /LSRVRPDO$PSKRWHULFLQ% PJNJ VLQJOHGRVH
K\SHUJOREXOLQDHPLDPRVWO\,J* LQ,9GULSYHU\VORZO\LVWKH¿UVWFKRLFH
XX ,PPXQRORJLFDOWHVWVIRULQGLUHFWHYLGHQFHRI.DODD]DU Alternative 1st line drugs
TT 'LUHFWDJJOXWLQDWLRQWHVW '$7 %HFRPHSRVLWLYH 7LWHU XX 0LOWHIRVLQHPJNJGD\RUDOO\LQWZRGLYLGHG
• DVHDUO\DVZHHNVDIWHULQIHFWLRQDQGUHPDLQ GRVHVDIWHUPHDOIRUGD\V
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TT ,PPXQR&KURPDWRJUDSKLF7HVW ,&7 $VLPSOHUDSLG XX Combination treatment
test based on rK39 antigen derived from L. chagasi. It TT 0LOWHIRVLQH3DURPRP\FLQLVWKHst choice

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UHPDLQVRIRU\HDUV
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TT 2WKHUWHVWV$OGHK\GHWHVW&RPSOHPHQW)L[DWLRQ7HVW
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may be done
XX 7HVWVIRUGLUHFWHYLGHQFHRISDUDVLWHV 2nd line drugs
TT Detection of LD bodies (amastigote form) in smears
XX $PSKRWHULFLQ%GHR[\FKRODWH PJNJ 'DLO\
SUHSDUHGIURPERQHPDUURZVSOHQLFDVSLUDWHVorO\PSK or on alternate day in IV infusion (5% Dextrose
QRGHDVSLUDWHV$PRQJWKHVHVSOHQLFSXQFWXUHKDVWKH solution 500 ml) for total 15 doses
highest rate of yielding LD bodies XX 6RGLXP6WLERJOXFRQDWH PJNJ ,0RQFHGDLO\
for 30 days

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and
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and
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Source: Internet

and
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or
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LD bodies in bone marrow
 160 Step on to Paediatrics

POST KALA-AZAR DERMAL Treatment of PKDL

LEISHMANIASIS (PKDL)
1st line
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Miltefosine
XX H/o Residing/travelling in the endemic areas
XX +RWUHDWPHQWRI.DODD]DUDQ\WLPHLQWKHSDVW
XX PJNJERG\ZHLJKWGD\LQWZRGLYLGHGGRVHVQRW
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XX Suggestive skin lesion with preservation of sensation,
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XX Exclusion of other skin diseases HJOHSURV\ XX Sodium Stibogluconate:PJNJERG\ZHLJKW
YLWLOLJRSLW\ULDVLVULQJZRUPHWF7KHFORVH''RI GDLO\IRUGD\VSHUF\FOH,0
3.'/LVOHSURV\ZKLFKLVFKDUDFWHUL]HGE\ORVVRI XX Amphotericin B Deoxycholate: 1mg/kg daily or on
VHQVDWLRQ µUN¶SRVLWLYH6OLWVNLQVPHDUSRVLWLYHPCR alternate days IV (in 500 ml of 5% DA) for 15 doses
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the cycles) are given with any one of the above
mentioned drugs.

Supportive treatment
XX (QVXUHDGHTXDWHQXWULWLRQ
XX &RQWUROVXSHUDGGHGLQIHFWLRQV
XX &RUUHFWDQDHPLDDQGLIUHTXLUHGEORRGWUDQVIXVLRQ
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be diagnosed by slit skin smear FDVH$VPDOOPLQRULW\PD\H[SHULHQFHUHODSVHGXULQJ
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XX (QODUJHPHQWRIVSOHHQ  Return of fever
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Kala-azar
 Step on to Paediatrics 161

References
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SELF ASSESSMENT
Short answer questions [SAQ]
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Multiple choice questions [MCQ]

1. Organs affected by P. falciparumDUH±
___ a) brain ___ b) kidney ___ c) lungs
___ d) gut ___ e) heart
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___ d) heart failure ___ e) secondary bacterial infections
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___ a) Stibogluconate ___ b) 0LOWHIRVLQH BBBF /LSRVRPDO$PSKRWHULFLQ%
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___ e) anaemia is common
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 162 Step on to Paediatrics

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 20
Jaundice
Acute viral hepatitis - - - - - - - - - - - - - 163
Fulminant hepatic failure - - - - - - - - - - - - 164
Chronic liver disease- - - - - - - - - - - - 166

:KHQHYHUDFKLOGSUHVHQWVZLWKMDXQGLFHRQHVKRXOG ACUTE VIRAL HEPATITIS

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Aetiology
A. Hepato-cellular
Organisms: 6L[KHSDWRWURSKLFYLUXVHV(Hepatitis A, B, C,
XX 9LUDOKHSDWLWLV +$9+%9+&9+(9 D, E, and G). $OODUH51$YLUXVHVH[FHSW%ZKLFKLV'1$
XX Chronic liver disease (CLD) HJGHFRPSHQVDWHG virus. +HSDWLWLV$ (YLUXVHVFDXVHDFXWHKHSDWLWLVRQO\
cirrhosis ZKHUHDV%&'FDXVHV&/'WKRXJKDFXWHSUHVHQWDWLRQ
XX $XWRLPPXQHKHSDWLWLV may occur.
XX 'UXJLQGXFHGKHSDWLWLVHJSDUDFHWDPROULIDPSLFLQ
Clinical Manifestations
B. Pre hepatic XX Asymptomatic: Only rise in serum transaminases
XX *HQHWLFGLVHDVHVHJ*LOEHUW VV\QGURPH&ULJOHU (6*376*27
Najjar syndrome XX Anicteric: Patients have no jaundice but suffer
XX Haemolytic anaemias e.g., thalassaemia, IURPDQRUH[LDQDXVHDYRPLWLQJDQGLQÀXHQ]DOLNH
VSKHURF\WRVLVDXWRLPPXQHKDHPRO\WLFDQDHPLD V\PSWRPV
XX Classical presentation2FFXUVLQSKDVHV
C. Post hepatic TT 3URGURPDOSKDVH7KLVSKDVHSUHFHGHVWKHLFWHULF

XX Biliary atresia SKDVHE\ZHHNVZLWKQRQVSHFL¿FV\PSWRPVOLNH

XX Choledocal cyst malaise, anorexia, nausea, vomiting, fever, headache,
XX ,GLRSDWKLFQHRQDWDOKHSDWLWLV myalgia, arthralgia etc.
XX Bile duct strictures
XX Stone in common bile duct

-DXQGLFHGXULQJQHRQDWDOSHULRGKDVGLIIHUHQWDHWLRORJ\
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(discussed in chapter 8)
Acute viral hepatitis
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discussed.

Transmission
XX +DHPDWRJHQRXV%&'*YLUXV
XX )DHFR2UDOURXWH$(YLUXV

Yellow sclerae
163
 164 Step on to Paediatrics

TT ,FWHULFSKDVH7KLVSKDVHLVFKDUDFWHUL]HGE\ FULMINANT HEPATIC FAILURE (FHF)

\HOORZVFOHUDWHQGHUKHSDWRPHJDO\ZLWKULJKW
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TT 5HFRYHU\SKDVH,QWKLVSKDVHFRQVWLWXWLRQDO ZHHNVGXUDWLRQ
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TT 37!VHFRU,15!QRWFRUUHFWHGE\9LWDPLQ.

Diagnosis LQWKHSUHVHQFHRIFOLQLFDOKHSDWLFHQFHSKDORSDWK\
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TT 37!VHFRU,15!UHJDUGOHVVRIWKHSUHVHQFHRI

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XX S. Bilirubin Aggravating factors
Liver XX 6*37 All markers are
function *,7EOHHGLQJ XX Uraemia
elevated
XX
XX 3URWKRPELQWLPH 37
tests XX +\SRYRODHPLD XX 6HSVLV
XX $ONDOLQHSKRVSKDWDVH
XX +\SRNDODHPLD XX +LJKSURWHLQGLHW
XX $QWL+$9,J0 XX +\SRJO\FDHPLD XX &RQVWLSDWLRQ
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XX HBsAg
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ascitis XX 6RPHSDWLHQWVSUHVHQWVZLWKUDSLGGHYHORSPHQWRI
GHHSHQLQJMDXQGLFHEOHHGLQJ(commonly haematemesis
& melaena)FRQIXVLRQDQGSURJUHVVLYHFRPD
Treatment XX 6RPHSDWLHQWVUHPDLQDV\PSWRPDWLFDWWKHRQVHW7KHQ
XX &RXQVHOSDUHQWVDERXWWKHQDWXUDOKLVWRU\RIWKHGLVHDVH VXGGHQO\EHFRPHVHYHUHO\LOOGXULQJWKHnd week of
XX 3URYLGHVXSSRUWLYHWUHDWPHQWRQO\DQGLQFOXGHV± the disease and jaundice, fever, anorexia, vomiting and
TT Rest: Outdoor activities should be restricted as much
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&OLQLFDOH[DPLQDWLRQUHYHDOV±
essential
TT Diet: Normal. High calorie diet is desirable.
XX 7HQGHUKHSDWRPHJDO\ZKLFKPD\EHIROORZHGE\
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XX +\SHUUHÀH[LDDQGSRVLWLYHH[WHQVRUSODQWHUUHVSRQVHV
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those who cannot tolerate oral feeding
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1
>1RUPDO,15@ XX Agitation
Fulminant hepatic failure

TT Purgatives, gut sterilizers orODFWXORVH1RWKHUDSHXWLF XX Drowsiness

XX Disorientation,
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convulsion, coma

Prevention
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Bleeding
XX 77+DHPDWHPHVLV
XX 77+DHPDWXULD
XX melaena
XX 77,QWUDFUDQLDO
 Step on to Paediatrics 165

Stages of Hepatic encephalopathy Treatment

Stages Symptoms Signs EEG
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mood swings,
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disorientation
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XX 7UHDWFRDJXORSDWK\ZLWK±
arousable, K\SHUUHIO[LD abnormal,
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References
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 21
Blood Vomiting
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 Step on to Paediatrics 171

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XX

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 Step on to Paediatrics 173

References
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Lymph node enlargement
Tubercular lymphadenopathy - - - - - - - - - - - 174
Lymphoma- - - - - - - - - - - - - - 175
Infectious mononucleosis - - - - - - - - - - - 177

/\PSKQRGHHQODUJHPHQW O\PSKDGHQRSDWK\ UHÀHFWV TUBERCULAR LYMPHADENOPATHY

diseases involving reticuloendothelial system.
It is mostly due to Organisms: M. tuberculosis,DW\SLFDOPLFREDFWHULDH
infections e.g. viral, /\PSKQRGH
EDFWHULDOSDUDVLWLF enlargement
or fungal. However, (scrofula) is the
malignancies, most common
autoimmunity, storage manifestation of
diseases etc. also H[WUDSXOPRQDU\
contribute. It may tuberculosis.
Generalized lymphadenopathy
be localized or Cervical glands
generalized ZKHQDGHQRSDWK\LQYROYH!QRQFRQWDJLRXV are affected
sites). It is not a diagnosis but the manifestation of many PRVWIUHTXHQWO\
underlying diseases. followed by
submandibular, Scrofula
:KHQHYHUDFKLOGSUHVHQWVZLWKO\PSKQRGHHQODUJHPHQW
WKHIROORZLQJGLVHDVHVVKRXOGFRQVLGHUHG± VXSUDFODYLFXODU
axillary and inguinal nodes. Sometimes, more than one
XX 7XEHUFXORVLV XX Systemic onset UHJLRQDUHLQYROYHG$EGRPLQDO PHVHQWHULF O\PSKQRGHV
XX /\PSKRPD MXYHQLOHLGLRSDWKLF are also involved e.g. tabes mesenterica.
XX Leukaemia arthritis
6\VWHPLFOXSXV
Characteristics of the lymph nodes in TB
XX Infectious XX

mononucleosis erythematosus (SLE) )LUPQRWKDUG

XX XX When caseation and
XX HIV infection XX Cat scratch disease 8VXDOO\SDLQOHVVDQG
XX
OLTXHIDFWLRQRFFXUV
QRQWHQGHU QRGHVEHFRPHÀXFWXDQW
Tubercular lymphadenopathy

$PRQJDOOFDXVHVWXEHUFXORVLVO\PSKRPDDQGLQIHFWLRXV XX 0DWWHGWKRXJKLQLWLDOO\ and may discharge

mononucleosis will be discussed in this section. mobile through the skin with
Lymph node (LN) examination: Points to note– XX 2IWHQ¿[HGWR the formation of a
underlying or overlying FROODUVWXGDEVFHVV and
XX 6LWHRIO\PSKQRGHHQODUJHPHQW
tissue sinus formation
XX Number: Single orPXOWLSOH
XX Size of the largest one
6\VWHPLFV\PSWRPVRWKHUWKDQORZJUDGHIHYHUDUHXVXDOO\
XX /RFDOWHPSHUDWXUH1RUPDOor raised
DEVHQW+RZHYHUVRPHWLPHVDORQJZLWKO\PSKQRGH
XX 7HQGHUQHVV3UHVHQWor absent
HQODUJHPHQWJURZWKIDLOXUHSDOORUKHSDWRVSOHQRPHJDO\
XX 1DWXUH0DWWHGor discrete
PD\EHSUHVHQW
XX &RQVLVWHQF\6RIWF\VWLFUXEEHU\¿UPor hard
XX Overlying skin colour: Normal or reddish Diagnosis
XX Discharging sinus: Present or not %DVHGRQFKDUDFWHULVWLFFOLQLFDODQGKLVWRORJ\SUR¿OHRI
XX $GMDFHQWVWUXFWXUHV)UHHor adherent O\PSKDGHQRSDWK\DQGRWKHUVXSSRUWLYHODEHYLGHQFHV
3UHVVXUHV\PSWRPVHJ5HVSLUDWRU\GLVWUHVVG\VSKDJLD
174

XX

IDFLDOSXI¿QHVVHWF: Present or not

 Step on to Paediatrics 175

Investigations Types
XX &RPSOHWHEORRGFRXQWV+E ORZ 7&DQG'&RI XX Hodgkin disease (HD)
:%&ZLOOVKRZO\PSKRF\WRVLV XX 1RQ+RGJNLQO\PSKRPD 1+/
XX 7XEHUFXOLQWHVW8VXDOO\SRVLWLYH
XX &KHVWUDGLRJUDSK\0RVWO\QRUPDOWKRXJKSDUDWUDFKHDO Pathology
KLODUDQGRWKHUO\PSKDGHQRSDWK\PD\EHSUHVHQW+LODU The net clinico-pathological
O\PSKDGHQRSDWK\LVFKDUDFWHULVWLF
consequences are–
XX /\PSKQRGHELRSV\ KLVWRSDWKRORJ\&HQWUDO
FDVHDWLRQQHFURVLVVXUURXQGHGE\HSLWKHOLRLGDQG XX 'HSUHVVLRQRIFHOOXODULPPXQLW\DQGLQFUHDVHG
multinucleated giant cells VXVFHSWLELOLW\WRLQIHFWLRQV
XX 3UHVVXUHV\PSWRPV

Clinical Manifestations
XX Painless nodular swellings in neck and other areas of
ERG\LVWKHFRPPRQHVWSUHVHQWDWLRQ
XX &RQVWLWXWLRQDOV\PSWRPV
TT Intermittent fever

TT Weight loss (>10%) during last 3 months

Source: Internet

TT Drenching night sweats

TT Others e.g. fatigue, lethargy, anorexia, urticaria

XX Pressure
V\PSWRPV
TT 5HVSLUDWRU\

distress
SUHVVXUH
Lymph node biopsy showing giant cells and caseation necrosis over trachea
SULQFLSDO
Treatment bronchi by
XX &RXQVHOWKHSDUHQWV mediastinal
XX $QWL7%GUXJV DVSHU1DWLRQDO7%*XLGHOLQHIRU O\PSK
&KLOGUHQnd ed.) nodes)
TT )DFLDO Cervical, submandibular and pre-
XX *RRGQXWULWLRQDOVXSSRUW auricular lymphadenopathy
oedema,
XX )ROORZXS
chemosis,
SOHWKRUDYHQRXVHQJRUJHPHQW SUHVVXUHRYHU
VXSHULRUYHQDFDYDLHVXSHULRUYHQDFDYDO
syndrome)
LYMPHOMA TT '\VSKDJLD SUHVVXUHRYHURHVRSKDJXV

TT Hoarseness of voice SUHVVXUHRYHUUHFXUUHQW

/\PSKRPDLVWKHPDOLJQDQWSUROLIHUDWLRQRIFHOOVQDWLYHWR laryngeal nerve)

O\PSKRLGWLVVXHLHO\PSKQRGHVDQGH[WUDQRGDOVLWHVOLNH TT $EGRPLQDOSDLQGLVFRPIRUW GLVWXUEDQFHVRIERZHO
:DOGH\HU¶VULQJOLYHUVSOHHQWK\PXV3H\HU¶VSDWFKHV habits SUHVVXUHRYHUERZHO
YHUPLIRUPDSSHQGL[HWF TT 3DUDSOHJLDDQGURRWSDLQ SUHVVXUHRYHUVSLQDOFRUG 
,QO\PSKRPDO\PSKRLGWLVVXHVDQ\ZKHUHLQWKHERG\PD\ nerve roots)
TT Cholestatic jaundice SUHVVXUHRYHUELOLDU\FKDQQHOV
be affected but cervical nodes are commonly affected and
OHVVIUHTXHQWO\WKHPHGLDVWLQDODQGVXEGLDSKUDJPDWLF DWSRUWDKHSDWLV 
Lymphoma

TT 6\PSWRPVGXHWRH[WUDQRGDOLQYROYHPHQW
nodes.
³³ &RXJKG\VSQRHD (lungs)
/\PSKRPDLVDOZD\VPDOLJQDQWQREHQLJQFDWHJRU\
³³ Ascites SHULWRQHXP 

³³ Pleural effusion SOHXUD

 176 Step on to Paediatrics

³³ Pericardial effusion SHULFDUGLXP 0HGLDVWLQDOO\PSKDGHQRSDWK\

³³ )HDWXUHVRIOHXNDHPLD(bone marrow) ZLGHQLQJ PD\EHSUHVHQW
³³ Pruritus (skin)
³³ Neurological manifestations (cerebral
involvement) ;5D\FKHVW$3
³³ Pain and swelling of jaw, testes Lateral view
Characteristics of lymph nodes
(LN) in Lymphoma
XX 1RQWHQGHU XX Discrete
XX )LUPWRUXEEHU\LQ XX 1RW¿[HGWRXQGHUO\LQJ 5HHG6WHUQEHUJ giant cell is the
consistency or overlying structures KDOOPDUNRIFODVVLFDO+' SLFEHORZ
Small round cell in case of NHL
Immunohistochemistry: Confirmatory
Difference between NHL and HD /\PSKQRGH
ELRSV\IRU IRUW\SHVRI1+/
Parameters NHL HD KLVWRSDWKRORJ\

Source: Internet
Complied by Zohora Jameela Khan
Short history and LPPXQR
Disease SKHQRW\SLQJ
UDSLGSURJUHVVLRQ Not so
SURJUHVVLRQ
of disease cytogenetics
Localized to molecular studies
/\PSKQRGH $WPXOWLSOH
a single axial
involvement SHULSKHUDOVLWHV
JURXS
Involvement of
Waldeyer ring and 7RGHWHFWLQYROYHPHQWRIRWKHUO\PSK
&7VFDQRIFKHVW
H[WUDQRGDOVLWHV QRGHJURXSVDVZHOODVH[WUDQRGDO
Common Uncommon DEGRPHQSHOYLV
e.g. thymus, liver, sites.
CNS, testis bone 05,RIVSLQH  7RHYDOXDWHERQH YHUWHEUDO 
PDUURZVSOHHQ bones involvement.
6SUHDG Non contiguous 2UGHUO\VSUHDG )RUGLVHDVHVWDJLQJWUHDWPHQW
3(7VFDQ
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0HVHQWHULFQRGHV
Common Rare Bone marrow 7RDVVHVVZKHWKHUPDUURZLQILOWUDWLRQ
involvement
examination occurs or not.
Diagnosis ,QGLFDWHGLQERQHSDLQor with high S
Bone scan
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%DVHGRQFKDUDFWHULVWLF&) VXSSRUWLYHODEHYLGHQFHV
Liver, renal 0D\EHDOWHUHGLIGLVVHPLQDWLRQ
Investigations function tests occurs to these organs.
&6) RWKHUERG\
TT Hb: Low 7RNQRZF\WRFKHPLFDOFKDUDFWHULVWLFV
fluids F\WRVSLQ
TT :%&&RXQWVYDULDEOH0D\KDYH of the malignant cells.
analysis)
QHXWURSKLOLDHRVLQRSKLOLD +' 
In advance stage, there may be
&%&3%)
O\PSKRDQGRWKHUF\WRSHQLDV
Treatment
ESR XX &RXQVHOLQJSDUHQWVDERXWWKHGLVHDVHWUHDWPHQWDQG
TT 3ODWHOHWV1RUPDO7KURPERF\WRVLV
SURJQRVLV
3%)1RUPRF\WLFQRUPRFKURPLF
Lymphoma

TT

anaemia. Hodgkin Disease

TT ESR: Very high XX 7UHDWPHQWFRQVLVWVRIFRPELQHG&KHPRWKHUDS\DQG
Blood for LDH Very high ORZGRVHLQYROYHG¿HOGUDGLDWLRQWKHUDS\ /',)57 LV
FRQVLGHUHGVWDQGDUGRIFDUH7KHYROXPHRIUDGLDWLRQDQG
 Step on to Paediatrics 177

WKHGXUDWLRQRIFKHPRWKHUDS\DUHGHWHUPLQHGE\ XX +HSDWRVSOHQRPHJDO\PD\EHSUHVHQW
WKHIROORZLQJSURJQRVWLFIDFWRUVDWSUHVHQWDWLRQ XX 0DFXORSDSXODUUDVKXVXDOO\DSSHDUHGDIWHULQWDNHRI
TT 3UHVHQFHRI%V\PSWRPV Amoxicilln
TT Initial stage of disease XX Petechiae at the junction of hard and soft palate is
TT Presence of bulky disease characteristic

Chemotherapy Complications
6WDQGDUGFKHPRWKHUDS\UHJLPHQDUH
XX CNS: 0HQLQJLWLVHQFHSKDOLWLVFUDQLDOQHUYHSDOV\*%6
DWD[LDSHUFHSWXDOGLVWRUWLRQVRIVL]HVKDSHV $OLFHLQ
XX $%9'F\FOHV UHSHDWHYHU\GD\V SOXV
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/',)57or
XX Respiratory: Airway obstruction due to swelling of tonsil
XX &233$%9K\EULGFRXUVHF\FOHV UHSHDWHYHU\
DQGRURSKDU\QJHDOVRIWWLVVXHLQWHUVWLWLDOSQHXPRQLD
GD\V SOXV/',)577KHVHUHJLPHQKDVDFXUH XX Haematological: +DHPRUUKDJHGXHWRWKURPERF\WRSDHQLD
UDWHXSWR
DXWRLPPXQHKDHPRO\WLFDQDHPLDDSODVWLFDQDHPLD
ABVD COPP XX Others: 6SOHQLFUXSWXUHP\RFDUGLWLV
Doxorubicin (Adriamycin) &\FORSKRVSKDPLGH
Diagnosis
Bleomycin Vincristine/Oncovine
0DLQO\FOLQLFDO)ROORZLQJLQYHVWLJDWLRQVZLOOEHVXSSRUWLYH
Vinblastine Procarbazine
Dacarbazine Prednisolone Investigations Results
&RPSOHWH%ORRG&RXQW /\PSKRF\WLFOHXNRF\WRVLV
Radiotherapy (/',)57
1RUPDOZLWKSUHVHQFHRIatypical
+HUH*\DUHXVHGZLWKPRGL¿FDWLRQEDVHG 3%)
lymphocytes.
RQSDWLHQW¶VDJHSUHVHQFHRIEXON\GLVHDVHQRUPDO
WLVVXHFRQFHUQVDQGSRWHQWLDODFXWHRUORQJWHUP 3RVLWLYH+HWHURSKLOHEHFDXVHLW
+HWHURSKLOHDQWLERG\
effects. agglutinate antigen from other
test
VSHFLHV
Non-Hodgkin Lymphoma ,J0DQWLERG\GHWHFWHGIRUVKHHS
8VXDOGXUDWLRQRIWUHDWPHQWZLWKFKHPRWKHUDS\LV 3DXO%XQQHOO'DYLGVRQ RBC agglutination.
test
DERXW\HDUVDFFRUGLQJWRNHL BFM-90 %HUOLQ 3RVLWLYHDIWHURQHZHHNDQGSHUVLVW
)UDQNIXUW0XQLFK SURWRFRO IRU7FHOO /0% for several months.
(for B cell). 0RQRVSRWWHVW UDSLG Horse RBC agglutination test.
&RPPRQO\XVHGGUXJVDUH± slide agglutination test) 5HPDLQSRVLWLYHIRU\HDUV
&\FORSKRVSKDPLGH  Vincristine

 Cytarabine (WRSRVLGH Treatment

0HWKRWUH[DWH /DVSDUDJLQDVH 6XSSRUWLYHRQO\DQGLQFOXGHV
XX %HGUHVW$YRLGFRQWDFWVSRUWVIRUZHHNVWRGHFUHDVHWKH
ULVNRIVSOHQLFUXSWXUH
XX $QWLS\UHWLF3DUDFHWDPRO
INFECTIOUS MONONUCLEOSIS XX Antiviral: Acyclovir
(GLANDULAR FEVER) XX 6WHURLG3UHGQLVRORQHPJNJIRUGD\VWKHQWDSHURYHU
DQRWKHUGD\V
Organism:(SVWHLQ%DUUYLUXVLQFDVHV
Indications of steroid
Incubation period: GD\V XX Airway obstruction
Glandular fever

Transmission:7KURXJKVDOLYDVH[XDOFRQWDFW XX 7KURPERF\WRSHQLDZLWKKDHPRUUKDJH
XX Auto immune haemolytic anaemia
Clinical Manifestations XX Seizure
XX )HYHU6RUHWKURDW XX 0HQLQJLWLV
XX *HQHUDOL]HGO\PSKDGHQRSDWK\ (SLWURFKOHDU
O\PSKDGHQRSDWK\LVVXJJHVWLYH Prognosis: Excellent.
 178 Step on to Paediatrics

References
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 *UDKDP'*HWDO1HRSODVWLFGLVHDVHV&XUUHQWGLDJQRVLV 7UHDWPHQWLQSHGLDWULFVrdHG0F*UDZ+LOOS
 .XUNXUH3$HWDO3HGLDWULF2QFRORJ\+RGJNLQ¶VGLVHDVH 1RQ+RGJNLQ¶VO\PSKRPD,Q3DUWKDVDUDWK\$HGLWRU,$3
7H[WERRNRI3HGLDWULFVthHG1HZ'HOKL-33
 3L]]R3$HWDO3ULQFLSOHV 3UDFWLFHRI3HGLDWULF2QFRORJ\thHGLWLRQS

SELF ASSESSMENT
Short answer questions [SAQ]
 :KDWDUHWKHFDXVHVRIJHQHUDOL]HGO\PSKDGHQRSDWK\"
 :KDWV\PSWRPVPD\GHYHORSGXHWRSUHVVXUHE\HQODUJHGO\PSKQRGHVLQO\PSKRPD"
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 :KDWUHOHYDQWLQYHVWLJDWLRQVZLOO\RXFRQVLGHULQDSDWLHQWZLWKO\PSKRPD"

Multiple choice questions [MCQ]

 7KHFKDUDFWHULVWLFVRIO\PSKQRGHVLQO\PSKRPDDUH±
___ a) rubbery consistency ___ b) discrete ___ c) matted
BBBG QHFURVLVRIWKHO\PSKQRGHV BBBH ¿[HGWRXQGHUO\LQJVWUXFWXUHV
 *HQHUDOL]HGO\PSKDGHQRSDWK\LVIRXQGLQ±
___ a) tuberculosis ___ b) systemic onset -,$  BBBF DSODVWLFDQDHPLD
BBBG NDODD]DU BBBH DFXWHO\PSKREODVWLFOHXNDHPLD
 3DWLHQWZLWKO\PSKRPDPD\SUHVHQWZLWKH[WUDQRGDOV\PSWRPVOLNH±
BBBD SOHXUDOHIIXVLRQ BBBE SHULFDUGLDOHIIXVLRQ BBBF SUXULWXV
___ d) neurological manifestations ___ e) swelling of jaw
 &KDUDFWHULVWLFFOLQLFRKDHPDWRORJLFDOIHDWXUHVRILQIHFWLRXVPRQRQXFOHRVLVDUH±
BBBD PDFXORSDSXODUUDVK BBBE HSLWURFKOHDUO\PSKDGHQRSDWK\ BBBF EODVWFHOOVLQ3%)
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___ a) Doxorubicin ___ b) Vincristine ___ c) (WRSRVLGH
___ d) 0HWKRWUH[DWH BBBH Dacarbazine
Self assessment
 23
Pallor or Anaemia
Iron deficiency anaemia (IDA) - - - - - - - - - - - 179
Hereditary haemolytic anaemias
¼¼ Į thalassaemia- - - - - - - - - - - - - 181
¼¼ ȕ thalassaemia major - - - - - - - - - - - - 182
¼¼ Haemoglobinopathies- - - - - - - - - - - - 182

Pallor (anaemia) is a common problem among children. It IRON DEFICIENCY ANAEMIA (IDA)
LVGH¿QHGDVWKHGHFUHDVHGFRQFHQWUDWLRQRIKDHPRJORELQ
IRUVSHFL¿FDJHDQGVH[RIWKHFKLOG 7KHPRVWFRPPRQFDXVHRIDQDHPLDLQFKLOGUHQ,WLV
associated with depressed motor and mental development
Haemoglobin levels of healthy RILQIDQWVDQGFKLOGUHQ
children at different ages
Age Haemoglobin (g/dl) Iron Metabolism
1 to 3 days 18.5 Sources

1 month 13.9 ,URQLVZLGHO\SUHVHQWLQDQLPDODQGSODQWIRRGVDV±

XX +HPHLURQ3UHVHQWLQPHDWOLYHU¿VKDQGSRXOWU\,W
6 months 12.6
LVUHDGLO\DEVRUEHGDQGDEVRUSWLRQLVQRWLQÀXHQFHGE\
6 months to 2 years 12.0 RWKHUGLHWDU\IDFWRUV
XX Non-heme iron: Present in beans, pulses, tubers, dried
2 to 6 years 12.5
IUXLWVDQGJUHHQYHJHWDEOHVe.g. banana, arum (kochu)
6 to 12 years 13.5 etc.
12 to 18 years 14.5 Daily requirement:PJRIHOHPHQWDOLURQ
Male/Female 14.0 Absorption: $WGXRGHQXPDQGMHMXQXPLQIHUURXVIRUP
Stored form of iron: Ferritin, haemosiderin
Whenever a child present with pallor, one should consider
WKHIROORZLQJFDXVHV± )DFWRUVLQÀXHQFHLURQDEVRUSWLRQ

XX ,URQGH¿FLHQF\DQDHPLD Factors enhance XX Vitamin C

Iron deficiency anaemia

XX Hereditary haemolytic anaemias e.g. thalassaemia absorption XX Proteins
syndrome, haemoglobinopathies
XX Helminthiasis XX 3K\WDWHV IRXQGLQXQUH¿QHG
XX Malnutrition cereals)
XX Chronic kidney diseases Factors inhibit XX 7DQQLQV IRXQGLQWHD OHJXPHV 
XX &KURQLFLQIHFWLRQe.g. tuberculosis, malaria, kala-azar absorption XX 3KRVSKDWHV IRXQGLQHJJV 
XX 'LVHDVHVRIWKHERQHPDUURZe.g. leukaemia, aplastic
XX 3RO\SKHQROV IRXQGLQFRIIHHDQG
anaemia spinach)
XX Others e.g. chronic liver disease, SLE, JIA

,QWKLVFKDSWHULURQGH¿FLHQF\DQDHPLD ,'$ DQG

hereditary haemolytic anaemia (HHA) will be discussed.
179
 180 Step on to Paediatrics

Aetiology

XX Preterm, LBW babies

XX Babies born to mothers with unusual perinatal

Source: Internet
haemorrhage
XX /DFWDWLRQIDLOXUH,URQLQEUHDVWPLONLVWLPHV
PRUHHI¿FLHQWO\DEVRUEHGWKDQWKDWLQFRZ¶VPLON
XX Inappropriate weaning
TT &RQVXPSWLRQRIODUJHDPRXQWRIFRZ¶VPLON PD\
Koilonychia
give rise to chronic intestinal blood loss due to a
KHDWODELOHSURWHLQSUHVHQWLQZKROHFRZ¶VPLON XX )HDWXUHVUHODWHGWRFKDQJHRIEHKDYLRXUe.g. Pica (the
TT 5HJXODUFRQVXPSWLRQRIIRRGVGH¿FLHQWLQLURQ
FRPSXOVLYHLQJHVWLRQRIQRQQXWULWLYHVXEVWDQFHVOLNH
e.g. rice gruel, suzi, barley etc. clay, dirt, paint or others)
XX ,QFUHDVHGGHPDQG'XULQJWKHSHULRGRIUDSLG XX 1HXURORJLFDO LQWHOOHFWXDOG\VIXQFWLRQVe.g.
JURZWKRILQIDQWVRUDGROHVFHQWV reduced attention span, alertness and reduced school
XX Occult bleeding: From gut as in peptic ulcer, SHUIRUPDQFH
0HFNHO¶VGLYHUWLFXOLWLVSRO\SDQDO¿VVXUH XX 5HGXFHGLPPXQLW\DQGIUHTXHQWLQIHFWLRQV
KDHPRUUKRLGKDHPDQJLRPDRULQÀDPPDWRU\ERZHO
disease etc ,QDGGLWLRQWKHDIIHFWHGFKLOGPD\KDYHbreath-holding
XX :RUPLQIHVWDWLRQe.g. hook worms in particular spells DUHEULHISHULRGVZKHQ\RXQJFKLOGUHQVWRS
XX 3HUVLVWHQWRUUHFXUUHQWDWWDFNVRIGLDUUKRHD EUHDWKLQJIRUXSWRPLQXWHDQGRIWHQFDXVHWKHFKLGWR
loose consciousness)

Diagnosis
Clinical Manifestations %DVHGRQ&) VXSSRUWVIURPUHOHYDQWLQYHVWLJDWLRQV
XX *HQHUDOV\PSWRPVRIDQDHPLDHJIDWLJXHGL]]LQHVV
OHVVDFWLYLWLHVLUULWDELOLW\SURIRXQGDQRUH[LDHWF Investigations
XX 3DOORURISDOPOLSVDQGFRQMXQFWLYD XX Complete blood counts: Hb% (reduced). TC and DC
XX 7KHFDUGLQDOIHDWXUHVRILURQGH¿FLHQF\DUH± (normal), reticulocyte counts (low or normal). Platelet
XX )HDWXUHVUHODWHGWRDWURSKLFFKDQJHVLQHSLWKHOLXPRI± counts usually normal but occasionally may be high
TT Mouth, lips (thrombocytosis)
e.g.cracking
TT Tongue e.g.

DWURSK\RI
papillae, smooth,

Target cell
pale and shiny
tongue
TT $QJOHRIPRXWK

e.g. redness,
soreness and
cracking Severely pale conjunctiva
Iron deficiency anaemia

TT 3KDU\Q[ 
oesophagus
e.g. dysphagia
(Plummer-
Vinson
syndrome)
TT Nails e.g.

ÀDWWHQLQJDQG
WKLQQLQJRIQDLOV Microcytic and Hypochromic red cells with few target cells
Courtesy: Dr Akhil Ranjon Biswas
koilonychia Cracked lips, angles of mouth, shiny tongue
 Step on to Paediatrics 181

XX 3HULSKHUDOEORRG¿OP6KRZVPLFURF\WLFK\SRFKURPLF Hereditary haemolytic anaemias (HHA)

RBC with anisocytosis, poikilocytosis and occasional
7KHVHDUHDJURXSRIJHQHWLFDOO\GHWHUPLQHGGLVRUGHUVRI
target cells
5%&FKDUDFWHUL]HGE\H[FHVVLYHKDHPRO\VLV7KHGHIHFWV
XX RBC indices: MCV, MCH are reduced but RDW (red
GH¿FLHQF\DWWULEXWHGWR5%&LVSUHVHQWHLWKHULQ±
cell distribution width) is high
XX 6HUXPLURQSUR¿OH6LURQDQGIHUULWLQDUHORZDQGTotal XX Membrane e.g. spherocytosis, eliptocytosis
Iron Binding Capacity (TIBC) is high XX Enzymes HJGH¿FLHQF\RI*3'S\UXYDWHNLQDVH
XX Other investigations: May be directed towards detecting XX Haemoglobin e.g.Thalassaemia syndromes,
DHWLRORJ\RILURQGH¿FLHQF\HJVWRRO50( IRU
haemoglobinopathies
RFFXOWEORRGWHVW PD\EHSRVLWLYH  IRUKHOPLQWK

2IWKHVH7KDODVVDHPLDV\QGURPHVDQGKDHPRJORELQ±
7KHFKDUDFWHULVWLF3%)IHDWXUHVRI,'$PD\PLPLFZLWK
opathies are the common haemolytic disorders, where the
WKDWRI±
GHIHFWLYHJHQHVDUHLQKHULWHGIURPWKHSDUHQWV

XX ĮȕWKDODVVDHPLDWUDLW
XX Hemoglobin E trait/ disease
XX Lead poisoning
XX $QDHPLDRIFKURQLFGLVHDVHe.g. JIA
XX Sideroblastic anaemia

Treatment
The objectives are to–
XX Restore haemoglobin level to normal
XX Replenish the depleted iron stores and
XX Treat the underlying causes
XX &RXQVHOWKHSDUHQWVDERXWWKHFDXVHFRQVHTXHQFHVDQG
LPSRUWDQFHRIWUHDWPHQWDQGSUHYHQWLRQRI,'$
XX 2UDOLURQWKHUDS\PJRIHOHPHQWDOLURQNJGD\LQ
GLYLGHGGRVHV,WVKRXOGEHJLYHQDERXWKDOIDQKRXU
EHIRUHPHDOWRPD[LPL]HDEVRUSWLRQ

NB: The choices are Ferrous sulphate, Ferrous fumarate

and Iron polymaltose complex.

Duration of treatment: ZHHNVDIWHUKDHPRJORELQ

Hereditary haemolytic anaemias

THALASSAEMIA SYNDROMES
indices return to normal
These are inherited abnormalities in globin synthesis
XX Diet
TT 6XSSOHPHQWDWLRQRIGLHWVULFKLQLURQ
where, there is a GH¿FLHQWSURGXFWLRQRIHLWKHUĮorȕ
TT $YRLGDQFHRIIRRGVGH¿FLHQWLQLURQ
chains and the globin chains are structurally normal.
TT $YRLGDQFHRIIRRGVWKRVHLQWHUIHUHZLWKLURQ %DVHGRQWKHGH¿FLHQF\RIHLWKHUĮorȕFKDLQV
absorption HJWHDFRIIHHHWF WKDODVVDHPLDVDUHRIW\SHV
XX 7UHDWPHQWRIWKHXQGHUO\LQJFDXVHe.g. anthelmintics
$ĮWKDODVVDHPLD (GH¿FLHQWSURGXFWLRQRIĮchain): It
PD\EH±
TT Homozygous e.g. K\GURSVIRHWDOLV Į0 or Hb Bart), or
TT Heterozygous HJVLOHQWFDUULHU Į ĮWKDODVVDHPLD
WUDLW Į RU+E+ Į 
 182 Step on to Paediatrics

%ȕWKDODVVDHPLD (GH¿FLHQWV\QWKHVLVRIȕ chains): It Haemoglobinopathies

PD\EH± 7KHVHDUHLQKHULWHGGLVRUGHURIKDHPRJORELQZKHUHJORELQ
TT ȕ7KDODVVDHPLDPDMRU7KH\DUHWUDQVIXVLRQ chains are structurally abnormal. The most important
dependent RIWKHVHDUH+E(+E6HbC and HbD Punjab and all are
TT ȕThalassaemia minor or trait: They carry the WKHUHVXOWVRIDPLQRDFLGVXEVWLWXWLRQVLQJORELQFKDLQV
GHIHFWLYHJHQHFRPSOHWHO\DV\PSWRPDWLFDQGDUH They may be either heterozygous or homozygous and their
LGHQWL¿HGLQFLGHQWDOO\
clinical presentations are variable.
TT ȕThalassaemia intermedia: Their clinical phenotype
is more than thalassaemia minor but milder than 2IWKHGLIIHUHQWW\SHVHbE is most prevalent in South
thalassaemia major. Their clinical behaviour is (DVW$VLDDQGLVLPSRUWDQWEHFDXVHRILW¶VFRPELQDWLRQ
ZLGHO\YDULDEOH6RPHRIWKHPPDLQWDLQ+E ZLWKEHWDWKDODVVDHPLDJHQHJLYLQJULVHWR+E(EHWDȕ
FRQFHQWUDWLRQRIDERXWJUDPZLWKRXWWUDQVIXVLRQ WKDODVVDHPLDDQGFKLOGUHQKDYLQJWKLVFRPELQDWLRQVXIIHU
but some may remain completely asymptomatic until IURPVHYHUHDQDHPLDOLNHWKDWRIWKDODVVDHPLDPDMRUDQG
DGXOWOLIH GHSHQGDQWRQUHJXODUEORRGWUDQVIXVLRQWRVXUYLYH

Prevalence
2YHUDOOSUHYDOHQFHRIȕWKDODVVDHPLDWUDLWDQG+E(WUDLW
LQ%DQJODGHVKDUH UHVSHFWLYHO\

BETA THALASSAEMIA MAJOR

Extra-medullary
Beta thalassaemia major

erythropoiesis
in liver

Hepatomegaly

3DWKRSK\VLRORJ\RIȕWKDODVVDHPLD0DMRU $GRSWHGIURP5REELQ¶V &RWUDQ¶VSDWKRORJ\µ

 Step on to Paediatrics 183

Pathogenesis TT *XPEOHHGLQJHSLVWD[LVHWFGXHWRhypersplenism
,QȕWKDODVVDHPLDPDMRUGXHWRDEVHQFHor decreased
TT 3DWKRORJLFDOIUDFWXUH
ȕFKDLQSURGXFWLRQWKHXQSDLUHGĮJORELQFKDLQVDUH
XX Sometimes, they may present with complications
DFFXPXODWHGDVµWR[LFLQFOXVLRQERGLHV¶LQWKHGHYHORSLQJ UHODWHGWRH[FHVVWLVVXHGHSRVLWLRQRILURQ±
erythroblasts and are causing their destruction within the XX ,VOHWVRI/DQJHUKDQV'LDEHWHVPHOOLWXV
bone marrow (LQHIIHFWLYHHU\WKURSRLHVLV . The remaining XX Liver : Chronic liver disease
GHIHFWLYH5%& FDUU\LQJLQFOXVLRQERGLHV WKRVH XX Heart: Cardiomyopathy, arrythmia, heart
escaping the destruction in the bone marrow, enter in the
XX Thyroid (hypothyroidism) Parathyroid
circulation and ultimately gets destroyed in the spleen
(hypoparathyroidism), Gonads (hypogonadism,
(splenomegaly). This premature haemolysis causes 2
delayed puberty) etc.
PDMRUFOLQLFRSDWKRORJLFDOFRQVHTXHQFHV± XX Brain: Epilepsy, neuropsychiatric problem
XX Severe anaemia
XX 3URGXFWLRQRIH[FHVVLURQIURPKDHPIUDFWLRQRI Physical Examination
KDHPRJORELQRIO\VHG5%&DQGWKHLUDFFXPXODWLRQ XX Moderate to severe pallor
LQWKHEORRGDVZHOODVLQYLWDORUJDQV FDXVLQJWKHLU
SURJUHVVLYHG\VIXQFWLRQ

7RFRPSHQVDWHVHYHUHDQDHPLDH[DJJHUDWHGHU\WKURSRLHVLV
occurs both in the marrow spaces (medullary
HU\WKURSRLHVLV DVZHOODVLQOLYHU H[WUDPHGXOODU\
HU\WKURSRLHVLV 7KHPDUURZVSDFHVWKXVH[SDQGGXHWR
HU\WKURLGK\SHUSODVLDZKLFKFDXVHVJUDGXDOWKLQQLQJRI
FRUWLFDOERQH7KHORQJERQHVLQSDUWLFXODUEHFRPHIUDJLOH
and results in pathological fractures0DUURZH[SDQVLRQ
RIWKHÀDWERQHVRIVNXOODQGIDFH HJPD[LOOD]\JRPD 
UHVXOWVLQ±
Pale palm
XX )DFLDOGHIRUPLWLHV
XX 0D[LOODU\SURWUXVLRQDQGPDODOLJQHGMDZ WHHWK XX Mild jaundice
XX 3URPLQHQFHRI)URQWDODQG3DULHWDO ERVVLQJ

In addition, the untreated or partially treated children grow

poorly (growth failure DQGGHYHORSPDVVLYHVSOHQR±
hepatomegaly.

Clinical Manifestations
$IIHFWHGFKLOGPD\EHQRUPDODWELUWKEXWGHYHORS
VLJQL¿FDQWDQDHPLDGXULQJWKHLU¿UVW\HDURIOLIH Beta thalassaemia major
7KHFRPPRQSUHVHQWDWLRQVDUH±
XX 3URJUHVVLYHSDOORUOHWKDUJ\DQGHIIRUWLQWROHUDQFH
XX Failure to thrive and growth retardation
XX Psychological depression
XX 5HFXUUHQWLQIHFWLRQV
XX 3UREOHPVLQPRYHPHQWDQGDEGRPLQDOGLVFRPIRUW
EHFDXVHRIPDVVLYHVSOHQRKHSDWRPHJDO\
XX 6RPHWLPHVSDWLHQWPD\SUHVHQWZLWKIHDWXUHVRI
FRPSOLFDWLRQVOLNH± Jaundice
TT 5HVSLUDWRU\GLVWUHVVGXHWRDQDHPLFKHDUWIDLOXUH
 184 Step on to Paediatrics

XX &KDQJHVLQIDFLDOSUR¿OHVOLNHIURQWDODQGSDULHWDO XX 3ODWHOHWFRXQW8VXDOO\QRUPDOH[FHSWLQhypersplenism
bossing, depressed nasal bridge, prominent zygoma, (Thrombocytopenia)
malaligned jaw and teeth 7KDODVVDHPLFIDFLHV XX Reticulocyte count: Relative reticulocytopenia,
commonly <8% (normal range 0.2-2%)
XX 3HULSKHUDOEORRG¿OP6KRZVPLFURF\WLFK\SRFKURPLF
SLFWXUHZLWKPDUNHGDQLVRF\WRVLV SRLNLORF\WRVLV
$SSHDUDQFHRIDEQRUPDOFHOOVlike target cells, tear
drop, pencil shaped cells, nucleated cells, schistocytes,
IUDJPHQWHGFHOOV

Courtesy: Dr. Akhil Ranjon Biswas

Prominent zygoma, misaligned jaw and teeth

XX *UHHQLVKEURZQFRPSOH[LRQGXHWRWKHHIIHFWRI
combined pallor, haemosiderosis and jaundice
XX *URZWKIDLOXUH Stunting)
XX Massive splenohepatomegaly.
Hypochromia with plenty of tear drop calls, schistocytes,
target cells and few nucleated RBC.

XX RBC indices (MCV, MCH, MCHC): Low

XX 6HUXPLURQDQG6IHUULWLQ,QFUHDVHG
XX 6WUDQVIHULQVDWXUDWLRQ,QFUHDVHG
XX S Total iron binding capacity (TIBC): Decreased
XX S unconjugated bilirubin: Usually increased
XX Haemoglobin electrophoresis: Shows markedly reduced
or absent HbA and raised HbF and HbA2

Massive hepatosplenomegaly
Beta thalassaemia major

Diagnosis
%DVHGRQ&) VXSSRUWVIURPUHOHYDQWLQYHVWLJDWLRQV

Investigations
A. Blood
XX +DHPRJORELQ/RZGHSHQGLQJRQWKHVHYHULW\RIWKH
disease
XX 7& '&1RUPDOH[FHSWZKHQDVVRFLDWHGLQIHFWLRQ
(leukocytosis) or hypersplenism (depleted)
 Step on to Paediatrics 185

Summary of haematological changes

in IDA & Thalassaemia major XX ;5D\RIORQJERQHVVKRZV±
TT Lacy increased trabecular, mosaic patterns and
Haematological ,URQGH¿FLHQF\ TT Osteopenia
Thalassaemia
parameter anaemia
XX Markedly
XX Haemoglobin XX Reduced
reduced
XX Platelet XX Thrombocytosis XX Normal or low
XX S. iron XX Reduced XX Raised
XX Ferritin XX Reduced XX Raised
XX TIBC XX Raised XX Reduced
XX RDW XX Raised XX Normal
XX MCHC XX Reduced XX Reduced
XX MCV XX Reduced XX Reduced

X-ray hands showing mosaic pattern

B. Radio-imaging
XX ;5D\VNXOOVKRZV±
Complications
TT Increased diploic space

TT Hair on end appearance

XX Growth retardation, Stunting
XX %RQ\GHIRUPLWLHV'HIRUPHGVNXOO IDFLHV
XX Organ damage related to iron overload:
TT Heart (cardiomyopathy), liver (CLD) and

endocrine system (hypothyroidism, diabetes

mellitus, hypogonadism etc.)
XX 5HFXUUHQWLQIHFWLRQVVHSVLVGXHWRORZLPPXQLW\
XX 0RUHFKDQFHRIIUDFWXUHVDVWKHERQHVDUHWKLQDQG
brittle
XX 6SLQDOFRUGFRPSUHVVLRQGXHWRH[WUDPHGXOODU\
haemopoiesis
XX 0DVVLYHVSOHQRPHJDO\FDXVLQJZRUVHQLQJRI
DQDHPLD PHFKDQLFDOGLVFRPIRUW
XX &&)IURPsevere anaemia and cardiomyopathy
XX &RPSOLFDWLRQVRIEORRGWUDQVIXVLRQe.g,
TT Allergic reaction
Beta thalassaemia major
TT Acute haemolytic reaction

Typical X-ray skull of thalassaemia Major
TT 75$/, 7UDQVIXVLRQ5HODWHG$FXWH/XQJ,QMXU\

TT 7$&2 7UDQVIXVLRQ$VVRFLDWHG&LUFXODWRU\

Overload)
TT 7UDQVPLVVLRQRILQIHFWLRXVDJHQWVe.g. HBV, HIV
 186 Step on to Paediatrics

Treatment 7KHDGRSWHGWUDQVIXVLRQSURJUDPPHVKRXOGPDLQWDLQ±
7KHDIIHFWHGFKLOGUHQDUHWUDQVIXVLRQGHSHQGHQW,Q TT 3UHWUDQVIXVLRQ+E!JPGO
DGGLWLRQWRUHJXODUEORRGWUDQVIXVLRQVWKH\UHTXLUHDQ TT 3RVWWUDQVIXVLRQ+EaJPGO
LQWHJUDWHGVXSSRUWVIURP3DHGLDWULFLDQ+DHPDWRORJLVW TT Mean Hb: 12.5 gm/dl
3V\FKRORJLVWDQG7UDQVIXVLRQVSHFLDOLVWV
+RZHYHUDKLJKHUSUHWUDQVIXVLRQ+ERIJPGOLV
XX &RXQVHOLQJSDUHQWV±
TT Help them to understand the illness
EHQH¿FLDOIRUWKDODVVDHPLFFKLOGZLWKFDUGLDFGLVHDVH
TT +HOSWKHIDPLO\WRFRSHXSZLWKWKHLOOQHVVDQGDQG The recommended blood productsIRUWUDQVIXVLRQDUH±
HQFRXUDJHVHOIHVWHHP TT Leuko-reduced packed RBC with a minimum
TT Genetic counseling and how to prevent the disease KDHPRJORELQFRQWHQWRIJPGO
XX 7KHPDMRURSWLRQVRIWUHDWPHQWDUH± TT Washed RBC
TT Frozen or cryopreserved RBC
XX Conventional method TT Neocyte or young red cell
XX Bone marrow transplantation
XX 3KDUPDFRORJLFDOPHWKRGVWRLQFUHDVHȖFKDLQ II. Iron chelation
synthesis
,URQFKHODWRUVDUHXVHGWRNHHS,URQLQDVDIH]RQHVR
XX Gene therapy
as to prevent its deposition in vital organs. The iron
FKHODWRUVDUH±
A. Conventional method: This includes± XX 'HVIHUULR[DPLQH')2 ,QM'HVIHUROPJ 
I. Blood transfusion XX 'HIHULSURQH &DS.HOIHUPJ
7RFRUUHFWDQDHPLDDQGWRPDLQWDLQVDWLVIDFWRU\ XX 'HIHUDVLUR[ 7DEAsunra 100, 400 mg)
KDHPRJORELQOHYHOVRDVWR±
XX Ensure normal growth and to increase physical activity
XX 0LQLPL]HH[SDQVLRQRIERQHPDUURZ Q. When to start iron chelation?
TT 8VXDOO\DIWHUWUDQVIXVLRQV25
TT :KHQ6IHUULWLQOHYHO!QJPO

7UHDWPHQWLVVWDUWHGZLWKDQ\RIWKHLURQFKHODWRUVor
ZLWKGLIIHUHQWFKHODWRUVFRPELQHGO\HJ')2DWWKHWLPH
RIWUDQVIXVLRQDQG'HIHULSURQHLQEHWZHHQWUDQVIXVLRQV
&RPELQHGWKHUDS\LVIRXQGPRUHHIIHFWLYH

III. Diet & Nutrition

XX 7KHFKLOGFDQHDW GULQNDOPRVWHYHU\WKLQJWKDWD
normal child can. But better to avoid red meat, liver etc.
Childrens getting XX 'ULQNVOLNHWHDFRIIHHGHFUHDVHVLURQDEVRUSWLRQKHQFH
EORRGWUDQVIXVLRQ GULQNLQJWKHVHMXVWDIWHUPHDOLVEHQH¿FLDO
XX 9LWDPLQ&LQFUHDVHVLURQH[FUHWLRQE\LQFUHDVLQJWKH
Beta thalassaemia major

DYDLODELOLW\RIFKHODWDEOHLURQ'RVHPJNJGD\DV
VXSSOHPHQWVWREHWDNHQDWWKHWLPHRI')2LQIXVLRQVR
WKDWLURQLVUDSLGO\FKHODWHGDQGH[FUHWHGWKURXJKXULQH
XX 9LWDPLQ(VKRXOGEHVXSSOHPHQWHGDVDQDQWLR[LGDQWWR
UHGXFHLURQLQGXFHGR[LGDWLYHGDPDJHRIFHOOV

N.B. Iron should not be Prescribed as supplement in

Thalassaemia.
Desferrioxamine infusion through pump
 Step on to Paediatrics 187

IV. Splenectomy B. Bone marrow or stem cell transplantation

XX ,QGLFDWLRQV± from a HLA identical sibling donor
TT 7UDQVIXVLRQUHTXLUHPHQWLV!PORISDFNHGFHOOV '' 7KHSUREDELOLW\RIKDHPDWRORJLFDOFXUHLV
kg/year !ZKHQWUDQVSODQWDWLRQLVGRQHSULRUWRWKH
TT 0DVVLYHVSOHQRPHJDO\LVDVVRFLDWHGZLWK± GHYHORSPHQWRIKHSDWRPHJDO\orSRUWDO¿EURVLV
³³ PHFKDQLFDOGLVFRPIRUW

³³ OHIWXSSHUTXDGUDQWSDLQ
C. Pharmacological methods
'' 7KLVLVGRQHWRLQFUHDVHȖFKDLQSURGXFWLRQVRDV
³³ IHDURIUXSWXUH
WRSURGXFHPRUH+E)WKURXJKPHWK\ODWLRQRIȖ
³³ early satiety
genes by drugs like Hydroxyurea, Sodium phenyl
EXW\UDWHDQGazacytidine. This helps to improve
XX Prerequisites of splenectomy KDHPRJORELQVWDWXVRISDWLHQWV
TT $JH0RUHWKDQ\HDUV WLPHQHHGHGIRU

PDWXULWLRQRILPPXQHV\VWHP D. Gene therapy

TT Vaccination: Four weeks prior to surgery against '' 5HWURYLUDOYHFWRUPHGLDWHGJHQHWUDQVIHULQWRWKH
6WUHSFRFFXVSQHXPRQLDH+LQIOXHQ]DHW\SHE KDHPRSRLHWLFVWHPFHOOVSURYLGHDSRWHQWLDOFXUHRI
and meningococcal meningitis VHYHUHȕ7KDODVVDHPLDEXWWKLVPRGDOLW\LVVWLOOLQWKH
XX Care after splenectomy H[SHULPHQWDOSKDVH
TT 2UDO3KHQR[\PHWK\O3HQLFLOOLQ OLIHORQJ
Thalassaemia: Prevention
SURSK\OD[LV XX Carrier detection among the general population
TT <2 years: 125 mg every 12 hours
WKURXJK/DEDVVHVVPHQWRIEORRG&%&3%)0&9
TT !\HDUVPJHYHU\KRXUV
0&+& +DHPRJORELQelectrophoresis. DNA analysis
TT 3URPSWWUHDWPHQWRIDQ\LQIHFWLRQ
LQFRQ¿UPDWRU\
XX Pre-marital counseling among the population,
specially among the carriers, how the disease is
V. Treatment of complicationsHJ5HSODFHPHQWRI±
WUDQVPLWWHGIURPRQHJHQHUDWLRQWRWKHQH[WDQGKRZWR
TT Insulin (diabetes mellitus) prevent
TT 7K\UR[LQ K\SRWK\URLGLVP HWF XX Antenatal detection: When a carrier mother becomes
SUHJQDQWWKHVWDWXVRIWKHIRHWXVZKHWKHUKDYLQJ
VI. Follow up thalassaemia major, carrier or normal can be detected
by chorionic villus sampling (CVS) and DNA analysis
Monthly XX Complete Blood Count
during 8-11thZHHNVRISUHJQDQF\
Every 3 XX 6IHUULWLQ5%6SGPT, albumin,
months creatinine

Every 6 XX Cardiac evaluation e.g. echocardiography,

months ECG
XX 6FUHHQLQJIRULQIHFWLRQ+%9+&9HIV
XX 6FUHHQLQJIRUHQGRFULQRSDWK\)7TSH,
Yearly
LH, Testosterone, Estradiol, GTT
XX $VVHVVPHQWRIYLVLRQDQGKHDULQJ
XX Other investigations to assess iron deposition in vital
organs e.g.
TT 05,RIKHDUWOLYHUHQGRFULQHJODQGV
Self assessment

TT 0HDVXUPHQWRIKRUPRQHVHJ76+)7 , GH, etc.

4
 188 Step on to Paediatrics

References
 1HOVRQWH[WERRNRI3DGLDWULFVthHG'LVHDVHVRIEORRGS
 .KDQ:$HWDO3UHYDOHQFHRIEHWDWKDODVVHPLDWUDLWDQG+E(WUDLWLQ%DQJODGHVKLVFKRROFKLOGUHQDQGKHDOWKEXUGHQRI
WKDODVVHPLDLQRXUSRSXODWLRQ'KDND6KLVKX+RVSLWDO-RXUQDO  
 5XQG'5DFKPLOHZLW](ȕWKDODVVHPLD7KH1HZ(QJODQG-RXUQDORI0HGLFLQH  
 &KRXGKU\931DLWKDQL5&XUUHQWVWDWXVRILURQRYHUORDG FKHODWLRQZLWKGHIHUDVLUR[,-3HGLDWULFV
5. Milner A D, Hull D. Blood In: Hospital Pediatrics. 3rd(GLWLRQ2[IRUG8.&KXUFKLO/LYLQJVWRQHS
 0ROODK0$+HWDO6HURSUHYDOHQFHRIFRPPRQ77,VDPRQJWKDODVVHPLFFKLOGUHQLQ%DQJODGHVK-+31  
 6KDOLJUDP'HWDO3V\FKRORJLFDOSUREOHPVDQGTXDOLW\RIOLIHLQFKLOGUHQZLWKWKDODVVHPLD,-3HGLDWULFV
/DQ]NRZVN\3,Q0DQXDORI3HDGLDWULF+DHPDWRORJ\DQG2QFRORJ\thHG8.(OVHYLHUS

SELF ASSESSMENT
Short answer questions [SAQ]
 :KDWDUHWKHFDUGLQDOIHDWXUHVRILURQGH¿FLHQF\LQ,'$"
 :ULWHGRZQWKHWUHDWPHQWRILURQGH¿FLHQF\DQDHPLDZLWKGXUDWLRQ
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 :KDWGR\RXPHDQE\WKHK\SHUWUDQVIXVLRQUHJLPHQRIEORRGWUDQVIXVLRQLQWKDODVVDHPLD"
5. What is the non-invasive way to assess iron-deposition in vital organs?
 :ULWHGRZQFRPSOLFDWLRQVRIWKDODVVHPLDPDMRU

Multiple choice questions [MCQ]

 1RUPDOIUDFWLRQVRIKDHPRJORELQRIDFKLOGLQFOXGH±
___ a) HbA ___ b) HbA2 ___ c) HbF ___ d) HbS ___ e) Hb Gower
 7KHEORRGSLFWXUHRIEHWDWKDODVVDHPLDPDMRUDUH±
___ a) microcytic hypochromic anaemia ___ b) target cells ___ c) nucleated RBC
___ d) normal reticulocyte count ___ e) high TIBC
 7KHUHFRPPHQGHGLURQFKHODWRUVDUH±
___ a) 'HVIHUULR[DPLQH BBBE 'HIHULSURQH BBBF 'HIHUDVLUR[
___ d) +\GUR[\XUHD BBBH azacytidine
 7KHSDWKRORJLFDOFRQVHTXHQFHVRIWKDODVVDHPLDPDMRUDUH±
BBBD KDHPRO\VLV BBBE RUJDQG\VIXQFWLRQ BBBF LURQRYHUORDG
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Self assessment

BBBD ORZVHUXPLURQ BBBE ORZVHUXPIHUULWLQ BBBF KLJKVDWXUDWLRQRILURQ

___ d) low total iron binding capacity ___ e) low marrow sideroblast
 3KDUPDFRWKHUDS\LQWKDODVVDHPLDFDXVHVLQFUHDVHGSURGXFWLRQRI±
___ a) alpha chain ___ b) beta chain ___ c) gamma chain ___ d) delta chain ___ e) theta chain
 7KHFRPPRQFOLQLFRKDHPDWRORJLFDOSUR¿OHRILURQGH¿FLHQF\DQDHPLDLQFOXGH±
___ a) clubbing ___ b) Microcytic hypochromic anaemia
 Step on to Paediatrics 189

BBBF ORZVHUXPWRWDOLURQELQGLQJFDSDFLW\ BBBG KLJKVHUXPIHUULWLQOHYHO BBBH ORZVHUXPLURQOHYHO

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 24
Pallor, Bleeding and Fever
Leukaemia - - - - - - - - - - - - - - 190
Aplastic anaemia - - - - - - - - - - - - - 195

Whenever, children present with pallor, mucocutaneous Pathogenesis

EOHHGLQJDQGIHYHUVLPXOWDQHRXVO\LHIHDWXUHVRI5%& /HXNDHPLDVDUHWKHSULPDU\PDOLJQDQFLHVRIERQH
platelets and WBC pathology, one should think that the marrow, where haemopoietic stem cells undergone
problem is possibly in the bone marrow. In such situation, PDOLJQDQWSUROLIHUDWLRQ7KHPDOLJQDQWFHOOV EODVWFHOOV 
WKHIROORZLQJFRPPRQERQHPDUURZGLVHDVHVVKRXOGEH VXEVHTXHQWO\UHSODFHDQGRFFXS\DPDMRUDUHDRIQRUPDO
FRQVLGHUHG± ERQHPDUURZSUHGRPLQDQWO\DIIHFWLQJWKHHU\WKRLGDQG
megakaryocyte population. As a result, there is decreased
XX Leukaemia
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XX Aplastic anaemia
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XX $Q\ERQHPDUURZLQ¿OWUDWLQJGLVHDVHV
XX 3DXFLW\RI5%& Anaemia
However, sometimes septicaemia/disseminated Immune suppression and
intravascular coagulation (DIC), hypersplenism also
XX 3DXFLW\RIPDWXUH:%&
LQIHFWLRQ
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XX 3DXFLW\RISODWHOHWV Bleeding
In this section acute leukaemia and aplastic anaemia will
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JUDGXDOO\VSLOORYHULQWREORRGIURPERQHPDUURZDQG
IURPZKHUHWKH\PD\LQ¿OWUDWHLQWRWKHH[WUDPHGXOODU\
sites like, lymph nodes, liver, spleen, bone, brain, eyes,
LEUKAEMIA testes and other tissue throughout the body.

/HXNDHPLDWKHFRPPRQHVWPDOLJQDQF\RIFKLOGUHQ,W
Types
FRQVWLWXWHVDERXWRIWKHWRWDOFKLOGKRRGFDQFHUV,Q Leukaemia may be acute or chronic and the common types
DGGLWLRQWROHXNDHPLDRWKHUFKLOGKRRGPDOLJQDQFLHVDUH± DUH±
XX $FXWHO\PSKREODVWLFOHXNDHPLD 
XX :LOP¶VWXPRU XX Acute myeloblastic leukaemia (12-15%)
XX CNS tumor
XX Retinoblastoma XX Chronic myelogenous leukaemia (5%)
XX Lymphoma
XX Sarcoma e.g. XX 2WKHUV  
XX Neuroblastoma
rhabdomyosarcoma,
XX Hepatoblastoma Clinical Manifestations
osteosarcoma
XX 1RQVSHFL¿F±
Leukaemia

TT 3URIRXQGORVVRIDSSHWLWHOHWKDUJ\LUULWDELOLW\
Aetiology
TT 3DLQLQGLIIHUHQWSDUWVRIERG\
XX Unknown
XX *HQHWLF FKURPRVRPDOGLVRUGHUV
XX 6SHFL¿F±
TT Fever: May be prolonged or intermittent. It results
XX (QYLURQPHQWDOIDFWRUVHJUDGLDWLRQYLUDOLQIHFWLRQV
IURPHLWKHUOHXNDHPLDLQGXFHGOLEHUDWLRQRI
H[SRVXUHWRFKHPLFDOVDQGF\WRWR[LFGUXJV
cytokines orVHFRQGDU\LQIHFWLRQVGXHWROHXNRSHQLD
immunosuppression
190

TT Progressive pallor
 Step on to Paediatrics 191

TT %OHHGLQJIURPJXPHSLVWD[LVSHWHFKLDHSXUSXUD XX 7HVWLFXODUVZHOOLQJIURPLQ¿OWUDWLRQRIOHXNDHPLFFHOOV
ecchymosis etc.
XX 6RPHWLPHVSDWLHQWVPD\KDYH±
TT &RQYXOVLRQDQGRWKHUQHXURORJLFDOPDQLIHVWDWLRQV

e.g. headache, vomiting, cranial nerve palsy etc.

EHFDXVHRI&16PHQLQJHDOLQ¿OWUDWLRQ
TT 3UREOHPVRIYLVLRQEHFDXVHRILQ¿OWUDWLRQWRUHWLQD

TT 5HVSLUDWRU\GLVWUHVVIURPWKHSUHVVXUHHIIHFWRI

mediastinal mass on airway orIURPDQDHPLFKHDUW

IDLOXUH
*XPEOHHGLQJ
Physical Examination
3K\VLFDO¿QGLQJVDWSUHVHQWDWLRQDUHZLGHO\YDULDEOH
UDQJLQJIURPQRUPDOWRKLJKO\VXJJHVWLYH7KHXVXDO
IHDWXUHVDUH±
XX 6LFNORRNLQJLUULWDEOHIHEULOHFKLOG

Infection at nose

XX Lymphadenopathy: Either localized or generalized

Pallor

Lymphadenopathy

XX Bony tenderness over sternum, tibia

Purpuric spots

XX 6LJQVUHODWHGWRERQHPDUURZG\VIXQFWLRQe.g.
TT UDLVHGERG\WHPSHUDWXUH LQIHFWLRQ 

TT pallor (depleting haemoglobin)

Leukaemia

TT SHWHFKLDHSXUSXUDJXPEOHHGLQJRUHSLVWD[LVGXHWR

platelet depletion
XX Hepatomegaly and splenomegaly Bony tenderness
XX ,QIHFWLRQVDQ\ZKHUHLQWKHERG\
 192 Step on to Paediatrics

Acute Myeloid Leukaemia (AML)

7KHFOLQLFRSDWKRORJLFDOEHKDYLRXURI$0/LVPRUH
aggressive and KDVDKLJKWHQGHQF\WRLQ¿OWUDWHLQWR
GLIIHUHQWRUJDQV+HUHERQHSDLQ WHQGHUQHVVDUHPRUH
VHYHUHWKDQ$//,QDGGLWLRQSDWLHQWVPD\SUHVHQWZLWK±
XX Gingival hypertrophy, parotid swelling
XX Proptosis
XX Mediastinal mass with pressure symptoms (e.g.
dyspnoea, superior vena caval syndrome) and
,Q¿OWUDWLRQRIOHXNDHPLFFHOOVWRH\H

Superior vena cava syndrome (SVCS), is a group

Aleukaemic/subleukaemic leukaemia
RIV\PSWRPVFDXVHGE\REVWUXFWLRQRIWKHVXSHULRU
YHQDFDYD69&6LVFKDUDFWHUL]HGE\± $W\SHRI
leukaemia
XX 6KRUWQHVVRIEUHDWK PRVWFRPPRQV\PSWRP
in which the
XX Headache
total leukocyte
XX Facial swelling
count remains
XX Venous distention in the neck and distended within normal
veins in the upper chest and arms limits or
XX Upper limb edema ORZDQGIHZ
Lightheadedness Chloroma
XX
abnormal
XX Cough IRUPV
XX (GHPD VZHOOLQJ RIWKHQHFNFDOOHGWKHFROODU appear in the
RI6WRNHV peripheral
blood.
Diagnosis
XX &KORURPD VROLGFROOHFWLRQRIOHXNDHPLFFHOOVRXWVLGH
the bone marrow) UHTXLUHVERQH
marrow study.
XX Hyperleukocytosis syndromeZLWKOLIHWKUHDWHQLQJ
FRPSOLFDWLRQVHJYHQRXVVWDVLV VOXGJLQJRIEODVW About 30%
FHOOVLQVPDOOYHVVHOVFDXVHK\SR[LDKDHPRUUKDJHDQG RIOHXNDHPLF
LQIDUFWLRQPRVWQRWDEO\LQOXQJVDQGEUDLQ patients may
XX :KHQOHXNDHPLFFHOOVLQ¿OWUDWHLQWKHVNLQ(leukaemia present in this /HXNDHPLDFXWLVLQDPRQWKVROGER\
cutis) way.

Aleukemic leukemia
$W\SHRIOHXNHPLDLQZKLFKWKHWRWDOOHXNRF\WH
count remains within normal limits or is low and
IHZDEQRUPDOIRUPVDSSHDULQWKHSHULSKHUDOEORRG
'LDJQRVLVUHTXLUHVERQHPDUURZELRSV\,WRFFXUVLQ
RIDOOSDWLHQWVZLWKOHXNHPLDUHJDUGOHVVRIWKH
VSHFL¿FW\SH

Differential Diagnoses
Leukaemia

XX Aplastic anaemia  ITP .DODD]DU

Gingival hypertrophy
 Step on to Paediatrics 193

Diagnosis XX &6)H[DPLQDWLRQ
%DVHGRQ&) VXSSRUWVIURPUHOHYDQWLQYHVWLJDWLRQV
TT $W\SLFDOEODVWFHOOVPD\EHIRXQGLQ&16OHXNDHPLD
XX Other investigations
Investigations TT X-Ray chest :May show mediastinal widening/

XX CBC with PBF DQWHULRUPHGLDVWLQDOPDVVWUDFKHDOFRPSUHVVLRQIURP

TT Haemoglobin level: Reduced lymphadeopathy orWK\PLFLQ¿OWUDWLRQVSHFLDOO\LQ7
TT 7RWDOFRXQWVRI:%&8VXDOO\KLJKEXWPD\EH cell leukaemia
TT ;5D\RIORQJERQHV VSLQHV'HPLQHUDOL]DWLRQ
normal or low (in aleukaemic leukaemia)
TT 'LIIHUHQWLDOFRXQWVRI:%&'HSHQGLQJRQWKH periosteal elevation, growth arrest lines, compression
W\SHRIOHXNDHPLDFHOOOLQHVPD\EHFKDQJHG RIYHUWHEUDOERGLHV
TT 8OWUDVRQRJUDPRIDEGRPHQ0D\VKRZNLGQH\
&KDUDFWHULVWLFIHDWXUHLVWKHSUHVHQFHRIblast cells
TT Platelet count: Low HQODUJHPHQWIURPOHXNDHPLFLQ¿OWUDWLRQLQWUD
TT 3HULSKHUDOEORRG¿OP5%&1RUPDOORZ:%&
abdominal lymphadenopathy
TT S Uric acid, S LDH: Uusually elevated
series shows blast cells SODWHOHWVUHGXFHG
TT S electrolytes, Ca, PO : May be altered
4
TT 6FUHDWLQLQH5DLVHGLQXULFDFLGQHSKURSDWK\IURP

UDSLGO\VLVRIEODVWFHOOVDQGPHWDEROLVPRIEDVHV
TT )ORZF\WRPHWU\RIPDUURZFHOOV7RFKDUDFWHUL]HWKH
Courtesy: Dr. Akhil Ranjon Biswas
W\SHVRIOHXNDHPLD

Treatment
Counsel parents about the disease, its management and
prognosis.

A. Supportive
TT 'LHW1XWURSHQLFGLHW IUHVKO\SUHSDUHGIRRGORZ
PLFURELDOGLHW 7KLQSHHOHGIUXLWVDUHUHVWULFWHG
3%)VKRZLQJO\PSKREODVW
TT 7RWUHDW SUHYHQWLQIHFWLRQVE\±
XX Bone marrow study ³³ Antibiotics: Broad spectrum covering both gram

TT Cellularity: Hypercellular
positive and gram negative organisms to treat any
TT M:E ratio: Increased
DVVRFLDWHGLQIHFWLRQ
TT Granulopoiesis: Increased ³³ &RWULPR[D]ROHKRXUO\WZLFHDZHHN

TT Erythropoiesis: Reduced throughout the treatment

TT Megakaryopoiesis: Reduced ³³ Clotrimazole/Nystatin drop, orally, 2.5 ml 6

TT Blast cells of >25% is diagnostic hourly throughout the treatment

³³ &KORUKH[LGLQHPRXWKZDVK PL[HGZLWKZDWHU 

hourly throughout the treatment

³³ $FULÀDYLQHKLSEDWK DFULÀDYLQPL[HGZLWKZDUP
Courtesy: Dr. Akhil Ranjon Biswas

water to clean the perinium), 12 hourly throughout

the treatment
³³ 0DLQWHQDQFHRIWRWDOK\JLHQHLQWKHOLYLQJDUHD

³³ Barrier nursing

TT Ranitidine IV/PO, 12 hourly when steroid is in regim

TT 7RFRUUHFWDQDHPLD WKURPERF\WRSHQLD7UDQVIXVLRQ
RIEORRGSURGXFWVRUZKROHEORRG
TT 7RWUHDWIHYHU2UDOSDUDFHWDPRO(not suppository)
Leukaemia

%RQHPDUURZVKRZLQJO\PSKREODVW
 194 Step on to Paediatrics

TT Pre-chemo measures
XX To reduce leukaemic cell XX ,9ÀXLG/P2GD\IRU %6SHFL¿F
induced aemoconcentration ¿UVWKRXUV TT Chemotherapy: This is a protocol based
(UKALL2003 Regimen A) multi-staged
XX Allopurinol 100 mg/m2/
poly-chemotherapy schedule, currently used in
XX 7RUHGXFHULVNRIXULFDFLG dose, 8 hrly (start 24 hours
Bangladesh.
nephropathy EHIRUHFKHPRDQGFRQWLQXH TT Bone marrow transplantation: The curative
IRUGD\V
WUHDWPHQWRIOHXNDHPLD
XX To reduce metabolic XX Inj. Sodi-bicarb 25ml in
acidosis PO,9ÀXLG
XX For emergency medical de- XX Tab Prednisolone 60 mg/
EXONLQJRIWXPRXUFHOOORDG m2/day, orally

Multi-stage poly Chemotherapy sehedule (UKALL 2003)

XX Vincristine, IV on D2,9,16,23 and 30

Induction of XX L-asparaginase IM on D4, 6, 8, 10, 12, 14, 16, 18, 20 (9 doses)
Remission
Weeks: 1-5 XX 7ULSOH,7 07;&\W+FW RQ'DQG
Phase: 1
XX 'H[DPHWKDVRQH32'WKHQWDSHUZLWKLQGD\V
XX 0HUFDSWRSXULQH32RQFHDWQLJKWIURP'

Early
,QWHQVL¿FDWLRQ XX 6-mercaptopurine PO, once daily
Weeks: 6-8 XX Triple IT (TIT) weekly
Phase: 2

Interim
XX 6-mercaptopurine PO, once daily up to week 15
maintenance XX 0HWKRWUH[DWH32RQ:HHN
Weeks: 9-16 XX TIT on week 11 and week 15
Phase: 3 XX 9LQFULVWLQH,9RQWKHVWGD\RIZHHNDQGZHHN
XX 7,7RQWKHVWGD\RI:HHN
Delayed XX 9LQFULVWLQH,9RQWKHQGGD\RIZHHN
,QWHQVL¿FDWLRQ
:HHNV XX 'R[RUXELFLQ,9RQQGGD\VRIZHHN
Phase: 4
XX /DVSHUDJLQDVH,0HYHU\DOWHUQDWHGD\IURP'RIZHHN
XX 'H[DPHWKDVRQH32IRUGD\VRQZHHNDQGZHHN
XX 7,7RQWKHVWGD\RIZHHNDQGZHHN
XX &\FORSKRVSKDPLGH,9RQWKHVWGD\RIZHHNZLWKPHVQDXURPLWR[DQUHVFXH
Delayed XX &\WDUDELQH,9IURP'RIZHHNDQGZHHN1%'H[DPHWKDVRQHH\HGURSV
,QWHQVL¿FDWLRQ
Weeks: 21-23 KRXUO\WREHVWDUWHGKRXUVEHIRUH&\WDUDELQWRKRXUVDIWHU&\WDUDELQH
Part-2, Phase: 4 WKHUDS\WRDYRLGFKHPLFDONHUDWLWLVDV&\WDUDELQHH[FUHWHVWKURXJKWHDUV
XX PHUFDSWRSXULQH32RQFHGDLO\IURPWKHVWGD\RIZHHNWRWKHODVWGD\RI
week 22
Aplastic anaemia

Weeks:
XX Vinristine IVmonthly
Maintenance TIT every 3 monthly
24-166 (Boys) XX

therapy XX 6-mercaptopurine PO daily

Weeks: 0HWKRWUH[DWH32ZHHNO\
Cycle: 1-12
XX

24-112 (Girls) XX 'H[DPHWKDVRQH32'IURPWKHGD\RI,99LQFULVWLQH

07;&\W+FW Methotrexate + &\WDUDELQH+\GURFRUWLVRQH ±Triple IT

 Step on to Paediatrics 195

Prognosis Pathogenesis
&KLOGUHQVZLWK$//DUHH[SHFWHGWRKDYHDORQJWHUP 7KHPHFKDQLVPRIPDUURZDSODVLDLVQRWIXOO\XQGHUVWRRG
VXUYLYDOUDWHRI!DW\HDUVIURPWKHGLDJQRVLV but is thought to be immune-mediated VXSSUHVVLRQ 
Poor prognostic criteriae (High risk) NLOOLQJRIKDHPDWRSRLHWLFSURJHQLWRUV,QDGGLWLRQWKHUH
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XX Age <1 year or!\HDUVDWGLDJQRVLV
SUROLIHUDWLYHDQGGLIIHUHQWLDWLYHFDSDELOLW\6RPHWLPHV
XX /HXNRF\WHFRXQWRI!ȝ/DWGLDJQRVLV
LQWULQVLFDEQRUPDOLW\RIVWHPFHOOVPD\DOVRSUHGLVSRVHWR
XX Slow response to initial chemotherapy
DNA damage and marrow aplasia.
XX Chromosomal abnormalities e.g. hypodiploidy, presence
RI3KLODGHOSKLDFKURPRVRPHDQGWUDQVORFDWLRQV>W
(1:19) or t (4:11)]
Stem cell
Good prognostic criteriae
XX Age: 1-9 years
XX Initial WBC count: <50,000/ mm3 Environmental insult
(viruses, drugs, etc.)
XX Early response to induction chemotherapy
XX &KURPRVRPDODOWHUDWLRQVHJFRPELQDWLRQVRI Genetically altered
WULVRPLHVRIFKURPRVRPHVDQG stem cells
XX $EVHQFHRI3KLODGHOSKLDFKURPRVRPH
XX %/\PSKREODVWLFW\SHRIOHXNDHPLD
XX $EVHQFHRI&16GLVHDVH

Express new antigens Reduced proliferative and

differentiative capacity
IFN
TNF
T-cell response
APLASTIC ANAEMIA Marrow
aplasia
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QXPEHURIFLUFXODWLQJEORRGFHOOVHJ5%&:%& 3DWKRJHQHVLVRIDSODVWLFDQDHPLD$GRSWHGIURP5REERQ
platelets, resulting in peripheral pancytopenia. &RWUDQµVSDWKRORJ\WKHGLWLRQ¶

Aetiology
Clinical Manifestations
XX ,GLRSDWKLF !FDVHV 7KHFDUGLQDOIHDWXUHVRIERQHPDUURZIDLOXUHDUHUHODWHGWR
XX Secondary SDQF\WRSHQLDWKDWLQFOXGHV±
TT 9LUDOLQIHFWLRQV e.g. HBV, EBV, HIV, parvovirus
Clinical features Related to
B19
TT Idiosyncratic reactions to drugs e.g. XX 3DOORUDQGQRQVSHFL¿FV\PSWRPVe.g. Low
3KHQ\OEXWD]RQH6XOIRQDPLGHV16$,'DQG ZHDNQHVVIDWLJXHDQRUH[LDHWF. haemoglobin
anticonvulsants XX %OHHGLQJLQ±
TT ([SRVXUHWRUDGLDWLRQDQGFKHPLFDOVe.g.
TT Skin: petechiae, purpura,

benzene,insectiside, heavy metals drugs and ecchymoses Low platelet

elements e.g. chloramphenicol phenylbutazone, TT Mucosa: gum,nose,conjunctiva etc.

gold TT Internal organs: brain, kidney, gut

Aplastic anaemia

XX Congenital e.g. Fanconi's anaemia etc.

XX )UHTXHQWVHYHUHLQIHFWLRQVe.g.
septicaemia, meningitis Low WBC
XX ,QIHFWLRQVZLWKIXQJXV XQXVXDO
pathogens
 196 Step on to Paediatrics

Source: Internet
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Diagnosis
$SODVWLFERQHPDUURZ
%DVHGRQ&) VXSSRUWVIURPWKHUHOHYDQWLQYHVWLJDWLRQV

Investigations
XX CBC with PBF
Treatment
TT Usually pancytopenia (low Hb, leukopenia and $&RXQVHOSDUHQWVDERXWWKHGLVHDVHLW¶VWUHDWPHQWDQG
thrombocytopenia). Occasionally bi/ monocytopenia WKHFRQVHTXHQFHV
TT Reticulocytes: Low
B. Comprehensive supportive care
TT PBF: Normocytic anaemia, Noabnormal cells
TT 4XLFNHYDOXDWLRQRIDIHEULOHFDVHDQGSURPSW
XX %RQHPDUURZ¿QGLQJV VWDUWLQJRIEURDGVSHFWUXPSDUHQWHUDODQWLELRWLFV
TT Cellularity:Markedly hypocellular marrow, largely &RQVLGHUDGGLQJDQWLIXQJDOGUXJVLIQHFHVVDU\
GHYRLGRIKDHPDWRSRLHWLFFHOOVRIWHQWKHUHLV TT 7UDQVIXVLRQRISHDNHGFHOOVWRDOOHYLDWHV\PSWRPVRI
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scattered lymphocytes and plasma cells threatening bleeding
TT Markedly reduction in granulopoiesis, erythropoiesis TT Diet: Neutropenic. 5DZPHDWVGDLU\SURGXFWVIUXLWV
and megakaryopoiesis and vegetables that are likely to be colonized with
XX Other investigations microbes should not be given to the patient
TT Chromosomal analysis: To assess chromosome break
&,PPXQRPRGXODWLRQZLWK±
UHDUUDQJHPHQWVLQSHULSKHUDOO\PSKRF\WHVDVVHHQ TT Anti-thymocyte globulin
in )DQFRQL¶VDQDHPLD TT Cyclosporine
TT &\WRJHQHWLFDQDO\VLVRIPDUURZSDUWLFOHVWRSUHGLFW
TT Tacrolimus (associated with a high response rate and
WKHVXEVHTXHQWGHYHORSPHQWRIOHXNDHPLD
overall survival)
TT Viral markers e.g. HBsAg

'+DHPDWRSRLHWLFVWHPFHOOWUDQVSODQWDWLRQ7KHVSHFL¿F
treatment

Prognosis
XX %RQHPDUURZWUDQVSODQWDWLRQ %07 IURP+/$
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Aplastic anaemia
 Step on to Paediatrics 197

References
 7XEHUJHQ'*HWDO7KH/HXNHPLDV1HOVRQ7H[WERRNRI3HGLDWULFVth(GLWLRQ1HZ'HOKL(OVHYLHU
 5REELQV &RWUDQ3DWKRORJLFEDVLVRIGLVHDVHth edition, 2015; 653-4.
 $PEUXVR'5HWDO+HPDWRORJLFGLVRUGHUV&XUUHQW'[ 7UHDWPHQWLQ3HGLDWULFVrd ed. McGraw-Hill; 2014: 891-944.
 .XUNXUH3$HWDO3HGLDWULF2QFRORJ\+RGJNLQ¶VGLVHDVH 1RQ+RGJNLQ¶VO\PSKRPD,$37H[WERRNRI3HGLDWULFVth ed.
'HOKL-%3

SELF ASSESSMENT
Short answer questions [SAQ]s
1. What are the common childhood cancers?
 :KDWDUHWKHGLIIHUHQWVWHSVRIWUHDWPHQWRIDFXWHOHXNDHPLD"
 1DPHFKHPRWKHUDSHXWLFDJHQWVXVHGIRUWUHDWPHQWRIDFXWHO\PSKREODVWLFOHXNDHPLD"
 :KDWDUHWKHSUHFKHPRPHDVXUHVWREHWDNHQGXULQJWUHDWPHQWRIDOHXNDHPLFFKLOG"
 2XWOLQHWKHSULQFLSOHVRIWUHDWPHQWRIDSODVWLFDQDHPLD
 :ULWHGRZQWKHFOLQLFDOIHDWXUHVRIDFXWHOHXNDHPLD
 +RZZLOO\RXLQYHVWLJDWHDFXWHOHXNDHPLD"
8. How will you investigate aplastic anaemia?
 $\HDUROGER\SUHVHQWHGZLWKIHYHUDQGSDOORUIRUODVWPRQWKVDORQJZLWKKHSDWRVSOHQRPHJDO\
D :ULWHWKUHHFRPPRQGLIIHUHQWLDOGLDJQRVLV E +RZZLOO\RXLQYHVWLJDWHWKHER\"

Multiple choice questions [MCQ]

 %ORRGSLFWXUHRIDFXWHOHXNDHPLDLQFOXGHV±
___ a) leukocytosis ___ b) thrombocytopenia ___ c) nucleated RBC
___ d) target cells ___ e) immature WBC (blast cells)
 7KURPERF\WRSHQLDLVIRXQGLQ±
___ a) ITP ___ b) haemophilia ___ c) von Willebrand disease
___ d) acute leukaemia ___ e) Henoch-Schönlein purpura
 $FKLOGZLWKDSODVWLFDQDHPLDPD\SUHVHQWZLWK±
 BBBD IHYHU BBBE VHYHUHDQDHPLD BBBF EOHHGLQJPDQLIHVWDWLRQ
___ d) hepatosplenomegaly ___ e) generalized lymphadenopathy
3RRUSURJQRVWLFFULWHULDHRI$//LQFOXGHVWKHDVVRFLDWHG±
___ a) chromosomal abnormality ___ b) high leukocyte count ___ c) thrombocytopaenia
 BBBG $//LQLQIDQWV BBBH UDSLGUHVSRQVHWRWKHUDS\
 ,PPXQRWKHUDSHXWLFDJHQWVIRUDSODVWLFDQHPLDLQFOXGH±
___ a) Anti Thymocytic Globulin ___ b) Granulocyte Colony Stimulating Factor
___ c) Tab. Cyclophosphamide ___ d) Cap. Cyclosporine ___ e) Tab. Prednisolone
 7KHGUXJVXVHGIRUPDLQWHQDQFHWUHDWPHQWRI$//LQFOXGH±
___ a) Etoposide ___ b) 0HWKRWUH[DWH BBBF Daunorubicin
Self assessment

BBBG &RWULPR[D]ROH BBBH Marcaptopurine

 &RPPRQFKLOGKRRGPDOLJQDQFLHVLQFOXGH±
___ a) Neuroblastoma ___ b) Hepatoblastoma ___ c) Adenocarcinoma
___ d) Lymphoma ___ e) Cholangiocarcinoma
 25
Bruising and Bleeding
Idiopathic thrombocytopenic purpura - - - - - - - - - 198
Haemophilia- - - - - - - - - - - - - - 201
Von willebrand disease- - - - - - - - - - - - 204

:KHQDFKLOGSUHVHQWVZLWKEOHHGLQJWKHIROORZLQJ platelet antibodies and these coat the circulating platelets

FRQGLWLRQVVKRXOGEHWDNHQLQWRFRQVLGHUDWLRQ± DQGWKHFRDWHGSODWHOHWVDUH¿QDOO\GHVWUR\HGDQGUHPRYHG
by the spleen.
XX Idiopathic thrombocytopenic purpura (ITP)
XX Leukaemia Clinical Manifestations
XX 'HQJXHKDHPRUUKDJLFIHYHU '+) XX 6XGGHQRQVHWRImuco-cutaneous bleeding
XX Aplastic anaemia GLVWLQJXLVKDEOHIURPFRDJXORSDWK\ LQDSUHYLRXVO\
XX Haemophilia A, B healthy child
TT Skin: petechiae, purpura, ecchymoses and easy
XX von Willebrand disease
bruising
XX Henoch Schönlein purpura
TT 0XFRVDEOHHGLQJIURPJXPQRVHFRQMXQFWLYD

menorrhagia
Rarely thrombasthenia e.g. Glanzmann disease and
Bernard Soulier syndrome may also present with bleeding.
In this chapter, ITP, haemophilia and von Willebrand
disease will be discussed.

IDIOPATHIC THROMBOCYTOPENIC
PURPURA (ITP)
7KLVLVWKHPRVWFRPPRQEOHHGLQJGLVRUGHURIFKLOGUHQ
where platelets are coated by a circulating antibody,
developed against platelet glycoprotein antigens and
eventually destroyed in the spleen.

Types 3HULRUELWDOHFFK\PRVLV JXPEOHHGLQJ

XX Acute ITP
XX Chronic ,73 SHUVLVWHQWWKURPERF\WRSHQLD!PRQWKV
XX Internal bleeding HJKDHPDWXULDKDHPDWHPHVLV 
Aetio-pathogenesis malaena, haemoptysis and intracranial bleeding are
Unknown. However, in about 50-60% cases, this uncommon but can occur in severe thrombocytopenia
SODWHOHWGHVWUXFWLRQPD\IROORZDQHSLVRGHRIYLUDOXSSHU DQGPD\EHIDWDO
ITP

UHVSLUDWRU\WUDFWLQIHFWLRQDERXWZHHNVSULRUWRWKH Physical Examination

bleeding episodes. The viruses commonly involved are XX (YLGHQFHRIEOHHGLQJLQ
(SVWHLQ±%DUUYLUXV EBV), Rubella, Varicella, Measles, TT Skin e.g. petechiae, purpura or ecchymosis
3DUYRYLUXV%DQG,QÀXHQ]D The viruses produce anti-
198

TT Mucosa e.g. nose, gum, oral cavity, conjunctiva

 Step on to Paediatrics 199

II. Skin lesions of acute meningococcaemia

/HVLRQVFRQVLVWRIWHQGHUSLQNPDFXOHVSHWHFKLDHDQG
SXUSXUD7KHVHDUHPRVWSURPLQHQWRQWKHH[WUHPLWLHV
DQGPD\SURJUHVVWRIRUPDUHDVRIIUDQNQHFURVLV

0XOWLSOHSXUSXULFVSRWVGRQRWEODQFKRQSUHVVXUH

+RZHYHUSDWLHQWVQHLWKHUKDYHVLJQL¿FDQWSDOORU
hepatosplenomegaly, lymphadenopathy nor bony
tenderness.

Differential Diagnoses Skin lesions of acute meningococcaemia

XX Henoch Schönlein purpura III. Skin lesions of Dengue fever

XX 'HQJXHKDHPRUUKDJLFIHYHU '+) 7UDQVLHQWPDFXODUUDVKLQ¿UVWGD\VPDFXORSDSXODU
XX Leukaemia VFDUOHWPRUELOOLIRUPIURPGD\
XX Aplastic anaemia
XX Meningococcal septicaemia

I. Skin rash of Henoch-Schönlein purpura

(Anaphylactoid purpura: Immune mediated vasculitis)
These rashes are characterized as palpable purpura that
HYROYHIURPUHGWRSXUSOHDQGWKHQWRUXVW\EURZQ

Skin rash of DHF

Clinical severity of acute ITP

XX Mild: Bruising and petechiae, occasional minor
HSLVWD[LVYHU\OLWWOHLQWHUIHUHQFHZLWKGDLO\OLYLQJ
Skin rash of HSP XX Moderate: More severe skin and mucosal lesions,
PRUHWURXEOHVRPHHSLVWD[LVDQGPHQRUUKDJLD
EHIRUHWKH\HYHQWXDOO\IDGH7KHVHDUHQRQWHQGHU
XX Severe: Bleeding episodes e.g. menorrhagia,
HSLVWD[LVPHOHQDUHTXLULQJWUDQVIXVLRQRU
do not blanch on pressure. Lesions usually involve
hospitalization6\PSWRPVLQWHUIHUHVHULRXVO\ZLWK
EXWWRFNORZHUH[WUHPLWLHVDQGWKHKDQGV waist down
WKHTXDOLW\RIOLIH
distribution).
ITP
 200 Step on to Paediatrics

Diagnosis B. Laboratory
,73LVGLDJQRVHGE\± Acute
Parameters Acute ITP Aplastic anaemia
XX ([FOXGLQJRWKHUFDXVHVRIWKURPERF\WRSHQLDe.g. acute leukaemia
leukaemia, aplastic anaemia Normal
$QDO\VLQJWKHFOLQLFDO ODERUDWRU\GDWDRIWKHFDVH Haemo-
XX
or slightly Low Low
globin reduced
Investigations
&%& 3%) Usually
XX
WBC count Normal Low
TT Haemoglobin: Usually normal unless massive
very high
haemorrhage Platelet
Low Low Low
TT 7&DQG'&RI:%&8VXDOO\QRUPDO counts
TT Platelet counts: Low
Presence Pancytopenia but
TT PBF: RBC (normal), WBC ( mature). No blast cells. %ORRGILOP Normal RI%ODVW cell morphology
Larger platelets may be seen cells are normal
XX &RDJXODWLRQSUR¿OH XVXDOO\QRWUHTXLUHGWRGR  Hypper Markedly
TT Bleeding time (BT): Prolonged Bone Increased cellular hypocellular
TT Prothrombin time (PT): Normal marrow mega- Blast cells PDUURZGHYRLGRI
TT aPTT: Normal ILQGLQJV karyocytes !LQ haematopopietic
diagnostic cells
XX %RQHPDUURZVWXG\*HQHUDOO\QRWUHTXLUHGIRUSDWLHQWV
ZLWKLVRODWHGWKURPERF\WRSHQLDZKR¿WWKHGLDJQRVWLF Treatment
FULWHULDHDERYHEXWLQGLFDWHGZKHQ±
Acute ,73LVDVHOIOLPLWLQJGLVHDVHDQG!RIFKLOGUHQ
XX 3DWLHQWVIDLOWRUHVSRQGWRWKHUHFRPPHQGHG UHTXLUHQRWKHUDS\2QO\±
WKHUDS\IRU,73 XX &RXQVHOLQJWRSDUHQWV SDWLHQWVDERXWWKHGLVHDVH
XX &HOOOLQHVRWKHUWKDQSODWHOHWVDUHDIIHFWHG XX &ORVHREVHUYDWLRQRIWKHSDWLHQWV
XX Steroid is planned to treat the case XX $YRLGDQFHRIDVSLULQ16$,'DQG
XX 5HVWULFWLRQIURPSK\VLFDOFRQWDFWDFWLYLWLHVDUH
TT %RQHPDUURZVWXG\¿QGLQJV0HJDNDU\RF\WHVDUH recommended.
increased. Erythroid and myeloid cellularity as well +RZHYHUZKHQSODWHOHWFRXQWIDOOVFPP
as myeloid erythroid ratio are normal WUHDWPHQWLVUHTXLUHGWRLQGXFHDUDSLGULVHRISODWHOHWVWR
WKHVDIHOHYHO7KHIROORZLQJGUXJVDUHUHFRPPHQGHGLQ
Differences between acute ITP,
WKLVVLWXDWLRQ±
leukaemia and aplastic anaemia
XX IVIG7KHWUHDWPHQWRIFKRLFHIRUVHYHUHDFXWH
A. Clinical
bleeding and may also be used as an alternative or
Acute Acute Aplastic adjunct to steroid in both acute and chronic ITP. Dose
Parameters JNJGD\ IRUGD\V,WLQGXFHVDUDSLGULVHRI
ITP leukaemia anaemia
SODWHOHWFRXQW !î9/ LQRISDWLHQWVZLWKLQ
TT Skin/gum/nose
Present Present Present 48 hours. IVIG appears to induce the response by down
bleeding
UHJXODWLQJ)FPHGLDWHGRQHSKDJRF\WRVLVRIDQWLERG\
Usually Usually Usually coated platelets
TT Fever
absent present present XX Prednisone3DWLHQWVZLWKFOLQLFDOO\VLJQL¿FDQWEXW
Sick, QRQOLIHWKUHDWHQLQJEOHHGLQJPD\EHQH¿WIURPDVKRUW
TT Appearance Normal Sick FRXUVHRIVWHURLG'RVH PJNJGD\ FRQWLQXHGIRU
irritable
Insigni- ZHHNVXQWLOSODWHOHWFRXQWLV!î9/L
TT Pallor Severe Severe IV anti-D to Rh-positive patients: Single dose (50-
¿FDQW XX

TT Lymph-adenopathy Absent Present Absent —JNJ LQGXFHVDUDSLGULVHRISODWHOHWFRXQW!

î9/ZLWKLQKRXUVLQRISDWLHQWV7KLV
TT Bony tenderness Absent Present Absent polyclonal immunoglobulin binds to the D antigen on
5%&V7KHVSOHQLFFOHDUDQFHRIDQWL'FRDWHG5%&
TT Liver size Normal Enlarged Normal
LQWHUIHUHVZLWKUHPRYDORIDQWLERG\FRDWHGSODWHOHWV
ITP

TT Spleen size Normal Enlarged Normal resulting in improvement in thrombocytopenia

 Step on to Paediatrics 201

XX 2WKHURSWLRQV± LVSHUKDSVGXHWRQHZPXWDWLRQRIJHQHVWKDWUHJXODWHWKH
TT 6SOHQHFWRP\5HVHUYHGIRUUHIUDFWRU\ V\QWKHVLVRIIDFWRU9,,,DQG,;
WKURPERF\WRSHQLDZLWKOLIHWKUHDWHQLQJKDHPRUUKDJH 7KHJHQHVIRUV\QWKHVLVRIERWKIDFWRU9,,, ,;DUH
TT 3ODWHOHWWUDQVIXVLRQ8VXDOO\QRWLQGLFDWHGLQacute
SUHVHQWRQ;FKURPRVRPH'XHWRPXWDWLRQRIWKHJHQHV
,73EHFDXVHWKHWUDQVIXVHGSODWHOHWVZLOOEHFRDWHG
WKHKDHPRSKLOLDFVKDYHUHGXFHGV\QWKHVLVRIHLWKHU9,,,or
ZLWKDQWLSODWHOHWDQWLERGLHVDQGGHVWUR\HG,ILWLV
,;7KLVDGYHUVHO\DIIHFWVWKHLQWULQVLFFRDJXODWLRQFDVFDGH
OLIHVDYLQJWUDQVIXVHDORQJZLWK,9,*or steroid
ZLWKGHOD\LQFORWIRUPDWLRQDQGFRQVHTXHQWSURORQJHG
Treatment of chronic ITP bleeding.
XX 6SOHQHFWRP\ SRVWVSOHQHFWRP\SHQLFLOOLQ 1HLWKHUIDFWRU9,,,QRU,;FURVVSODFHQWDDQGWKXVEOHHGLQJ
SURSK\OD[LVLQGXFHVFRPSOHWHUHPLVVLRQLQRI may present since birth or even in utero.
cases
7KHPRGHRILQKHULWHQFHRIKDHPRSKLOLD&RQWKH
XX Monoclonal anti-B cell antibodyHJ5LWX[LPDE
RWKHUKDQGLVDXWRVRPDOUHFHVVLYHZKHUHERWKPDOHV 
XX Drug that stimulates thrombopoiesis e.g. Romiplostin
IHPDOHVFDQVXIIHUIURPWKHGLVHDVH
XX IVIG (1g/kg/dose), every 2-6 weeks
XX Immunosuppressive drugs Azathioprine, Cyclosporin Coagulation Cascade
Intrinsic pathway Extrinsic pathway
Prognosis
XII Tissue factor
$ERXWRIFKLOGUHQZLWKDFXWHITP will achieve a XI
IX VII
remission and 20% may turn into chronic ITP and the
VIII
SUHGLFWRUVRIFKURQLFLW\DUH IHPDOHJHQGHU DJH!
O O
Common
aPartial pathway Prothrombin
years at presentation LQVLGLRXVRQVHWRIEUXLVLQJDQG
O
Thromoboplastin Time
OSUHVHQFHRIRWKHUDXWRDQWLERGLHV Time X
V
Ca++
Lipids
Prothrombin Thrombin
(II)
Fibrinogen Fibrin clot
HAEMOPHILIA (I)
(XIII)
7KHFRPPRQHVWKHUHGLWDU\FRDJXORSDWK\IURPGH¿FLHQF\ Clinical Severity
RIIDFWRU9,,,,;DQG;,7KHSUHYDOHQFHRIKDHPRSKLOLD
6HYHULW\RIKDHPRSKLOLDLVUHODWHGWRWKHFRQFHQWUDWLRQRI
DUHDVIROORZV±
IDFWRU9,,,or,;SUHVHQWLQSODVPDDQGLVH[SUHVVHGDV
XX Haemophilia A (Classical):1 in 5,000 males percentage orOHYHORIDFWLYLW\
XX Haemophilia B (Christmas disease):1 in 30,000 males
)RUH[DPSOH±
These, along with YRQ:LOOHEUDQGGLVHDVHDFFRXQWVIRU
!RIKHUHGLWDU\FRDJXORSDWKLHV ,IXQLWRIHLWKHUIDFWRU9,,,,;LVSUHVHQWLQPORI
SODVPDWKHQLWLVHTXLYDOHQWWRIDFWRUDFWLYLW\
XX Haemophilia CFRQWULEXWHVDERXWRIDOO
haemophiliacs
7\SHVGH¿FLHQWIDFWRUVDQGLQKHULWHQFH Level of VIII
Severity Patterns of Haemorrhage
or IX activity
XX Haemophilia A:'H¿FLHQF\RIIDFWRU9,,, ;5
XX Haemophilia B: 'H¿FLHQF\RIIDFWRU,; ;5 Spontaneous'HHSVRIW
XX Haemophilia C:'H¿FLHQF\RIIDFWRU;, $5 Severe <1% WLVVXHKDHPRUUKDJH 
haemarthrosis
,QWKLVVHFWLRQZHZLOOFRQFHQWUDWHRQKDHPRSKLOLD$ % Mild to moderate trauma:
Gross bleeding. Seldom
Pathogenesis Moderate 1-<5%
spontaneous haemorrhage.
Haemophilia

%RWKKDHPRSKLOLD$ %H[KLELWX-liked Recessive Sometimes, haemarthrosis

FKDUDFWHUVZKHUHPDOHVVXIIHUDQGIHPDOHVFDUU\WKH
GLVHDVH)DPLO\KLVWRU\RIEOHHGLQJLQUHODWLYHVRQ Moderate haemorrhage
maternal side is present in about 80% cases. In about Mild 5-25% RQO\IROORZLQJPRGHUDWHWR
FDVHVIDPLO\KLVWRU\RIEOHHGLQJLVDEVHQWDQGWKLV severe trauma or Surgery
 202 Step on to Paediatrics

Clinical Manifestations IV. CNS

XX %OHHGLQJLVWKHPDLQV\PSWRP'HSHQGLQJRQWKHH[WHQWRI '' /LIHWKUHDWHQLQJDQGSDWLHQWVSUHVHQWZLWK
IDFWRUGH¿FLHQF\EOHHGLQJPD\EHHLWKHUVSRQWDQHRXVor altered consciousness, convulsions and other
IROORZLQJWUDXPD,WPD\RFFXUDWDQ\DJHDQGDQ\ZKHUHLQ QHXURORJLFDOPDQLIHVWDWLRQV
the body V. Other sites
XX Deep-seated bleeding induced by relatively minor trauma '' Abdomen
DUHFKDUDFWHULVWLFVRIFRDJXORSDWK\ IRUPDWLRQ
RIELJ
Neonatal, Infancy & childhood bleeding
haematoma
XX 7KHUHPD\EHKLVWRU\RIEOHHGLQJIURPXPELOLFDOFRUG
and
cephalhaematoma or intracranial haemorrhage in newborn
complicated
XX (DV\EUXLVLQJIRUPDWLRQRIKDHPDWRPDor haemarthrosis by
PD\RFFXUDWFUDZOLQJZDONLQJDQGIROORZLQJYDFFLQDWLRQ circulatory
XX ([FHVVLYHEOHHGLQJIROORZLQJFLUFXPFLVLRQPD\EHWKH¿UVW IDLOXUH
SUHVHQWDWLRQRIKDHPRSKLOLD Bleeding in inguinal area and
shock and scrotum with haematoma formation
XX 3URORQJHGEOHHGLQJPD\DOVRRFFXUDWWKHWLPHRIWHHWKLQJ presssure IROORZLQJULGLQJRQELF\FOHURG
over vital
Sites of Bleeding structures in abdomen
I. Joints '' Gut (haematemesis and melaena)

HaemarthrosisLVWKHKDOOPDUNRIKDHPRSKLOLD XX Nose HSLVWD[LV

Haemarthrosis begins in toddler age and ankle joints are XX Urinary tract (haematuria)
DIIHFWHG XX Upper airway (severe respiratory distress, cyanosis)
earliest. When XX However, bleeding in skin (petechiae) is usually
child tries uncommon
to maintain
upright
posture, the
knee joints are
second most
common joint
Haemarthrosis at left knee joint
DIIHFWHG$V
the age advances the common bleeding sites become knees
DQGWKHHOERZV3DWLHQWVZLWKKDHPRSKLOLDRIWHQGHYHORSD
target jointZKHUHUHSHWLWLYHHSLVRGHVRIEOHHGLQJRFFXU ([WHQVLYHHFFK\PRVLVRYHUWKHOHIWDUP PXVFOHEOHHGLQJ
Chronic arthropathyLVWKHPDMRUORQJWHUPPRUELWLW\RI
haemophilia. Complications
II. Muscles & Soft tissue
XX +DHPRG\QDPLFLQVWDELOLW\EHFDXVHRIPDVVLYH
bleeding
TT 0RVWO\RFFXUVLQJDVWURFQHPLXVTXDGULFHSVDQG
LOLRSVRDVDQGIRUPKDHPDWRPD
XX Severe pallor
XX 3DLQDQGSUHVVXUHHIIHFWVIURPKDHPDWRPDRYHUWKH
III. Oral cavity (teeth & gum)
vital organs
Prolonged bleeding XX 3HUPDQHQWMRLQWGDPDJHGXHWRIUHTXHQWEOHHGLQJ
IURPPLQRUWUDXPDWLF inside the joint cavities
laceration in mouth XX 'HYHORSPHQWRIDQWLERGLHVLQWKHUHFLSLHQW¶VEORRG
orIROORZLQJWRRWK DJDLQVWWKHLQIXVHGIDFWRU9,,, ,;
H[WUDFWLRQPD\RFFXU 7UDQVIXVLRQWUDQVPLWWHGLQIHFWLRQV
Haemophilia

XX

in many patients.
Diagnosis
%DVHGRQWKURXJKFOLQLFDOHYDOXDWLRQDQGVXSSRUWIURP
relevant investigations.
Bleeding following tooth extraction
 Step on to Paediatrics 203

XX &OLQLFDOHYDOXDWLRQZLWKSDUWLFXODUHPSKDVLVRQ±
Types of
Dosage of factor VIII
haemorrhage
XX $JHRIRQVHWRI XX 6LWHRIEOHHGLQJ
bleeding XX 7DUJHWMRLQWVLIDQ\
TT 50 U/kg stat on day 1, then
XX &KDUDFWHULVWLFVRI XX )DPLO\KLVWRU\RI Haemarthrosis TT 20 U/kg on days 2, 3, 5 until the joint
bleeding similar disease IXQFWLRQQRUPDOL]HVor back to baseline
TT 50 U/kg on Day 1 then
Intramuscular
20 U/kg every other day until haematoma
Investigations
TT
haematoma
is well resolved
Investigations Results Major surgery, TT 6WDW,8NJ
Haemoglobin: Low and OLIHWKUHDWHQLQJ TT 1H[WGD\V,8NJKRXUO\WR
XX Complete Blood LVUHODWHGWRH[WHQWRI bleeding (e.g. PDLQWDLQWURXJKOHYHO!,8GO
Count haemorrhage. WBC, CNS, GI TT 1H[WGD\V,8NJRQFHGDLO\WR
platelet counts: Normal bleeding etc) PDLQWDLQWURXJK!,8GO

XX Peripheral blood :KHQIDFWRU9,,,or,;DUHQRWDYDLODEOH±

Normal XX
Film TT &U\RSUHFLSLWDWH GRHVQRWFRQWDLQIDFWRU,;

TT )UHVKIUR]HQSODVPD
XX Bleeding time (BT)
TT Whole blood may be given
XX Prothrombin Normal
time (PT) XX /LIHVW\OHPRGL¿FDWLRQ Avoiding contact sports e.g.
IRRWEDOOKRFNH\EDVNHWEDOOHWF
XX Activated partial XX Prophylactic factor VIII infusion (2-4 times weekly) may
Prolonged
thromboplastin SUHYHQWGHYHORSPHQWRIDUWKURSDWK\LQVHYHUHKDHPRSKLOLDFV
(Normal: 25-36 sec)
time (aPTT)
B. Supportive Treatment of haemarthrosis
XX Factor VIII Reduced in Haemophilia A TT RICE (rest, ice, compression, elevation): The bleeding
joints and muscles can be kept at rest by splinting or by
XX Factor IX Reduced in Haemophilia B
casting
TT Analgesics: Paracetamol or ,EXSURIHQPD\EHVXI¿FLHQW
XX 7KHGLDJQRVLVRIKDHPRSKLOLD$LVFRQ¿UPHGE\ Aspirin and narcotic analgesics should be avoided
GHFUHDVHGIDFWRU9,,,DFWLYLW\ZLWKQRUPDOY:) TT Ice therapy: It relieves pain and reduces bleeding by
activity SURPRWLQJYDVRFRQVWULFWLRQ,WLVDSSOLHGWRWKHVNLQIRUD
XX ,QDPDOHIRHWXVorQHZERUQZLWKDIDPLO\KLVWRU\ SHULRGRIKRXUVZUDSSLQJLFHLQDWKLFNWRZHOQRW
RIKDHPRSKLOLD$FRUGEORRGVDPSOLQJIRUIDFWRU directly
VIII is accurate and important in diagnosis TT Physiotherapy: Should be initiated as soon as active
bleeding stops and pain is diminished. However,
Treatment SURSK\ODFWLFIDFWRU9,,,FRQFHQWUDWHPD\EHUHTXLUHGWR
XX Counsel SDUHQWVDERXWWKHQDWXUDOKLVWRU\RIWKH prevent physiotherapy-induced haemorrhage
disease C. Other haemostatic measures
A. Replacement therapy TT Desmopressin acetate: Used in mild cases. It helps
von willebrand disease

UHOHDVHRIHQGRJHQRXVO\SURGXFHGIDFWRU9,,,
Factor VIII (in Haemophilia A) and Factor IX
'HVPRSUHVVLQLVQRWHIIHFWLYHLQIDFWRU,;GH¿FLHQW
(in +DHPRSKLOLD% FRQFHQWUDWHIROORZLQJWKH haemophilia
standard protocol. TT Tranexamic acid or Aminocaproic acid: These
Dose calculation for haemophilia A & B DQWL¿EULQRO\WLFDJHQWVDUHXVHGORFDOO\LQFDVHRIPRXWK
XX 'RVHRI)9,,, ,8  GHVLUHG ULVHLQ)9,,, î and dental bleeding
%RG\ZHLJKW NJ î Carrier detection&DUULHUVRIKDHPRSKLOLDLVVXVSHFWHGE\
XX 'RVHRI),; ,8  GHVLUHG ULVHLQSODVPD) GHWHUPLQLQJWKHUDWLRRIIDFWRU9,,,DFWLYLW\WRY:)DQWLJHQDQG
,; î%RG\ZHLJKW NJ î GH¿QLWHO\E\PROHFXODUJHQHWLFWHFKQLTXH
 204 Step on to Paediatrics

VON WILLEBRAND DISEASE (VWD) Differential Diagnoses

OHaemophilia A and B O ITP OThrombasthenia
Inheritance:0RVWRIWHQWUDQVPLWWHGDVDQDXWRVRPDO
dominant trait but sometimes autosomal recessive Diagnoses
&KURPRVRPH 7KHGLVHDVHPD\DOVREHDFTXLUHG
developing in association with hypothyroidism, Wilms Investigations
tumor, SLE, patient reeceiving valproic acid. Investigations Results
Sex:&KLOGUHQRIERWKVH[HVDUHHTXDOO\DIIHFWHGXQOLNH TT CBC with PBF Usually normal
WKDWRIKDHPRSKLOLD$DQG%
TT Bleeding time (BT) Prolonged
Pathophysiology TT Prothrombin time (PT) Normal
1RUPDOO\YRQ:LOOHEUDQGIDFWRU Y:) ±
TT Activated partial thromboplastin
Prolonged
time (aPTT)
Functions of vWF

XX 6XSSRUWVFDUULHVDQGGHOLYHUVIDFWRU9,,,WRWKH
VLWHRILQMXU\ TT YRQ:LOOHEUDQGIDFWRU Y:) DVVD\ Reduced
XX +HOSVDGKHVLRQEHWZHHQWKHSODWHOHWVWRIRUP
platelet plugs
&RDJXODWLRQSUR¿OHRI,73
+HOSVDGKHVLRQRISODWHOHWVWRWKHVXE
Haemophilia, vWD
XX

HQGRWKHOLDOFRQQHFWLYHWLVVXHDWWKHVLWHRI
vascular injury Bleeding Prothrombin
Diseases aPTT
time time
%XWLQLWVGH¿FLHQF\WKHVHIXQFWLRQVGRQRWRFFXUDQGDVD
TT ITP Prolonged Normal Normal
result, haemorrhage occurs.
TT Haemophilia Normal Normal Prolonged
Types
XX 7\SH  3DUWLDOTXDQWLWDWLYHGH¿FLHQF\RI TT vWD Prolonged Normal Prolonged
vWF
XX 7\SH4XDOLWDWLYHGH¿FLHQF\RIY:) Treatment
XX 7\SH1HDUO\FRPSOHWHGH¿FLHQF\RIY:) &RXQVHOLQJSDUHQWVDERXWWKHGLVHDVHLW¶VWUHDWPHQWDQG
Clinical Manifestations prognosis.
XX $IIHFWHGFKLOGUHQPD\EHDV\PSWRPDWLF
XX Mild case
XX Symptomatic patient usually have muco-cutaneous
TT Desmopressin Acetate (DDAVP): It helps release
bleeding HJHDV\EUXLVLQJUHFXUUHQWHSLVWD[LVJXP RIY:)IURPHQGRWKHOLDOVWRUDJHVLWHV,QWUDQDVDO
bleeding, menorrhagia, bleeding in postoperative cases DDAVP (Stimate)—J SXII IRUFDVHVNJ
SDUWLFXODUO\DIWHUWRQVLOOHFWRP\RUWRRWKH[WUDFWLRQV DQG—J SXII IRUWKRVH!NJ
TT $QWL¿EULQRO\WLFDJHQWV(SVLORQDPLQRFDSURLFDFLG
XX 0D\KDYHSRVLWLYHIDPLO\KLVWRU\
XX 3DWLHQWVQHLWKHUKDYHSDOORUQRUKHSDWRVSOHQRPHJDO\  XVHIXOIRUPXFRVDOEOHHGLQJ
TT (VWURJHQFRQWDLQJFRQWUDFHSWLYHWKHUDS\IRU
their haemodynamic status are usually stable
menorrhagia
XX Severe Case
TT Plasma-derived vWF is recommended
von willebrand disease

Prognosis
:LWKWKHDYDLODELW\RIHIIHFWLYHWUHDWPHQWDQGSURRK\OD[LV
IRUEOHHGLQJOLIHH[SHFWDQF\LQY:'LVQRUPDO
 Step on to Paediatrics 205

References
 6FRWW-3HWDO+HUHGLWDU\&ORWWLQJ)DFWRU'H¿FLHQFLHV1HOVRQ7H[WERRNRI3HGLDWULFVth Ed. Elsevier; 2016: 2384-2391.
 $PEUXVR'5HWDO%OHHGLQJGLVRUGHUV&XUUHQWGLDJQRVLV 7UHDWPHQWLQ3HGLDWULFVrd ed. McGraw-Hill; 2015: 891-944.
3. Sachdeva A, et al. Hemophilia. Advances in Pediatrics. 1stHG-D\SHH%URWKHUV0HGLFDO3XEOLVKHUVOWGSS
 .KDQ055DKPDQ0((VVHQFHRI3HGLDWULFVth ed. Elsevier; 2011. Chapter 15, Hematology; p. 291-302.

SELF ASSESSMENT
Short answer question [SAQ]
&ODVVLI\KDHPRSKLOLDDFFRUGLQJWRVHYHULW\
:KDW¿QGLQJVGR\RXH[SHFWWRJHWLQFRDJXODWLRQSUR¿OHRIDFKLOGZLWKvon Willebrand disease?
$JLUOKDVEHHQKRVSLWDOL]HGZLWKEOHHGLQJIURPJXPDQGJHQHUDOL]HGSXSXULFUDVK
a) what are the clinical possibilities?
E ZKDWDUHWKHLQYHVWLJDWLRQVUHTXLUHGIRUGLDJQRVLQJWKHFDVH"
F RXWOLQHWKHPDQDJHPHQWRIDFKLOGZLWK,73.

Multiple choice questions [MCQ]

1. %OHHGLQJWLPHLVSURORQJHGLQ±
___ a) haemophilia ___ b) YRQ:LOOHEUDQGGLVHDVH BBBF GHQJXHKDHPRUUKDJLFIHYHU
BBBG +HQRFK6FKRQOHLQSXUSXUD BBBH IXOPLQDQWKHSDWLFIDLOXUH
7KHFOLQLFDOIHDWXUHVRIDFXWH,73LQFOXGHV±
___ a) petechiae ___ b) mild pallor ___ c) lymphadenopathy
___ d) splenomegaly ___ e) bony tenderness.
7KHUHFRPPHQGHGWUHDWPHQWRSWLRQVRIDFXWH,73DUH±
___ a) prednisolone ___ b) cyclophosphamide ___ c) IVlg
BBBG DQWL'LPPXQRJOREXOLQ BBBH SODWHOHWWUDQVIXVLRQ
7KHKDHPDWRORJLFDOSUR¿OHRIKDHPRSKLOLD$LQFOXGHV±
___ a) thrombocytopenia ___ b) prolonged bleeding time ___ c) prolonged aPTT
___ d) prolonged prothrombin time ___ e) normal reticulocyte counts
7KHKDHPDWRORJLFDOSUR¿OHRIYRQ:LOOHEUDQGGLVHDVHLQFOXGH±
___ a) thrombocytopenia ___ b) reticulocytosis ___ c) prolonged bleeding time
___ d) normal prothrombin time ___ e) normal aPTT
6. ''$93LVUHFRPPHQGHGWRWUHDW±
___ a) von Willebrand disease ___ b) haemophilia ___ c) ITP
___ d) Henoch-Schonlein purpura ___ e) thrombasthenia
 $\HDUVROGER\FOLQLFDOO\GLDJQRVHGDVDFDVHRIKDHPRSKLOLDKDV±
___ a) prolonged clotting time ___ b) prolonged PT
___ c) normal bleeding time ___ d) prolonged PTT ___ e) reduced vWF activity
 7KHFRDJXODWLRQIDFWRUVFRQVXPHGLQ',&LQFOXGH±
Self assessment

___ a) Factor II ___ b) Factor VII ___ c) Factor VIII

___ d) Factor V ___ e) Factor IX
 26
Puffy Face and Scanty Urine
Acute post streptococcal Glomerulonephritis - - - - - - - - 206
Nephrotic syndrome - - - - - - - - - - - - 208
Acute kidney injury (AKI) - - - - - - - - - - - - 212
Chronic kidney disease- - - - - - - - - - - - 214

3XI¿QHVVRIIDFHDQGORZXULQHRXWSXWLVWKHXVXDO VWUHSWRFRFFDODQWLJHQV$QWLJHQDQWLERG\FRPSOH[HVDUH
FOLQLFDOSUHVHQWDWLRQRIUHQDOGLVHDVHV7KHWZRPRVW WKXVIRUPHGLQWKHEORRGGHSRVLWHGLQWKHJORPHUXOL
FRPPRQNLGQH\GLVHDVHVDIIHFWLQJFKLOGUHQZLWKWKHVH ZKHUHWKH\LQFLWHJORPHUXODULQÀDPPDWLRQDQGDFWLYDWH
SUHVHQWDWLRQVLQFOXGH± WKHFRPSOHPHQWFDVFDGH$VDUHVXOWRIWKLVLQÀDPPDWLRQ
WKHIROORZLQJFOLQLFRSDWKRORJLFDOHYHQWVRFFXU±
XX Acute glomerulonephritis (AGN)
XX 5HGXFHGUHQDOEORRGÀRZZLWKFRQVHTXHQWORZGFR
XX Nephrotic syndrome (NS)
and oliguria
XX 3DVVDJHRI5%&LQXULQH(haematuria)
,QDGGLWLRQRWKHUOLIHWKUHDWHQLQJNLGQH\GLVHDVHVDUH XX $FFXPXODWLRQRIZDWHUHOHFWURO\WHVWR[LFZDVWH
acute kidney injury ($., DQGFKURQLFNLGQH\GLVHDVH materials and acids in the body, leading to acidosis,
(&.' ,QWKLVVHFWLRQZHZLOOGLVFXVV$*116$., azotaemia and hyperkalaemia
&.' XX Intravascular volume overload systemic giving rise
to systemic hypertension DQGLW¶V
XX Sudden rise may increase cardiac workload and
ensues acute left heart failure and hypertensive
Acute post streptococcal glomerulonephritis

ACUTE POST STREPTOCOCCAL

encephalopathy
GLOMERULONEPHRITIS
(APSGN OR AGN)
Clinical Manifestations
Acute post streptococcal glomerulonephritis (APSGN) is XX $JH%HWZHHQ\HDUV8QFRPPRQEHIRUH\HDUV
WKHPRVWFRPPRQFDXVHRIJURVVKDHPDWXULDLQFKLOGUHQ XX H/o skin orWKURDWLQIHFWLRQV0D\EHSUHVHQWZHHNV
,QDGGLWLRQWRKDHPDWXULDSXII\IDFHVFDQW\XULQHDQG SULRUWRGLVHDVHPDQLIHVWDWLRQV
hypertension are other common presentations. XX 7KHPDQLIHVWDWLRQVDUH
variable and are related
Aetio-pathogenesis WRVHYHULW\RIUHQDO
AGN is an LQYROYHPHQWUDQJLQJIURP
LPPXQHFRPSOH[ asymptomatic microscopic
mediated disease haematuria with normal
that occurs UHQDOIXQFWLRQWRDFXWH
IROORZLQJDQ kidney injury ($., 7KH
Smoky urine
DIIHFWHGFKLOGXVXDOO\
LQIHFWLRQLQ
SUHVHQWVZLWK±
the skin or in
XX 3DVVDJHRI scanty high coloured urine. Sometimes,
throat by certain
may have anuria
nephritogenic
6FDELHVLQIHFWHGZLWKVWUHSWRFRFFL
XX 3XI¿QHVVRIIDFH
strains (e.g. 49-
XX )HYHU8QFRPPRQEXWPD\KDYHORZJUDGHIHYHU
skin, 12-throat)RI
XX 1RQVSHFL¿FV\PSWRPVe.g. malaise, lethargy, headache
group A beta haemolytic streptococci.
206

or vomiting may be present

$IWHULQIHFWLRQDQWLERG\LVSURGXFHGDJDLQVWWKH
 Step on to Paediatrics 207

XX 6RPHWLPHVSDWLHQWVPD\SUHVHQWZLWKIHDWXUHVRI Investigations
FRPSOLFDWLRQVOLNH±
Investigations Results
XX Sudden severe respiratory distress DFXWHOHIW TT RBC
8ULQHIRU
YHQWULFXODUIDLOXUH TT RBC cast FRDJXDODWHGSURWHLQ Mild
R/M/E
XX &RQYXOVLRQ XQFRQVFLRXVQHVV(hypertensive proteinuria
encephalopathy) TT Hb: Mildly reduced
XX &RPSOHWHFHVVDWLRQRIXULQH(DFXWHUHQDOIDLOXUH 
Complete TT 7& '&0LOGSRO\PRUSKRQXFOHDU
blood counts leukocytosis
Physical Examination TT PBF: Normochromic anaemia ESR: High
XX )DFH3XII\i.e.
%ORRGIRUASO/
VZHOOLQJRIH\HOLGV Elevated
anti DNase B
(periorbital) and also
RIIDFH %ORRGIRUC3 Low
XX Pallor : Mild
S. Electrolytes May show hyperkalaemia, acidosis
XX 6NLQ(YLGHQFHRI
LQIHFWHGVFDELHVor S. Creatinine May be elevated
VFDUVRISUHYLRXV $XVHIXODQGVLPSOHGLDJQRVWLFWHVWWKDW
LQIHFWHGVFDELHV Streptozyme
detects antibodies to streptolysin O,
XX Oedema: Present test
DNAse B, hyaluronidase, streptokinase
XX Blood Pressure: May show cardiomegaly with promiment
High Puffy face X-Ray chest SXOPRQDU\YDVFXODWXUHVXJJHVWLQJOHIW
XX )HDWXUHVRIheart KHDUWIDLOXUH
failure (LVF)
TT 6HYHUHUHVSLUDWRU\GLVWUHVVRUWKRSQRHDIHHGLQJ
Treatment
GLI¿FXOWLHVWDFK\SQRHD XX &RXQVHOSDUHQWVDERXWWKHQDWXUHRIWKHGLVHDVHLWV
TT Pulse: Tachycardia
complications, treatment and prognosis
TT Jugular Venous Pressure (JVP): Raised
XX 7UHDWPHQWPDLQO\VXSSRUWLYHDQGLQFOXGHV±
TT Precordium: Hyperdynamic
TT Bed rest

TT $SH[EHDW0D\EHVKLIWHGWRWKHOHIW
TT 'LHW5HVWULFWLRQRI±

TT Gallop rhythm: May be present

³³ Protein to 0.5 gm/kg/day

Acute post streptococcal glomerulonephritis

TT Lung bases: Crepitations on auscultation
³³ Salt: No added salt in the diet

TT Liver: Enlarged and tender

³³ 3RWDVVLXP .  .ULFKIRRGDQGIUXLWV
XX )HDWXUHVRIK\SHUWHQVLYHencephalopathy ³³ Fluid: 400 ml/m 2XWSXWRISUHYLRXVGD\
2

 Headache Nausea, Vomiting


TT Diuretics: Frusemide (1-2 mg/kg/day)

 Blurred vision Restlessness


TT Antibiotics

 Convulsion Alterad sensoriu


³³ 2UDO3KHQR[\PHWK\O3HQLFLOOLQ PJNJGD\ LQ

 Papilloedema GLYLGHGGRVHVIRUGD\V
XX )HDWXUHVRI renal failure
 Oliguria Anuria
 3HQLFLOOLQGRHVQRWDOWHUWKHFRXUVHRIWKHGLVHDVHEXWLWSUHYHQWV
 Vomiting Drowsiness
 VSUHDGLQJRIUHPDLQLQJQHSKULWRJHQLFVWUDLQRIVWUHSWRFRFFXVWR
the contacts.
Other causes of haematuria XX Antihypertensives

XX IgA nephropathy XX Wilms tumour TT )RUUDSLGUHGXFWLRQRI%3±

XX Renal TB XX Coagulopathy ³³ 1LIHGLSLQH PJNJ VXEOLQJXDO

XX Renal calculi XX SLE, HSP, UTI TT )RUPDLQWHQDQFHRIQRUPDO%3

³³ Captopril (0.25-6 mg/kg/day) in 2-4 doses

Diagnosis ³³ 1LIHGLSLQH PJNJGD\ LQGRVHV

XX )ROORZXS'DLO\WRDVVHVVFOLQLFDOUHVSRQVHDQGWRVHDUFKIRU
%DVHGRQW\SLFDO&) VXSSRUWLYHODERUDWRU\
¿QGLQJV any complications
 208 Step on to Paediatrics

Prognosis 2IWKHGLIIHUHQWW\SHVminimal change nephrotic

8VXDOO\JRRGZLWKFRPSOHWHUHFRYHU\LQ!FDVHV syndrome (MCNS) is the most common type among
Recurrences are rare. children and will be discussed in this section

Pathogenesis

'DPDJHRIWKHSRGRF\WHV effacement of foot process)

NEPHROTIC SYNDROME (NS)
XX The commonest kidney problem in children
,QFUHDVHVSHUPHDELOLW\RI*)%
XX ,QFLGHQFHSHUFKLOGUHQ\HDUVRIDJH
XX 3HDNDJHRIRQVHW$URXQG\HDU
ĹĹSDVVDJHRIDOEXPLQDFURVV*)%LQWRWKHXQLQDU\VSDFH
XX 0DVVLYHSURWHLQXULD !JPP2/day)
4 Cardinal
features

XX Hypoalbuminaemia (<2.5 gm/dl) This massive albumin loss in urine (Albuminuria) gives
XX Generalized oedema and rise to hypoalbuminaemiaZLWKIDOORISODVPD&ROORLGDO
XX +\SHUOLSLGDHPLD !PJGO RVPRWLFSUHVVXUH$VDUHVXOWÀXLGVKLIWVIURPSODVPDWR
LQWHUVWLWLDOVSDFHUHVXOWLQJLQ±
To understand the disease it is essential to know the
KLVWRORJLFDOFRPSRQHQWVRIJORPHUXODU¿OWUDWLRQEDUULHU XX Generalized Oedema$FFXPXODWLRQRIÀXLGLQ
*)% ,WFRQVLVWVRI± VHURXVFDYLWLHVJLYLQJULVHWRDVFLWHVSOHXUDO 
SHULFDUGLDOHIIXVLRQ
XX &RQWUDFWLRQRILQWUDYDVFXODUYROXPH
(Haemoconcentration)

The reduced intravascular volume compromises renal

SHUIXVLRQZLWKFRQVHTXHQWORZGFR and oliguria. This
activates renin-angiotensin-aldosterone system and
SURPRWHVUHOHDVHRI$'+UHVXOWLQJLQUHDEVRUSWLRQRI
VRGLXPIURPWXEXOHVDQGZDWHUIURPFROOHFWLQJGXFWVDQG
WKLVIXUWKHUDJJUDYDWHVRHGHPD,QDGGLWLRQ
Hypoalbuminaemia induces lipoprotein synthesis in liver
*ORPHUXODU¿OWUDWLRQEDUULHU *)%
ZKLFKFDXVHVHOHYDWLRQRIcholesterol and triglycerides in
XX Fenestrated capillary XX Podocytes (with blood.
endothelium IRRWSURFHVVHVDQG
intercalated slit
The Essential Characteristics of MCNS±
XX Glomerular basemen†
membrane diaphragm) XX No appreciable glomerular pathology, noted in light
PLFURVFRS\EXWHIIDFHPHQWRIIRRWSURFHVVHVRI
Aetiology & Types of Nephrotic syndrome podocytes in GBM seen under electron microscope
XX Prompt response to steroid but high tendency to
Idiopathic Secondary relapse
Types XX ,QIHFWLRQ+%9+&9HIV, XX Not associated with hypertension, haematuria and
0DODULD6\SKLOLV7R[RSODVPD azotaemia
Nephrotic syndrome

XX Minimal
change disease XX Drugs: Penicillamine, Gold
XX Mesangial NSAIDs, Na Stibogluconate Clinical Manifestations
SUROLIHUDWLRQ XX System illnesses: SLE, Henoch- XX $JH&RPPRQLQEHWZHHQWR\HDUVSHDNa\HDUV
XX Focal Schönlein purpura (HSP) XX 7KHDIIHFWHGFKLOGUHQPD\SUHVHQWDVLQLWLDOFDVHor may
segmental XX Malignancy: Leukaemia, SUHVHQWZLWKKRUHFXUUHQWDWWDFNV UHODSVH ZLWK±
glomerulo- lymphoma TT )DFLDOSXI¿QHVVPDVVLYHSHULRUELWDOVZHOOLQJ

sclerosis XX Allergic reaction: Bee stings TT Generalized oedema

TT Scanty urination (colour usually normal)

 Step on to Paediatrics 209

XX 6RPHWLPHVSDWLHQWVPD\DGGLWLRQDOO\SUHVHQWZLWKIHDWXUHV
RIFRPSOLFDWLRQVOLNH±

XX &RXJK UHVSLUDWRU\ XX Haematuria (NS other

distress (pneumonia, than MCD, UTI, renal
SOHXUDOHIIXVLRQKXJH vein thrombosis)
ascites) XX Diarrhoea (impaired
XX Abdominal pain (gut DEVRUSWLRQRIIRRGVGXH
ischaemia, peritonitis, WRRHGHPDRIWKHERZHO
renal vein thrombosis) wall)
XX 3DLQUHGQHVV  XX 1HXURGH¿FLWOLNH
WHQGHUQHVVRIVNLQ hemiplegia VWURNHIURP
(cellulitis) thrombo-embolism due to Ankle and pedal oedema
XX )HYHU G\VXULD(UTI) haemoconcentration)
II. Signs related to diminished circulatory volume
Physical Examination XX Pulse: Weak, low volume
I. Signs secondary to hypoalbuminaemia XX %RG\H[WUHPLWLHV0D\EHFROG
XX 6ZHOOLQJRIH\H
XX BP: Usually low
OLGVH[WHQGLQJ XX &DSLOODU\UH¿OOWLPH3URORQJHG !VHFRQGV
to chin and neck
(double chin) III. Signs related to complications
XX 6KLQ\DEGRPLQDOZDOOULJLGLW\ WHQGHUQHVV
XX Huge ascites and absent bowel sounds SHULWRQLWLVIURP6WUSW
with or without pneumoniae)
parietal oedema XX 3DOSDEOHNLGQH\ KDHPDWXULD(renal vein
thrombosis)
XX Oedema and
VZHOOLQJRI
XX $OWHUDWLRQVRIFRQVFLRXVQHVVKHPLSOHJLD stroke)
VFURWXP SHQLV 3XII\IDFH3HULRUELWDOVZHOOLQJDQGGRXEOHFKLQ
IV. Signs related to steroid toxicity
ZLWKFUDFNV 
¿VVXULQJRIVNLQ XX &XVKLQJRLGIDFLHV XX Cataract
ZLWKH[XGDWLRQ XX %XIIDORKXPS XX Muscular weakness
XX &OLQLFDOIHDWXUHV XX Abdominal striae (due to steroid
RISOHXUDO XX Hirsutism LQGXFHGSUR[LPDO
HIIXVLRQDQG XX Hypertension myopathy)
increased
respiratory rate

XX 2HGHPDRI
DQNOHV EDFN
e.g. sacral area
+XJHDVFLWHVZLWKWUDQVYHUVHO\VOLWXPELOLFXV
XX Oedematous
Nephrotic syndrome

chest wall with

IXOOLQWHUFRVWDO
spaces and

XX 2HGHPDRIVFDOS

Cushingoid face from prolonged steroid use

Peno-scrotal swelling
 210 Step on to Paediatrics

Diagnosis Indications for Renal Biopsy

%DVHGRQW\SLFDO&) VXSSRUWLYHODERUDWRU\HYLGHQFHV
At Onset
Investigations XX $JHRIRQVHWRI16\HDURU!\HDUV
XX Urine XX Gross haematuria, persistent microscopic haematuria
TT 5RXWLQH  or low serum C3
Microscopic XX Sustained hypertension
H[DPLQDWLRQ XX 5HQDOIDLOXUHQRWDWWULEXWDEOHWRK\SRYRODHPLD
³³ Albuminuria (done
XX 6XVSHFWHGVHFRQGDU\FDXVHVRIQHSKURWLFV\QGURPH
E\$OEXVWL[or Heat
After Initial Treatment
coagulation test)
³³ Granular and
XX 3URWHLQXULDSHUVLVWLQJGHVSLWHZHHNVRIGDLO\
hyaline casts corticosteroid therapy
³³ Pus cells, when
XX %HIRUHVWDUWLQJWUHDWPHQWZLWK&\FORVSRULQ$RU
associated with UTI Tacrolimus
³³ RBC and RBC cast

usually absent in Positive heat

Treatment
$OEXVWL[
MCNS coagulation test &RXQVHOSDUHQWVDERXWWKHQDWXUHRIWKHGLVHDVHLWV
treatment and prognosis.
TT 24 hours urinary total protein (UTP): Proteinuria
H[FHHGLQJ!JPGD\
$6SHFL¿F3UHGQLVRORQH
or
TT Spot urinary SURWHLQFUHDWLQLQHUDWLR,I!VXJJHVWV I. First attack
VLJQL¿FDQWSURWHLQXULDLQGLFDWLQJ16 Prednisolone 60 mg/m2/day in a single morning
GRVHIRUZHHNV IROORZHGE\PJP2 as single
Urine protein (mg)
PRUQLQJGRVH RQDOWHUQDWHGD\IRUDQRWKHUZHHNV
Urine creatinine (mg) The alternate day dose then slowly tapered and
XX Blood: Biochemistry GLVFRQWLQXHGRYHUWKHQH[WZHHNV
TT Serum total protein: Reduced
II. Relapse cases
TT Serum albumin: Reduced
(When urine DOEXPLQLVRURUSURWHLQXULD!
TT Serum albumin globulin ratio: Altered
mg/m2KRXUIRUFRQVHFXWLYHGD\VLQSDWLHQWVZKR
TT Serum cholesterol: Elevated
had been in remission previously).
TT Serum C : Normal in MCNS, but when decreased
3
LQGLFDWHV16RIRWKHUW\SHV Prednisolone 60 mg/m2/day in a single morning dose till
TT Serum urea/creatinine/BUN: Usually normal
XULQHLVIUHHRIDOEXPLQIRUFRQVHFXWLYHGD\VIROORZHG
TT Serum electrolytes: Usually normal
by 40 mg/m2DVVLQJOHPRUQLQJGRVHRQDOWHUQDWHGD\IRU
XX CBC another 4 weeks and gradually tapered over 4-8 weeks.
TT 7&'&RI:%&8VXDOO\QRUPDO
B. Supportive
TT Haematocrit and ESR: Increased

TT 3HULSKHUDOEORRG¿OP1RUPDO
TT Diet
³³ 1RUPDOIDPLO\GLHWDGHTXDWHLQSURWHLQ J
XX 2WKHULQYHVWLJDWLRQVWRDVVHVVDHWLRORJ\WKHH[WHQWRI
NJGD\ ”RIFDORULHIURPIDW
WKHGLVHDVHFRPSOLFDWLRQ WRFRQ¿UPWKHGLDJQRVLV
Nephrotic syndrome

³³ Salt restriction: a µQRDGGHGVDOW¶VDOWIUHH diet is

TT %ORRGIRUHBsAg, Anti HCV
XVXDOO\VXI¿FLHQW
TT 8ULQHIRU&6:KHQ87,LVVXVSHFWHG
³³ 3DWLHQWFDQWDNHULFHYHJHWDEOHVPHDW¿VKHJJ
TT ;5D\&KHVW7RORRNIRUSOHXUDOHIIXVLRQ
without yolk, dal, milk, sugar etc.
pneumonia TT Fluid
TT 8OWUDVRQRJUDPRIFKHVWDEGRPHQ7RVHHSOHXUDO
³³ /LEHUDOÀXLGLQWDNHLQPLOGRHGHPD
HIIXVLRQDVFLWHVDQGWRDVVHVVWKHNLGQH\PRUSKRORJ\
³³ Severe oedema: Restricted to 400 ml/m22XWSXW
TT Renal biopsy: To determine the histological type
RIWKHSUHYLRXVGD\
 Step on to Paediatrics 211

TT 0DQDJHPHQWRIRHGHPD III. Frequent relapses **

³³ Diuretics should be avoided in mild oedema TT Two or more relapses in initial 6 months or
³³ ,QFDVHRIVHYHUHDQGSHUVLVWHQWRHGHPD
TT !UHODSVHVLQDQ\PRQWKV
Oral Frusemide (1-2 mg/kg/day)
O

IV. Infrequent relapse **

Oral Spironolactone (3 mg/kg/day)
O

³³ Hypovolaemic patients should receive normal

TT 2QHUHODSVHZLWKLQPRQWKVRIWKHLQLWLDOUHVSRQVH
saline bolus and/or DOEXPLQLQIXVLRQSULRUWR UHODSVHLQPRQWKVIRULQLWLDODWWDFN or
diuretic administration TT One to 3 relapses within any 12 months period
TT Antibiotics: Oral Penicillin, 50 mg/kg/day till (<4 relapse in one year)
PDVVLYHRHGHPDSHUVLVW XVXDOO\IRUGD\V  V. Steroid dependent *
,ISDWLHQWLVIHEULOHor systemically unwell or TT Two consecutive relapses when on alternate day
VKRZLQJHYLGHQFHRILQIHFWLRQSDUHQWHUDODQWLELRWLFV steroids orZLWKLQZHHNVRIGLVFRQWLQXDWLRQRI
like, Ampicillin with Gentamycin (renal dose) or steroid
&HIWULD[RQHPD\EHVWDUWHG
VI. Steroid resistance *
TT 6XSSRUWWRVFURWXPLILWLVWHQVHDQGVXVFHSWLEOHWR
ulceration
TT )DLOXUHWRDFKLHYHUHPLVVLRQDIWHUZHHNRIVWHURLG
therapy
TT Prescribe other medication e.g.
³³ Antacid or5DQLWLGLQHLIXSSHU*,GLVFRPIRUW

³³ 6XSSOHPHQW&DOFLXPLIWKHFKLOGJHWWLQJVWHURLG Difference between AGN and MCNS

IRU!PRQWKV Characteristics AGN MCNS
C. Follow up TT $JHRIRQVHW 5-12 years 2-8 years
TT ,Q+RVSLWDO.HHSUHFRUGVRIYLWDOVLJQV e.g. pulse,
BP, resp. rate, weight, oedema, abdominal girth, TT H/O sore throat
More pertinent May present
LQWDNHRXWSXWEHGVLGHXULQHIRUalbumin, etc. orVNLQLQIHFWLRQ
TT $IWHUGLVFKDUJHZHHNO\IROORZXSWRFKHFN± TT ([WHQWRI 8VXDOO\FRQ¿QHG
Generalized
³³ Albuminuria, to assess response to drugs swelling WRIDFH
³³ &XVKLQJRLGIHDWXUHVWRDVVHVVGUXJWR[LFLWLHV
TT Ascites Unlikely Usually present
³³ Any complications HJLQIHFWLRQ

³³ 5HQDOIXQFWLRQDOVWDWXV
TT Urine Colour High/Reddish Normal
TT Hypertension Present Usually absent
Prognosis TT Proteinuria Mild Massive
Usually good. But children <1 year or!\HDUVZKR
RBC, RBC cast:
have haematuria or hypertension, prognosis is guarded. RBC, RBC Absent
TT Urine R/M/E
cast: Present Hyaline, granular
Spectrum of nephrotic syndrome cast: Present
I. Remission
TT S Albumin Normal Decreased
TT 8ULQH3URWHLQ&UHDWLQLQHUDWLRRIor
TT SURWHLQRQXULQHGLSVWLFNWHVWIRUFRQVHFXWLYH TT S Cholesterol Normal Increased
days TT Serum C3 Decreased Normal
II. Relapse*
Nephrotic syndrome

TT 5HODSVH 
TT 8ULQH3URWHLQ&UHDWLQLQHUDWLRRI!or Rare Common
Remission
TT 3SURWHLQRQXULQHGLSVWLFNWHVWIRUFRQVHFXWLYH
days
 212 Step on to Paediatrics

ACUTE KIDNEY INJURY (AKI) AKI Gradings

,QFKLOGUHQH[WHQWRI$.,DUHJUDGHGDFFRUGLQJWR±
$.,GHQRWHVVXGGHQLQDELOLW\RINLGQH\VWRH[FUHWH
XULQHRIVXI¿FLHQWTXDQWLW\or composition, to maintain L ([WHQWRIIDOORIGFR as measured by estimated
ERG\ÀXLGKRPHRVWDVLV creatinine clearance (eccl) and
LL 8ULQHRXWSXWDVEHORZ±
Aetiology
Urine output
Stages Creatinine criteria
I. Pre renal (UO) criteria
Ischaemia Increased creatinine 
XX
82”PONJ
I: Risk WLPHVRIQRUPDO or
TT Hypovolaemia e.g. acute diarrhoea with severe KUîKUV
*)5GHFUHDVHV!
dehydration, vomiting, acute haemorrhage
Increased creatinine
TT Hypotension 82”PONJ
II: Injury WLPHVRIQRUPDO or
TT Sepsis KUîKUV
*)5GHFUHDVHV!
TT ,QJHVWLRQRIQHSKURWR[LFGUXJe.g. diethyl
Increased creatinine
glycol in paracetamol 82”PONJ
WLPHVRIQRUPDO or
KUîKUV
XX 7R[LQVHJZDVSVWLQJVQDNHELWHSODQWWR[LQHWF III: Failure *)5GHFUHDVHV!
or
or
DQXULDîKUV
*)5P/PLQP 2
II. Renal
XX Glomerulonephritis (GN) e.g. PSGN, SLE, HSP IV: Loss 3HUVLVWHQWIDLOXUHIRU!ZHHNV
XX Vascular e.g. HUS, renal vein thrombosis, renal V: Endstage 3HUVLVWHQWIDLOXUHIRU!PRQWKV
arterial thrombosis
XX Acute pyelonephritis How to calculate eccl? By Schwartz formula
XX Acute interstitial nephritis NîKHLJKW FP
HFFO  -----------------------------
S. creatinine (mg/dl)
III. Post renal (Obstructive uropathy)
XX Structural • Post. urethral valve • PUJ obstruction N  IRUFKLOGUHQ
XX Crystalluria Clinical Manifestations
XX Calculi, blood clot in urinay tract XX Scanty urine (oliguria) orFRPSOHWHFHVVDWLRQRIXULQH
DQXULD WKHKDOOPDUNRI$.,
XX 2WKHUPDQLIHVWDWLRQVe.g. vomiting, convulsions
Pathogensis
%HFDXVHRILQVDXOWIURPWKHDERYHPHQWLRQHGFDXVHV Assessment
WKHUHLVUDSLGGHFFOLQHLQ*)5DQGZKLFKUHVXOWVLQ± History
TT $FFXPXODWLRQRIQLWURJHQRXVZDVWHVLQWKHERG\ TT H/o anuria/oliguria, vomiting
and TT +LVWRU\WR¿QGRXWWKHFDXVHVEHKLQG$.,±
TT ,PSDLUPHQWRIZDWHUHOHFWURO\WHVDQGDFLGEDVH ³³ Fluid loss e.g. diarrhoea, severe vomiting

balances ³³ 3UHH[LVWLQJNLGQH\GLVHDVHe.g. AGN, NS

7KHQHWFOLQLFRELRFKHPLFDOPDQLIHVWDWLRQVDUH± ³³ ,QJHVWLRQRIQHSKURWR[LFGUXJe.g. diethyl glycol in

paracetamol
XX Oliguria, anuria Physical Examination
5HWHQWLRQRIQLWURJHQRXVZDVWHSURGXFWVLQ
Acute kidney injury

XX
TT )HDWXUHVRIÀXLGRYHUORDG±
WKHERG\DVHYLGHQWLQHOHYDWLRQRIEORRGXUHD ³³ )DFLDOSXI¿QHVVRHGHPDK\SHUWHQVLRQ
creatinine, blood urea nitrogen (BUN) ³³ +HDUWIDLOXUH(hepatomegaly, pulmonary oedema)
XX Dyselectrolyteaemia e.g. hyperkalaemia TT )HDWXUHVRIVHYHUHGHK\GUDWLRQe. g. drowsiness, skin
XX Acid-base imbalance e.g. metabolic acidosis
SLQFKQRWJRLQJEDFNTXLFNO\XULQHRXWSXW
XX Fluid overload, hypertension TT Haemodynamic status HJSXOVH%3FDSLOODU\UH¿OWLPH
­­­­ TT )HDWXUHVRI$.,e.g. unconsciousness, arrhythmia,
vomiting, convulsion etc.
 Step on to Paediatrics 213

Investigations Indications of Peritoneal Dialysis (PD)

XX Complete blood counts with PBF
XX Blood biochemistry XX Volume overload with hypertension and/or pulmonary
TT S electrolytes: hyperkalaemia, acidosis RHGHPDUHIUDFWRU\WRGLXUHWLFWKHUDS\
TT S creatinine, urea, BUN: Raised XX Severe metabolic acidosis unresponsive to medical
TT Arterial blood gas: Metabolic acidosis management
XX Urine R/M/E: RBC, pus cells, crystal, cast
XX Persistent hyperkalaemia
XX (&*7RQRWHDQ\FKDQJHIURPG\VHOHFWURO\WDHPLD
XX 6\PSWRPVRIXUDHPLDe.g CNS depression
XX 7R¿QGRXWFDXVHASO titre,C3,C4, ANA, Anti-ds
XX %81RI!PJGO
DNA XX Calcium/phosphorus imbalance with hypocalcaemic
XX Others tetany
TT &KHVW;5D\7RVHHSXOPRQDU\RHGHPD FDUGLDF
enlargement 5. Nutrition
TT USG abdomen: To assess renal anatomy TT Encourage high calorie diet, rich in carbohydrate and
XX Renal biopsy IDWWRUHGXFHSURWHLQFDWDEROLVP
TT Restrict protein intake
³³ 0-6 mo: 1.8 g/kg/day   
Treatment
³³ 6 mo-3yrs: 1.0-1.5 g/kg/day   
XX 6WDJH, ,,2QO\VXSSRUWLYHWUHDWPHQW
³³ &KLOGUHQ DGROHVFHQWVJNJGD\   
XX 6WDJH,,,(QVXUHWKHIROORZLQJWUHDWPHQW±
³³ 3URWHLQLQWDNHVKRXOGEHPRUHLISHULWRQHDOor

A. General haemodialysis is going on

TT Counseling parents about the nature, treatment TT 5HVWULFWH[WUDVDOWLQWDNHLQWDNH
RSWLRQVDQGSURJQRVLVRIWKHGLVHDVH TT $YRLGIRRGVULFKLQSRWDVVLXPHJFLWUXVIUXLWVWRPDWR
TT 8UJHQWUHIHUUDOWRDSDHGLDWULFQHSKURORJLVWWHUWLDU\ paste, chocolates and potato crisps
centre
6. Management of associated conditions
B. Supportive TT Hyperkalaemia: Management is discussed in chapter
TT Discontinue nephrotoxic agentsLIDQ\
39: p 323
TT Fluid resuscitation TT Metabolic acidosis: Sodibicarb (1ml/kg), IV
³³ ,IWKHFKLOGLVGHK\GUDWHGJLYHEROXVQRUPDO
TT Hypocalcaemia: Calcium gluconate (1-2 ml/kg), IV
VDOLQH#PONJRYHUPLQ$IWHUYROXPH
resuscitation, hypovolaemic patients generally
TT Hyponatraemia, most commonly dilutional
³³ 5HVWULFWÀXLGLQWDNH
void within 2 hours
³³ Symptomatic hyponatraemia e.g. seizures, lethargy

3. Diuretic therapy and S NaLIP(T/VKRXOGEHFRUUHFWHGDV

TT $IWHUHVWDEOLVKLQJDGHTXDWHFLUFXODWRU\YROXPHLI mentioned in chapter 39: p 321
no voiding. Give Frusemide IV, 1-5 mg/kg/dose
TT Hypertension
³³ $V\PSWRPDWLFFDVHV1LIHGLSLQHPJNJ32
TT ,IQRUHVSRQVHVHHQZLWKLQDQKRXURIPD[LPXP
³³ Symptomatic hypertension e.g. hypertensive
GRVHRI)UXVHPLGHRULIWKHXULQHRXWSXWUHPDLQV
ORZ PONJKRXU WKHQ± encephalopathy1D1LWURSUXVVLGH ȝJNJ
³³ 6WRSIXUWKHUDGPLQLVWUDWLRQRIGLXUHWLFV min) or/DEHWDORO PJNJKRXU E\LQIXVLRQ
³³ 5HVWULFWÀXLGWRLQVHQVLEOHORVVHV POP
XQGHUVXSHUYLVLRQRISHGFDUGLRORJLVW
KRXUV SOXVXULQHRXWSXWRIWKHSUHYLRXVGD\
TT Seizures: 'LD]HSDP PJNJ35 PRVWHIIHFWLYH
Acute kidney injury

³³ 0RQLWRUÀXLGLQWDNHXULQHDQGVWRRORXWSXW
TT Anaemia
³³ ,I+EJGOWUDQVIXVLRQRISDFNHGUHGEORRGFHOOV
body weight, and s electrolytes, creatinine,
BUN daily PONJ YHU\VORZO\RYHU±KRXUV
4. Peritoneal dialysis (PD): Start as soon as possible
7. Treatment of underlying cause of AKI: If any.
 214 Step on to Paediatrics

CHRONIC KIDNEY DISEASE (CKD) Investigations

&.'LVWKHJUDGXDOORVVRINLGQH\IXQFWLRQRYHUD Parameters Results
SHULRGRIWLPH,QFKLOGUHQLWFRPPRQO\UHVXOWVIURP Normocytic normochromic
XX CBC, PBF
GHYHORSPHQWDOPDOIRUPDWLRQV,WLVGH¿QHGDVUHQDO anaemia
injury/proteinuria and/or GFR <POPLQP2 XX Blood urea nitrogen (BUN)
IRUPRUHWKDQPRQWKV Raised
XX S Creatinine, Urea
Aetiology Hyperkalaemia,
XX S Electrolytes
Hyponatraemia
XX Idiopathic Hypocalcaemia,
&RQJHQLWDOPDOIRUPDWLRQVe.g. XX S Ca, PO4---, Alkaline
Hyperphosphatemia, Raised
XX

TT Hypoplastic or dysplastic kidneys phosphatase, Parathormone

$/3 37+
TT Polycystic kidney disease
XX )DVWLQJ/LSLGSUR¿OH Hyperlipidaemia
XX Chronic glomerulonephritis
XX ,UUHYHUVLEOHQHSKURWR[LFLQMXU\ XX ,URQSUR¿OH ,URQGH¿FLHQF\
XX Obstructive uropathy e.g. XX Urine R/M/E Proteinuria
TT 3RVWHULRUXUHWKUDOYDOYH 389

TT 38-REVWUXFWLRQ
Bilateral shrunken echogenic
XX 86*.8%
TT %ODGGHUQHFNREVWUXFWLRQ
kidneys /Hydronephrosis
TT 9HVLFRXUHWHULFUHÀX[ 985 Renal scarring/impaired
XX DTPA/DMSA scan
UHQDOH[FUHWLRQ
To evaluate PUV (posterior
XX MCU/VCUG
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Pathological Events To evaluate VUR, urinary
XX IVU
WUDFW VWDWXVRINLGQH\V
XX 'DPDJHORVVRIQHSKURQV GLVUXSWLRQRI XX Creatinine clearance to
FRQFHQWUDWLQJDELOLW\RIQHSKURQpolyuria, Reduced
assess GFR
polydipsia
0&8±0LFWXUDWLQJ&\VWRXUHWKURJUDP
XX $FFXPXODWLRQRIQLWURJHQRXVZDVWHSURGXFWV
9&8*±9RLGLQJ&\VWRXUHWKURJUDP
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,98±,QWUDYHQRXV8URJUDSK\
XX )OXLG (OHFWURO\WHLPEDODQFH
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TT 9ROXPHRYHUORDG 1DUHWHQWLRQ H[FHVV
'06$±'LPHUFDSWRVXFFLQLF$FLGVFDQ
Renin production) - hypertension
TT $FFXPXODWLRQRI.: Hyperkalaemia Posterior urethral
XX 5HGXFHGSURGXFWLRQRIHU\WKURSRLHWLQ anaemia valve in a 7-year-old
XX 'HFUHDVHGDFWLYHIRUPRIYLWDPLQ' PDOHFKLOG$QREOLTXH
renal osteodystrophy, hypocalcaemia, 9&8*LPDJHVKRZV
hyperphosphataemia a dilated posterior
XX *URZWKUHWDUGDWLRQ )77: Renal XUHWKUD DUURZ ZLWK
RVWHRG\VWURSK\ DQDHPLD DQDEUXSWWUDQVLWLRQ
Chronic kidney disease

WRDQRUPDOFDOLEUH
XX 3ODWHOHWG\VIXQFWLRQDQGRWKHUFRDJXORSDWK\
anterior urethra.
leading to bleeding especially in GIT
1RWHWKHEODGGHU
XX Seizures: Untreated hypertension or
neck hypertrophy, the
hypocalcaemia
LUUHJXODUWUDEHFXODWHG
XX Hypertension, uraemia: CCF, pulmonary EODGGHUZDOODQGWKH
oedema and pulmonary hypertension left-sided grade III
YHVLFRXUHWHULFUHÀX[
FXUYHGDUURZ
 Step on to Paediatrics 215

Management TT Correct Anaemia

³³ Human recombinant erythropoietin (50-150 U/kg/

A. Supportive dose), 3 times a week, subcutaneously

TT &RXQVHOSDUHQWVDERXWWKHQDWXUHDQGIXWXUHRIWKH ³³ Iron supplementation (2-6 mg/kg/day)

GLVHDVHWUHDWPHQWRSWLRQVDQGSURJQRVLV5HIHUWKH ³³ 3DFNHG5HGFHOO WUDQVIXVLRQ PONJ ZKHQ+E

child to a paediatric nephrologist/tertiary centre < 6gm/dl

TT Diet TT Immunize the child with all routine vaccines along
³³ 5HVWULFW3URWHLQWRJNJGD\IURP
with
animal source to reduce muscle wasting ³³ MMR

³³ 'RQ¶WDOORZDQ\DGGHGVDOWor DQ\.ULFKIRRGV
³³ Pneumococcal conjugate vaccine

HJFLWUXVIUXLWVWRPDWRSDVWHFKRFRODWHVDQG ³³ Meningococcal conjugate vaccine

potato chips, banana etc in the diet ³³ ,QflXHQ]DYDFFLQHDQQXDOO\
TT Supplement Calcium TT 7UHDWDVVRFLDWHGLQIHFWLRQVZLWKQRQQHSKURWR[LF
³³ Age 1-10 years: 500-600 mg/day
antibiotics
³³ Age 11-18 years: 800-1000 mg/day

TT Control hypertension % 6SHFL¿FRenal Transplantation

³³ )UXVHPLGH PJNJGD\ ,I%3LVQRWFRQWUROOHG

³³ ACE inhibitor e.g. Captopril (0.25-6 mg/kg/day)

in 2-4 divided doses,orally End Stage Renal Disease

TT Treat Renal osteodystrophy When GFR <POPLQP2DQGSURJUHVVLRQRI
³³ Rocaltrol, Calcitriol: 1, 25 (OH) FKROHFDOFLIHURO
2 disease can no longer be managed by medical means then
VXSSOHPHQWDWLRQ±
WUHDWPHQWRSWLRQVLQFOXGH±
—JNJGD\32\HDUVRIDJH
O

—JGD\32!\HDUVRIDJH
O
XX Peritoneal dialysis, or
³³ &DOFLXPFDUERQDWH JUDPJLYHVPJRI
XX +DHPRGLDO\VLV SUHIHUDEOH or
HOHPHQWDO&D WRIDFLOLWDWHSKRVSKDWHH[FUHWLRQ XX Renal transplantation
TT Correct Hyperkalaemia:$VPHQWLRQHGLQFKDSWHU
TT Correct Metabolic acidosis
³³ ,QM6RGLELFDUE P(TNJ +DOIVKRXOGEH

JLYHQLPPHGLDWHO\DQGWKHUHPDLQLQJKDOILQ,9
LQIXVLRQRYHUQH[WKRXUV

References
Chronic kidney disease

 0HOLVVD$HWDO.LGQH\ 8ULQDU\WUDFW&XUUHQW3HGLDWULF'LDJQRVLV 7UHDWPHQWrdHG3

 3DQ&*HWDO$FXWH3RVWVWUHSWRFRFFDO*ORPHUXORQHSKULWLV1HOVRQ7H[WERRNRI3HGLDWULFVth Edition. 2016: 2498-2500.
 3DLV3HWDO1HSKURWLF6\QGURPH1HOVRQ7H[WERRNRI3HGLDWULFVthHG(OVHYLHU
 $EH\DJXQDZDUGHQD$67UHDWPHQWRIVWHURLGVHQVLWLYHQHSKURWLFV\QGURPH,QGLDQ-RXUQDORI3HGLDWULFV
 %DJJD$HWDO5HYLVHGJXLGHOLQHVIRUPDQDJHPHQWRIVWHURLGVHQVLWLYHQHSKURWLFV\QGURPH,-1  
6. Nephrotic syndrome. In: Srivastava RN, Arvind Bagga. Pediatric nephrology. 5th ed. ; 2011
 'LO\V$HWDO&KURQLF.LGQH\'LVHDVHLQ&KLOGUHQ3HGLDWULFVLQ5HYLHZ
8. Liborio AB et al. $.,LQQHRQDWHVIURPXULQHRXWSXWWRQHZELRPDUNHUV%LRPHG5HVHDUFK,QW$ULFOH,'
 216 Step on to Paediatrics

SELF ASSESSMENT
Short answer question [SAQ]
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:KDWLQYHVWLJDWLRQVZLOO\RXGRDQGZKDWDUHWKHH[SHFWHG¿QGLQJVLQDFDVHRIQHSKURWLFV\QGURPH"
3. How will you treat a child with 1stDWWDFNRIPLQLPDOFKDQJHQHSKURWLFV\QGURPH"
$\HDUVROGER\SUHVHQWVZLWKSXII\IDFHDQGVPRN\XULQHIRUGD\V+LV%3LVPP+J
a) What is the probable diagnosis?
E :KDWFRPSOLFDWLRQVFDQGHYHORSLIWKHFKLOGUHPDLQVXQWUHDWHG"
F :KDWLQYHVWLJDWLRQVZLOO\RXSODQDQGZKDW¿QGLQJVDUHH[SHFWHG"
d) How will you treat the child?

Multiple choice questions [MCQ]

7KHFKDUDFWHULVWLFIHDWXUHVRI0&16DUH±
___ a) heavy proteinuria ___ b) haematuria ___ c) azot emia
___ d) hypertension ___ e) hyperlipidaemia
%ORRGELRFKHPLVWU\RI0&16LQFOXGHV±
___ a) low C3 level ___ b) high BUN ___ c) hyperkalaemia
___ d) hypoalbuminaemia ___ e) hypercholesterolaemia
&RPSOLFDWLRQVWKDWPD\RFFXULQXQWUHDWHG$*1DUH±
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___ d) thrombo-embolism ___ e) gut ischaemia
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EDFNDQGLPSURYHGZLWKSUHGQLVRORQH+LV%3LVPP+J%HGVLGHXULQHVKRZVDOEXPLQ&KRRVHWKHFRPPRQHVW
SDWKRORJLFDOW\SHRIWKLVSUREOHPLV±
___ a) MCNS ___ b) FSGS ___ c) membranous GN
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___ d) generalized oedema ___ e) haematuria
 7KHGLDJQRVWLFFULWHULDRIQHSKULWLFV\QGURPHLQFOXGH±
___ a) generalized edema ___ b) hypertension ___ c) hypercholesterolaemia
___ d) haematuria ___ e) hypoalbuminaemia
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 &DXVHVRIKDHPDWXULDLQFOXGH±
Chronic kidney disease

___ a) AGN ___ b) UTI ___ c) &.'

___ d) Renal TB ___ e) CLD
 )HDWXUHVRIK\SHUWHQVLYHHQFHSKDORSDWK\±
___ a) Headache ___ b) Vomiting ___ c) Slurred speech
___ d) Convulsion ___ e) Unconsciousness
 27
Smoky/Red urine
Renal Tuberculosis - - - - - - - - - - - - - 217
IgA Nephropathy - - - - - - - - - - - - - 218
Alport Syndrome - - - - - - - - - - - - - 218
Polycystic kidney disease- - - - - - - - - - - - 218

Whenever a child presents with red or smoky urine, one XX Others e.g. Henoch Schonlen purpura, SLE, renal vein
should consider it as haematuria, i.e.SUHVHQFHRIEORRGLQ WKURPERVLV$OSRUWVV\QGURPHKHDY\H[HUFLVH
WKHXULQHHLWKHUIURPNLGQH\RUIURPDQ\SDUWVRIXULQDU\ One thing should be mentioned here, that smoky urine
WUDFW FRPLQJIURPUHQDOSHOYLVWRXUHWKUD ,QVXFK FDQDOVRRFFXUGXHWRSUHVHQFHRIKDHPRJORELQLQXULQH
VLWXDWLRQWKHIROORZLQJFRQGLWLRQVVKRXOGEHFRQVLGHUHG IURPH[FHVVLYHLQWUDYDVFXODUKDHPRO\VLVDVRFFXULQ
XX Glomerulonephritis (GN) e.g. acute post-strptococcal, DXWRLPPXQHKDHPRO\WLFDQDHPLDIDOFLSDUXPPDODULD
PHPEUDQRXVPHPEUDQRSUROLIHUDWLYH WUDQVIXVLRQUHDFWLRQHWF
XX 8ULQDU\WUDFWLQIHFWLRQ   Renal TB
Sometimes, children can pass red urine without RBC as
XX Severe thrombocytopenia  Coagulopathy
RFFXUVLQLQJHVWLRQRIIHZGUXJVG\HVLQIRRGVHWFZKLFK
XX :LOP¶VWXPRU   IgA nephropathy
PD\FUHDWHFRQIXVLRQZLWKKDHPDWXULD
XX Polycystic kidney disease  Renal stones

Traits Upper urinary tract Lower urinary tract

XX Origin XX Pelvi-caliceal system, ureter,
TT Nephron (glomerulus, tubules, interstitium)
XX &RORXURIXULQH bladder, urethra
TT Brown, cola or tea colored
XX Haematuria in relation XX Bright red or pink colour
TT 7KURXJKRXWWKHZKROHSKDVHRIPLFWXULWLRQ
WRWLPHRIPLFWXULWLRQ XX $WWKHHQGRIPLFWXULWLRQ
TT Usually painless
XX Pain XX Associated with dysuria
TT Absent
XX Clot in the urine XX May be present
TT Dysmorphic
XX RBC morphology XX Normal
TT !PJGO
XX Proteinuria XX Minimal proteinuria (<100mg/dl)
TT RBC case, leukocyte or tubular cast may be present
XX Cellular cast XX Cellular cast absent

Types
XX Gross haematuria: Urine looks as smoky, pink or RENAL TUBERCULOSIS
tea-coloured in naked eye
Renal tuberculosis
XX Microscopic haematuria: Urine looks normal in naked 5DUHLQFKLOGUHQEHFDXVHRIORQJLQFXEDWLRQSHULRG
eyes, but RBC seen under microscope
TT ,QXQFHQWULIXVHGXULQH5%&!—/25
Transmission: Lymphohaematogenous
TT ,QFHQWULIXVHGXULQH5%&!KLJKSRZHU¿HOG
Pathogenesis
$IWHUUHDFKLQJNLGQH\WKHEDFLOOLIRUPVPDOOFDVHDWLQJIRFL
We have already discussed acute post-streptococcal
LQWKHUHQDOSDUHQFK\PDIURPZKLFKEDFLOOLDUHUHOHDVHGLQ
*187,WKURPERF\WRSHQLDFRDJXORSDWK\IDOFLSDUXP
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UHQDOSHOYLVWKURXJKD¿VWXODDQGPD\VSUHDGWRDGMDFHQW
217

$OSRUW¶VV\QGURPHDQGSRO\F\VWLFNLGQH\GLVHDVH
structures like ureter, prostate, epididymis etc.
 218 Step on to Paediatrics

Clinical Manifestations Treatment

XX Asymptomatic 6\PSWRPDWLFHJFRQWURORIK\SHUWHQVLRQDQGSURWHLQXULD
XX +DHPDWXULD6RPHWLPHVG\VXULDÀDQNSDLQDEGRPLQDO with ACE inhibitors
pain
Prognosis
Investigations
5LVNRISURJUHVVLYHUHQDOG\VIXQFWLRQOHDGLQJWR(65'
XX 8ULQH50(RIPRUQLQJVDPSOH6WHULOHS\XULD HDUO\
stage), RBC
XX 8ULQHVHGLPHQWIRU$)%VWDLQ5HYHDOVWKHEDFLOOLLQ
FDVHV
XX Urine C/S: Positive in 80-90% cases
XX MT: May be negative in 20% cases POLYCYSTIC KIDNEY DISEASE
XX 3\HORJUDP&7VFDQ0DVVOHVLRQGLODWHGSUR[LPDO
XUHWHUK\GURQHSKURVLV PRVWRIWHQXQLODWHUDO Genetic (AD, AR) kidney disorder characterized by
GHYHORSPHQWRIPXOWLSOHF\VWVLQWKHNLGQH\VDQGOLYHU
Treatment 7KHFDUGLQDOIHDWXUHVDUH
Anti tubercular drugs. XX 1HRQDWDOSHULRG,8*5SRWWHUIDFLHVUHVSLUDWRU\
GLVWUHVVVSRQWDQHRXVSQHXPRWKRUD[
XX Hypertension, proteinuria, haematuria
XX +HSDWLFGLVHDVHPDQLIHVWDWLRQDVSRUWDOK\SHUWHQVLRQ
variceal bleeding, hepatosplenomegaly.
IGA NEPHROPATHY XX 6RPHWLPHVELODWHUDOÀDQNSDLQDEGRPLQDOPDVVDQG
hypertension
,PPXQHFRPSOH[PHGLDWHGFKURQLFJORPHUXODU
How to evaluate a child with haematuria
GLVHDVHRFFXUVDIWHUGD\VIROORZLQJDYLUDO
UHVSLUDWRU\WUDFWRU*,7LQIHFWLRQ 7KHDLPRIHYDOXDWLRQLVWR¿QGRXWWKHVRXUFHRIEOHHGLQJ
,WQHHGVFDUHIXOKLVWRU\WKRURXJKSK\VLFDOH[DPLQDWLRQ
Clinical manifestations and relevant investigations.
XX Painless gross haematuria, moderate proteinuria, mild
to moderate hypertension History
XX Recurrent gross haematuria: IgA nephropathy, Alport
Diagnosis syndrome, thin glomerular basement membrane disease
XX &RQ¿UPHGE\UHQDOELRSV\WKDWVKRZV,J$LQWKH XX 3UHVHQFHRIIHYHU3\HORQHSKULWLV
mesangial cells XX 3UHVHQFHRIXULQDU\V\PSWRPXUJHQF\IUHTXHQF\
Cystitis
Treatment XX +DHPDWXULDLQUHODWLRQWRWLPHRIPLFWXULWLRQ
XX ACE inhibitors, corticosteroids
TT Throughout the whole micturition: Glomerular cause

Prognosis TT $WWKHHQGRIPLFWXULWLRQ8ULQDU\EODGGHU

XX End stage renal disease (rare) XX Abdominal pain:

TT Lower abdominal pain: Cystitis,
Polycystic kidney disease

TT Colicky pain: Nephrolithiasis

XX 3DVVDJHRIEORRGFORWV+DHPRUUKDJLFF\VWLWLV
XX 6ZHOOLQJRIWKHERG\VFDQW\XULQHKHDGDFKHEOXUULQJ
ALPORT SYNDROME RIWKHYLVLRQ$*1
XX 3UHVHQFHRIUDVKMRLQWVZHOOLQJ6/(+63
Hereditary nephritis, characterized by- XX +LVWRU\RIWUDXPD
XX Haematuria XX %OHHGLQJIURPRWKHUVLWHVRIWKHERG\&RDJXORSDWK\
XX Mild to moderate proteinuria severe thrombocytopenia
XX Bilateral sensori-neural hearing loss (not congenital)
XX +LVWRU\RISUHFHGLQJRUUHFHQWUHVSLUDWRU\WUDFWVNLQRU
*,LQIHFWLRQ$36*1+86,J$QHSKURSDWK\
XX Ocular abnormalities
 Step on to Paediatrics 219

XX )DPLO\KLVWRU\RIKDHPDWXULD+HUHGLWDU\QHSKURSDWK\ Investigations
thin glomerular basement membrane disease, IgA XX Urine R/M/E:
nephropathy TT Proteinuria, RBC, RBC cast and dysmorphic RBC:
XX +LVWRU\RIYLVXDORUKHDULQJSUREOHP$OSRUWV\QGURPH Glomerular diseases
TT 6LJQL¿FDQWSXVFHOOV:%&FDVW87,
General Physical examination
TT Crystalluria: Urolithiasis, nephrocalcinosis
XX Appearance, any dysmorphism: Syndromic renal
problems, hereditary nephropathy
XX 8ULQH&6*URZWKRIPLFURRUJDQLVP 87,
XX 3XII\IDFH+71RHGHPD*ORPHUXORQHSKULWLV
XX 86*RIWKH.8%UHJLRQ5HQDOF\VWLFGLVHDVH
XX 3DOORU6/(FRDJXODWLRQGLVRUGHUV+86&.' hydronephrosis, tumour, urolithiasis, nephrocalcinosis
XX Malar rash, photosensitive rash, oral ulcer: SLE
XX CBC with PBF:
TT When anemia, thrombocytopenia: SLE
XX Palpable purpura: HSP
TT Leukocytosis, thrombocytosis: HSP
XX %HGVLGHXULQHIRUDOEXPLQ 3URWHLQXULD *ORPHUXODU
diseases
XX Blood biochemistry
TT Serum electrolytes, calcium may be altered
XX ([DPLQDWLRQIRUKHDULQJDQGYLVLRQ
TT 5HQDOIXQFWLRQWHVW

Abdomen TT Serum protein, albumin

XX Suprapubic tenderness: Cystitis TT Serum cholesterol

XX Renal angle tenderness: Pyelonephritis, renal vein TT Spot urinary protein creatinine ratio

thrombosis TT C3, ASO titre, streptozyme test, anti DNase b :

XX 3DOSDEOHÀDQNPDVV+\GURQHSKURVLVUHQDOYHLQ APSGN
thrombosis, polycystic kidney diseases, renal tumours TT C3,C4, ANA, Anti dsDNA antibody: SLE

XX Palpable urinary bladder: Obstructive uropathy XX Renal biopsy

XX Ascites: Glomerulonephritis XX &RDJXODWLRQVFUHHQLQJDQGIDFWRUDVVD\&RDJXODWLRQ
XX /LYHU KHSDWRPHJDO\ +HDUWIDLOXUH GHIHFW
XX Genitalia: Meatal stenosis XX ,QYHVWLJDWLRQVWR¿QGRXWRWKHUFDXVHVRIKDHPDWXULD
Other systems TT 8ULQDO\VLVRIVLEOLQJVDQGSDUHQWV7KLQJORPHUXODU

XX Musculoskeletal system (Arthritis): HSP, SLE basement membrane disease

TT 8ULQHFDOFLXPFUHDWLQLQH!LQLGLRSDWKLF
XX Cardiovascular system (Tachycardia, galloping):
)HDWXUHVRIKHDUWIDLOXUH hypercalciuria.
TT KRXUVXULQHIRU&DXULFDFLGR[DODWH)RU
XX 2WKHUV\VWHPV)RUFRQJHQLWDODQRPDOLHVLQGLIIHUHQW
PDOIRUPDWLRQV\QGURPHV urolithiasis and nephrocalcinosis
TT &\VWRJUDPDQGUHQDOVFDQ,IKXGURQHSKURVLVIRXQG

in USG

Polycystic kidney disease

 220 Step on to Paediatrics

References
 &\QWKLD*(OOLV'$YQHU(GLWRUV&OLQLFDOHYDOXDWLRQRIFKLOGUHQZLWKKDHPDWXULD1HOVRQWH[WERRNRI3DHGLDWULFVth ed.
New Delhi; Elsevier; 2016.
 &UDLJ&3RUWHU(OOLV'$YQHU(GLWRUV$QDWRPLFDEQRUPDOLWLHVDVVRFLDWHGZLWKKDHPDWXULD1HOVRQWH[WERRNRI3DHGLDWULFV
20th ed. New Delhi; Elsevier; 2016.
 -DFN6(OGHU(GLWRU8ULQDU\OLWKLDVLV1HOVRQWH[WERRNRI3DHGLDWULFVth ed. New Delhi; Elsevier; 2016.

SELF ASSESSMENT
Short answer questions (SAQ):
 'H¿QHKDHPDWXULD(QXPHUDWHWKHFRPPRQFDXVHVRIKDHPDWXULDLQFKLOGUHQ
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3. How will you investigate a child with haematuria?
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 :KDWDUHWKHIHDWXUHVRIVWRQHLQWKHXULQDU\WUDFW"+RZZLOO\RXLQYHVWLJDWHDQGWUHDWVXFKDFDVH"

Multiple choice questions (MCQ)

 )ROORZLQJDUHWKHFDXVHVRIKDHPDWXULD±
___ a) UTI ___ b) Myoglobin ___ c) Renal stone
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 :KLFKVWDWHPHQWVDUHFRUUHFWUHJDUGLQJWKHDHWLRORJ\RIKDHPDWXULD±
___ a) Abdominal lump in AGN ___ Suprapubic tenderness in cystitis ___ c) Fever in renal stone
BBBG 3RVLWLYHIDPLO\KLVWRU\LQFRDJXORSDWK\ BBBH )DFLDOG\VPRUSKLVPLQ6/(
 :KDWDUHWKHEDVHOLQHLQYHVWLJDWLRQVIRUSDLQIXOKDHPDWXULD±
BBBD 8ULQH50( BBBE 86*RI.8%UHJLRQ BBBF 5HQDOELRSV\
BBBG '06$VFDQ BBBH 3ODLQ;UD\RIDEGRPHQ
 )ROORZLQJLVDUHWKHLQIHFWLRXVFDXVHVRIKDHPDWXULD±
___ a) APSGN ___ b) Pyelonephritis ___ c) Cystitis
___ d) Ig A nephropathy ___ e) Renal TB
Self assessment
 28
Dysuria
Urinary tract infection- - - - - - - - - - - - 221

'\VXULDXVXDOO\UHSUHVHQWVXULQDU\WUDFWLQIHFWLRQ 87, 
ZKLFKLVDFRPPRQFDXVHRIPRUELGLW\LQFKLOGUHQ0DQ\
UTI cases have an underlying urinary tract anomaly e.g.
YHVLFRXUHWHULFUHÀX[ 985 REVWUXFWLRQHWFDQGLIWKDW
remains untreated, may predispose to renal damage. In this
chapter we will highlight UTI.

URINARY TRACT INFECTION (UTI)

Aetiology & Risk factors

9LUWXDOO\87,VDUHWKHDVFHQGLQJLQIHFWLRQVZKHUH
EDFWHULDIURPIDHFDOÀRUDFRORQL]HLQWKHSHULQHXPDQG
VXEVHTXHQWO\HQWHULQWREODGGHUYLDXUHWKUD(cystitis) and
Organism
¿QDOO\¿QGWKHLUZD\WRWKHNLGQH\V(pyelonephritis).
Most common (&ROL  .OHEVLHOOD3URWHXV
Risk factors
Pseudomonas, enterococcus, coagulase
XX 9RLGLQJG\VIXQFWLRQ Less common
IURPEDFNWRIURQWLQ negative staph, Strept. faecalis
XX Obstructive uropathy
IHPDOHV
XX Urethral instrumentation XX Female gender Types & Clinical Features of UTI
XX 9HVLFRXUHWHULFUHÀX[ XX Uncircumcised males Acute XX +LJKIHYHUFKLOOVDQGULJRU
(VUR) XX Tight clothing Pyelonephritis DEGRPLQDORUÀDQNSDLQQDXVHD
XX Neuropathic bladder XX Bubble bath ,QIHFWLRQ persistent vomiting, dehydration,
XX Constipation XX Poor perineal hygiene of renal renal angle tenderness
XX 3LQZRUPLQIHVWDWLRQ
SDUHQFK\PD XX 3UHVHQWDWLRQVRIneonates are
XX :LSLQJRISHULQHXP QRQVSHFL¿F7KH\XVXDOO\SUHVHQWV
ZLWKIHDWXUHVRIVHSVLVHJIHYHU
vomiting, lethargy, hypothermia,
Pathogensis SRRUIHHGLQJLUULWDELOLW\IDLOLQJWR
thrive and sometimes prolonged
7KHULVNIDFWRUVPHQWLRQHGDERYHLQWHUIDUHZLWKFRPSOHWH
neonatal jaundice
HPSW\LQJRIXULQDU\EODGGHUDQGWKHUHE\IDFLOLWDWHXULQDU\ XX 3DVVDJHRIIRXOVPHOOLQJRUFORXG\
VWDVLV7KLVSURPRWHVFRORQL]DWLRQRIXULQDU\EODGGHU
urine
ZLWKEDFWHULDDQGVXEVHTXHQWO\LQIHFWLRQ(cystitis).
7KHQLQIHFWLRQDVFHQGVXSWRSHOYLFDOHFLDOV\VWHP Acute Cystitis XX '\VXULDXUJHQF\IUHTXHQF\
(pyelitis),QIHFWLRQLQUHQDOSHOYLVDOVRGDPDJHVWKH ,QIHFWLRQ incontinence, suprapubic pain and
adjacent nephrons (pyelonephritis)6XEVHTXHQWO\scars of urinary malodorous urine
UTI

DUHIRUPHGLQWKHGDPDJHGUHQDOWLVVXHVFRQWULEXWLQJ EODGGHU XX Fever usually not common

GHYHORSPHQWRIhypertension, renal dysfunction as well
as renal failure. XX BP should be measured in every case of UTI as it
may increase when complicated
221
 222 Step on to Paediatrics

Asymptomatic Bacteriuria TT DMSA (dimercaptosuccinic acid): Done to asses

UHQDOPRUSKRORJ\SDUWLFXODUO\WKHSUHVHQFHRIDQ\
'H¿QHGDVLVRODWLRQRIDVSHFL¿HGTXDQWLWDWLYHFRXQWRI
scar, renal masses etc.
EDFWHULDLQDQDSSURSULDWHO\FROOHFWHGXULQHVSHFLPHQIURP
DQLQGLYLGXDOZLWKRXWV\PSWRPVRUVLJQVRI87,

Diagnosis
%DVHGRQ&) VXSSRUWVIURPWKHUHOHYDQWLQYHVWLJDWLRQV

Investigations
XX 8ULQH50(6KRZVPDQ\SXVFHOOV ! +3)Sample

Source: Internet
VKRXOGEHVHQWWRODERUDWRU\ZLWKLQPLQXWHVRI
collection
XX 8ULQHIRU&6:LOOLGHQWLI\WKHRUJDQLVPVDQGWKHLU
antibiotic sensitivity pattern '06$VFDQVKRZLQJ87,UHODWHGVFDUULQJRIWKHULJKWNLGQH\
'LDJQRVWLFVLJQL¿FDQFHRIFRORQ\FRXQWLQXULQH
Treatment
Method of Probability of
Colony count A. Supportive
Collection infection
XX &RXQVHOSDUHQWVDERXWWKHQDWXUH IXWXUHRIWKHGLVHDVH
Clean
TT VSHFLPHQ!5 XX 80%
XX
XX (QFRXUDJHWKHSDWLHQWWRGULQNPRUHOLTXLG
voided TT VSHFLPHQ!5 XX 95% XX 7HDFKSDUHQWVRQKRZWRDYRLGWKHULVNIDFWRUV
TT !5 XX 95% %6SHFL¿F
XX Catheter- TT 10 -10
4 5 XX ,QIHFWLRQOLNHO\ XX 6HOHFWLRQRIDSSURSULDWHDQWLELRWLFV
ization UTI Treatment
XX ,QIHFWLRQ Antibiotics, Route, Dose
TT <103 Types Duration
XX unlikely
Gram-Ve bacilli: Acute &HIWULD[RQH,9PJNJGD\RU
TT
10-14
Any number Pyelo- &HIRWD[LPH,9PJNJGD\RU
XX Suprapubic days
XX 99% nephritis Gentamicin, IV, 5 mg/kg/day
XX puncture TT *UDP9HFRFFL
&RWULPR[D]RORU$PR[LFLOOLQRU
!IHZWKRXVDQG
Acute &R$PR[LFODYRU 
Cystitis &HIDGUR[LORU days
XX CBC: Neutrophilic leukocytosis
&LSURIOR[DFLQ/HYRIOR[LQ
XX ,PDJLQJVWXGLHV7R¿QGRXWWKHFDXVHDVZHOODVH[WHQW
RIUHQDOGDPDJH Recurrent UTI
TT Renal ultrasound
XX &KLOGUHQZLWK!DWWDFNVRI87,LUUHVSHFWLYHRIDJH
TT Voiding/micturating cystourethrogram (MCU)
is called recurrent UTI. They should be evaluated with
TT '73$UHQRJUDP'RQHWRXQGHUVWDQGWKHIXQFWLRQDO
ultrasound, '06$VFDQDQG0&8WR¿QGRXWWKHFDXVH
VWDWXVRINLQH\VE\DQDO\VLQJWKHDUULYDOXSWDNHDQG RIUHFXUUHQFHDQGWRDVVHVWKHH[WHQWRIUHQDOGDPDJH
HOLPLQDWLRQRILQMHFWHG'73$ 'LHWK\OHQH7ULDPLQR
Pentaacetic Acid) Risk factors

XX 9HVLFRXUHWHULFUHÀX[ 985
XX Urinary tract abnormalities
XX Diseases e.g. diabetes mellitus, neurogenic bladder,
LPPXQHGH¿FLHQF\GLVRUGHUHWF
UTI
 Step on to Paediatrics 223

Treatment XX Duration of Prophylaxis

9DULHVDFFRUGLQJWRWKHXQGHUO\LQJFDXVHRISHUVLVWHQW
A. Supportive LQIHFWLRQ3URSK\OD[LVPD\EHGLVFRQWLQXHGLIWKHFDXVH
XX Counsel the parents, about recurrent UTI, its
is removed and the repeat urine C/S shows no growth.
complications and outcome
6RPHWLPHVLWPD\EHGLVFRQWLQXHGDIWHU\HDUVRI
XX (QFRXUDJHWKHSDWLHQWWRGULQNPRUHOLTXLG
DJHHYHQLIORZJUDGHUHÀX[SHUVLVWV
XX 7HDFKSDUHQWVRQKRZWRDYRLGWKHULVNIDFWRUV
TT &RUUHFWLRQRIFRQVWLSDWLRQ Complete voiding

Prevention of UTI
TT :DVKLQJRISHULQHXPIURPIURQWWREDFNDIWHU XX Avoiding constipation. A healthy eating diet which
GHIDHFDWLRQLQIHPDOHV LQFOXGHVKLJK¿EUHVKRXOGEHHQFRXUDJHG6RPHWLPHV
XX ,GHQWL¿FDWLRQ HOLPLQDWLRQRIWKHXQGHUO\LQJFDXVHRI OD[DWLYHVPD\EHSUHVFULEHG
recurrent UTI XX (QFRXUDJHFKLOGUHQWRGULQNSOHQW\RIZDWHUDQGHPSW\
XX Emphasize Antibiotic prophylaxis,QGLFDWLRQV± WKHEODGGHUDGHTXDWHO\6RPHWLPHVFKLOGUHQKDYHWREH
TT )LUVWIHEULOH87, reminded to use the toilet every 2-3 hours. Also ensure
TT 87,ZLWKERZHOEODGGHUG\VIXQFWLRQ that the child is using the toilet at break-time at school
TT *UDGH,,,RU,9YHVLFRXUHWHULFUHÀX[
XX ,Q\RXQJJLUOVSURSHUZLSLQJIURPIURQWWREDFNDIWHU
XX Drugs used for Prophylaxis they have been to the toilet may also be important
XX Ensure that your children wear loose cotton underwear
XX &RWULPR[D]ROHPJRI7ULPHWKRSULPNJGD\or rather than tight nylon underwear
XX 1LWURIXUDQWRLQPJNJGD\or XX Foreskin should be kept clean in uncircumcised boys
XX &HSKDOH[LQPJNJGD\or
XX &HIDGUR[LOPJNJGD\

UTI
 224 Step on to Paediatrics

References
 0HQRQ68ULQDU\WUDFWLQIHFWLRQDQXSGDWH,Q'XWWD$.6DFKDGHYD$HGLWRUV$GYDQFHVLQ3HGLDWULFVst ed. Delhi: Jaypee
%URWKHUV0HGLFDO3XEOLVKHUVS
 (OGHU-68ULQDU\WUDFWLQIHFWLRQ1HOVRQ7H[WERRNRI3HGLDWULFVth ed.. New Delhi: Elsevier; 2016: 2556-62.
 3UDMDSDWL%6HWDO$GYDQFHVLQWKHPDQDJHPHQWRIXULQDU\WUDFWLQIHFWLRQV,QGLDQ-RXUQDORI3HGLDWULFV

SELF ASSESSMENT
Short answer question [SAQ]
 :KDWDUHWKHPLFURRUJDQLVPVUHVSRQVLEOHIRU87,"
 :ULWHGRZQWKHWUHDWPHQWRIDFXWHS\HORQHSKULWLV
 $\HDUROGJLUOKDVFRPSODLQWVRIG\VXULDLQFUHDVHVIUHTXHQF\RIPLFWXULWLRQDQGIHYHU
a) What is your probable diagnosis?
b) How to investigate the child?
3) Write down her management.

Multiple choice question [MCQ]

 7KHNQRZQULVNIDFWRUVRI87,DUH±
BBBD YHVLFRXUHWHULFUHÀX[ BBBE REVWUXFWLYHXURSDWK\ BBBF QHXURSDWKLFEODGGHU
BBBG FRQVWLSDWLRQ BBBH SLQZRUPLQIHVWDWLRQ
 7KHUHFRPPHQGHGGUXJVIRUSURSK\OD[LVRIUHFXUUHQW87,DUH±
___ a) 1LWURIXUDQWRLQ BBBE 7ULPHWKRSULP BBBF &HSKDOH[LQ
___ d) Ampicillin ___ e) Erythromycin
 7KHUHFRPPHQGHGGUXJIRUSURSK\OD[LVRIUHFXUUHQW87,DUH
BBBD 1LWURIXUDQWRLQ BBBE 7ULPHWKRSULP BBBF &HSKDOH[LQ
___ d) Amphicillin ___ e) Erythromycin
 7KHIROORZLQJDUHFDXVHVRIVWHULOHS\XULD
___ a) Renal stones ___ b) membranous glomerulonephritis
___ c) Renal tuberculosis ___ d) Chlamydia ___ e) Appendicitis
 $FKLOGSUHVHQWHGZLWKKLJKIHYHUDQGG\VXULD3XVFHOOVDUHSUHVHQWDQGFXOWXUHVKRZV4 FRORQLHVRI(FORLZKDWZRXOGEH
appropriate
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BBBF 5HSHDWXULQH5(DQG&6 BBBG 86*DEGRPHQWRUXOHRXWIHDWXUHVRI87,
 $\UROGJLUOSUHVHQWVZLWKFXOWXUHSRVLWLYH87,:KDWLQLWLDOLQYHVWLJDWLRQZRXOG\RXVXJJHVWIRUKHU
BBBD 86*RIDEGRPHQ BBBE 86*0&8
BBBF 86*'06$ BBBG 86*0&8'06$
Self assessment
 29
excessive urine output (polyuria)
Diabetes Mellitus (DM) - - - - - - - - - - - - 225
Diabetes Ketoacidosis - - - - - - - - - - - - 226

:KHQHYHUDFKLOGSUHVHQWVZLWKKLVWRU\RISDVVDJH Pathogenesis
RIH[FHVVXULQH !POP2GD\ WKHIROORZLQJ In DM, the body is unable to utilize glucose to generate
FRQGLWLRQVVKRXOGEHWDNHQLQWRFRQVLGHUDWLRQ± DGHTXDWHHQHUJ\GXHWRLQVXOLQGH¿FLHQF\RUUHVLVWDQFH7R¿OO
XX Diabetes Mellitus (DM) WKLVHQHUJ\JDSIDWDQGSURWHLQV IURPPXVFOH DUHEURNHQGRZQ
XX Diabetes Insipidus (DI) resulting in weight loss. Whenever the elevated glucose level in
XX &KURQLF.LGQH\GLVHDVH &.' EORRGH[FHHGWKHUHQDOWKUHVRXOGWKHH[FHVVJOXFRVHLVH[FUHWHG
XX Renal tubular acidosis (RTA) in the urine (glycosuria), dragging water with it resulting
XX Psychogenic polydipsia LQH[FHVVLYHXULQDWLRQ polyuria)DQGZLWKH[FHVVLYHWKLUVW
,QWKLVVHFWLRQ'0RIFKLOGUHQDQGLWVOLIH (polydipsia)<RXQJHUFKLOGUHQRIWHQUHVXPHbedwetting.
threatening complication like diabetic ketoacidosis %UHDNGRZQRIIDWFDXVHVH[FHVVNHWRQHSURGXFWLRQDQG
'.$ ZLOOEHGLVFXVVHG7KHFDUGLQDOIHDWXUHVRIWKH accumulation in the blood (ketosis/acidosis),IWKHGLDJQRVLV 
RWKHUFDXVHVRISRO\XULDZLOODOVREHKLJKOLJKWHG WUHDWPHQWLVGHOD\HGH[FHVVJOXFRVHDQGNHWRQHVDUHH[FUHWHGLQ
urine, resulting in severe dehydrationDQGORVVRIHOHFWURO\WHV
IURPWKHERG\7KLVLVFDOOHG'.$
7KHSUHVHQFHRINHWRQHVDQGWKHDFFRPSDQ\LQJDFLGRVLV
DIABETES MELLITUS (DM) may cause an acetone/sweet smell on the breath, vomiting,
DEGRPLQDOSDLQGHFUHDVHGOHYHORIFRQVFLRXVQHVVDQGUDSLG
It is a chronic metabolic disorder characterized by deep breathing (Kussmaul respiration ,IXQWUHDWHGVKRFN
DVXVWDLQHGHOHYDWLRQRIEORRGJOXFRVHGXHHLWKHUWR cerebral oedema, coma and death may occur.
GH¿FLHQF\RILQVXOLQVHFUHWHGE\ȕFHOOVRISDQFUHDV
RUGHIHFWLQLWVDFWLRQ7KHIXQFWLRQRILQVXOLQLVWR
IDFLOLWDWHWKHHQWU\RIJOXFRVHIURPEORRGLQWRWKH
Clinical Manifestations
cells where it is metabolized to produce energy.
When ȕFHOOVIDLOWRSURGXFHDGHTXDWHDPRXQWRI More
Less common Features of DKA
common
LQVXOLQRUWKHHIIHFWRUFHOOVKDYHLQVXOLQUHVLVWDQFH
DM occurs. XX Weight loss XX ([FHVVLYH XX )UHTXHQWYRPLWLQJ
hunger Acute abdominal pain
Diabetes Mellitus (DM)
XX Polyuria; XX

Diabetes Mellitus: Types bed wetting XX Blurred XX Cheek: Flushed

XX Type 1:0RVWFRPPRQDPRQJFKLOGUHQ  in younger vision XX Breathing: Acetone
DGROHVFHQWVGXHWRDEVROXWHLQVXOLQGH¿FLHQF\ children XX Mood smell
7KH\DUHSURQHWRGHYHORS'.$ changes
XX ([FHVV XX Dehydration with
XX Type 2:&RPPRQDPRQJSHRSOHRYHU\HDUVRI thirst XX 6NLQLQIHFWLRQ continuing polyuria
DJHPRVWO\LQVXOLQUHVLVWDQWPD\UXQLQIDPLOLHV XX Tiredness- XX Oral or XX Altered consciousness
DQGRIWHQDVVRFLDWHGZLWKRYHUZHLJKW7KH\KDYH
not want to vaginal thrush XX .XVVPDXOUHVSLUDWLRQ
OHVVFKDQFHRI'.$
work or to XX Abdominal XX Shock, Cerebral
XX Other types play pain oedema,Coma
TT Malnutrition-related DM

TT Fibrocalculous pancreatopathy

TT Neonatal DM etc.
225
 226 Step on to Paediatrics

Complications DIABETIC KETOACIDOSIS (DKA)

XX $FXWH'.$K\SRJO\FDHPLDK\SHUJO\FDHPLF
hyperosmolar state '.$LVDPHGLFDOHPHUJHQF\DQGRFFXUVZKHQHYHUWKHUHLV
XX Chronic: SURIRXQGLQVXOLQGH¿FLHQF\,WPD\EHWKH¿UVWSUHVHQWDWLRQ
TT Microvascular:Neuropathy, retinopathy, nephropathy RI'0RURFFXUVZKHQLQVXOLQLVPLVVHGRUGLVFRQWLQXHG
TT Macrovascular:cerebro-vascular disease, coronary LQDNQRZQGLDEHWLFFKLOGRULILQDGHTXDWHGRVHRILQVXOLQ
artery disease, peripheral vascular disease. LVJLYHQDWWLPHVRIDFXWHLOOQHVV&HUHEUDORHGHPDLVWKH
TT 2WKHUVJURZWKIDLOXUHGHOD\HGSXEHUW\ PRVWGDQJHURXVHYHQWRI'.$

Diagnosis Diagnosis
'LDJQRVLVLVEDVHGRQFODVVLFDOFOLQLFDOIHDWXUHVDQG %DVHGRQFDUGLQDOFOLQLFDOIHDWXUHV PHQWLRQHGLQWKHWDEOH 
Persistently elevated blood sugar level DQGRQWKHIROORZLQJ%LRFKHPLFDOFULWHULDH±
XX %ORRGJOXFRVH•  PPRO/ PJG/
2 hrs PG after
Fasting plasma a 75 g IRU
XX 9HQRXVEORRGS+
Category HbA1C S Bicarbonate: <15 mmol/L
glucose (FPG) FKLOGUHQJ XX

NJ glucose XX .HWRQDHPLD NHWRQXULD

<5.6 mmol/L PPRO/ Management
Normal <6.5%
(100 mg/dl) (140 mg/dl)
I. Quick Clinical & Laboratory assessment e.g.
Impaired TT /HYHORIFRQVFLRXVQHVV
Fasting 5.6-6.9 mmol/L Normal TT 6WDWXVRIGHK\GUDWLRQ
glucose (100-125mg/dl) PPRO/ TT 3UHVHQFHRUDEVHQFHRIVKRFNand
(IFG) TT $Q\HYLGHQFHRILQIHFWLRQ
Impaired
glucose 
Normal
mmol/L
tolerance <5.6 mmol/L
(140-200 mg/dl)
(IGT)
•  PPROO •  PPROO
DM
(126 mg/dl) (200 mg/dl) •  

Management
III. Send bloodIRUO CBC, PBF O.HWRQHERGLHVLQ
I. Supportive: Counsel– blood and in urine O Glucose, ABG, S electrolytes,
TT 3DUHQWVDERXWWKHQDWXUH IXWXUHRIWKHGLVHDVH Urea, Creatinine, HBA1C
complications
III. Rehydration
TT 2QGLIIHUHQWDVSHFWVRIPDQDJHPHQWHJLQVXOLQ
DGMXVWPHQWRIGRVHPRQLWRULQJJOXFRVHHWF
TT ,ILQVKRFN,QIXVH1RUPDOVDOLQH 16 #
TT )RU/LIHVW\OHPRGL¿FDWLRQHJUHJXODUH[HUFLVHHWF PONJEROXVDVTXLFNO\DVSRVVLEOHDORQJZLWK
DSSURSULDWHOLIHVXSSRUW $%& $GGLWLRQDOPONJ
Diabetic ketoacidosis (DKA)

TT )RUSHUVRQDOK\JLHQHHJIRRWFDUH
EROXVLQIXVLRQVPD\EHQHHGHGRQFHRUWZLFHXQWLO
TT 7R6HOHFWDSSURSULDWHGLHW7KHFDORU\PL[WXUHZLOO
circulation is stable.
EHDVIROORZV&DUERK\GUDWH  )DW  DQG TT ,IQRVKRFNEXWGHK\GUDWLRQRI!UHVXVFLWDWHZLWK
Protein (15%)
Normal Saline @ 10 ml/kg bolus over 1 hour.
,,6SHFL¿F
1%7KHPRUHLOOWKHFKLOGWKHVORZHUWKHUDWHRI
TT Type 1 DM: Subcutaneous Insulin, mainly short UHK\GUDWLRQWRDYRLGWKHULVNRIFHUHEUDORHGHPD
DFWLQJ LQWHUPHGLDWHDFWLQJ
TT Type 2 DM : Oral hypoglycaemic agents IV. Monitoring

III. Regular Follow up:7RDVVHVVFRQWURORI'0

TT /HYHORIFRQVFLRXVQHVV
TT +RXUO\RIYLWDOVLJQV Intake-output chart
IV. Treatment of complications TT Hourly, Capillary blood glucose status
HJ'.$K\SRJO\FDHPLD TT .HWRQHVLQHYHU\VDPSOHRIXULQHSDVVHG
 Step on to Paediatrics 227

³³ Once circulating blood volume is restored, VII. Treatment of cerebral oedema

FDOFXODWHRQJRLQJÀXLGUHTXLUHPHQWVDVIROORZV )HDWXUHV+HDGDFKHYRPLWLQJRUVORZLQJRIKHDUWUDWH
Requirement H[LVWLQJGH¿FLW0DLQWHQDQFH
high BP, alterated sensorium, abnormal respiratory pattern
ÀXLGIRUQH[WKRXUV
³³ Once blood glucose is <15 mmol/l, change NS to
TT Supportive: (OHYDWLRQRIKHDGUHVSLUDWRU\VXSSRUW
ÀXLGUHVWULFWLRQ
5% DNS
³³ :KHQRUDOÀXLGLVWROHUDWHG,9ÀXLGVKRXOGEH
TT Mannitol (0.5-1 g/kg) IV over 10-15 minutes
reduced accordingly.
TT Hypertonic saline (3%), 2.5-5 ml/kg over 10-15
³³ 2QFHVKRFNVHYHUHGHK\GUDWLRQLVFRUUHFWHGDIWHU
minutes may be given as an alternative to mannitol,
HVSHFLDOO\LIWKHUHLVQRLQLWLDOUHVSRQVHWRPDQQLWRO
KRXUVRI,9UHK\GUDWLRQVWDUW
TT Insulin in IV Infusion DVHDUOLHUVWDUWRILQVXOLQ VIII. Monitoring of the child
EHIRUHUHK\GUDWLRQLVDVVRFLDWHGZLWKFHUHEUDO XX )ROORZXS+RXUO\DIWHUVWDUWLQJWUHDWPHQWWKHQ
oedema,WLVVWDUWHGDWDGRVHRIXQLWNJKRXU KRXUO\RQ±
using insulin pump TT Monitoring vital signs  Intake output chart

TT Blood glucose, S electrolytes, ABG

V. Potassium replacement, LISDWLHQWLVK\SRNDODHPLF
³³ 2QFH'.$KDVEHHQDGHTXDWHO\WUHDWHG(hydration
'RVHPPROOLQ,9PDLQWHQDQFHÀXLGRQFHXULQH
output has been documented corrected, glucose controlled, ketones cleared) the
child can be transitioned to Subcutaneous (SC)
VI. Broad spectrum Antibiotics, IV in suspected sepsis
LQVXOLQ7KH¿UVW6&GRVHRIVKRUWDFWLQJLQVXOLQ
1%1D+&2LVQRW5RXWLQHO\XVHGH[FHSWZKHQWKHFKLOG VKRXOGEHJLYHQKRXUVEHIRUHVWRSSLQJWKH
is in shock with severe acidaemia (pH <6.9). LQVXOLQLQIXVLRQ

Patho-physiology, cardinal features & treatment of other causes of polyuria

Diabetes mellitus Diabetes insipidus RTA CKD

'HFUHDVHOHYHORI /DFNRI$'+ )DLOXUHRI+ secretion/
Patho- Renal loss involving both
insulin in blood/ VHFUHWLRQODFNRI$'+ decreased HCO3
physiology glomeruli and tubule
ODFNRILQVXOLQ action absorption
,QDELOLW\RIWKHUHQDO 7XEXORSDWK\LQWHUIHULQJ
Inability to utilise Inability to
(IIHFW tubules to maintain ZLWKVDOW ZDWHU
glucose concentrate urine
normal acid-base balance reabsorption
Pituitary, Renal 3UR[LPDO GLVWDOUHQDO
$IIHFWHG6LWH 3DQFUHDWLFȕFHOO Glomeruli and renal tubules
collecting tubule tubules
Metabolic acidosis,
Hyperglycaemia, Heamoconcentration, Non anion gap metabolic
Biochemical high BUN, creatinine
ketonemia, ketonuria, hypernatreamia, dilute acidosis, hypercalciurea,
changes hyperkalaemia,
ketoacidosis urine phosphoturia, glycosuria
hyponatreamia, anaemia

Polyuria(enormous Respiratory distress, Respiratory distress,

Diabetic ketoacidosis (DKA)
Polyuria, polydipsia,
Clinical diluted urine), JURZWKIDLOXUHIHDWXUHV K\SHUWHQVLRQJURZWKIDLOXUH
polyphagia, weight
FRQVHTXHQFHV polydipsia, weight RIULFNHWVSRO\XULD DQDHPLDIHDWXUHVRIULFNHWV
ORVVIHDWXUHVRI'.$
loss±, dehydration polydipsia polyuria, polydipsia

Serum osmolality,
Blood glucose level, Arterial blood gas
Investigation urinary osmolality, 5HQDOIXQFWLRQWHVWVHUXP
urinary sugar, urinary analysis, serum
WRFRQILUP XULQDU\VSHFLILF electrolyte, Hb%, Imaging
acetone, blood gas HOHFWURO\WHXULQDU\S+ 
the diagnosis gravity, Water study
analysis electrolyte
deprivation test
Insulin, oral Desmopressin acetate, Sodium bicarbonate,
Treatment Renal replacement therapy
hypoglycaemic drug thiazide diuretics 6KRKO¶VVROXWLRQ
 228 Step on to Paediatrics

DKA Management - Recommended Care

Clinical Signs
• Accesss dehydration
• 'HHSVLJKWLQJUHVSLUDWLRQ .XVVPDXO Biochemical featured &
• 6PHOORINHWRQHV investigations
• Lethargy/drowsiness ± vomiting • .HWRQHVLQXULQH
• Elevated blood glucose
• 'LDJQRVLVFRQ¿UPHG • Acidemia
• 'LDEHWLF.HWRDFLGRVLV • Blood gases, urea, electrolytes
• &RQWDFW6HQLRU6WDII • Other investigations as indicated

• 'HK\GUDWLRQ•
• Not in shock Minimal dehydration,
• $FLGRWLF>K\SHUYHQWLODWLRQ@ WROHUDWLQJRUDOÀXLG
• ±YRPLWLQJ
• 6KRFN>UHGXFHGSHULSKHUDOSXOVHV@
• Reduced conscious level/coma Therapy
0.9% saline 10mls per kg IV over 1 hour
• .6WDUWZLWK6&LQVXOLQ
Resuscitation IV Therapy • Continue oral hydration
• $LUZD\±1*WXEH • &DOFXODWHÀXLGUHTXLUHPHQWV
• %UHDWKLQJ>2[\JHQ@ • Correct over 48 hours No improvement
• &LUFXODWLRQ>6DOLQHPONJDV • Saline 0.9%
TXLFNO\DVSRVVLEOHDGGLWLRQDOPO • (&*IRUDEQRUPDO7ZDYHV
kg boluses until circulation is stable] • $GG.&/PPROSHUOLWUHÀXLG

&RQWLQXRXVLQVXOLQLQIXVLRQ8NJKUVWDUWHG
KRXUVDIWHUÀXLGWUHDWPHQWKDVEHHQLQLWLDWHG

Critical Observations
• Hourly blood glucose
• +RXUO\ÀXLGLQSXW RXWSXW
• Neurological ststus at least hourly
• (OHFWURO\WHVKRXUO\DIWHUVWDUWRI,9WKHUDSK\
• 0RQLWRU(&*IRU7ZDYHFKDQJHV Neurological deterioration
Acidosis not improving
WARNING SIGNS:
%ORRGJOXFRVHPPROO>PJGO@ Headache, Slowing Heart rate,
or Irritability, Decreased continence,
EORRGJOXFRVHIDOOV•PPROOKSXU>•PJGOK@
Re-evaluate 6SHFL¿FQHXURORJLFDOVLJQV
• ,9ÀXLGFDOFXNDWLRQV
IV Theraphy
• ,QVXOLQGHOLYHU\V\VWHP GRVH ([FOXGHK\SRJO\FDHPLD
• 1HHGIRUDGGLWLRQDOUHVXVFLWDWLRQ • &KDQJHWRVDOLQHJOXFRVH Is it cerebral edema?
• Consider sepsis • $GMXVWVRGLXPLQIXVLRQWRSURPRWHDQ
increase in measured serum sodium
Management
Improvement • Give mannitol 0.5-1 g/kg
&OLQLFDOO\ZHOOWROHUDWLQJRUDOÀXLGV • 5HVWULFW,9ÀXLGVE\RQHWKLUG
* Bolus added when dehydration
• &DOOVHQLRUVWDII
•DVSUHVHQWDWLRQVDUHRIWHQODWH • Move to ICU
Transition to S/C Insulin • Consider cranial imaging only
in less-resourced setting
Srart SC insulin then stop IV insulin DIWHUSDWLHQWVWDELOLVHG
DIWHUDQDSSURSULDWHLQWHUYDO
,63$'*XLGHOLQHVµ
DKA Management

Psychogenic polydipsia 7KHGLDJQRVLVRISV\FKRJHQLFSRO\GLSVLDLVRQHRI

Psychogenic polydipsia is an uncommon clinical disorder H[FOXVLRQDQGUHTXLUHVVSHFLDOLVWLQYHVWLJDWLRQDQG
FKDUDFWHUL]HGE\H[FHVVLYHZDWHUGULQNLQJLQWKHDEVHQFH management; the most important test is the water
RIDSK\VLRORJLFVWLPXOXVWRGULQN7KHH[FHVVLYH GHSULYDWLRQWHVWZKLFKVKRXOGEHXQGHUWDNHQFDUHIXOO\
water-drinking is well tolerated unless hyponatraemia
Treatment
supervenes. XX 5HVWULFWLRQRIÀXLG  Behavioural therapy

XX 7UHDWPHQWRIDQ\RWKHUXQGHUO\LQJFDXVH
 Step on to Paediatrics 229

References
 1HOVRQ7H[WERRNRI3HGLDWULFVth ed.. New Delhi: Elsevier; 2016: 2556-62.
2. ISPAD Guidelines ‘2016

SELF ASSESSMENT
Short answer question [SAQ]
1.
2.
a)

Multiple choice question [MCQ]

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 230 Step on to Paediatrics

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Self assessment
 30
Sudden Paralysis of limbs
Poliomyelitis - - - - - - - - - - - - - - 231
Guillain–Barré syndrome - - - - - - - - - - - - 233
Transverse myelitis - - - - - - - - - - - - - 235

:KHQHYHUDFKLOGSUHVHQWVZLWKVXGGHQRQVHWRISDUDO\VLV Clinical Manifestations

RQHVKRXOGWKLQNRIWKHIROORZLQJSRVVLEOHSUREOHPV Presentations are variable.
LQYROYLQJ±
A. Asymptomatic: $ERXWRISDWLHQWV
XX Spinal cord: Poliomyelitis, transverse myelitis B. Symptomatic: About 5-10% cases and they present as
(TM), spinal cord tumor RQHRIWKHIROORZLQJZD\V±
XX Peripheral nerves*XLOODLQ±%DUUpV\QGURPH GBS) TT Abortive polio:
diphtheria, porphyria ³³ Like
XX Neuromuscular junction: Tick, botulism
any viral
XX Brain: Stroke LQIHFWLRQ
³³ No paralysis

³³ Recovery is
,QWKLVFKDSWHUGLVHDVHVWKRVHJLYHULVHWRDFXWHÀDFFLG
paralysis e.g. Poliomyelitis, GBS, TM will be highlighted. complete
TT Nonparalytic
aseptic
meningitis:
Characterized
POLIOMYELITIS E\IHYHU
headache and
Aetio-pathogenesis QHFNVWLIIQHVV
without
Organism: Polio virus type 1, 2, 3.
paralysis
All the 3 types can cause paralysis but type 1 is associated TT Paralytic
ZLWKPRVWRIWKHPDMRUHSLGHPLFVDQGVKRZVWKHJUHDWHVW poliomyelitis:
SURSHQVLW\WRFDXVHSDUDO\WLFIRUPRIWKHGLVHDVH According
Transmission: Faecal-oral route to the site
RIOHVLRQV
Incubation period: 1-3 weeks paralytic
7KHDUHDVRIVSLQDOFRUGDQGEUDLQDIIHFWHGE\SROLRYLUXV poliomyelitis
DUH± DUHRIW\SHV
³³ Spinal
Poliomyelitis

XX Spinal cord Anterior horn cells ³³ Bulbar

XX 0HGXOOD 3RQV Motor cranial nerve nuclei ³³ Polio

A child with paralyzed right
encephalitis ORZHUOLPEIURPSROLR
XX Cerebellum 1XFOHLLQWKHURRIDQGYHUPLV
Substantia nigra, and occasionally
XX Pons
the red nucleus
231
 232 Step on to Paediatrics

Cardinal features of 3 types of Paralytic Poliomyelitis

Parameters Spinal poliomyelitis Bulbar poliomyelitis Polio encephalitis

6LWHRIOHVLRQ $QWHULRUKRUQFHOOVRIVSLQDOFRUG 0RWRUFUDQLDOQHUYHQXFOHLDW0HGXOOD 3RQV Brain

XX ,QLWLDOO\KLJKIHYHUVHYHUH XX 1DVDOLQWRQDWLRQRIYRLFH
P\DOJLDKHUDOGSURJUHVVLRQWR± XX 1DVDOUHJXUJLWDWLRQRIVDOLYD ÀXLGVGXULQJ
TT /RVVRIWHQGRQUHÀH[HVDQG swallowing
XX Higher center
VXEVHTXHQW)ODFFLGSDUDO\VLV XX $EVHQFHRIHIIHFWLYHFRXJKLQJ
RIEUDLQ
XX Paralysis,usually asymmetrical XX 'HYLDWLRQRIWKHSDODWHXYXODRUWRQJXH
involved
Presentation

XX 3UR[LPDOOLPEPXVFOHVPRUH XX ,QYROYHPHQWRIYLWDOFHQWHUVLQWKHPHGXOOD XX Cranial nerve

DIIHFWHGWKDQGLVWDO ZKLFKXVXDOO\PDQLIHVWDV±
involvement
XX /RZHUOLPEVDUHDIIHFWHGPRUH TT ,UUHJXODULWLHVLQUDWHGHSWKDQGUK\WKPRI
XX Irritability/
than the upper limbs respiration
drowsiness
XX $IIHFWHGPXVFOHVDUHÀRSS\ TT Changes in Blood pressure
XX Seizure
XX Sensation remains intact TT Cardiac arrhythmias
XX Coma
XX +\SHUDHVWKHVLDRIVNLQ TT Flactuations in body temperature

overlying paralyzed muscles is TT 3DUDO\VLVRIRUERWKYRFDOFRUGVFDXVLQJ

FRPPRQ SDWKRJQRPRQLF KRDUVHQHVVDSKRQLDDQGXOWLPDWHO\DVSK\[LD

TT Bladder distension and marked constipation UHKDELOLWDWLYH7KHDLPRIWUHDWPHQWLVWR±

accompany paralysis XX 6WUHQJWKHQDOOWKHDIIHFWHGPXVFOHV
TT Paralysis is complete by the time temperature XX 3UHYHQWFRQWUDFWXUHVDQGGHIRUPLWLHV
normalize XX 0DNHWKHSDWLHQWDVVHOIVXI¿FLHQWDVSRVVLEOH
TT Muscle atrophy evident by 4-8 weeks XX Provide emotional and psychological support
TT 0RVWLPSURYHPHQWRISDUDO\VLV
Treatment in the acute stage of
Complications muscle paralysis (7-10 days)
XX 5HVSLUDWRU\SKDU\QJHDODQGERZHOPDOIXQFWLRQ XX *LYH1*WXEHIHHGLQJLIXQDEOHWRIHHGRUDOO\
'HDWKLVXVXDOO\WKHFRQVHTXHQFHRIUHVSLUDWRU\ XX $SSO\PRLVWKRWSDFNVWRWKHDIIHFWHGPXVFOHVDORQJZLWK
G\VIXQFWLRQ
analgesics to treat pain
Diagnosis XX 6XSSRUWWKHVSLQHKLSNQHHIRRWDQGRWKHUMRLQWVWRSUHYHQW
XX &KDUDFWHULVWLFFOLQLFDOPDQLIHVWDWLRQV FRQWUDFWXUHVRUHVDQGGHIRUPLWLHVHJ
TT Change posture 2 hourly
XX ,VRODWLRQRIYLUXVIURPVWRROLVFRQ¿UPDWRU\
TT 5HVWRQD¿UPPDWWUHVVZLWKEDFNVXSSRUWHGRQDOXPEDU

$IWHUUHFHLYLQJWKHSDWLHQWLWKDVWREHQRWL¿HGWR ERDUG(DUO\VSLQDOEUDFLQJLIEDFNLVZHDN
$)3VXUYHLOODQFHRI¿FHDQGVWRROVDPSOHVKRXOG TT 6XSSRUWWKHIHHWE\ULJLGERDUGVDWÛDQJOH

EHVHQW VDPSOHVRIJPVWRROHDFKWR TT $SSO\SDVVLYHUDQJHRIPRYHPHQWIRUWKHMRLQWV

EHFROOHFWHGKRXUVDSDUWZLWKLQGD\VRI TT 3RVLWLRQKLS NQHHVDVVWUDLJKWDVSRVVLEOHDQGDUPVLQ

RQVHWRI$)3 WREHVHQWLQFROGER[DWƒ&WR abduction with mild support
1DWLRQDO/DEIRU3ROLR Measles at IPH building, TT $YRLGIRUFHIXOH[HUFLVHDVWKLVPD\LQFUHDVHSDUDO\VLV

Mohakhali, Dhaka). XX No IM injection during acute phase

XX 'RLQWXEDWLRQRUWUDFKHRVWRP\IRUYHQWLODWLRQDQGVHFUHWLRQ
XX 3&5LVWKHPHWKRGRIFKRLFHIRUSROLRGHWHFWLRQ control
Poliomyelitis

XX 'RFDWKHWHUGUDLQDJHRIXULQDU\EODGGHULIUHTXLUHG
Treatment XX 7UHDWSXOPRQDU\DWHOHFWDVLVDQGLQIHFWLRQVZLWKDQWLELRWLFV
Counsel parents that polio is a non curable disease and chest physiotherapy
and the treatment is mainly supportive and
 Step on to Paediatrics 233

Treatment in the convalescent mediated demyelinating neuropathy where there is

stage (upto 2 years) GDPDJHRIP\HOLQVKHDWKDQGDOVRGHJHQHUDWLRQRI
XX (QFRXUDJHVLWWLQJXSLIWKHSDUDO\VLVLVQRWVHYHUH WKHD[RQ7KLVGDPDJHRIP\HOLQVKHDWKRISHULSKHUDO
XX 6WDUWSDVVLYHH[HUFLVH¿UVWDQGWKHQEHJLQDFWLYHDVVLVWHG QHUYHVEORFNVLQWHUIHUHVZLWKFRQGXFWLRQRIQHUYH
WRDFWLYHUHVLVWHGH[HUFLVHV impulse.
XX *UDGXDOO\LQWURGXFHVLWWLQJEDODQFHWUDLQLQJ VWDQGLQJ
balance training in parallel bars, gait training etc. Types
XX Crutches, leg brace (calipers) and other devices may
help the child to move better and prevent contractures or
XX $FXWHLQÀDPPDWRU\GHP\HOLQDWLQJ
GHIRUPLWLHV polyneuropathy (AIDP)
XX Introduce active games, swimming and other activities to
XX $FXWHPRWRUD[RQDOQHXURSDWK\ AMAN)
keep limb moving XX $FXWHPRWRUVHQVRU\D[RQDOQHXURSDWK\
(AMSAN)
Prevention XX Miller-Fisher syndrome (MFS)
XX ,PPXQL]HZLWKSROLRYDFFLQHDFFRUGLQJWR(3, 1,' XX *%6ZLWKVHYHUHEXOEDUDQGIDFLDOSDUDO\VLV
programme XX Congenital GBS
Prognosis
XX Paralyzed muscles generally recover power to a variable
GHJUHHRYHUWLPH,IQRUHFRYHU\E\PRQWKVWKHQLWZLOO Clinical Manifestations
be parmanent XX 3DLQ WHQGHUQHVVLQPXVFOHVRIQHFNEDFNEXWWRFN
XX Mortality is about 5-10%, mostly due to cardio-respiratory and leg at the onset
G\VIXQFWLRQ XX $EUXSWRQVHWRI±
TT Symmetrical weakness usually in the lower

H[WUHPLWLHV
TT Progressive ascending paralysis gradually

LQYROYLQJWKHWUXQNDQGXSSHUOLPEVDQGIQDOO\
GUILLAIN–BARRÉ SYNDROME
the bulbar muscles, a pattern known as Landry
(GBS) ACUTE POST-INFECTIOUS ascending paralysis
DEMYELINATING POLYNEUROPATHY TT 'LVWDOPXVFOHVPRUHDIIHFWHGWKDQSUR[LPDO

muscles
GBS is a SRVWLQIHFWLRXVSRO\QHXURSDWK\involving mainly
XX $IIHFWHGPXVFOHVVKRZVLJQVRIORZHUPRWRUQHXURQ
motor but sometimes sensory and autonomic nerves as well.
paralysis e.g.
Aetiology
XX 3URIRXQGPXVFOH
7KHSDWKRJHQLFWULJJHUVDUH± XX /RVVRIGHHS
weakness
WHQGRQUHÀH[HV
XX /RVVRIPRYHPHQW
XX &DPS\OREDFWHUMHMXQL XX $EVHQFHRISODQWHU
virus, Cytomegalovirus, XX Reduced tone and
(most common) UHÀH[HV
Enteroviruses, Hepatitis strength
XX Mycoplasma pneumoniae
A and B, Varicella
XX Viruses e.g. Epstein-Barr
XX 5HVSLUDWRU\IDLOXUHGXHWRSDUDO\VLVRIGLDSKUDJP 
RWKHUPXVFOHVRIUHVSLUDWLRQDQGSUHVHQWVDV±
Guillain–Barré syndrome

Pathogenesis
The syndrome usually XX Dyspnoea
develops 1-4 weeks XX 3URPLQHQFHRIDFFHVVRU\PXVFOHVRI
DIWHUDJDVWURLQWHVWLQDO respiration
QDWL th
GHP lin she to
RQ
a
mye mage

&DPS\OREDFWHU XX Cyanosis
Source: Internet
\HOL

MHMXQL or respiratory 3URJUHVVLYHHOHYDWLRQRIWKHUHVSLUDWRU\UDWH

Da

XX

tract 0\FRSODVPD XX Tachycardia

pneumoniae LQIHFWLRQ XX $JLWDWLRQFRQIXVLRQFRPD
The major pathological
event is an immune
 234 Step on to Paediatrics

XX %XOEDUSDOV\5HVXOWVIURPWKHZHDNQHVVSDUDO\VLV Treatment
RIPXVFOHVVXSSOLHGE\WKHPRWRUQXFOHLRI99,,
IX-XII, cranial nerves. Muscles involved are: $6SHFL¿F
TT 0XVFOHVRIMDZ IDFH XX ,QWUDYHQRXVLPPXQRJOREXOLQ ,9,* PJNJGD\IRU
TT 6WHUQRFOHLGRPDVWRLGDQGXSSHUSDUWRI7UDSH]LXV consecutive days (total dose 2 g/kg)
TT 0XVFOHVRIWRQJXHSKDU\Q[DQGODU\Q[SUHVHQWV
XX Plasmapheresis +HUHZKROHEORRGGUDZQIURPSDWLHQWLV
DV± separated into plasma and blood cells; the plasma is replaced
with saline/albumin or specially prepared donor plasma,
XX Dysarthria UHFRQVWLWXWHGZLWKEORRGFHOOVDQGUHWUDQVIXVHGLQWRWKH
XX '\VSKDJLD RIWHQZLWKFKRFNLQJHSLVRGHV patient):+HOSVVSHHG\UHFRYHU\,WLVPRUHEHQH¿FLDOZKHQ
DQGQDVDOUHJXUJLWDWLRQRIÀXLGV VWDUWHGZLWKLQVHYHQGD\VRIWKHGLVHDVHRQVHW
XX '\VSKRQLD QDVDOLQWRQDWLRQRIYRLFH  XX &RPELQDWLRQRI,9,*DQGLQWHUIHURQ
XX Poor cough and susceptibility to aspiration XX Corticosteroids: No role
pneumonia
B. Supportive
XX Counsel parents about the disease, prognosis and to provide
XX 0DQLIHVWDWLRQVRIDXWRQRPLFLQYROYHPHQWDUH± psychological support
XX %HGUHVW SQHXPDWLFEHGLVSUHIHUDEOH DQGIUHTXHQWFKDQJH
XX )OXFWXDWLRQRI%3DQGKHDUWUDWH RISRVWXUHWRDYRLGEHGVRUHV
XX )OXFWXDWLRQRIERG\WHPSHUDWXUH XX )HHGLQJ1*WXEHIHHGLQJLIXQDEOHWRWDNHRUDOO\
XX Maintain personal hygiene e.g. bathing, hand washing etc.
XX %ODGGHUG\VIXQFWLRQ8VXDOO\DEVHQWEXWPD\ XX &DUHRIERZHO%\HQVXULQJUHJXODUERZHOPRYHPHQWE\D
occur on about 20% cases, sometimes there may KLJK¿EHUGLHWDGHTXDWHDQGWLPHO\ÀXLGLQWDNHPHGLFDWLRQV
be pain at the back (radiculopathy) to regulate bowel evacuations e.g. /DFWXORVHHQHPDLI
XX &RPSOLFDWLRQVRILPPRELOLW\Aspiration necessary
pneumonia, bed sore etc. XX &DUHRIWKHEODGGHU%\FDWKHWHUL]DWLRQZLWKUHJXODUFKHFNXS
XX $YRLGDQFHRIDVSLUDWLRQSQHXPRQLDE\FOHDULQJWKHWKURDWRII
secretions by oropharyngeal suction, chest physiotherapy
Diagnosis XX $VVLVWHGYHQWLODWLRQLIUHVSLUDWRU\IDLOXUH(arterial PO2IDOOV
'LDJQRVLVEDVHGRQFOLQLFDOZLWKVXSSRUWIURPWKU EHORZPP+J
relevant investigations XX 0DQDJHPHQWRISDLQZLWK16$,'Ve.g. ,EXSURIHQ
XX Physiotherapy
Investigations TT 6KRXOGEHVWDUWHGEHIRUHUHFRYHU\EHJLQVE\PRYLQJ

XX CSF study: characteristic Albumino-Cytological SDWLHQWV¶OLPEVPDQXDOO\WRKHOSNHHSWKHPXVFOHVÀH[LEOH

GLVVRFLDWLRQHYLGHQWDIWHUGD\VRIRQVHWRI and strong
symptoms
TT Cytology: Usually normal (<10 cells/cmm)
Follow up
TT Biochemistry: Increased protein (may be as high
XX Improvement usually occurs in 2-3 weeks but may need 1 to
2 months
as 400-500 mg/dl). Increased CSF protein is
WKRXJKWWRUHÀHFWWKHZLGHVSUHDGLQÀDPPDWLRQ
XX Sometimes complete recovery may occur in 1-2 years
RIWKHQHUYHURRWV Prognosis
TT Glucose: Normal
XX 0RUHWKDQRIFKLOGUHQUHFRYHUIXOO\ZKLOHDVPDOO
XX Stool culture: &MHMXQLPD\EHIRXQG minority has mild weakness. PredictorsRISRRURXWFRPH
Motor nerve conduction velocity: Reduced
Transverse myelitis

XX
DUH±
XX (OHFWURP\RJUDP (0* 6KRZVHYLGHQFHRIDFXWH TT Cranial nerve involvement

GHQHUYDWLRQRIPXVFOH TT 5HTXLUHGLQWXEDWLRQ

XX Sural nerve biopsy: Shows segmental TT 0D[LPXPGLVDELOLW\DWWKHWLPHRILQLWLDOSUHVHQWDWLRQ

GHP\HOLQDWLRQIRFDOLQÀDPPDWLRQDQG:DOOHULDQ XX 0RUWDOLW\LVORZ ± DQGJHQHUDOO\UHVXOWVIURP

GHJHQHUDWLRQ±ZKLFKLVGLDJQRVWLFBut virtually UHVSLUDWRU\IDLOXUHFDUGLDFDUUK\WKPLDKHPRG\QDPLF
QHYHUUHTXLUHGIRUGLDJQRVLV instability etc.
 Step on to Paediatrics 235

TRANSVERSE MYELITIS (TM) Investigations

XX 05,RIVSLQH0LOG
The term transverse means across the width, IXVLIRUPVZHOOLQJ
P\HOLWLVUHIHUVWRLQÀDPPDWLRQRIWKHVSLQDOFRUG6R RIFRUGRYHUVHYHUDO
WUDQVYHUVHP\HOLWLVPHDQVLQÀDPPDWLRLQDFURVVWKH segment, most
ZLGWKRIRQHOHYHORUVHJPHQWRIVSLQDOFRUG IUHTXHQWO\LQWKRUDFLF
segments
Aetio-Pathogenesis XX CSF study
,QÀDPPDWLRQRIVSLQDOFRUGFDXVHV± TT Cytology:

XX 'DPDJHRUGHVWUXFWLRQRIQHUYHFHOOVLQWKH Moderate

Source: Internet
LQÀDPHGVHJPHQW pleocytosis (50-
XX ,QWHUUXSWLRQRIFRQQHFWLRQEHWZHHQEUDLQDQG 100 lymphocytes/
VSLQDOQHUYHVEHORZWKHOHYHORIOHVLRQ mm3).
TT Biochemistry:

Elevated protein
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DUH±
Treatment Fusiform swelling of spinal cord in TM
XX $WWKHOHYHORIOHVLRQ 6LJQVRI/01OHVLRQ
XX %HORZWKHOHYHORI
A. Supportive
6LJQVRI801OHVLRQ XX Counsel parents about the disease, its prognosis and provide
lesion
psychological support
XX $ERYHWKHOHYHORI %HGUHVW SQHXPDWLFEHGLVSUHIHUDEOH DQGFKDQJHRISRVWXUH
1RUPDOQHUYHIXQFWLRQ XX
lesion 2 hourly to avoid bed sores
/01/RZHUPRWRUQHXURQ8018SSHUPRWRUQHXURQ XX Maintain personal hygiene e.g. bathing, hand washing etc.
XX Ensure chest physiotherapy to prevent hypostatic pneumonia
Clinical Manifestations XX &DUHRIXULQDU\EODGGHU%\FDWKHWHUL]DWLRQ
XX 1RQVSHFL¿FV\PSWRPV± XX &DUHRIERZHO(QVXULQJUHJXODUERZHOPRYHPHQWE\±
TT ,QLWLDOO\SDUDHVWKHVLDVDVFHQGLQJIURPWKHIHHW
TT +LJK¿EHUGLHW
or
TT $GHTXDWHDQGWLPHO\ÀXLGLQWDNH
TT %DFNSDLQDWWKHOHYHORIP\HOLWLV XVXDOO\DW
TT Medications to regulate bowel evacuations e.g. Lactulose
thoracic level)
TT (QHPDLIQHFHVVDU\
XX Sensory loss: /RVVRIVHQVDWLRQ ZLWKDGH¿QLWH
upper level. Pain, temperature, and light touch
XX Physiotherapy
TT Should be started when pain subsides. It is done by passive
VHQVDWLRQDUHDIIHFWHGEXWMRLQWSRVLWLRQDQG
vibration sense may be preserved PRYHPHQWRISDWLHQWV¶OLPEV
XX 0RWRUG\VIXQFWLRQ&KDUDFWHUL]HGE\ÀDFFLG XX Anti-spasticity drugs e.g. oral/intrathecal %DFORIHQ
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TT Sweating
improvement with IV steroids
TT Urinary retention with dribbling

TT No spontaneous bowel movement Prognosis

XX 5HFRYHU\PD\RFFXURYHUDSHULRGRIZHHNVRUPRQWKV
XX One third completely recovers, one third live with residual
symptoms and the remaining show no improvement at all
 236 Step on to Paediatrics

Differences between the common causes of AFP

Parameters Poliomyelitis GBS TM

Asymmetric paralysis, Symmetrical ascending paralysis,
,QLWLDOO\/01VXEVHTXHQWO\
Paralysis SUR[LPDOPXVFOHVDUHPRUH GLVWDOPXVFOHVDUHPRUHDIIHFWHGWKDQ
UMN paralysis
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6LWHRIOHVLRQ cord and motor cranial nerve Peripheral nerves RIRQHOHYHORUVHJPHQWRI
nuclei at medulla spinal cord
3UHVHQWZLWKDGHILQLWHXSSHU
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level
Cranial
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nerve Usually absent
FRPPRQO\,; ; are VII, IX, X, XI, XII
involvement
Respiratory 3UHVHQWLQERWK%XOEDU 
3UHVHQW /LIHWKUHDWHQLQJ Usually absent
LQVXIILFLHQF\ Bulbo-spinal polio
Autonomic May be present HJIOXFWXDQW%3
Absent May be present
involvement ERG\WHPSHUDWXUHH[FHVVLYHVZHDWLQJ
Bladder
Present Usually absent Usually present
G\VIXQFWLRQ
Cytology: Moderate
Cytology: Pleocytosis, mostly Cytology: Usually normal (<10/cmm)
pleocytosis
CSF changes lymphocyte Biochemistry: Protein
Biochemistry: Mild elevation
Biochemistry : Protein normal (Albumino-Cytological dissociation)
RISURWHLQ

References
Transverse myelitis

 6DUQDW+%*XLOODLQ±%DUUHV\QGURPH,Q1HOVRQ7H[WERRNRI3HGLDWULFVth Ed. New Delhi: Elsevier; 2016: 3010-3012.

 5HNDWH+/7UDQYHUVHP\HOLWLV,Q1HOVRQ7H[WERRNRI3HGLDWULFVth Edition. New Delhi: Elsevier; 2016: 2958-2959.
 +XJKHV5$&HWDO,9,*IRU*%6&RFKUDQH'DWDEDVHRI6\VWHPDWLF5HYLHZV,VVXH$UW1R&'
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5. Levin MJ. Current Pediatric diagnosis and Treatment, 23rdHG
 Step on to Paediatrics 237

SELF ASSESSMENT
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Self assessment
 31
Convulsion
Febrile convulsion/seizure - - - - - - - - - - -
- 238
Meningitis - - - - - - - - - - - - - - 240
Tubercular meningitis - - - - - - - - - - - - 244
Viral encephalitis- - - - - - - - - - - - - 245
Epilepsy/Recuraent seizures
¼¼ Status epilepticus- - - - - - - - - - - - - 248
Intracranial space occupying lesions - - - - - - - - - - 250

Convulsion represents many serious underlying

Convulsions
neurological illnesses. Convulsions not associated
associated with
with fever
It is a sudden, fever
transient brain XX Epilepsy
G\VIXQFWLRQ XX Febrile XX Encephalopathy e.g.
PDQLIHVWHGE\ convulsion TT hypertensive, hepatic or

involuntary motor, XX Acute XUDHPLFK\SR[LFLVFKDHPLF

sensory, autonomic meningitis- XX Trauma e.g. head injury
or psychic bacterial or XX Acute stroke syndrome
phenomena alone viral
XX Intracranial space occupying
or in combination, XX Cerebral
lesions
RIWHQDFFRPSDQLHG malaria
XX Metabolic abnormalities e.g.
by loss/alteration XX Viral
TT Hypoglycaemia,

in consciousness. encephalitis
hypocalcaemia
Convulsions may
XX Tubercular
TT Hypo or hypernatraemia

occur either with meningitis

TT Hypomagnesaemia
(TBM)
IHYHURUZLWKRXW TT 3\ULGR[LQHGH¿FLHQF\

IHYHU
XX Brain abscess
dependency
The conditions
JLYHQLQWKHER[
should be taken
into consideration
Febrile convulsion

whenever a child FEBRILE CONVULSION/SEIZURE (FS)

presents with
Febrile seizure are seizures that occur between the age
convulsion. In
RIPRQWKVDQGPRQWKVZLWKDWHPSUDWXUHRIƒ&
this section, the
ƒ) or higher, that are not due to
common causes
RIFRQYXOVLRQLQ
TT &16LQIHFWLRQRU
children will be
TT Any metabolic imbalance and
GLVFXVVHGEULHÀ\ &RQYXOVLQJFKLOGZLWK¿[HGVWDUHDQGULJLGLW\
TT WKDWRFFXULQWKHDEVHQFHRIDKLVWRU\RISULRU
$IHEULOHVHL]XUH
7HPS& UHIFXUUHQWSHGGLDJ WUHDWUGHGS 
238
 Step on to Paediatrics 239

Types Diagnosis
Pattern of %DVHGRQFKDUDFWHULVWLFFOLQLFDOIHDWXUHVDQGDEVHQFHRI
Types Duration Recurrence DQ\HYLGHQFHRIPHQLQJLWLVFOLQLFDOO\ LQ&6)SUR¿OH
seizure

< 15 No recurrence Investigations

Simple GTCS
minutes within 24 hours While managing such a case, the most important
decision is to rule out meningitis by CSF study. Other
Focal
&RPSOH[ • Recurrence LQYHVWLJDWLRQVDUHSODQQHGWR¿QGRXWWKHFDXVHRIIHYHU
seizures
(Atypical) minutes within 24 hours DQGDOVRRIFRQYXOVLRQ7KHVHDUH±
(usually)
Febrile status ! Focal or
XX %ORRGIRU&%&3%)&6
epilepticus minutes generalized XX Random blood sugar (RBS)
XX Serum Calcium
Febrile Serum electrolytes
Recurrence within 24 hours XX
seizure plus XX 7KURDWVZDEIRU&6
GTCS: Generalized tonic clonic seizure XX X-Ray chest
XX Urine R/M/E, C/S
Characteristics of Simple FS XX ((*1RWUHTXLUHGLQVLPSOHIHEULOHVHL]XUH
XX Neuro-imaging: No role
XX Convulsion/seizure occurs among children between
PRQWKVWR\HDUVZLWKDSHDNDJHRIDURXQG Indications of CSF study in febrile seizure
months
XX Seizures are mostly generalized, occurs usually once
XX $Q\VXVSLFLRQRIPHQLQJLWLV
LQKRXUVODVWIURPIHZVHFRQGVWRIHZPLQXWHV XX )LUVWDWWDFNRI)6RFFXUVDWDDJHRIPRQWKV
EXWQRWH[FHHGLQJPLQXWHVRFFXUHDUO\LQWKH XX &RPSOH[VLH]XUH
LOOQHVVFDXVLQJIHYHU XX Altered sensorium
XX $EVHQFHRIVLJQVRIPHQLQJLWLVe.g. bulging XX Recovery is slow or prolonged post-ictal sleep
IRQWDQHOOHVWLIIQHFNVWXSRUDQGLUULWDELOLW\
XX 1RUHVLGXDOQHXURGH¿FLW
XX 0D\KDYHIDPLO\KLVWRU\RIIHEULOHFRQYXOVLRQ
Treatment
XX &RXQVHOSDUHQWVDERXWWKHQDWXUHDQGIXWXUHRIWKH
Clinical Evaluation disease
History XX Maintain airway, breathing and circulation (see status
XX $JHRIWKHFKLOG epilepticus p 254)
XX 1DWXUHRIIHYHU
XX 6WRSVHL]XUHE\HLWKHU±
TT Inj. Diazepam (0.5 mg/kg) per rectal (PR) or 0.2-0.3
XX 7\SHV GXUDWLRQRIVHL]XUH
mg/kg slow IV or
XX )DPLO\KLVWRU\RIVHL]XUHGLVRUGHURUIHEULOHVHL]XUH
TT Inj. Midazolam (0.2 mg/kg) smeared on buccal
XX 'HYHORSPHQWDOVWDWXVRIWKHFKLOG
mucosa or instilled intranasally
Physical Examination XX 5HGXFHERG\WHPSHUDWXUHE\±
TT Paracetamol (15 mg/kg/dose), 6 hourly, orally or per
XX 7RDVVHVVSDWLHQW¶VQHXURORJLFVWDWXVHJOHYHORI
consciousness rectally
TT Tepid sponging
XX To check airway, breathing and circulation
Febrile convulsion

XX 7RFKHFNDQWHULRUIRQWDQHOOH XX $SSURSULDWHDQWLELRWLFVWRWUHDWDVVRFLDWHGLQIHFWLRQ
XX 7RFKHFNVLJQVRIPHQLQJHDOLUULWDWLRQe.g. neck 2QHLPSRUWDQWFKDUDFWHULVWLFVRI)6LVLW¶Vhigh tendency
VWLIIQHVVSRVLWLYH.HUQLJ¶VVLJQ %UXG]LQLVNL¶VVLJQ WRUHFXUGXULQJIXWXUHIHEULOHHSLVRGHV.7KHIROORZLQJ
XX Assess others HJ2)&VWDWXVRIFUDQLDOQHUYHVHWF are the Risk factorsIRUWKHUHFXUUHQFHV±
XX 7R¿QGRXWWKHFDXVHRIIHYHUe.g. otitis media,
pneumonia, UTI, tonsilitis, pharyngitis or any viral
H[DQWKHP
 240 Step on to Paediatrics

ACUTE PYOGENIC MENINGITIS

XX MajorULVNIDFWRUV
TT Age <1 yr
$FXWHS\RJHQLFPHQLQJLWLVLVWKHOHDGLQJFDXVHRIGHDWK
TT 'XUDWLRQRIIHYHUKU(i.e. have a shorter
and neurodisability among children.
LQWHUYDOEHWZHHQWKHRQVHWRIIHYHUDQGWKH
seizure) Risk factors
TT )HYHUƒ& ƒ)i.e. have a lower XX Neonates
GHJUHHRIIHYHUEHIRUHWKHLUVHL]XUH TT 0DWHUQDOXURJHQLWDOLQIHFWLRQ
XX MinorULVNIDFWRUV TT Prematurity

TT )DPLO\KLVWRU\RIIHEULOHVHL]XUHV TT 1HXUDOWXEHGHIHFW VSLQDEL¿GD

TT )DPLO\KLVWRU\RIHSLOHSV\ XX ,QIDQWV &KLOGUHQ

TT &RPSOH[IHEULOHVHL]XUH TT Septicemia, pneumonia,otitis media, mastoiditis

TT Daycare TT Head trauma

TT Male gender TT Asplenia / splenectomy

TT Lower S NaDWWLPHRISUHVHQWDWLRQ

Organisms
5HFXUUHQFHVLQUHODWLRQWRSUHVHQFHRIULVNIDFWRU XX Neonatal period: E. coli, Gr. B Streptococci,
1R•
L. monocytogenes
XX Beyond neonatal period: H. influenzae, Strept.
How to Prevent future recurrence of FS? pneumoniae, N. meningitides
XX 5HGXFWLRQRIERG\WHPSHUDWXUHE\DGHTXDWHGRVHRI Route of entry of organisms in CNS
paracetamol and tepid sponging XX Through blood (bacteremia/septicaemia)
XX $QWLFRQYXOVDQWSURSK\OD[LV XX 'LUHFWH[WHQVLRQIURPWKHVXUURXQGLQJLQIHFWLRQe.g.
TT &RQWLQXRXVSURSK\OD[LVQRWUHFRPPHQGHG
otitis media, mastoiditis etc
TT Intermittent prophylaxis ZLWKHLWKHURIWKH

IROORZLQJGUXJLVUHFRPPHQGHGWLOO\HDUVRIDJH Pathogenesis
³³ Oral 'LD]HSDPPJNJGD\ PD[PJ LQ
$IWHUHQWU\LQWRWKHFKRURLGSOH[XVRIODWHUDOYHQWULFOH
GLYLGHGGRVHVIRUKRXUV25 WKHRUJDQLVPVQH[WHQWHULQWRWKHH[WUDFHUHEUDO&6)
³³ Oral &ORED]DPPJNJGD\ PD[PJ DV
and sub-arachnoid space, where they multiply and cause
VLQJOHEGGRVHVIRUKRXUV LQÀDPPDWLRQRIWKHDGMDFHQWPHQLQJHV PHQLQJLWLV DQG
Prognosis UHOHDVHPDQ\LQÀDPPDWRU\PHGLDWRUVZKLFKDOVRDIIHFW
XX Good, as it is a benign condition and leaving behind no DQGLUULWDWHDGMDFHQWQHUYHURRWV7KHLQÀDPPDWRU\SURFHVV
death or neuro-disability WKHQIXUWKHUVSUHDGVWRWKHDGMDFHQWEUDLQWLVVXHDQGFDXVHV
XX +RZHYHURQO\RIFKLOGUHQZKRH[SHULHQFH)6 their damage to
SURFHHGWRGHYHORSHSLOHSV\ODWHULQWKHLUOLIH TT Brain FHUHEULWLVFHUHEUDOLQIDUFWLRQVWURNH
TT Blood vessels (vasculitis, vasodilatation, vasospasm,
vascular occlusion) etc.
The net clinico-pathological effects of this
MENINGITIS
LQÀDPPDWLRQDUH±
5HIHUVWRLQÀDPPDWLRQRIleptomeninges HJSLD  XX Signs of meningeal irritationGXHWRLUULWDWLRQRI
arachnoid mater and CSF within the subarachnoid spaces. spinal nerve roots
vPyogenic meningitis

It is usually caused by microorganisms and is broadly XX Raised intra cranial pressure (ICP) due to
JURXSHGDV± '' &\WRWR[LFFHUHEUDOHGHPDIURPFHOOGHDWK

a) Acute pyogenic meningitis '' Vasogenic cerebral edema due to increased

b) Acute viral meningitis vascular permeability

'' Interstitial cerebral edema due to increased
c) Chronic (TB, spirichetal) meningitis hydrostatic pressure
In this chapter, we will discuss acute pyogenic and
tubercular meningitis.
 Step on to Paediatrics 241

TT 6LJQVRIPHQLQJHDOLUULWDWLRQe.g.
XX Hydrocephalus ³³ Neck rigidity
'' ,QLWLDOO\FRPPXQLFDWLQJLHREVWUXFWLRQRI
³³ .HUQLJ¶VVLJQ PD\QRWEHSUHVHQWPRQWKV
DUDFKQRLGYLOOLDURXQGFLVWHUQDWWKHEDVHRIWKH
³³ %UXG]LQVNL¶VVLJQ
EUDLQE\SXUXOHQWPHQLQJHDOH[XGDWH
'' /DWHUQRQFRPPXQLFDWLQJGXHWR¿EURVLVDQG

JOLRVLVRIDTXHGXFWRI6\OYLXVIRUDPHQRI/XVKND
DQGIRUDPHQRI0DJHQGL
XX Convulsion GXHWRFHUHEUDOLQIDUFWLRQFHUHEULWLV
electrolyte imbalance
XX &HUHEUDOLQIDUFWLRQVWURNHFUDQLDOQHUYHSDOV\GXHWR
YDVRVSDPYDVFXODURFFOXVLRQ WKURPERVLV

Clinical Manifestations
A. Older children: &ODVVLFDOO\SUHVHQWVZLWK±
Neck rigidity
XX +LJKIHYHU XX Recurrent convulsions
XX Vomiting XX $OWHUDWLRQRI
XX Headache consciousness

B. Neonates: 3UHVHQWDWLRQVDUH1RQVSHFL¿F±
XX 5HOXFWDQWWRIHHG XX %XOJHGIRQWDQHOOH
XX High-pitched cry XX 6WLIIQHVVRIOLPEV
XX Vacant look XX Convulsions
XX Hypo/hyperthermia XX Respiratory distress
XX Jitteriness XX (YLGHQFHRIVHSVLV

Physical Examination
XX 1HXURORJLFDOH[DPLQDWLRQWRDVVHVV
TT Altered sensorium/unconsciousness, stupor (a
Kernig's sign
VWDWHRIOHWKDUJ\DQGLPPRELOLW\ZLWKGLPLQLVKHG
responsiveness to stimuli)

Source: Internet
TT $QWHULRUIRQWDQHOOHWRDVVHVVDQ\EXOJLQJDPRQJ

QHRQDWHVDQGLQIDQWV

Brudzinski's sign
Pyogenic meningitis

TT 0XVFOHWRQHVWUHQJWKMHUNVSODQWHUUHÀH[ VLJQVRI
UMN lesion may be present, when complicated)
TT 3XSLODU\OLJKWUHÀH[

TT &UDQLDOQHUYHVWRDVVHVVIRUDQ\SDOV\

XX Fever: Usually high grade

XX (DU(YLGHQFHRIHDULQIHFWLRQPDVWRLGLWLV
XX +HPRG\QDPLFVWDWXV3XOVH%3FDSLOODU\UH¿OOWLPH
Bulged anterior fontanelle XX 6NLQIRUDQ\UDVKDVIRXQGLQPHQLQJRFRFFDHPLD
 242 Step on to Paediatrics

Features of cranial nerve palsy

Left 7th cranial nerve palsy

0LFURFHSKDO\DQGODWHUDOVTXLQW Hydrocephalus
OHIWUGFUDQLDOQHUYHSDOV\

Diagnosis
%DVHGRQ&) VXSSRUWVIURPUHOHYDQWLQYHVWLJDWLRQV

Investigations
I. Blood
TT CBC shows polymorphonuclear leukocytosis
TT &XOWXUH VHQVLWLYLW\WRNQRZWKHRUJDQLVPDQGWKH
antibiotic sensitivity pattern
7\SLFDOVNLQUDVK GLIIHUHQWVKDSHLUUHJXODUPDUJLQUHGGLVK
SHULSKHU\ZLWKQHFURWLFEODFNLVKFHQWUH RI0HQLQJRFRFFDOVHSVLV
2. CSFVWXG\7RFRQ¿UPWKHGLDJQRVLV
XX In Meningococcal infectionLQDGGLWLRQWRIHDWXUHVRI 3UHFDXWLRQVEHIRUHGRLQJ/3±
PHQLQJLWLVSDWLHQWPD\DGGLWLRQDOO\KDYH±
TT 0DUNHGWR[LFLW\ XX )XQGXVH[DPLQDWLRQWRUXOHRXWSDSLOORHGHPD
TT Purpura, petechiae, and occasionally bright pink XX 1RLQIHFWLRQDWWKHVLWHRI/3
WHQGHUPDFXOHVRUSDSXOHVRYHUWKHH[WUHPLWLHVDQG XX %OHHGLQJGLDWKHVLVWREHH[FOXGHG
trunk
TT Fulminant meningococcemia is characterized by

DIC, massive skin and mucosal haemorrhage and XX Physical appearance

TT )HDWXUHVRIVKRFNHJ/RZYROXPHSXOVHORZ%3 TT Pressure: Usually
QDUURZSXOVHSUHVVXUHSURORQJHG&57!VHF elevated
TT Colour: Hazy, cloudy

Complications or purulent 1RUPDO

&6)FU\VWDOFOHDU 
Immediate Long-term XX Cytological
XX Hydrocephalus XX Cerebral palsy TT Neutrophilic
Pyogenic meningitis

XX 6XEGXUDOHIIXVLRQ XX 'HDIQHVV leukocytosis usually Clear vs Purulent CSF

XX Subdural empyema XX Intellectual disability 300-2000 cells/cmm
XX Ventriculitis XX Epilepsy QRUPDOO\PSKRF\WHVFPP 
XX Cerebral abscess XX Visual impairment
XX &HUHEUDOLQIDUFWLRQe.g. XX Learning and language
1%&6)PXVWEHH[DPLQHGZLWKLQKRXURI/3WR
acute stroke disability
obtain correct results
XX Cranial nerve palsy
 Step on to Paediatrics 243

XX Biochemical Treatment
TT Glucose: Decreased, usually <40 mg/dl QRUPDOCSF

JOXFRVHPJGO RUOHVVWKDQUGRIEORRG A. Supportive

glucose. Corresponding blood sugar estimation is XX &RXQVHOSDUHQWVDERXWWKHQDWXUH IXWXUHRIWKH
UHFRPPHQGHGKDOIDQKRXUEHIRUH/3IRUWKLVSXUSRVH disease, treatment, prognosis etc
TT Protein: Increased, usually 100-500 mg/dl QRUPDO XX 1RWKLQJSHURUDOLIFRQYXOVLRQ DOWHUHGFRQFLRXVQHVV
PJGO XX Maintain airway, breathing and circulation (details
TT Chloride: Decreased,102-120 mmol/L QRUPDO given in status epilepticus, p-254)
PPRO/ XX To stop convulsion, give Inj. Diazepam 0.5 mg/kg per
XX Microbiological rectal (PR) or 0.2-0.3 mg/kg slow IV
TT Gram staining: May reveal the organisms XX 6WDUW,9ÀXLG1RUPDOGDLO\DOORZDQFHEXWUHVWULFW
TT 'HWHFWLRQRIEDFWHULDODQWLJHQV%\ODWH[ ZKHQSDWLHQWKDVIHDWXUHVRI6,$'+
TT GH[WURVHLQ1D&O %DE\VDOLQH RU
agglutination or by PCR.
TT Culture: May grow the causative organism TT GH[WURVHLQ1D&O -XQLRUVDOLQH

3. Other investigations
XX $GGPDLQWHQDQFHGRVHRI., 1-2 mmol/kg/day (not to
H[FHHGPHT/ WLOOSDWLHQWLVRQ132
TT Blood glucose, S. calcium
XX Give Paracetamol (15 mg/kg/dose) 6 hourly and tepid
TT S. electrolytes HJK\SRQDWUDHPLD K\SRFKURODHPLD
VSRQJLQJLIIHYHU
due to SIADH
XX *LYH1*WXEHIHHGLQJZKHQSDWLHQWLVVWDEOHe.g. no
TT *UDPVWDLQLQJ &XOWXUHRIVZDEWDNHQIURPWKHVNLQ
convulsion
UDVK7RVHDUFKIRUPHQLQJRFRFFDOLQIHFWLRQ
XX Monitor vital signs e.g. heart rate, respiration, urine
TT ;5D\FKHVW7RORRNIRUHYLGHQFHRISQHXPRQLD
output, BP or Capillary refill time 4-6 hourly during
TT 8ULQH50( &6WRH[FOXGH87, WKH¿UVWKRXUVRIWUHDWPHQW

%6SHFL¿F3DUHQWHUDO$QWLELRWLFV
Organisms Antibiotics of choice Duration
XX 8QNQRZQ &HIWULD[RQH&HIRWD[LPHSOXV9DQFRP\FLQ 10 days
XX Meningococcus Penicillin G GD\V
XX Pneumococcus &HIWULD[RQH9DQFRP\FLQ 10-14 days
XX H. influenzae &HIWULD[RQHRU&HIRWD[LPH GD\V
XX *UDP±YHEDFWHULD ,PPXQRFRPSURPL]HGSW 0HURSHQHPRU&HIRWD[LPH$PLNDFLQ 21 days
XX Pseudomonas &HIWD]LGLPH 14-21 days
XX L. monocytogenes &HIWULD[RQH$PSLFLOOLQ
&HIWULD[RQHPJNJGD\2QFHRUKRXUO\
Meropenem: 40mg/kg/dose 8 hourly
&HIRWD[LPHPJNJGD\KRXUO\
Amikacin: 20-30mg/kg/day 8 hourly
&HIWD]LGLPHPJNJGD\KRXUO\
Ampicillin: 300 mg/kg/day 6 hourly
Penicillin G: 300,000 units/kg/day 6 hourly
Tubercular meningitis

C. Adjunctive therapy XX UHGXFHVFHUHEUDORHGHPDQHXWURSKLOLQ¿OWUDWLRQDQG

XOWLPDWHO\SUHYHQWV±
,QPHQLQJLWLVPXFKRIWKHQHXURQDOGDPDJHUHVXOWV
TT Further neurologic damage particularly the
IURPhigh host immune responseDQGXVHRILPPXQH
sensorineural hearing loss
suppresants e.g. DexamethasoneLQWKLVUHJDUGLVIRXQG
TT Adhesion between meninges
EHQH¿FLDO,W±
XX VXSUHVVHVF\WRNLQHPHGLDWHGLQÀDPPDWRU\FDVFDGHWKDW Dose: PJNJGRVH,9KRXUO\IRUKRXUV,WRIIHUV
RFFXUVDIWHUUDSLGNLOOLQJRIEDFWHULDE\DQWLELRWLFV PD[LPXPEHQH¿WLIJLYHQKRXUVEHIRUHVWDUWLQJ
antibiotics.
 244 Step on to Paediatrics

D. Treatment of complications Clinical Manifestations

:KHQHYHUGHVSLWHVXI¿FLHQWWUHDWPHQWIHYHUSHUVLVWV 2QVHWRIWKHGLVHDVHLVJUDGXDODQGV\PSWRPVSURJUHVV
(brain abscess) or head size is increased (hydrocephalous) over several weeks and present through 3 stages:
RUDQ\HYLGHQFHRI(cranial nerve palsy) noted, evaluate
the cases thoroughly to detect and treat the complication.
XX 1RQVSHFL¿FV\PSWRPVe.g. low
Stage I JUDGHIHYHUKHDGDFKHPDODLVH
XX SIADH: Fluid restriction 6WDJHRI
irritability, behavioural change,
XX Raised ICP invasion/
drowsiness
TT (OHYDWHKHDGHQGRIEHGE\ƒ Prodromal stage
XX Focal neurological signs are absent
TT ,QIXVHK\SHUWRQLFVDOLQH

TT Frusemide (1mg/kg) XX 1HXURORJLFDOIHDWXUHVe.g. lethargy,

TT 0DQQLWRO JP.J  convulsions, vomiting
TT (7LQWXEDWLRQ +\SHUYHQWLODWLRQ 6LJQVRIPHQLQJHDOLUULWDWLRQ
Stage II XX

XX 6XEGXUDOHIIXVLRQ 6WDJHRI HJQHFNULJLGLW\.HUQLJ VRU

TT $VSLUDWHÀXLGWKURXJKRSHQDQWHULRUIRQWDQHOOH meningitis Brudzinski's signs, hypertonia
XX Cranial nerve palsies present
E. Follow up: 7RGHWHFWDQ\IXWXUHQHXURGH¿FLW XX Focal neurological signs present
F. Prophylaxis for Contacts of meningococci XX Marked by coma, hemiplegia or
XX 5LIDPSLFLQ PJNJGRVH RUDOO\HYHU\KRXUVIRU paraplegia
48 hours, OR Stage III
6WDJHRIFRPD XX Decerebrate/decorticate posturing
XX &LSURÀR[DFLQ PJ RUDOO\DVDVLQJOHGRVHIRU Terminal stage XX 'HWHULRUDWLRQRIYLWDOVLJQVDQG
SHUVRQV!\HDUV
XX Eventually death
G. Prevention:%\YDFFLQDWLRQZLWK±
XX Meningococcal conjugate vaccine: 2 doses are
UHFRPPHQGHGDQ\WLPHDIWHU\HDUVRIDJH
XX ([DPLQDWLRQRIIXQGXVChoroid tubercle is highly
XX +DHPRSKLOXVLQÀXHQ]DHW\SH%YDFFLQHGRVHVIURP VSHFL¿FIRU7%0
òPRQWKVRIDJH JLYHQLQ(3,VFKHGXOH
XX 3QHXPRFRFFDOFRQMXJDWHYDFFLQHGRVHVIURPò
PRQWKVRIDJH JLYHQLQ(3,VFKHGXOH

TUBERCULAR MENINGITIS (TBM)

$OVRGLVFXVVHGLQFKDSWHUDORQJZLWK7%

The most dangerous form of TB infection

Pathogenesis &KRURLGWXEHUFOHLQ7%0
7%EDFLOOLUHDFK&16E\KDHPDWRJHQRXVURXWHIURPD
SULPDU\7%IRFLLQOXQJV PLOOLDU\7% RUDQ\ZKHUHLQ Diagnosis
the body. Initially, small tuberculous lesion 5LFK¶VIRFL
%DVHGRQ±
Viral encephalitis

develop in the CNS (meninges, subpial or subependymal

VXUIDFHRIYHQWULFOHRURIVSLQDOFRUG which may remain
XX 7\SLFDOFOLQLFDOIHDWXUHVDVPHQWLRQHGLQWKHFKDUW
GRUPDQWWKHUHIRU\HDUV/DWHURQUXSWXUHRIWKHVHIRFL
XX +2FRQWDFWZLWKDQDGXOWLQIHFWLRXV7%SDWLHQW
into the subarachnoid space or into the ventricular system
XX $EVHQFHRISULRUBCG vaccination
results in meningitis.
XX (YLGHQFHRI7%LQIHFWLRQHOVHZKHUHLQWKHERG\e.g.
lungs and
XX 6XSSRUWVIURPUHOHYDQW,QYHVWLJDWLRQV
 Step on to Paediatrics 245

Investigations VIRAL ENCEPHALITIS

XX &6)VWXG\&ODVVLFDOIHDWXUHVLQ7%0DVZHOODVRWKHU
W\SHVRIPHQLQJLWLVDUHJLYHQLQWKHWDEOHEHORZ± ,WLVWKHLQÀDPPDWLRQRIEUDLQSDUHQFK\PD3DWLHQWV
KRZHYHUKDYHVRPHGHJUHHRIPHQLQJHDOLQÀDPPDWLRQ
CSF Pyogenic Tubercular Viral
as well.
May be
Pressure Elevated Elevated Aetiology
elevated
Hazy, cloudy Organism: (QWHURYLUXVHV+HUSHV6LPSOH[9LUXV
Colour Straw Usually clear (SVWHLQ%DUU9LUXVNipah, Japanese B encephalitis.
or purulent
PL[HG
Neutrophilic
cells initially; Clinical Manifestations
leukocytosis 10-500
Cells becoming 7KHRQVHWRIWKHGLVHDVHLVXVXDOO\DEUXSW$IWHUDÀXOLNH
300-2000/ lymphocytes
lymphocytic SURGURPHWKHUHLVDUDSLGGHWHULRUDWLRQRI&16IXQFWLRQ
cmm
by 36 hours DQGPRUHWKDQRISDWLHQWVVXFFXPELQWRFRPD
< 40 mg/dl
or <50% Seizure
Glucose < 40 mg/dl PJGO
RIEORRG
glucose
Epileptic Non
100-500 100-3,000 50-200
Protein
mg/dl mg/dl mg/dl
Gram May show May show Provoked Unprovoked HCR
stain/AFB the organism the bacilli Breath holding
Febrile seizure More than Attack
May be Gene-Xpert
one Syncope
detected &6)IRU Meningitis
Bacterial TICS
E\ODWH[ adenosine Encephalitis
antigen
agglutination de aminase Dyselectrolytemia Epilepsy
or PCR (ADA) Metabolic
disturbance
Culture May grow the organism

XX 0DQWRX[WHVW1RQUHDFWLYHLQDERXWRIFDVHV 7KHSDWLHQWVFRPPRQO\KDYH±
XX CBC: Hb% (reduced), DC (lymphocytosis), ESR (high) TT Fever, worsening headache, vomiting
XX X-Ray chest: May show miliary mottling TT 'URZVLQHVVFRQIXVLRQDQGEHKDYLRUDOFKDQJH
XX 05,RIEUDLQ$EQRUPDOPHQLQJHDOHQKDQFHPHQWLQ TT Convulsions and lethargy also develops rapidly
EDVDOFLVWHUQWKHSDWKRJQRPRQLFIHDWXUHRI7%0 TT Physical and neurological signs are variable
Treatment
XX &RXQVHOLQJSDUHQWVDERXWWKHQDWXUH IXWXUHRIWKH Diagnosis
disease. %DVHGRQ&) VXSSRUWVIURPUHOHYDQWLQYHVWLJDWLRQV
XX $QWL7%GUXJV GUXJV  +5= 6DQG +5 IRUWRWDO
12 months or more Investigations
XX 3UHGQLVRORQH PJNJGD\ IRULQLWLDOZHHNVDQG XX CSF study
gradual tapering by another 2 weeks TT 5RXWLQHH[DPLQDWLRQ

³³ Modest lymphocytic pleocytosis

Prognosis ³³ 0LOGULVHRISURWHLQ

&RUUHODWHVPRVWO\ZLWKWKHFOLQLFDOVWDJHRILOOQHVV  ³³ Glucose level remain normal

when treatment is initiated. It is good in 1st stage but most TT 3&5IRUYLUXVHVLQCSF

Epilepsy

patients in 3rd stage die and who survive have permanent TT Antibodies against viruses in CSF

disabilities OLNHEOLQGQHVVGHDIQHVVLQWHOOHFWXDOGLVDELOLW\
PRWRUGLVDELOLWLHVHWF
 246 Step on to Paediatrics

XX 05,RIEUDLQ %6SHFL¿F
TT Focal change XX Inj. $F\FORYLULIHerpes simplex encephalitis
³³ Temporal TT )RUROGHUFKLOGUHQ PJNJGRVH KRXUO\IRU
lobe days
pathology TT )RU1HRQDWHV PJNJGRVH KRXUO\IRUGD\V

is seen in
Herpes Precautions for contacts and health workers

Courtesy: Dr Narayan Saha

6LPSOH[ XX Close contacts and medical personnel should maintain
encephalitis
standard safety protocols like hand washing, using
³³ Bilateral
gloves and masks while attending the patients
thalamic
haemorrhage
seen as Eyes
RI3DQGDin CEREBRAL MALARIA
Japanese B Panda sign
encephalitis 'LVFXVVHGLQWKHFKDSWHU

Treatment
&RXQVHOSDUHQWVDERXWWKHQDWXUH IXWXUHRIWKHGLVHDVH
A. Supportive EPILEPSY/RECURAENT SEIZURES
XX 1RWKLQJSHU2UDOLIFRQYXOVLRQ
XX 0DLQWHQDQFHRIDLUZD\EUHDWKLQJDQGFLUFXODWLRQ (SLOHSV\WKHFRPPRQHVWQHXURORJLFDOGLVRUGHUDIIHFWLQJ
(details given in page 254) 50 million people globally. Over 60% has its onset in
XX To control convulsion, give Inj. Diazepam 0.5 mg/kg childhood and the incidence is highest in the neonatal
per rectal or 0.2-0.3 mg/kg slow IV LIQRWFRQWUROOHG period.
WUHDWDVSHUDOJRULWKPGLVFXVVHGLQVWDWXVHSLOHSWLFXV
ESLOHSV\LVGH¿QHGDVWZRVHL]XUHVWKDWDUHVHSDUDWHGE\DW
XX *LYH,9ÀXLGôRIGDLO\PDLQWHQDQFHZLWK±
least 24 hours.
TT GH[WURVHLQ1D&O25

TT GH[WURVHLQ1D&O
A seizureLVDVXGGHQWUDQVLHQWGLVWXUEDQFHRIEUDLQ
IXQFWLRQPDQLIHVWHGE\LQYROXQWDU\PRWRUVHQVRU\
XX $GGPDLQWHQDQFHGRVHRI. @ 1-2 mmol/kg/day (not
WRH[FHHGPHT/ WLOOSDWLHQWLV132 autonomic or psychic phenomena, alone or in any
XX Paracetamol (15 mg/kg/dose 6 hourly) and tepid FRPELQDWLRQRIWHQDFFRPSDQLHGE\DOWHUDWLRQRUORVV
VSRQJLQJLIIHYHU RIFRQVFLRXVQHVV,WFDQEHFDXVHGE\DQ\IDFWRUWKDW
XX $OORZ1*WXEHIHHGLQJZKHQSDWLHQWLVVWDEOH GLVWXUEVEUDLQIXQFWLRQ7KH\PD\RFFXUDIWHUDPHWDEROLF
XX (QVXUHDGHTXDWHQXUVLQJHVSHFLDOO\WDNLQJFDUHRI± WUDXPDWLFDQR[LFRULQIHFWLRXVLQVXOWWRWKHEUDLQRU
spontaneously without prior known CNS insult.
XX (\HV$SSO\H\HGURSV RLQWPHQWWRSUHYHQW Aetio-pathogenesis
H[SRVXUHNHUDWLWLV&ORVHWKHH\HVZLWKFRWWRQSDG
LIQHFHVVDU\ XX Idiopathic
XX 0RXWK&OHDUPRXWKIURPVHFUHWLRQDSSO\ XX ,QWUDXWHULQHLQIHFWLRQe.g. TORCH, HIV
DQWLIXQJDOGURSVLIUHTXLUHG XX Abnormal brain development
XX Skin: Change posture 2 hourly. Gentle massage XX +\SR[LFLVFKDHPLFHQFHSKDORSDWK\
over pressure points to prevent bed sores XX &16LQIHFWLRQVe.g. meningitis, encephalitis
XX %ODGGHU&DWKHWHUL]DWLRQLIQHFHVVDU\ XX %UDLQLQMXU\ EUDLQWXPRU
XX Bowel: Ensure regular bowel movement.Give XX 1HXURPHWDEROLF QHXURGHJHQHUDWLYHGLVHDVHV
HQHPDLIQHFHVVDU\
XX Chromosomal disorders e.g. Fragile X, Trisomies
Epilepsy

XX Give appropriate Antibiotic to prevent secondary

LQIHFWLRQDVSLUDWLRQSQHXPRQLDDQG87,
 Step on to Paediatrics 247

&ODVVL¿FDWLRQ Clinical manifestations

(International League Against Epilepsy, 1981) XX 5HFXUUHQWDWWDFNVRIDIHEULOHVHL]XUHV7KH
FKDUDFWHULVWLFIHDWXUHVRIGLIIHUHQWW\SHVDUHGLVFXVVHG
Epileptic seizure previously
XX Sometimes patient may present with status
epilepticus.
Partial seizures Generalized seizures 8QFODVVL¿HGVHL]XUHV

Whenever, a child is suspected to have epilepsy, he/she

Simple &RPSOH[ Partial seizures VKRXOGEHHYDOXDWHGFOLQLFDOO\DVEHORZ±
with secondary
generalization
Clinical evaluation
Absence Myoclonic Tonic Clonic Atonic (drop attack) XX 3URYRFDWLRQRUWULJJHUIDFWRUVe.g., sleep
GHSULYDWLRQÀLFNLQJRIOLJKWPLVVLQJRU
A. Partial seizures:2QHFHUHEUDOKHPLVSKHUHLVDIIHFWHGDQG ZLWKGUDZDORIDQWLFRQYXOVDQWGUXJVHWF
FRQYXOVLRQVSUHVHQWRQRQHVLGHRIWKHERG\ XX Warning phase or Aura e.g. epigastric pain,
DEQRUPDOEHKDYLRXUIHHOLQJRIIHDUXQZHOOQHVV
Types Characteristics QXPEQHVVWLQJOLQJLQWKH¿QJHUVRUEULJKWOLJKWVLQ
RQHYLVXDO¿HOGHWF
6HL]XUHLQYROYHVRQHVLGHRIWKHERG\ )HEULOHRUDIHEULOH
Simple partial XX

and the patient remains consciousDIWHU Single or recurrent

seizure XX

the seizure XX Gap between two seizure events

&RPSOH[SDUWLDO 6HL]XUHLQYROYHVRQHVLGHRIWKHERG\ XX 0RWRUH[SUHVVLRQe.g. atonic, tonic, clonic,
seizure but the patient become unconscious myoclonic, athetoid etc.
XX 6HQVRU\H[SUHVVLRQe.g. pain, paresthesia
Partial seizures
6HL]XUHVWDUWVRQRQHVLGHRIWKHERG\  XX 'LVWULEXWLRQRIVHL]XUHVHJIRFDORUJHQHUDOL]HG
with secondary
then spreads throughout the whole body XX 5HVSRQVLYHQHVVRIWKHSDWLHQWe.g. alteration in
generalization
consciousness
XX 'XUDWLRQRIVHL]XUHDWWDFNV
B. Generalized seizures: Both cerebral hemispheres are
XX $VVRFLDWHGIHDWXUHVHJWRQJXHELWLQJORVVRI
DIIHFWHGDQGVHL]XUHVHYLGHQWRQERWKVLGHVRIWKHERG\
sphincter control etc.
Types Characteristics
XX Recovery phase e.g. post ictal stage (headache,
FRQIXVLRQDPQHVLDVOHHS SURPSWUHFRYHU\HWF
6XGGHQLQWHUUXSWLRQRIRQJRLQJDFWLYLWLHV 0LOHVWRQHVRIGHYHORSPHQW
Absence XX

EODQNVWDUHXSZDUGUROOLQJRIWKHH\HV
6XGGHQEULHIVKRFNOLNHPXVFOHFRQWUDFWLRQV
Myoclonic

ZKLFKPD\EHJHQHUDOL]HGRUFRQILQHGWRWKH Diagnosis
IDFHDQGWUXQNRURQHPRUHH[WUHPLWLHVRUWR %\FOLQLFDOHYDOXDWLRQ UHOHYDQWODERUDWRU\VXSSRUWV
JURXSRIPXVFOHVHYHQLQGLYLGXDOPXVFOH
5LJLGYLROHQWPXVFXODUFRQWUDFWLRQIL[LQJ
Investigations
XX Electroencephalogram (EEG) is sometimes
the limb in some strained position. There is
Tonic diagnostic. $QRUPDO((*GRHVQRWH[FOXGHHSLOHSV\
XVXDOO\GHYLDWLRQRIWKHH\HVDQGRIWKHKHDG
XX Neuro-imaging: Indicated in all suspected cases,
towards one side
ZKHUHWKHFDXVHLVQRWREYLRXVDIWHUFOLQLFDO
Clonic Repetitive clonic jerks HYDOXDWLRQ05,RIEUDLQLVPRUHVHQVLWLYHWKDQ&7
scan and is strongly recommended in partial epilepsy
Atonic %ULHIORVVLQPXVFOHWRQHODVWLQJIRU
GURS
VHFRQGVUHVXOWLQJLQIDOO
Epilepsy

DWWDFN

&8QFODVVL¿HGHJQHRQDWDOVHL]XUHLQIDQWLOHVSDVP
 248 Step on to Paediatrics

Treatment The Characteristics of True & Pseudoseizures

XX Counsel SDUHQWVDERXWWKHQDWXUHRIWKHGLVHDVH
SUHFLSLWDWLQJIDFWRUVFKDQFHRIUHFXUUHQFHDQG Epilepsy: True
Characteristics Pseudoseizures
LPSRUWDQFHRIUHJXODUPHGLFDWLRQV SURJQRVLV seizures
XX 6HOHFWLRQRIDQWLHSLOHSWLFGUXJ $('  2IWHQHPRWLRQDO
No association
DSSURSULDWHIRUVHL]XUHW\SH7KHWDEOHEHORZ XX Precipitating IDFWRUV$WWDFNV
ZLWKSUHVHQFHRI
VKRZLQJDOLVWRIDSSURSULDWH$('EDVHGRQWKH IDFWRUV VLWXDWLRQV generally occur in
others
seizure types SUHVHQFHRIRWKHUV
XX Movement pattern 9DULDEOHQRVSHFL¿F Similar pattern in
Seizure types Anti-epileptic drug of choice
during the attacks pattern GLIIHUHQWHSLVRGHV
XX Partial CBZ, PHT May have e.g.
XX +2VHOILQMXU\ No
XX GTCS SVA, CBZ,PHT,PB tongue biting

XX Absence SVA, ESM, CZP, CLB

XX Occurrence in sleep No May occur

XX Myoclonic SVA, CZP, CLB

XX H/O bowel
or bladder No 2IWHQSUHVHQW
XX Tonic SVA incontinence
XX Atonic SVA XX 5HFDOORIGHWDLOV Generally can Can not
XX 0L[HG SVA Preserved; may
Loss.
appear unresponsive
CBZ = &DUEDPD]HSLQH3+7 Phenytoin, XX Consciousness Unresponsive to
but response to
69$ 6RGLXP9DOSURDWH pain
SDLQIXOVWLPXOL
ESM = Ethosuximide PB = 3KHQREDUELWRQH
Bizarre,
CZP = Clonazepam, CLB = &ORED]DP Typical
nonsynchronous or
generalized
XX Movements may lie motionless
XX /LIHVW\OHPRGL¿FDWLRQ3DWLHQWVVKRXOG± tonic clonic
RUVWLIIQHVVRIOLPEV
TT EHDZD\IURPEULJKW ÀDVKLQJOLJKWVe.g. TV, movements
IRUORQJWLPH
9LGHRJDPHVPRELOHSKRQH¿UHSODFH
Post ictal
TT avoid driving, swimming, climbing tree etc.
XX 6WDWHRIFKLOGDIWHU 1RFRQIXVLRQQR FRQIXVLRQRU
XX 3HULRGLFPRQLWRULQJRIWKHFDVHWUHDWPHQWWR the ictal phase QHXURGH¿FLW Todds paralysis
QRWH± may occur
TT +RZLVWKHFRQWURORIVHL]XUH E\VHL]XUH
Hyperactive deep
diary) WHQGRQUHÀH[HV
No pathological
TT :KHWKHUDQ\VLGHHIIHFWVRIGUXJV XX 5HÀH[HV and Babinski
UHÀH[HV
UHÀH[DIWHU
Duration of treatment & seizure
Drug withdrawal XX Demonstration on
,IWKHSDWLHQWUHPDLQVseizure freeIRUDWOHDVW 2IWHQSRVVLEOH Not possible
XX
UHTXHVW
years, AED may be withdrawn gradually over the XX Stop on command &DQRIWHQVWRS Cannot stop
QH[WZHHNV
XX Secondary gain Generally present None
Prognosis
XX RIFKLOGUHQZLWKHSLOHSV\ZLOODFKLHYH
seizure remission with appropriate AED
medication
XX RIFDVHVPD\KDYHUHODSVH UHPDLQ
STATUS EPILEPTICUS (SE)
uncontrolled
6(LVGH¿QHGDVFRQWLQXRXVVHL]XUHDFWLYLW\RUUHFXUUHQWVHL]XUH
XX DUH³'LI¿FXOWWRWUHDWFRQWURO´IURPWKH
DFWLYLW\ZLWKRXWUHJDLQLQJRIFRQVFLRXVQHVVODVWLQJIRU!
outset
Epilepsy

minitus. Some authors advocated 5 minutes (rather than 30

6RPHWLPHVWUXHVHL]XUHVPD\EHFRQIXVHGZLWK minutes) as the time limit. This is a medical emergency and the
pseudo or psychogenic seizures major concern is irreversible brain injury.
 Step on to Paediatrics 249

Precipitating factors XX Others e.g.

XX Underlying neurologic disorders e.g. l sleep deprivation LQWHUFXUUHQWLQIHFWLRQHWF
l

TT &16LQIHFWLRQWXPRXU
Management
TT Metabolic abnormalities e.g. hypoglycaemia, hypo or
,QFOXGHVWKHIROORZLQJ6WHSVLQVHTXHQFH
hypernatraemia, hypocalcaemia, hypomagnesaemia
XX 6XGGHQZLWKGUDZDORI$('IURPDQHSLOHSWLFFKLOG,W XX 0DLQWHQDQFHRI$LUZD\%UHDWKLQJDQG&LUFXODWLRQ
FDQDOVRKDSSHQLIWKH$('DUHWDNHQLUUHJXODUO\ XX &RQWURORIFRQYXOVLRQ
XX ([SRVXUHWRÀXVKHGOLJKWIURP XX $VVHVVPHQWWR¿QGRXWWKHFDXVHRI6(
l video game TV computer etc.
l l
XX 3UHYHQWLRQRIUHFXUUHQFH

A. Management of Airway, Breathing and Circulation

A±Airway B–Breathing C–Circulation
XX Assess airway by looking at XX Assess breathing by looking XX Assess circulatory status by looking
TT Nose TT Respiratory rate (Tachypnoea/ TT Pulse e.g. volume, rate, rhythm
ASSESSMENT

TT Oral cavity apnoea) TT Blood pressure

TT Throat TT )ODULQJRIDODHQDVL TT Pulse pressure

TT 3KDU\Q[ TT Cyanosis TT &DSLOODU\UH¿OOWLPH

TT &KHVWPRYHPHQWH[SDQVLELOLW\ !VHFRQGV
IRUDQ\VHFUHWLRQRUYRPLWXV
that could obstruct the airway and recession
TT O saturations (SpO <90%)
2 2

XX Maintain airway by ,IWKHSDWLHQWKDYHG\VSQRHDRU XX Secure an IV line and start IV crystalloid

TT &OHDULQJWKHDLUZD\RI cyanosis ÀXLG(Baby saline/Junior saline/Normal
secretions, vomitus by XX Give O2 through saline)
suction with sucker or by TT Face mask (5L/min) ,ISDWLHQWLVLQVKRFNHJORZV\VWROLFEORRG
¿QJHUVZHHSPDQHXYHU or SUHVVXUHDQGFDSLOODU\UHILOOWLPH!VHFRQGV
TT Opening up the airway
TT Nasal catheter (1-2 L/min) XX Give IV Normal saline bolus (20 ml/kg)
ACTION

by KHDGWLOWFKLQOLIW rapidly
,IIHDWXUHVRILPSHQGLQJUHVSLUDWRU\
maneuver (to keep
IDLOXUH DSQRHD XX 5HDVVHVVDQGLIQRLPSURYHPHQWUHSHDWWKH
head and neck slightly
bolus
H[WHQGHG TT %DJ 0DVNYHQWLODWLRQRU
XX ,IVKRFNVWLOOSHUVLVWVJLYH±
TT Putting airway tube TT (QGRWUDFKHDOLQWXEDWLRQ
TT Inj. 'RSDPLQH —JNJPLQ and/or
TT Endotracheal intubation, TT Mechanical ventilation
TT Inj. 'REXWDPLQH —JNJPLQ
may be necessary to
maintain the airway

B. Control of Convulsion using the following algorithm

Status Epilepticus
([FOXGHFRQFRPLWDQWK\SRJO\FDHPLD 

35 'LD]HSDPPJNJPD[PJ
Status continue
other metabolic derangement

5HSHDWGRVHRI35 'LD]HSDPDIWHUPLQXWHV
Status continue
,93+7 GULSPJNJ 0D[PJKU#
Status epilepticus

”PJNJPLQ 0D[PJPLQ RURYHUPLQXWHV

Status continue
3% PJNJ 0D[PJ #”PJNJPLQ 0D[PJPLQ RURYHUPLQV
Status continue**
0LGD]RODPPJNJEROXV 0D[PJNJ WKHQPJNJKU
increase every 15 minutes up to 2 mg/kg
Status continue

353HUUHFWDO3+73KHQ\WRLQ3%3KHQREDUELWRQH 3URSRIROPJNJEROXV 0D[PJNJ 

*LYH,9JOXFRVH6RGLELFDUEDQWLRHGHPD0HDVXUHV then 2-10 mg/kg/hr Intubation under GA
HJFRUWLFRVWHURLG PDQQLWRO
 250 Step on to Paediatrics

Monitoring
XX Clinical e.g. heart rate, blood pressure, capillary
UH¿OOLQJWLPH &57 6S22UHVSLUDWRU\UDWH 
pattern
XX Laboratory e.g. CBC, glucose, calcium, magnesium,
ABG, anti-epileptic drugs level
XX Continuous EEG monitoring

&6FUHHQLQJWR¿QGRXWWKHFDXVHRI6(
TT CSF study
TT Sepsis screening
TT Neuroimaging
TT Metabolic screening
Clinical Manifestations
D. Prevention of recurences XX &DUGLQDOIHDWXUHVRIUDLVHG,&3
&RXQVHOSDUHQWVHPSKDVL]LQJWKHLPSRUWDQFHRI TT Headache
TT 5HJXODULQWDNHRIDQWLHSLOHSWLFGUXJV TT Nausea, vomiting

TT $YRLGLQJWKHULVNIDFWRUVRI6( TT Visual problem

TT Papilloedema

XX Cranial nerve palsy

XX 1RQVSHFL¿FIHDWXUHV
INTRACRANIAL SPACE OCCUPYING TT Change in

LESIONS (ICSOL) personality,

mentation and
ICSOL are the 2ndPRVWIUHTXHQWPDOLJQDQF\DPRQJ speech
children and adolescents. TT 'LVRUGHURI
Right 7th cranial nerve palsy
HTXLOLEULXPJDLWDQG
Aetiology coordination

XX Unknown, mostly Diagnosis

XX Radiation %DVHGRQ&)DQGVXSSRUWIURPUHOHYDQWLQYHVWLJDWLRQV
XX Hereditary syndromes
Investigations
XX CT scan/MRI
RIEUDLQ
Pathology
Tumor can occur anywhere inside the cranial cavity e.g.
cerebrum, brain stem, cerebellum, etc. Grossly, these Treatment
DUHFODVVL¿HGDVHLWKHUVXSUDWHQWRULDODQGLQIUDWHQWRULDO According to the
DQGWKHFOLQLFDOSUHVHQWDWLRQDUHUHODWHGWRWKHIROORZLQJ site and stage
FRQVHTXHQFHV± RIGLVHDVH7KH
Status epilepticus

RSWLRQVDUH±
XX Raised intra-cranial pressure (ICP) XX 6XUJHU\ RU
XX )RFDOEUDLQG\VIXQFWLRQ XX Radiotherapy
XX ,PSDLUPHQWRICSF circulation

Coronal section of contrast-enhanced

MRI scan showing the lesion
 Step on to Paediatrics 251

References
 .HGLD6HWDO1HXURORJLF 0XVFXODUGLVRUGHU,Q&XUUHQWGLDJQRVLV 7UHDWPHQW3HGLDWULFVrd(G¶
 0LNDWL0$6HL]XUHVLQFKLOGKRRG1HOVRQ7H[WERRNRI3HGLDWULFVth Edition. New Delhi: Elsevier; 2016: 2823-2856
3. Singhi P. Seizures and epilepsy in children: a practical guide. 1st ed. Publisher Noble Vision; 2008.
 0RH3*HWDO1HXURORJLFDQG0XVFXODUGLVRUGHUV&XUUHQW'LDJQRVLV 7UHDWPHQWLQ3HGLDWULFVrd ed. NY; 2015.
 ,QGLDQ$FDGHP\RI3HGLDWULFV ,$3 JXLGHOLQHVRQGLDJQRVLVDQGPDQDJHPHQWRIFKLOGKRRGHSLOHSV\
 1DWLRQDO*XLGHOLQHIRU7XEHUFXORVLVLQ&KLOGUHQRI%DQJODGHVK'*+6%DQJODGHVKndHGLWLRQ0DUFK
 3UDFWLFDO3HGLDWULF1HXURORJ\3URI9HHQD.DOUDnd edition , Arya publication, Delhi.

SELF ASSESSMENT
Short answer questions [SAQ]
 :ULWHGRZQWKHWUHDWPHQWRI\HDUROGER\ZLWKS\RJHQLFPHQLQJLWLV
 +RZZLOO\RXPDQDJHVHL]XUHRIDFKLOGZLWKVWDWXVHSLOHSWLFXV"
 :ULWHGRZQWKHFKDUDFWHULVWLFIHDWXUHRIIHEULOHFRQYXOVLRQ
 :KDWDUHWKHFDXVHVRIFRQYXOVLRQZLWKRXWIHYHU"+RZZLOO\RXSUHYHQWUHFXUUHQFHRIIHEULOHFRQYXOVLRQ"
 :ULWHGRZQWKHFOLQLFDOIHDWXUHRIS\RJHQLFPHQLQJLWLV
6. Write down the comparative &6)¿QGLQJVRIS\RJHQLFPHQLQJLWLVZLWK7%0
 :ULWHGRZQWKHGLIIHUHQFHEHWZHHQSVHXGRVHL]XUH VHL]XUH
 $PRQWKVROGFKLOGDGPLWWHGZLWKIHYHUIRUGD\VDQGVHYHUDOHSLVRGHVRIFRQYXOVLRQVIRUODVWGD\2QH[DPLQDWLRQWKH
FKLOGZDVIRXQGGURZV\DQGKDGEXOJHGDQWHULRUIRQWDQHOOH
i) What is the probable diagnosis?
LL :ULWHWKHUHOHYDQWLQYHVWLJDWLRQVZLWKH[SHFWHG¿QGLQJV
iii) Outline the management.
 +RZZLOO\RXGLIIHUHQWLDWHIHEULOHFRQYXOVLRQIURPPHQLQJLWLVFOLQLFDOO\"

Multiple choice questions [MCQ]

 7KHFKDUDFWHULVWLFIHDWXUHVRIQRUPDO&6)LQFOXGH±
___ a) colour: straw ___ b) pressure: 100-300mmH2O ___ c) protein: 20-45mg/dl
BBBG JOXFRVHPJGO BBBH FHOOFRXQWFXPP
 7KHFRQGLWLRQVSUHVHQWZLWKIHYHUDQGFRQYXOVLRQVDUH±
___ a) meningitis ___ b) cerebral malaria ___ c) acute stroke syndrome
___ d) hepatic encephalopathy ___ e) encephalitis
3. The classic &6)¿QGLQJVRIS\RJHQLFPHQLQJLWLVDUH±
___ a) hazy appearance ___ b) neutrophilic leukocytosis ___ c) normal protein
Status epilepticus

___ d) low chloride level ___ e) low glucose level

 7KHSUHFLSLWDWLQJIDFWRUVRIVWDWXVHSLOHSWLFXVDUH±
BBBD K\SRJO\FDHPLD BBBE K\SRFDOFDHPLD BBBF LQWHUFXUUHQWLQIHFWLRQ
BBBG VOHHSGHSULYDWLRQ BBBH VXGGHQZLWKGUDZORIDQWLHSLOHSWLFGUXJV
 )ROORZLQJDUHWKHIHDWXUHVRIW\SLFDOIHEULOHVHL]XUH±
BBBD VHL]XUHSHUVLVWLQJ!PLQXWHV BBBE RFFXU!RQFHLQKRXUV
BBBF HSLOHSV\LVDFRPPRQVHTXHODH BBBG CSF protein is elevated
 252 Step on to Paediatrics

BBBH DVVRFLDWHGZLWKLQWUDFUDQLDOLQIHFWLRQ
 )HDWXUHVRIVWDJH7%0DUH±
BBBD QRQVSHFL¿F BBBE QHFNULJLGLW\ BBBF FUDQLDOQHUYHSDOV\
___ d) decerebrate rigidity ___ e) behavioural change
 &6)¿QGLQJRI7%0DUH±
BBBD FRORXU±FOHDU BBBE SURWHLQ±PJGO BBBF FHOOV±PRVWO\O\PSKRF\WHV
BBBG JOXFRVH±PJGO BBBH SUHVVXUH±HOHYDWHG
 7KHFRPPRQRUJDQLVPVIRUFKLOGKRRG !PRQWKV PHQLQJLWLVDUH±
___ a) Listeria monocytogen ___ b) H. influenzae ___ c) Pneumococcas
___ d) E. coli ___ e) Meningococcas
 &DUGLQDOV\PSWRPVRIUDLVHG,&3±
___ a) Headache ___ b) Nausea ___ c) Convulsion
___ d) Visual problem ___ e) Cranial nerve palsy
&LUFXODWRU\VWDWXVFDQEHDVVHVVHGE\DWORRNLQJ±
___ a) O2 saturition ___ b) Blood pressure ___ c) Pulse pressure
BBBG &DUGLDFPXUPXU BBBH &DSLOODU\UH¿OOWLPH
'UXJRIFKRLFHIRUDEVHQFHVHL]XUHLQFOXGH±
BBBD 6RGLXP9DOSURDWH BBBE (WKRVX[LPLGH BBBF Phenobarbitone
___ d) Clonazepam ___ e) Clobazam
 &RPPRQPHWDEROLFDEQRUPDOLWLHVWKDWFDQFDXVHVHL]XUHLQFOXGH±
___ a) hypoglycaemia ___ b) hypernatraemia ___ c) hypocalcaemia
___ d) hypochloremia ___ e) hypomagnesaemia
Self assessment
 32
Developmental Delay
Developmental delay - - - - - - - - - - - - 253
Hypothyroidism - - - - - - - - - - - - - 254
Down syndrome - - - - - - - - - - - - - 256

DEVELOPMENTAL DELAY OHDUQLQJGLVDELOLWLHVDUHG\VOH[LD SUREOHPVLQUHDGLQJ 

,WUHIHUVWRIDLOXUHRQWKHSDUWRIDFKLOGWRDFTXLUHDJH dyscalculia (problem in mathematics), dysgraphia
DSSURSULDWHPLOHVWRQHVRIGHYHORSPHQWLQDQ\RILW¶V (problems in writing) etc.
domains. )RUH[DPSOHD\HDUVROGFKLOGZKRFDQQRW When to suspect Developmental Delay?
sit independantly from lying position.This is a delay in
,IDFKLOGKDVQRWDFKLHYHG±
development in motor domain
Parameter by
Types Social smile 3 months
Delay restricted to a particular domain Neck control 5 months
Isolated
e.g. speech and language, motor etc.
Sits without support 12 months
Global 6LJQLILFDQWGHOD\LQ•GRPDLQV Stands without support 18 months
Walks well 20 months
Intellectual disability (ID) 2-3 words sentence 36 months
Intellectual disability (once called mental retardation) is a 7HOOVVHOIQDPH 48 months
FOLQLFDOVLWXDWLRQFKDUDFWHUL]HGE\VLJQL¿FDQWOLPLWDWLRQLQ
Toilet control 60 months
both-
TT ,QWHOOHFWXDOIXQFWLRQLQJe.g. learning, reasoning, :KHQHYHUDFKLOGLVEURXJKWZLWKKLVWRU\RIGHOD\LQ
SUREOHPVROYLQJVNLOOVHWFand achieving age-appropriate developmental milestone, one
TT Adaptive behavior e.g. such as conceptional, social VKRXOGFRQVLGHUWKHIROORZLQJGLVHDVHVDVWKHFDXVHRI
and practical skillsZKLFKDIIHFWPDQ\HYHU\GD\µV developmental delay -
social and practical skills.
XX Idiopathic
,'RULJLQDWHVEHIRUH\HDUVRIDJHDQGLW¶VVHYHULW\LV
XX 725&+(6LQIHFWLRQ
FDWHJRUL]HGE\PHDVXULQJ,4VWDWXVRIWKHFKLOG
XX Chromosomal abnormalities e.g. Down syndrome,
Normal Reference value,I,4LV .OLQHIHOWHU¶VV\QGURPHFragile X syndrome
TT 85-114:Average intelligence XX Genetic disorders e.g. Hurler syndrome,
TT %RUGHUOLQHLQWHOOLJHQFH Phenylketonuria
Hypothyroidism
l 55-69: Mild ID l 40-54: Moderate ID XX Endocrine disorders e.g. congenital hypothyroidism
l 25-39: Severe ID and l,4RI3URIRXQG,' XX 3HULQDWDODVSK\[LD K\SR[LFLVFKDHPLF
encephalopathy)
Learning disability (LD) XX &16LQIHFWLRQVe.g. meningitis, encephalitis
XX Protein energy malnutrition
,WLVDQHXURORJLFDOGLVRUGHUZKHUHEUDLQ¶VFRPPXQLFDWLRQ
FKDQQHOVDUHDIIHFWHGHJDELOLW\WRUHFHLYHSURFHVV
VWRUHDQGUHVSRQVHWRLQIRUPDWLRQ3HRSOHZKRKDYH/' In this chapter, Congenital Hypothyroidism, Down
JHQHUDOO\KDYHDYHUDJHRUDERYHDYHUDJH,47KHVSHFL¿F syndrome will be discussed.
253
 254 Step on to Paediatrics

HYPOTHYROIDISM XX Prolonged jaundice (jaundice persists beyond 2 weeks

RIDJH
$FRPPRQHQGRFULQHGLVRUGHUWKDWUHVXOWVIURPDGHIHFW XX 5HIUDFWRU\
anywhere in the hypothalamic-pituitary-thyroid D[LV constipation
XX Little cry,
Aetiology & Classifications somnolence,
H[FHVVLYHVOHHS\
A. Based on the site of pathology sluggishness
XX Primary: 3URORQJHGMDXQGLFH SURWUXGHGWRQJXH
XX )HHGLQJGLI¿FXOWLHV
Pathology is in
XX &RDUVHIDFLHVHJSURWUXGHGWRQJXHSXII\H\HOLGV
thyroid gland
ZULQNOHGIRUHKHDGGHSUHVVHGQDVDOEULGJH
ZLWKGH¿FLHQW
SURGXFWLRQRI
XX 2HGHPDRIH[WUHPLWLHV JHQLWDOV
WK\UR[LQH XX Subnormal body temperature
XX Secondary: XX :LGHO\RSHQDQWHULRUIRQWDQHOOHDQGRSHQSRVWHULRU
Pathology is IRQWDQHOOHDWELUWK
either in pituitary
gland or in
Physical Examination
hypothalamus, XX Normal head size with widely open
and is Head DQWHULRUDQGSRVWHULRUIRQWDQHOOHV
characterized XX +DLUGU\ VFDQW\
E\GH¿FLHQW
SURGXFWLRQRI75+76+DVZHOODVWK\UR[LQH
XX &RDUVHZLWKZULQNOHGIRUHKHDGDQGORZ
hairline
B. Based on the time of onset XX /DUJHWRQJXHSURWUXGLQJIURPWKHPRXWK
of illness and aetiology Face XX 'HSUHVVLRQRIQDVDOEULGJH
XX Delayed dentition
Congenital Acquired XX Swollen eyelids with narrow palpebral
XX Aplasia, hypoplasia or ¿VVXUHV
XX Autoimmune thyroiditis
HFWRS\RIWK\URLGJODQG XX $SSHDUVVKRUWEHFDXVHRIWKHSUHVHQFH
XX Endemic iodine
XX ,QERUQHUURUVRIWK\URLG Neck RIP\[RHGHPDWRXVSDGVRIIDWDERYHWKH
GH¿FLHQF\
hormone biosynthesis clavicles
XX ([SRVXUHWRJRLWURJHQ
XX ,QVHQVLWLYLW\RIWKHWLVVXH XX Irradiation or surgery to XX Feels dry, thick, cold and mottled (cutis
receptors to thyroid Skin
thyroid gland marmorata)
hormone
Abdomen XX Distended and umbilical hernia
+DQGV  XX Broad and stumpy
¿QJHUV
CONGENITAL HYPOTHYROIDISM (CH) XX Usually hypotonic
Muscles XX $QNOHMHUNVKRZVVORZUHOD[DWLRQ
Pathogenesis
Congenital hypothyroidism

'XHWRGH¿FLHQF\RIWK\UR[LQHWKHUHLVLPSDLUHG
XX Pulse slow
GHYHORSPHQWRI&16 OHDGLQJWRPHQWDOUHWDUGDWLRQ DQG CVS XX Cardiomegaly, murmur
skeletal system (short stature). XX $V\PSWRPDWLFSHULFDUGLDOHIIXVLRQ
XX Markedly stunted
development
Growth and

Clinical Manifestations
XX Maintain LQIDQWLOHERG\SURSRUWLRQ
XX 0LOHVWRQHVRIGHYHORSPHQWVDUHGHOD\HG
3UHVHQWDWLRQRIFRQJHQLWDOK\SRWK\URLGLVPDWELUWKPD\EH XX 6H[XDOPDWXUDWLRQLVGHOD\HGRUPD\QRW
overt, may be sub-clinical or asymptomatic. However, one
take place at all
should not miss to suspect CH, when a newborn presents
with - XX Mentally retarded. About 20% have
Intelligence
sensory neural hearing loss
XX 'HOD\HGSDVVDJHRIPHFRQLXP !KRXUVDIWHUELUWK
 Step on to Paediatrics 255

XX Skeletal survey:
TT $EVHQWGLVWDOIHPRUDODQGSUR[LPDOWLELDOHSLSK\VHV
$ERXWRI
babies with Coarse ZKLFKLVVXSSRVHGWRSUHVHQWDWZHHNVRIJHVWDWLRQ
TT (SLSK\VHDOG\VJHQHVLVIRUROGHUFKLOGUHQ
CH may have facies
associated Protruded
congenital tongue
anomalies e.g.
cong heart
disease

Umbilical
hernia $EVHQW Normal

7\SLFDOSUR¿OHVRIDFKLOGZLWK
congenital hypothyroidism

XX Anthropometry
TT Length or height

(stunted)
TT 5DWLRRIXSSHU

to lower body
segments reveals
,QIDQWLOHERG\
proportion Dysgenetic femoral epiphysis
GLVSURSRUWLRQDWH
VKRUWVWDWXUH 7KHVHUDGLRORJLFDO¿QGLQJVJLYHFOXHVWRWKHGLDJQRVLVDW
places, where TSH, FT4 assay is not readily available.
Courtesy: Dr Laila Yeasmin

$JHVSHFL¿F1RUPDO
body proportion Treatment
XX &RXQVHOLQJSDUHQWVDERXWWKHFRQVHTXHQFHVRIXQWUHDWHG
'' $WELUWK
FDVHVDQGWKHLPSRUWDQFHRIUHJXODUFRQWLQXDWLRQRI
'' At 6 years: 1.4:1
WUHDWPHQWZLWK7K\UR[LQH
'' At 11 years: 1:1 XX 6RGLXP/WK\UR[LQHVKRXOGEHVWDUWHGZLWKRXWGHOD\DIWHU
Short stature compared to a normal birth or at diagnosis
child of same age and sex

Diagnosis Dose & Duration

Based on characteristic symptoms, classical physical Age group Dose Duration
¿QGLQJV VXSSRUWVIURPWKHUHOHYDQWLQYHVWLJDWLRQV
Neonate ±ȝJPNJGD\
/LIHORQJ
Investigations Beyond neonatal period ȝJPNJGD\
Congenital hypothyroidism
XX Serum FT4, TSH: Low FT4 and high TSH (Primary
K\SRWK\URLGLVP ,IERWKTSH and FT4 are low, then
problem is in pituitary or in hypothalamus
XX CBC, PBF: Microcytic anaemia, UHIUDFWRU\WR
treatment with haematinics
XX Thyroid Scan: Iodine-123 (I-123) or Sodium
pertechnetate 99 m (Tc99 m) uptake and scan:
To detect an ectopic gland, thyroid hypoplasia or
thyroid aplasia
XX 7K\URLGXOWUDVRQRJUDSK\7RDVVHVVWKHDQDWRP\RI
thyroid whether enlarged or absent glands 3UR¿OHEHIRUHDQGZHHNVDIWHUWUHDWPHQW
 256 Step on to Paediatrics

Course & Prognosis DOWN SYNDROME

Depends on the age at which the treatment is started. Early
WKHUDS\ZLWKLQ¿UVWZHHNRIOLIHJLYHVDJUHDWHUFKDQFH The commonest chromosomal anomaly. Overall incidence
IRUQRUPDOOLQHDUJURZWKDQGLQWHOOHFWXDODFKLHYHPHQW LVDERXWLQOLYHELUWKVDQGWKHLQFLGHQFHLQFUHDVHV
But delay to start therapy even by 2 months may cause with advanced maternal age.
VLJQL¿FDQWLQWHOOHFWXDOGLVDELOLW\ Aetio-pathogenesis
Follow up: Assessment 7KHH[DFWFDXVHLVQRWNQRZQ7KHGLVHDVHLVFKDUDFWHUL]HG
A. Biochemical: S. FT4 and TSH levels as follows- E\WKHSUHVHQFHRIDQextra copy of genetic material on
chromosome 21, either whole or in part and occurs in 3
Age of baby Frequency ways-

0-6 months Every 6 weeks XX Chromosomal QRQGLVMXQFWLRQ LQRIFDVHV 

6 months-3 years Every 3 months
XX 5REHUWVRQLDQWUDQVORFDWLRQ LQRIFDVHV 
XX 0RVDLFLVP LQRIFDVHV
!\HDUV Every 6 months

B. Clinical: Height, development and hearing Clinical Manifestations

XX ([SHFWHGUHVSRQVHLQZHHNV Regions Features
TT Regular bowel movement

TT 5HGXFWLRQLQZHLJKWDQGSXI¿QHVV
%UDFK\FHSKDO\PLFURFHSKDO\IODW
+HDG IDFH
TT Increase in the pulse rate
nasal bridge
XX ([SHFWHGUHVSRQVHLQPRQWKV 8SZDUGVODQWLQJRISDOSHEUDOILVVXUH
TT 5HGXFWLRQLQKRDUVHQHVVRIYRLFH Eyes HSLFDQWKLFIROG%UXVKILHOGVSRW
TT &RUUHFWLRQRIDQDHPLD congenital cataract
TT Changes in skin and hair
Low set ears, chronic otitis media (glue
Ears
ears)
How to identify CH at the earliest? 2UDOFDYLW\  Macroglossia, dental abnormalities like
Teeth malposition and enamel hypoplasia etc.
Neonatal screening (NS)
,WLVDLPHGWRGHWHFWFDVHVRI&+LPPHGLDWHO\DIWHUELUWKVR Broad and short hands, clinodactyle
as to start treatment early and to prevent irreversible brain VKRUWLQFXUYHGOLWWOHILQJHUV VLQJOH
GDPDJHRIWKHDIIHFWHGFKLOG +DQGV IHHW palmar crease (simian crease) increased
gaps between 1st and 2nd toes and
planter crease between them in the sole
Method )LOWHUSDSHUVSRWWHFKQLTXHE\KHHOSULFN
,QWHOOHFWXDOGLVDELOLW\ ,4UDQJHVIURP
Neuro-
Timing GD\VDIWHUELUWK  DYHUDJH GHOD\LQPLOHVWRQHV
psychologic
RIGHYHORSPHQWDIILQLW\IRUPXVLF
)7ȝJP/dl
76+!P8PO Muscle Generalized hypotonia
Results
Borderline TSH level (20-40 mU/ml): should
be repeated Endocrine Hypothyroidism

'HOD\LQGHYHORSPHQWRIVHFRQGDU\
Down syndrome

7RDYRLGIDOVHSRVLWLYHUHVXOWGXHWRSK\VLRORJLFDO 6H[XDO
VXUJHRITSH causing increased T4 upto 48 hours VH[XDOFKDUDFWHULVWLFV$GXOWPDOHVDUH
development
LQIHUWLOHEXWIHPDOHVDUHIHUWLOH
 Step on to Paediatrics 257

Simian crease
Brachycephaly

Down syndrome

&UHDVHEHWZHHQQGDQGJUHDWWRH
8SZDUGVODQWLQJRISDOSHEUDO¿VVXUH
 258 Step on to Paediatrics

Investigations to screen out complications

XX &%&3%)3RO\F\WKHPLDLQIHFWLRQLQFUHDVHG0&9
XX CXR: Heart anomalies or pneumonia
XX ECG: Ventricular hypertrophy
XX (FKRFDUGLRJUDSK\'RQHZLWKLQ¿UVWPRQWKRIOLIHWR
UXOHRXWFDUGLDFGHIHFW
XX TSH, FT4: To rule out hypo or hyperthyroidism
XX Developmental and psychological assessment:
,4YDULHVIURPZLWKPHDQ

Ante-natal diagnosis
7KHULVNRIKDYLQJDFKLOGZLWK7ULVRP\LVKLJKHVWLQ
ZRPHQZKRFRQFHLYHDW!\HDUVRIDJH(YHQWKRXJK
\RXQJHUZRPHQKDYHDORZHUULVNWKH\UHSUHVHQWKDOIRI
DOOPRWKHUVZLWK'RZQEDELHVEHFDXVHRIKLJKHURYHUDOO
birth rate.
$QWHQDWDOGLDJQRVLVRI'RZQV\QGURPHLVGRQHE\
screening tests during ¿UVW and second trimesters
XX First trimester
Common associated illnesses TT Foetal nuchal translucency (NT) thickness
XX Congenital heart diseases HJ96'$9FDQDOGHIHFW TT Beta hCG level
XX GIT anomalies e.g. Hirschsprung disease, duodenal TT Pregnancy-associated plasma protein-A (PAPP-A) in
DWUHVLDLQFUHDVHGFKDQFHRIcoeliac disease
maternal serum
XX )UHTXHQWLQIHFWLRQVe.g. recurrent respiratory tract XX Second trimester (Quad screening in maternal serum)
LQIHFWLRQV
TT Free beta hCG
XX Endocrinopathies e.g. hypothyroidism, diabetes mellitus
TT Unconjugated estriol
XX Malignancy HJWLPHVPRUHFKDQFHVRI
TT Inhibin
leukaemia
TT $OIDIHWRSURWHLQ
XX Musculoskeletal HJDWODQWRRFFLSLWDOVXEOX[DWLRQ
GLVORFDWLRQRIKLS
XX Others e.g. Alzheimers disease Management
XX &RXQVHOLQJSDUHQWVDERXWWKHQDWXUH IXWXUHRIWKH
Diagnosis problem
0DGHRQWKHEDVLVRI XX (DUO\ UHJXODUVWLPXODWLRQRIWKHFKLOGHJH[SRVXUHWR
XX +LVWRU\RIDGYDQFHGPDWHUQDODJH games, music, interactions etc.
XX 7\SLFDOFOLQLFDOIHDWXUHV XX 7UHDWPHQWRIDQ\DVVRFLDWHGLOOQHVVe.g. cardiac
XX .DU\RW\SLQJFRQ¿UPDWRU\ SUREOHPVLQIHFWLRQVWK\URLGUHSODFHPHQWHWF
XX Special education and occupational training to
overcome mental subnormality

Prognosis
Around 20% patients die within 1st year, 45% survive
XSWR\HDUVRIDJHDQGPDQ\RIWKHPVXIIHUIURP
Down syndrome

$O]KHLPHU¶VGLVHDVHDW\HDUVRIDJH

.DU\RW\SLQJVKRZLQJWULVRP\
 Step on to Paediatrics 259

References
 6FRWW0HWDO0DQDJHPHQWRI&KLOGUHQZLWK$6'XWLVP3HGLDWULFV
.DOUD93UDFWLFDO3DHGLDWULF1HXURORJ\ndHG1HZ'HOKL$U\D3XEOLFDWLRQVS
3. Huang SA, LaFranchi S. Congenital +\SRWK\URLGLVP1HOVRQ7H[WERRNRI3HGLDWULFVth Ed. : Elsevier; 2016:2684-85.
 0ROOD057KH&RQFLVH7H[WERRNRI3HGLDWULFVnd edition, Dhaka: &KLOG)ULHQGO\3XEOLFDWLRQV
 (OLDV(5HWDO*HQHWLF G\VPRUSKRORJ\&XUUHQW'LDJQRVLV 7UHDWPHQWLQ3HGLDWULFVrd ed. NY; 2015. P. 1031-32.
6. Hutchinson JH, Cockburn F. Practical Pediatric Problems. 6th ed. Singapore: PG Asian Economy Edition; 1989.

SELF ASSESSMENT
Short answer questions [SAQ]
:ULWHGRZQWKHFOLQLFDOPDQLIHVWDWLRQRI&RQJHypothyroidism.
1DPHWKHLQYHVWLJDWLRQVRI&RQJK\SRWK\URLGLVP
:ULWHGRZQWKHW\SLFDOFOLQLFDOIHDWXUHVRIDown syndrome.
4. Write short note on : Mental Retardation.

Multiple choice questions [MCQ]

 )HDWXUHVRI'RZQV\QGURPHDUH±
BBBD EUDFK\FHSKDO\ BBBE K\SRWRQLD BBBF %UXVK¿HOGVSRWVLQH\HV
BBBG GRZQZDUGVODQWLQJRISDOSHEUDO¿VVXUHV BBBH LQFXUYLQJRIOLWWOH¿QJHUV
 )HDWXUHVRIFRQJHQLWDOK\SRWK\URLGLVPDUH±
___ a) irritability ___ b) constipation ___ c) prolonged physiological jaundice
BBBG FRDUVHZULQNOHGIRUHKHDG BBBH DSSHDUDQFHRIORZHUIHPRUDOHSLSK\VHVDWELUWK
 &DUGLQDOELRFKHPLFDO UDGLRORJLFDOIHDWXUHVRISULPDU\K\SRWK\URLGLVPDUH
___ a) delayed bone age ___ b) epiphyseal dysgenesis ___ c) low TSH
___ d) low FT4 ___ e) low T3 level
 $PRQWKROGER\LVDGPLWWHGEHFDXVHKHFDQQRWVLW\HW2QH[DPLQDWLRQ\RXQRWHGWKDWKHLVK\SRWRQLFKLVH\HVDUH
VOXQWHGXSZDUGVDQGKDYHHSLFDQWKLFIROGV±
&KRRVHWKHPRVWFRPPRQPHFKDQLVPIURPWKHFKDUWJLYHQEHORZLVDVVRFLDWHGZLWKWKHFKLOG¶VSUREOHP
___ a) translocation ___ b) non-dysjunction ___ c) mosaicism
___ d) single gene mutation ___ e) deletion
 $ZHHNVROGEDE\LVEURXJKWWR\RXEHFDXVHRISHUVLVWDQW\HOORZIDFHDQGVFOHUDDQGFRQVWLSDWLRQ7KHIROORZLQJ
LQYHVWLJDWLRQVDUHUHOHYDQWWRUHDFKDGLDJQRVLVRIWKHEDE\¶VSUREOHP±
___ a) X-ray knee joint ___ b) X-ray wrist joint ___ c) Serum TSH estimation
___ d) karyotyping ___ e) Serum growth hormone estimation
 $ZHHNROGEDE\LVDGPLWWHGZLWKSHUVLVWHQWMDXQGLFH7KHIROORZLQJFOLQLFDOIHDWXUHVDUHUHOHYDQWIRUFRQJHQLWDO
K\SRWK\URLGVP±
BBBD EUDFKLFHSKDO\ BBBE QRLV\UHVSLUDWLRQ BBBF H[FHVVLYHVOHHSLQHVV
___ d) Simian crease ___ e) constipation
Self assessment

 7KHIROORZLQJIHDWXUHVDUHFKDUDFWHULVWLFVRIFRQJHQLWDOK\SRWK\URLGLVPRI\HDUVROGER\±
BBBD VKRUWVWDWXUH BBBE FDUSDOERQHV BBBF %UXVK¿HOGVSRWV
BBBG HSLSK\VHDOG\VJHQHVLV BBBH XSSHUVHJPHQWWRORZHUVHJPHQWRIERG\UDWLRRI
260 Step on to Paediatrics
 33
Abnormal Behaviour
Common Psychiatric Disorders
¼¼ Autism - - - - - - - - - - - - - - 262
¼¼ Attention deficit hyperactivity disorder - - - - - - - - - - 263

Whenever, a child is brought with an abnormal behaviour XX Mood disorders e.g. Depressive disorder
RUDQ\GHYLDWLRQIURPDJHDSSURSULDWHEHKDYLRXUe.g. XX Eating disordersHJ$QRUH[LDQHUYRVDEXOLPLD
UHVWOHVVQHVVODFNRILQWHUDFWLRQSRRUFRPPXQLFDWLRQHWF nervosa, binge eating disorder
WKHQRQHVKRXOGFRQVLGHUWKHSRVVLELOLWLHVRISV\FKLDWULF XX Elimination disorder e.g. Enuresis, encopresis
SUREOHPV7KHIROORZLQJDUHWKHFRPPRQSV\FKLDWULF XX Disorder of impulse control e.g. Temper tantrum,
GLVRUGHUVRIFKLOGUHQ breath holding attack
XX Somatic symptom related disorder e.g. Conversion XX Autism sprectrum disorder
GLVRUGHUVRPDWLFV\PSWRPGLVRUGHU¿FWLWLRXVGLVRUGHU XX Neurobehavioral and learning disorder e.g. attention
XX Rumination and pica GH¿FLWK\SHUDFWLYHGLVRUGHU $'+' LQWHOOHFWXDO
XX Motor disorders e.g. Tics, stereotype movement disability
disorder In this chapter, we will discuss autism and ADHD
XX Habit disorder e.g. Thumb sucking, nail biting, head DWWHQWLRQGH¿FLWK\SHUDFWLYHGLVRUGHU7KHFDUGLQDOIHDWXUHV
EDQJLQJEUX[LVP RIVRPHRIWKHSV\FKLDWULFSUREOHPVDUHDOVRKLJKOLJKWHGLQ
XX Anxiety disorder e.g. Obsessive compulsive disorder, the table below.
school phobia, panic disorder

COMMON PSYCHIATRIC DISORDERS IN CHILDREN

Cardinal features
Disorders Clinical features
XX Pica 3HUVLVWHQWHDWLQJRIQRQQXWULWLYHVXEVWDQFHVe.g. plaster, charcoal, clay, ashes, paint, earth etc.

Common psychiatric disorders

XX

XX 1RUPDODPRQJLQIDQWVDQGWRGGOHUVEXWLIFRQWLQXHGWKHQLWLVFRQVLGHUHGDVKDELWGLVRUGHU
7KXPEVXFNLQJSURYLGHDSOHDVXUDEOHVHQVDWLRQ7KLVKDELWPD\LQWHUIHUHZLWKGHQWDODOLJQPHQW
XX Thumb sucking
PD\LQFUHDVHWKHLQFLGHQFHRIKHOPLQWKLDVLV$ELWWHUVROXWLRQPD\EHDSSOLHGRQWKHWKXPEWR
FRQWUROWKXPEVXFNLQJ DQWKHOPLQWLFVPD\EHJLYHQ

XX Head banging XX %DQJLQJRIKHDGDJDLQVWWKHEHGRUZDOOZKHQWKHFKLOGLVXQGHUVWUHVV

XX Body rocking XX Body rocking against bed during stress

XX 1DLOELWLQJLVDQH[SUHVVLRQRIDQ[LHW\EXWLILWLVQRWDVVRFLDWHGZLWKRWKHUV\PSWRPVLWVKRXOG
XX Nail biting
QRWEHDPDWWHURIFRQFHUQ

XX Teeth grinding / XX 0D\EHDVVRFLDWHGZLWKDQ[LHW\3HUVLVWHQWEUX[LVPFDQPDQLIHVWDVGHQWDORFFOXVLRQGHIHFW

%UX[LVP muscular or temporomandubular joint pain
261
 262 Step on to Paediatrics

XX Hair pulling / XX 5HOHDVHRIWHQVLRQDIWHUKDLUSXOOLQJ,UUHJXODUDUHDVRIKDLUORVVFRPPRQO\VHHQRYHURFFLSLWDO

Trichotillomania DQGSDULHWDODUHDRIVFDOSDQGH\HEURZVRUH\HODVKHV

Disorders Clinical features

XX ,VDQH[SUHVVLRQRIDQJHUDQGIUXVWUDWLRQ,QWKLVFRQGLWLRQFKLOGO\LQJRUWKURZLQJKLPVHOIGRZQ
XX Temper tantrums
kicking, screaming, throwing things or hitting

XX Sudden, rapid, recurrent, nonrhythmic, stereotype motor movement or vocalization e.g. eye
XX Tics blinking, neck jerking, shoulder shrugging, cough, throat clearing. Can be controlled voluntarily.
$EVHQWGXULQJVOHHSRUSK\VLFDODFWLYLW\DQGH[DFHUEDWHGGXULQJHPRWLRQDOVWUHVV
XX )ROORZLQJDWUDXPDRUDQHPRWLRQDOVWUHVVWKHFKLOGFULHVEULHÀ\ KROGVWKHEUHDWKLQ
XX Breath-holding H[SLUDWLRQ7KLVHYHQWVPD\EHF\DQRWLFRUDF\DQRWLF7KHVSHOOPD\UHVROYHRUWKHFKLOGPD\
spells GHYHORSFRQYXOVLRQRUEHFRPHXQFRQVFLRXV1RVSHFL¿FWUHDWPHQWLVQHFHVVDU\RUHIIHFWLYH
Parents should be reassured
XX 6FKRROSKRELDLVFDXVHGE\XQZDUUDQWHGIHDURULQDSSURSULDWHDQ[LHW\DERXWOHDYLQJKRPHRULQ
XX School phobia SDUWLFXODUWKHFKLOG¶VPRWKHU7KHSKRELDLVRIWHQDFFRPSDQLHGE\DYDJXHDEGRPLQDOSDLQRU
headache alleviated by school absence

XX Enuresis/ XX 9RLGLQJRIXULQHLQWRFORWKHVRUEHGWZLFHRUPRUHLQDZHHNIRUDWOHDVWWKUHHFRQVHFXWLYH
XX Bed-wetting PRQWKVDIWHU\HDUVRIDJH

XX (QFRSUHVLVLVXVXDOO\GH¿QHGDVYROXQWDU\RULQYROXQWDU\SDVVDJHRIIDHFHVLQWRLQDSSURSULDWH
XX Encopresis SODFHVDWOHDVWRQFHDPRQWKIRUFRQVHFXWLYHPRQWKVLQWKHDEVHQFHRIDQ\SK\VLFDOSDWKRORJ\
DIWHU\HDUVRIDJH
XX Encopresis is 4-5 times more common in boys than in girls and tends to decrease with age

Clinical Characteristics
AUTISM SPECTRUM XX Fails to respond to his or her name
DISORDERS
Defects in social interaction and

XX Resists cuddling and holding

XX 8QDZDUHRIRWKHUVIHHOLQJ
Autism spectrum disorders are XX 6HHPVWRSUHIHUSOD\LQJDORQHOLYHVLQKLVRUKHURZQOLIH
communitation

neurodevelopmental disorder characterized XX 6WDUWVWDONLQJODWHUWKDQRI\HDUVRIDJH

by XX /RVHVSUHYLRXVO\DFTXLUHGDELOLW\WRVD\ZRUGVRU
TT Impaired social interaction and sentences
communication and XX 'RHVQRWPDNHH\HFRQWDFWVXSRQUHTXHVW
TT 5HVWULFWHGDQGUHSHWLWLYHSDWWHUQRI XX May use a singsong voice or robot like speech while
behavior or interest talking
Aetiology
XX &DQ¶WLQLWLDWHDFRQYHUVDWLRQRUNHHSRQJRLQJ
XX Mostly unknown
XX May repeat words or phrases
XX Genetic XX 3HUIRUPVUHSHWLWLYHPRYHPHQWVsuch as rocking,
Restricted and repetitive

XX 5LVNIDFWRUVLQFOXGH spinning or hand-flapping

pattern of behavior

TT 3UHQDWDOUXEHOODRU&09LQIHFWLRQRI XX 'HYHORSVVSHFL¿FURXWLQHVRUULWXDOV
mother XX Disturbed at the slightest change in routines or rituals
TT $GYDQFHGDJHRIHLWKHUSDUHQW
XX Moves constantly
TT Gestational diabetes mellitus
XX 0D\EHIDVFLQDWHGE\SDUWVRIDQREMHFWsuch as the
TT 8VHRISV\FKLDWULFGUXJVE\WKHPRWKHU
spinning wheels of a toy car
Autism

during pregnancy XX May be unusually sensitive to light, sound and touch and
yet oblivious to pain
 Step on to Paediatrics 263

Diagnosis ATTENTION-DEFICIT HYPERACTIVITY

0DLQO\FOLQLFDO+RZHYHUGLDJQRVLVLVIXUWKHUVWUHQWKHQHG DISORDER (ADHD)
ZLWKGDWDIURPWKHIROORZLQJWRROV
$'+'LVRQHRIWKHPRVWFRPPRQQHXUREHKDYLRXUDO
A. Screening tools GLVRUGHUVRIFKLOGKRRGFKDUDFWHUL]HGE\DQDJH
TT 0RGL¿HG&KHFNOLVWIRUAutism in Toddlers (MCHAT) inappropriate hyperactivity, impulsiveness and inattention.
TT Communication and Symbolic Behavioural Scale
(CSBS) Clinical Characteristics
B. Diagnostic Tool XX 'LI¿FXOWWRKROGDQGVRRWKHDVDQLQIDQW
TT Autism Diagnosis Observation Schedule (ADOS) XX Careless mistakes at school

Persistent pattern of
inattentiveness and
TT Autism Diagnostic Interview Revised (ADI-R) XX Easily distracted

hyperactivity
XX 8QDEOHWR¿QLVKWDVNV
Management XX 'RHVQRWIROORZLQVWUXFWLRQV
Current interventions include XX 'RQ¶WUHPDLQVWLOOLQWKHFODVVURRP
XX 3V\FKRHGXFDWLRQDO EHKDYLRUDOLQWHUYHQWLRQVHJ XX &DQQRWVXVWDLQDWWHQWLRQIRUHLWKHUSOD\RU
TT 7HDFKWUHDWPHQWDQGHGXFDWLRQRIDXWLVWLFDQGUHODWHG work
handicapped children XX ([FHVVLYHUXQQLQJRUFOLPELQJ
TT Applied behavioral analysis communication XX 7DONVH[FHVVLYHO\
TT Alternative communication

Poor impulse
TT 6RFLDOVNLOOWHFKQLTXH
XX %OXUWRXWDQVZHUEHIRUHTXHVWLRQVKDYHEHHQ

control
completed
TT Parental involvement
XX Risky acts without considering
XX Psychopharmacological e.g. antidepressants, selective FRQVHTXHQFHV
VHURWRQLQUHXSWDNHLQKLELWRUVEHWDEORFNHUVPRRG
VWDELOL]HUVHWF
XX 7KHVHV\PSWRPVPXVWVWDUWEHIRUH\HDUV
XX Others e.g. megavitamin therapy, gluten and casein free
diet, sensory and auditory integration etc.
XX 7KHV\PSWRPVPXVWSUHVHQWLQWZRRIPRUHGLIIHUHQW
settings(school, home, work place)
XX 7KHV\PSWRPVVKRXOGSHUVLVWVDWOHDVWIRUPRQWKV

Diagnosis
0DLQO\FOLQLFDO+RZHYHUGLDJQRVLVLVIXUWKHUVWUHQWKHQHG
ZLWKGDWDIURPWKHIROORZLQJVFUHHQLQJWRROV

Screening tools

Attention-deficit hyperactivity disorder

XX &RQQHU¶V5DWLQJ6FDOHV
XX ADHD Rating Scale
XX Vanderbilt ADHD Rating Scale
XX Child Behavioral Checklist

Management
XX %HKDYLRXUDOWKHUDS\SDUHQWVDUHWDXJKWKRZWR±
TT 5HLQIRUFHSRVLWLYHEHKDYLRXUE\SUDLVLQJRUE\XVLQJ

daily contingency charts

TT ([WLQJXLVKQHJDWLYHEHKDYLRXUVE\DFWLYHLJQRULQJ

XX Pharmacotherapy includes
TT Methylphenidate (5-20 mg bd )

TT $WRPR[HWLQH PJNJGD\2'
 264 Step on to Paediatrics

References
1. Huang SA, LaFranchi S. Congenital +\SRWK\URLGLVP1HOVRQ7H[WERRNRI3HGLDWULFVth Ed ; 2016:2684-85.
6FRWW0HWDO0DQDJHPHQWRI&KLOGUHQZLWK$XWLVP6SHFWUXP'LVRUGHUV3HGLDWULFV
 0ROOD057KH&RQFLVH7H[WERRNRI3HGLDWULFVnd ed, Dhaka: &KLOG)ULHQGO\3XEOLFDWLRQV
 .KDQ055DKPDQ0((VVHQFHRI3HGLDWULFVthHG(OVHYLHU1XWULWLRQDO3UREOHPVS
 .DKDQ6HWDOAutism Spectrum Disorder In A Page Pediatrics, 2ndHG
3DUWKDVDUDWK\$HWDO,$37H[WERRNRI3HGLDWULFVth ed. New Delhi: Jaypee Brothers; 2013. P 394-95.

SELF ASSESSMENT
Short answer questions [SAQ]
1. What are the common psychiatric disorders in children?
 :ULWHGRZQWKHFKDUDFWHULVWLFVRIDXWLVWLFFKLOG
 0HQWLRQWKHHWLRORJ\RIDXWLVP
4. How will you treat a child with autism?
 :ULWHGRZQWKHFOLQLFDOPDQLIHVWDWLRQRIADHD.
 :ULWHGRZQWKHWUHDWPHQWSODQRIDFKLOGZLWKADHD.

Multiple choice questions [MCQ]

 +DELWGLVRUGHUVDUH±
__ a) Autism __ b) Head banging __ c) Trichotillomenia
__ d) ADHD __ e) Breath holding attacks
 ,QDXWLVP±
BBD ,PSDLUHGVRFLDOLQWHUDFWLRQ FRPPXQLFDWLRQ BBE /DQJXDJHGHYHORSPHQWLVQRUPDO
BBF 5HVWULFWHG UHSHWLWLYHEHKDYLRU BBG WKHUHPD\EHXQGHUO\LQJRUJDQLFFDXVHV
 BBH IDLOVWRUHVSRQVHWRKLVKHUQDPH
 &KDUDFWHULVWLFVIHDWXUHVRI$'+'±
BBD ,QDWWHQWLYHQHVV BBE K\SHUDFWLYLW\ BBF 5HVWULFWHG UHSHWLWLYHEHKDYLRU
BBG SRRULPSXOVHFRQWURO BBH /DFNRIFRPPXQLFDWLRQV
Self assessment
 34
Short Stature
Constitutional growth delay - - - - - - - - - - - 265
Familial short stature (FSS) - - - - - - - - - - - 265
Growth hormone deficiency - - - - - - - - - - - 266
Turner syndrome - - - - - - - - - - - - - 266

Whenever a child presents with short stature i.e the delayed but height age WKHDJHDWZKLFKWKHH[LVWLQJ
KHLJKWRUOHQJWKRIWKHFKLOGLVPRUHWKDQ6'¶VIRUWKDW KHLJKWRIWKHFKLOGIDOOVRQth centile) corresponds with
VSHFL¿FDJHDQGVH[RQHVKRXOGFRQVLGHUWKHIROORZLQJ bone age.
SRVVLELOLWLHVDVWKHDHWLRORJ\RIVKRUWVWDWXUH7KH
+2 SD (97th Centile)
possibilities can be grouped under two headings- 190 -
180 - Mean
170 - -2 SD (3rd Centile)
A. Normal variants 160 -

Height in cm
150 -
TT Familial (genetic) short stature 140 -
TT Constitutional growth delay 130 -
120 -
B. Pathological causes 110 -
100 - Constitutional Delay
TT Idiopathic short stature 50 -
TT Endocrinopathies e.g. JURZWKKRUPRQHGH¿FLHQF\ 0 3m 6m 12m 3y 6y 12y 18y
WK\URLGKRUPRQHGH¿FLHQF\GLDEHWHVPHOOLWXV Age in years
diabetes insipidus, cushing syndrome
TT Psychogenic e.g. psychosocial deprivation
TT 1XWULWLRQDOGH¿FLHQF\e.g. malnutrition, rickets
TT Chronic illnesses HJLQÀDPPDWRU\ERZHO FAMILIAL SHORT STATURE (FSS)
disease, coeliac disease, chronic kidney disease
TT Chromosomal abnormalities e.g. Down syndrome, ,QWKLVFRQGLWLRQVKRUWVWDWXUHRIWKHFKLOGLVFRQVLGHUHG
Turner syndrome, Noonan syndrome WREHWKHLQÀXHQFHRISDUHQW¶VKHLJKW JHQHWLFLQÀXHQFH .
TT Skeletal dysplasias e.g. achondroplasia, &KLOGUHQZLWK)66KDYHVKRUWSDUHQWVDQGWKHFKLOG¶V
mucopolysaccharidosis height commensurate with his/her genetic potential.
They are born small and adopt a place below 3rd centile

Constitutional growth delay

In this section, we will discuss constitutional growth and continue to grow along that channel with a normal
GHOD\IDPLOLDOVKRUWVWDWXUH*+GH¿FLHQF\DQGTurner growth velocity. Their bone ages as well as puberty are
V\QGURPH7KHRWKHUFDXVHVRIVKRUWVWDWXUHOLNH age appropriate but height age is less. The adult height is
hypothyroidism, rickets, &.'Down syndrome, VKRUWEXWFRQVLVWHQWZLWKWKHIDPLOLDOSDWWHUQ
malnutrition etc. are discussed in other sections. +2 SD (97th Centile)
190 -
Mean
Constitutional growth delay 180
170
-
- -2 SD (3rd Centile)
In this condition, babies are born with normal size and 160 -
150 -
grow normally during the 1stIHZPRQWKVRIOLIH+RZHYHU
Height in cm

140 -
EHWZHHQPRQWKVRIDJHWKHLUJURZWKUDWHVORZVIRU 130 -
QRDSSDUHQWUHDVRQDQGWKHLUKHLJKWIDOOVEHORZrd centile 120 -
110 -
and continue to grow below 3rdFHQWLOH,QODWHUSDUWRI 100 - Familial SS
puberty, growth spurt occur and growth curves re-enter 50 -

above 3rd centile and results in achieving normal adult 0 3m 6m 12m 3y 6y 12y 18y
265

Age in years
KHLJKWDVZHOODVVH[XDOGHYHORSPHQW7KHbone age is
 266 Step on to Paediatrics

7RGHWHUPLQHWKHFDXVHVRIVKRUWVWDWXUHHLWKHUJHQHWLFRU Clinical Manifestations

RWKHULVHYDOXDWHGDWEHGVLGHE\FDOFXODWLQJ LQWHUSUHWLQJ XX Short stature
Mid Parental Height (MPH). XX )HDWXUHVRISLWXLWDU\LQVXI¿FLHQF\HJPDQLIHVWDWLRQRI
DGUHQDOWK\URLGDQGJRQDGDOLQVXI¿FLHQF\
XX )HDWXUHVRIUDLVHG,&3DVLQSLWXLWDU\WXPRUe.g.
Mid Parental Height (MPH) headache, vomiting, visual diturbances, polyurea,
seizure etc.
,WLVWKHDYHUDJHKHLJKWRIERWKIDWKHUDQGPRWKHU6LQFH
men are genetically pre determined to be taller than Diagnosis
ZRPHQE\DERXWFPRQHPXVWDGGFPWRPRWKHU¶V %DVHGRQ&) VXSSRUWVIURPWKHUHOHYDQWLQYHVWLJDWLRQV
KHLJKWEHIRUHDYHUDJLQJLWZLWKIDWKHU¶VKHLJKWWRFDOFXODWH
03+IRUDER\2QWKHRWKHUKDQGFDOFXODWLQJ03+IRUD Investigations
JLUOFPQHHGWREHVXEWUDFWHGIURPWKHIDWKHU¶VKHLJKW
Parameters Results
EHIRUHDYHUDJLQJLWZLWKPRWKHU¶VKHLJKW
XX Bone age is delayed than
7KXVIRUPXODIRU03+LVDVIROORZV
XX ;UD\ZULVW KDQG
chronological age
03+IRUDER\ XX RBS XX Low
)DWKHUVKHLJKW PRWKHU¶VKHLJKWFP XX X-Ray skill:
2 'LVWRUWLRQRIVHOOD XX &DOFL¿FDWLRQWXPRURI
turcica pituitary region
MPH for a girl XX &705,RIEUDLQ
)DWKHU¶VKHLJKWFP PRWKHU¶VKHLJKW
XX Insulin like growth XX 'HFUHDVHG LIQRUPDOLW
2 IDFWRU H[FOXGHV*+GH¿FLHQF\
How to assertain genetic or true short stature? XX Growth hormone XX &RQ¿UPDWRU\
$IWHUFDOFXODWLQJ03+ZHQHHGWRFDOFXODWHWKHtarget provocation test
heightUDQJHE\WKHIROORZLQJIRUPXODMPH±8.5 cm.
Treatment
The target height range is then plotted on the line
Replacement therapy with Recombinant Human Growth
FRUUHVSRQGVWR\HDUVRIDJHRQWKHJURZWKFKDUW$IWHU
Hormone (rhGH). Dose: ,8NJGD\JLYHQGDLO\
that, the existing height RIWKHFKLOGLVSORWWHGRQWKHDJH
RUHYHU\DOWHUQDWHGD\VXEFXWDQHRXVO\DWQLJKWWLOODGHTXDWH
VSHFL¿FOLQHRIWKHJURZWKFKDUW$OLQHLVWKHQGUDZQIURP
growth.
WKLVSRLQWRIH[LVWLQJKHLJKWDQGH[WHQGLQJOLQHWRZDUGVWKH
18 years age line to determine the adult Projected height
RIWKLVFKLOG,IWKHSURMHFWHGKHLJKWRIWKHFKLOGSDVV
below the target height range, then this child has true or
pathological short statureEXWLIFKLOG¶VSURMHFWHGKHLJKW TURNER SYNDROME
SDVVZLWKLQWKHUDQJHRItarget height range then his height XX .DU\RW\SH;
will be considered as genetic short stature. XX ,QFLGHQFHLQIHPDOHELUWKV+RZHYHULWLV
HVWLPDWHGWKDWRIFRQFHSWXVHVZLWKPRQRVRP\;
Growth hormone deficiency

are miscarried and only 5% are liveborn.

XX 6H[)HPDOH

Aetio-pathogenesis
GROWTH HORMONE DEFICIENCY XX Idiopathic 0DWHUQDODJHLVQRWDSUHGLVSRVLQJIDFWRU
&OLQLFDOEHKDYLRXURI7XUQHUV\QGURPHLVGXHWRDPLVVLQJ
Aetiology RULQFRPSOHWH;FKURPRVRPH$VVRPHRIWKHJHQHV
XX Idiopathic LQYROYHGLQSK\VLFDOJURZWK VH[XDOGHYHORSPHQWSUHVHQW
XX Secondary e.g. CNS irradiation, histiocytosis, on the X chromosome, girls with this disorder are shorter
craniopharyngioma
WKDQQRUPDODQGKDYHLQFRPSOHWHO\GHYHORSHGVH[XDO
characteristics.
 Step on to Paediatrics 267

Clinical Manifestations
XX Short stature
XX &KDUDFWHULVWLFFOLQLFDOIHDWXUHV JLYHQRQWKHWDEOH
Regions Features
XX Eyes ,QQHUFDQWKDOIROGVSWRVLVEOXHVFOHUDH
XX Ears, Nose Low-set prominent auricles, high arch
Mouth palate, narrow mandible
XX Neck Low posterior hairline, webbing
Shield chest e.g. Broad, widely spaced
XX Chest
nipples.3HFWXVH[FDYDWXP
6KRUWVWDWXUHFXELWXVYDOJXVVKRUWIRXUWK
XX Skeleton metacarpal and/or metatarsal, scoliosis,
hypoplastic nails
XX +DQG  Turner child with :HEELQJRIQHFN
/\PSKRHGHPDRIKDQGDQGIHHW DWELUWK
Feet Courtesy: Dr Iffat Ara Shamshad

Courtesy: Dr Maliha Alam

7XUQHU1HZERUQZLWKRHGHPDRIKDQG
Turner child with low posterior hair line

Turner syndrome

7XUQHU1HZERUQZLWKRHGHPDRIOHJDQGIRRW 7XUQHUFKLOGZLWKZLGHO\VSDFHGQLSSOHV VKLHOGFKHVW

 268 Step on to Paediatrics

Diagnosis
9LUWXDOO\FOLQLFDODQGNDU\RW\SLQJLVFRQ¿UPDWRU\

7XUQHU1HZERUQZLWKUHGXQGDQWQXFKDOVNLQ

Co-morbidities of Turner syndrome

TT Learning disabilities Treatment
TT 'HOD\HGSXEHUWDOGHYHORSPHQWDQGIDLOXUHRIVH[XDO
XX &RXQVHOLQJSDUHQWVDERXWWKHQDWXUH IXWXUHRIGLVHDVH
maturation XX *URZWKKRUPRQHUHSODFHPHQWE\\HDUVRIDJHWR
TT *RQDGDOG\VJHQHVLVDQGLQIHUWLOLW\ LQFUHDVHWKHKHLJKWRIWKHDIIHFWHGJLUO
TT Congenital heart diseases HJFRDUFWDWLRQRIDRUWD
XX )HPDOHVH[KRUPRQH 2HVWURJHQ 3URJHVWHURQH 
replacement during adolescence to develop secondary
TT 5HQDOPDOIRUPDWLRQVe.g. horse-shoe kidney
VH[FKDUDFWHULVWLFVDQGQRUPDOPHQVWUXDWLRQDQGWR
TT Endocrinopathies e.g. Hypothyroidism, diabetes
prevents osteoporosis
mellitus
TT Most have normal intelligence Prognosis
TT May have behavioural problem )HPDOHVZLWK;RU;PRVDLFLVPKDYHDORZIHUWLOLW\
UDWHDQGWKRVHZKREHFRPHSUHJQDQWKDYHDKLJKULVNRI
IRHWDOZDVWDJHHJPLVFDUULDJHVWLOOELUWK)XUWKHUPRUH
WKHLUOLYHERUQRIIVSULQJVKDYHDQLQFUHDVHGIUHTXHQF\RI
FKURPRVRPDODEQRUPDOLWLHVDQGPDOIRUPDWLRQV
Turner syndrome
 Step on to Paediatrics 269

References
 6DHQ]06*HQHWLFV '\VPRUSKRORJ\&XUUHQW3HGLDWULFGLDJQRVLVDQG7UHDWPHQWrd(G¶
 &RKHQ35RJRO$''HDO&/HWDO:LW-0,66&RQVHQVXV:RUNVKRSSDUWLFLSDQWV&RQVHQVXVVWDWHPHQWRQWKH
GLDJQRVLVDQGWUHDWPHQWRIFKLOGUHQZLWKLGLRSDWKLFVKRUWVWDWXUHDVXPPDU\RIWKHGrowth Hormone Research Society,
WKH/DZVRQ:LONLQV3HGLDWULF(QGRFULQH6RFLHW\DQGWKH(XURSHDQ6RFLHW\IRU3DHGLDWULF(QGRFULQRORJ\:RUNVKRS-&OLQ
(QGRFULQRO0HWDE
 0HOLVVD//RVFDO]R7XUQHU6\QGURPH3HGLDWULFVLQ5HYLHZ
 $JDUZDO.1HWDO7KH*URZWK,QIDQF\WRDGROHVFHQFHndHGµ&%63XEOLVKHU1HZ'HOKLSS

SELF ASSESSMENT
Short answer questions [SAQ]
 1DPH¿YHLPSRUWDQWFDXVHVRIVKRUWVWDWXUH
2. How will you diagnose and treat a child with Turner syndrome?
 :KDWDUHWKHFRPPRQSK\VLFDO¿QGLQJVRITurner syndrome?
4. A 10 years old girl presented with short statures
D :ULWHGRZQLPSRUWDQWGLIIHUHQWLDOV
E :KDWUHOHYDQWKLVWRU\ZLOO\RXH[SHFW"
c) How will you investigate the child?

Multiple choice questions [MCQ]

 7KHPDMRUFOLQLFRSDWKRORJLFDORXWFRPHRI7XUQHUV\QGURPHDUH±
BBBD GLDEHWHVPHOOLWXV BBBE VKRUWVWDWXUH BBBF UHQDOIDLOXUH
BBBG LQIHUWLOLW\ BBBH K\SRWK\URLGLVP
 7XUQHU¶VV\QGURPHLVFKDUDFWHUL]HGE\±
BBBD IHPDOHGRPLQDQFH BBBE 7DOOVWDWXUH BBBF ;2NDU\RW\SH
BBBG DEVHQFHRIDQWLDQGUR]HQWKHUDS\UHVSRQVH± BBBH K\SHUWHQVLRQ
 7KHFKDUDFWHULVWLFFOLQLFDOIHDWXUHVRI7XUQHU¶VV\QGURPHDUH
BBBD VKLHOGFKHVW BBBE LQIHUWLOLW\ BBBF ZHEELQJRIQHFN
___ d) simian crease ___ e) EUXVK¿HOGVSRWV
 7KHIROORZLQJDUHWKHQRUPDOYDULDQWVKRUWVWDWXUH±
BBBD FRQVWLWXWLRQDOJURZWKGHOD\ BBBE JHQHWLFVKRUWVWDWXUH BBBF *+GH¿FLHQF\
___ d) phychosocial deprivation ___ e) achondroplasia

Self assessment
 35
Difficulties in Movement and Posture
Cerebral palsy - - - - - - - - - - - - - - 276
Duchenne muscular dystrophy - - - - - - - - - - 278
Wilson disease - - - - - - - - - - - - - 279

:KHQDFKLOGSUHVHQWVZLWKGLI¿FXOWLHVLQPRYHPHQW Aetiology & Risk factors

SRVWXUHLHactivity limitation, one should consider ,QPDQ\FDVHVQRGH¿QLWHFDXVHLVLGHQWL¿HG ,GLRSDWKLF 
cerebral palsy (CP) as the commonest possibility. However, the known causes are-
+RZHYHUGLVHDVHVRIPXVFOHVe.g. Duchenne muscular
dystrophy (DMD)DQGRIEUDLQ VSLQDOFRUGe.g. XX Abnormal brain development
VSLQRFHUHEHOODUDWD[LDVXEDFXWHVFOHURVLQJSDQHQFHSKDOLWLV XX ,QWUDXWHULQHH[SRVXUHWRPDWHUQDOLQIHFWLRQ
(SSPE), Wilson disease, adrenolukodystrophy etc. also XX ,QWUDXWHULQHK\SR[LD
gives rise to such presentation. In this chapter CP, DMD XX 3HULQDWDODVSK\[LD K\SR[LFLVFKDHPLF
and Wilson disease is highlighted. encephalopathy (HIE)
XX ,QWUDFHUHEUDOKDHPRUUKDJHLQIDUFWLRQSHULYHQWULFXODU
leukomalacia
XX Neonatal sepsis
XX ([WUHPHORZELUWKZHLJKW SUHPDWXULW\
CEREBRAL PALSY (CP)
XX Hypoglycaemia or other metabolic abnormalities
&HUHEUDOSDOV\ &3 LVDQRQVSHFL¿FWHUPXVHGWRGHVFULEH XX .HUQLFWHUXV
DFKURQLFGLVRUGHUVRIPRYHPHQWDQGSRVWXUHFDXVLQJ
activity limitation. The condition is non-progressive Clinical Manifestations
DQGRULJLQDWHGIURPVRPHW\SHRIFHUHEUDOLQVXOWRULQMXU\
EHIRUHELUWKGXULQJGHOLYHU\RULQWKHSHULQDWDOSHULRG Symptoms
2WKHUQHXURORJLFGH¿FLWVRUGLVRUGHUVHJEOLQGQHVV
XX Not achieving or delay in achieving age appropriate
deafness, or epilepsyPD\FRH[LVW Motor skills i.e. neck control, sitting, standing,
crawling, walking, holding things etc.
7KHIXQGDPHQWDOFRXUVHVHYHULW\SUHFLVHPDQLIHVWDWLRQV XX Involuntary movements e.g. choreoathetoid movements
and prognosis vary widely. XX 'URROLQJRIVDOLYD
Types
XX 2WKHUV\PSWRPVRFFXULQJLQYDULDEOHIUHTXHQFLHVDUH
TT Seizure (50%)
XX 6SDVWLFLW\RIOLPEV UHODWHGWRGDPDJHLQWKHZKLWH
TT Intellectual disability PLOGVHYHUH
PDWWHU WKHPRVWFRPPRQIRUPRI&3  e.g.
TT Abnormal behaviour
6SDVWLFTXDGULSOHJLD6SDVWLFKHPLSOHJLD6SDVWLF
paraplegia,Spastic diplegia, Spastic monoplegia TT 'LVRUGHUVRI

XX $WD[LD UHODWHGWRGDPDJHLQFHUHEHOOXPRULWV ³³ Language, Speech e.g. dysarthria, dysrrhythmia

Cerebral palsy

pathways) is the 2ndFRPPRQIRUPRI&3  +HUH ³³ VisionHJVTXLQWUHIUDFWLYHHUURUGHIHFWLQ

¿QHFRRUGLQDWHGPRYHPHQWVRIERWKXSSHUORZHU choroid/retina and blindness

H[WUHPLWLHVDQGWUXQNDUHDIIHFWHGDQGWKHEDE\PD\ ³³ Hearing

present with early hypotonia poor balance an

l l
³³ Sensory perception
l delayed motor development intension tremor etc.
l
³³ Interaction
XX Dyskinetic movement (related to damage in basal XX Feeding problem
JDQJOLDRUWKHLUDVVRFLDWHGSDWKZD\V DQGWKHDIIHFWHG
child presents with involuntary movements e.g. chorea,
athetosis, dystonia and poor postural control(5%)
270

XX Persistent hypotonia without spasticity (1%)

 Step on to Paediatrics 271

Physical Examination B. The Integrated managementLVRIIHUHGE\DJURXS

7KH¿QGLQJVDUHYDULDEOHDQGDUHUHODWHGWRLQYROYHPHQWRI RIH[SHUWVIURPGLIIHUHQWGLVFLSOLQHV+HUHWKH
S\UDPLGDOH[WUDS\UDPLGDOV\VWHPDQGFHUHEHOOXP Paediatrician plays the pivotal role. This group will
FROOHFWLYHO\RIIHUPD[LPXPVSHFLDOL]HGVHUYLFHV
7KHXVXDO¿QGLQJVDUH
WRDWWDLQPD[LPDOQHXURORJLFIXQFWLRQLQJZLWKDQ
XX $SSHDUDQFH'XOO YDFDQW appropriate and integrated approach emphasizing on
XX Posturing: Abnormal physical, occupational and speech therapy.
XX Spasticity e.g. scissoring, tight tendoachilis
7KHUROHRIGLIIHUHQWVSHFLDOWLHVDUHJLYHQLQWKHWDEOH
XX +\SHUUHÀH[LDEULVNRUH[DJJHUDWHGGHHSUHÀH[HVe.g.
knee, ankle jerks XX Ensure appropriate nutrition
XX Involuntary movements XX Treat common illnesses
e.g. chorea, tremor etc. Paediatrician XX Ensure complete immunization
XX Hypotonia, sometimes XX 0DNHWLPHO\UHIHUUDOWRDSSURSULDWH
but deep tendon authority
UHÀH[HVDUHEULVNas in
hypertonic CP
XX 6SHFL¿FWUDLQLQJe.g. sitting,
XX Gait: Abnormalities, VWDQGLQJVWHSSLQJ ZDONLQJ
PD\EHDWD[LF
XX ([HUFLVHGHVLJQHGWRLQFUHDVH
Physiotherapist
XX 2WKHU¿QGLQJV muscle strength
TT Microcephaly
XX 3UHYHQWLRQRIFRQWUDFWXUHV
2)&6'IRUDJH 
XX &RQWURORIPRYHPHQW
TT 6TXLQWSRRU¿[DWLRQ Speech language XX Develop communication skills
RIH\HVGXHWRFUDQLDO therapist especially speaking
nerve palsy XX 'HYHORS¿QHPRWRUVNLOOVe.g.
TT 3HUVLVWHQFHRI Occupational
GUHVVLQJIHHGLQJZULWLQJDQGRWKHU
SULPLWLYHUHÀH[HVe.g. therapist
daily activities
palmar grasp, moro
UHÀH[HWF beyond the XX Improve cognitive and behavioural
&3ZLWKK\SHUWRQLFLW\RIERWK Psychologist
DJHRIGLVDSSHDUDQFH development
XSSHUDQGORZHUOLPEV ¿VWLQJ
TT Limb length
Audiologist XX Assist in hearing problems
discrepancy as noted in spastic hemiplegia
TT (YLGHQFHRIFRQJHQLWDOLQIHFWLRQVE\&095XEHOOD XX &RUUHFWUHIUDFWLYHHUURUVTXLQWDQG
Ophthalmologist
e.g. CHD, cataract, retinopathy etc. DGYLFHRQH\HH[HUFLVH
TT 0DOQXWULWLRQ )77 GXHWRIHHGLQJGLI¿FXOWLHV
XX &RUUHFWGHIRUPLWLHVZKLFKDUH
Orthopaedic beyond medical treatment
Diagnosis
surgeon XX 6XUJLFDOUHOHDVHRIKHHOFRUG
'LDJQRVLVRI&3LVYLUWXDOO\FOLQLFDODQGE\H[FOXVLRQRI contractures
other neurological disorders. Investigations have limited
value. However, XX Mild CP may attend normal school
Special school
XX MRI VFDQPD\EHKHOSIXOWRXQGHUVWDQGWKHIXOOH[WHQW XX Moderate to severe CP needs
and teachers
RIFHUHEUDOLQMXU\DQGRFFDVLRQDOO\WKHSDWKRORJ\RI special schools
FRQJHQLWDO&09LQIHFWLRQRUEUDLQPDOIRUPDWLRQ XX Create social awareness to
XX *HQHWLF PHWDEROLFVFUHHQLQJPD\JLYHVRPHFOXHDQG HVWDEOLVKWKHULJKWRIWKHDIIHFWHG
VKRXOGEHSODQQHGEDVHGRQKLVWRU\RU05,¿QGLQJV Social worker FKLOGUHQ DUUDQJHYDULRXV
Management economic aids and legislative
Cerebral palsy

support
A. Counseling parents regarding the disease, its treatment
and outcome. Make it clear to parents that it is- &0DQDJHPHQWRIIHHGLQJGLI¿FXOW\
XX A non progressive disease TT 8VHDVKDOORZVSRRQDQGJLYHVRIWIRRG
XX Not a mental illness and TT 3ODFHWKHIRRGRQWKHPLGGOHRIWKHWRQJXH
XX Not curable TT 1DVRJDVWULFWXEHIHHGLQJLIQHHGHG
 272 Step on to Paediatrics

D. Pharmacotherapy Pathogenesis
TT For spasticity - 'XHWRPXWDWLRQRIWKHJHQHRQ;FKURPRVRPHWKHUH
³³ Drugs: Tizanidine, %DFORIHQClonazepam,
LVGH¿FLHQWSURGXFWLRQRIPXVFOHF\WRVNHOHWRQSURWHLQ
Diazepam etc. µ'\VWURSKLQ¶ZKLFKFDXVHVSURJUHVVLYHZHDNQHVVRI
³³ ,QM%RWR[LVXVHGWRWUHDWVSDVWLFLW\,WEORFNV
PXVFOHVSDUWLFXODUO\WKHSUR[LPDOPXVFOHV SUR[LPDO
WKHWUDQVPLVVLRQRIRYHUDFWLYHQHUYHLPSXOVHV myopathy).
to the targeted muscle by selectively preventing
WKHUHOHDVHRIAcetylcholine (ACh) at the 0XWDWLRQVLQVDPHJHQHWKDWUHVXOWVLQSDUWLDOH[SUHVVLRQ
neuromuscular junction RIG\WURSKLQSURWHLQSURGXFHDOHVVVHYHUHSKHQRW\SH
³³ '\VNLQHWLF&37ULKH[LSKHQLG\OK\GURFKORULGH µ%HFNHUPXVFXODUG\VWURSK\¶
(Pacitane)
TT Convulsion: Give standard anticonvulsants (avoid
Clinical Manifestations
Phenobarbitone)
XX 1RUPDODWELUWKRUGXULQJHDUO\LQIDQF\
XX &OLQLFDOPDHQLIHVWDWLRQVXVXDOO\DSSHDUE\\HDUVRI
E. Follow up:7RDVVHVVHI¿FDF\RIWUHDWPHQWE\ORRNLQJ
age, HJIUHTXHQWIDOOVWURXEOHUXQQLQJGLI¿FXOWLHVLQ
DWVWDWXVRIGLVDELOLWLHV FOLPELQJVWDLUVDVZHOODVULVLQJIURPÀRRUEHG
Prognosis
XX +2UHFXUUHQWUHVSLUDWRU\LQIHFWLRQV
XX &OLQLFDOH[DPLQDWLRQVKRZV
'HSHQGVJUHDWO\RQFKLOG¶V,4VHYHULW\RIPRWRUGH¿FLWV TT 3VHXGRK\SHUWURSK\RIFDOYHV GXHWRK\SHUWURSK\RI
HWLRORJ\RI&3DQGGHJUHHRILQFDSDFLW\,QVHYHUHO\
VRPHPXVFOH¿EHUVLQ¿OWUDWLRQRIPXVFOHE\IDWDQG
DIIHFWHGFKLOGUHQDVSLUDWLRQSQHXPRQLDDQGRWKHU SUROLIHUDWLRQRIFROODJHQ
LQWHUFXUUHQWLQIHFWLRQVDUHWKHPRVWFRPPRQFDXVHVRI
death. In contrast, children with mild CP, may improve
with age.

DUCHENNE MUSCULAR DYSTROPHY

,QWKLVGLVHDVHER\VVXIIHUDQGIHPDOHVFDUU\WKHGLVHDVH
RQO\H[FHSWLRQLV7XUQHUVZKHUHIHPDOHDUHVXIIHUHUV
XX Incidence: 1 in 3600 male births Pseudohypertrophy of calf muscle
XX 'HIHFW0XWDWLRQRIWKHJHQHDW;SORFXV
XX 0RGHRILQKHULWDQFH;OLQNHGUHFHVVLYHWUDLW
TT :DVWLQJRIWKLJKPXVFOHV SUR[LPDOP\RSDWK\

1 2 3
Duchenne muscular dystrophy

Gower sign Gower sign Gower sign

 Step on to Paediatrics 273

TT Lordotic posture XX ;5D\FKHVW0D\VKRZHYLGHQFHRISQHXPRQLDDQGRU

TT Trendelenburg gait or hip waddle (Waddling gait) cardiomyopathy (cardiomegaly)
TT 3UHVHQFHRIGower sign, the characteristic posture XX (&* (FKRFDUGLRJUDP(YLGHQFHRI&DUGLRP\RSDWK\
TT 3UHVHQFHRIslip through sign DVWKHER\LVOLIWHG XX 0XVFOHELRSV\VKRZV±
XSE\KROGLQJDURXQGWKHVLGHVRIKLVFKHVWULJKWXS TT (QGRP\VLDOFRQQHFWLYHWLVVXHSUROLIHUDWLRQ

under his arms, the weak shoulders move upward, TT 6FDWWHUHGGHJHQHUDWLQJDQGUHJHQHUDWLQJP\R¿EULOV

DOPRVWDOORZLQJKLPWRVOLSWKURXJKWKHSK\VLFLDQ¶V TT )RFLRIPRQRQXFOHDUFHOOLQ¿OWUDWLRQ

hands) XX Molecular analysis has largely replaced muscle biopsy

TT 3UHVHQFHRIwinging sign ZLQJLQJRIVFDSXOD WRFRQ¿UPWKHGLDJQRVLV

Treatment
&RXQVHOSDUHQWVDERXWWKHQDWXUH IXWXUHRIWKHGLVHDVH

Supportive
XX Diet
TT Maintain good nutrition and to prevent obesity
TT 0LQLPL]HRVWHRSRURVLVE\DGHTXDWHFDOFLXPDQG

ÀXRULGHVXSSOHPHQWDWLRQ
XX Physiotherapy to delay contractures
XX 3URPSWWUHDWPHQWRI
TT 3XOPRQDU\LQIHFWLRQV

TT &DUGLDFGHFRPSHQVDWLRQ 'LJR[LQ

XX 6WHURLGDUHXVHIXOLQPDLQWDLQLQJPXVFOHVWUHQJWK,W
does not slow the disease progression. Prednisolone,
PJGDLO\IRUGD\VRIHDFKPRQWKPD\EHJLYHQ
XX ,PPXQL]DWLRQDJDLQVWLQÀXHQ]DYLUXVLQDGGLWLRQWR
other routine vaccinations

Prognosis
Winging of scapula 7KHUHOHQWOHVVSURJUHVVLRQRIZHDNQHVVFRQWLQXHVLQWRWKH
2nd decade. Most patients continue to walk with increasing
TT +\SHUWURSK\RIWRQJXHDQGIRUHDUPPD\EHSUHVHQW
GLI¿FXOW\XQWLO\HDUVRIDJHDQGVRPHDUHZKHHOFKDLU
EXWQRIDVFLFXODWLRQ
ERXQGE\\HDUV
XX OtherIHDWXUHV
TT &RQWUDFWXUHVLQYROYLQJDQNOHVNQHHVKLSV HOERZV 'HDWKRFFXUVXVXDOO\DURXQG\UVRIDJH7KH
TT Scoliosis
FRPPRQFDXVHVRIGHDWKDUHUHVSLUDWRU\IDLOXUHLQWUDFWDEOH
TT Cardiomyopathy, presenting DVFDUGLDFIDLOXUH
KHDUWIDLOXUHSQHXPRQLDRURFFDVLRQDOO\DVSLUDWLRQDQG
persistent tachycardia, murmur airway obstruction.

Duchenne muscular dystrophy

TT Intellectual impairment

Diagnosis
%DVHGRQFKDUDFWHULVWLF&)DQGVXSSRUWVIURPWKHUHOHYDQW WILSON DISEASE
investigations. XX Incidence: 1/5000 to 1/100,000 population
XX 0RGHRILQKHULWDQFH$XWRVRPDO5HFHVVLYH
Investigations XX 'HIHFW0XWDWLRQRI$73%JHQHRQFKURPRVRPH
XX 6HUXP&.OHYHOGreatly elevated (15,000 -35,000 FRGLQJIRUDVSHFL¿F3W\SHDGHQRVLQHWULSKRVSKDWDVH
IU/L, (normal: < 150 IU/L) involved in copper transport.
XX Electromyogram (EMG): Characteristics myopathic To learn Wilson disease, it is important to understand
IHDWXUHEXWQRWVSHFL¿FIRU'0'
normal copper metabolism.
 274 Step on to Paediatrics

Normal Copper (Cu) metabolism Clinical Manifestations

+HSDWLF KDHPDWRORJLFDOPDQLIHVWDWLRQVDSSHDUHDUO\ 
,QJHVWLRQRI&XFRQWDLQLQJIRRG ODWHURQQHXURORJLFDOPDQLIHVWDWLRQV

$EVRUSWLRQRILQJHVWHG&X  LQGXRGHQXP  Organs Manifestations

SUR[LPDOJXW LW¶VHQWU\LQWRSRUWDOYHQRXVV\VWHP XX Acute hepatitis e.g. jaundice
Liver XX )XOPLQDQWKHSDWLFIDLOXUH
%LQGLQJRIDEVRUEHG&XZLWKZLWKDOEXPLQDQG XX Chronic liver disease, portal hypertension,
histidine in portal blood ascites
XX ([WUDS\UDPLGDOPDQLIHVWDWLRQV e.g.
7UDQVSRUWDWLRQRI&XDOEXPLQFRPSOH[WROLYHU tremor, dysarthria, drooling, dystonia,
Nervous choreoathetosis
'LVVRFLDWLRQRI&XIURPDOEXPLQDQGKLVWLGLQH  system XX 3V\FKLDWULFPDQLVIHVWDWLRQVe.g. dementia
WDNHQXSRI&XE\KHSDWRF\WHV XX 'HWHULRUDWLRQRIKDQGZULWLQJVFKRRO
SHUIRUPDQFH
Within hepatocytes Cu binds with
XX Speech disturbances
DSRFHUXORSODVPLQWRIRUPFHUXORSODVPLQ XX KF (Kayser-Fleischer) ring (Greenish
brown ring due to Copper deposition in
Eyes
5HOHDVHRIFHUXORSODVPLQ ZLWK&X  GHVFHPHW¶VPHPEUDQHRIVFOHURFRUQHDO
in the systemic circulation junction (limbus)
XX 6XQÀRZHUFDWDUDFW
$IWHULW¶VIXQFWLRQLVRYHULQEORRG XX Haemolytic anaemia
FHUXORSODVPLQWDNHQXSE\WKHOLYHUIURPFLUFXODWLRQ
XX Rickets
XX Renal tubular acidosis
'LVLDO\ODWLRQDQGGHJUDGDWLRQRIFHUXORSODVPLQ
Others XX Arthritis
within hepatic lysosomes
XX Cardiomyopathy
XX Endocrinopathy e.g. Hypoparathyroidsm
5HOHDVHG&XIURPFHUXORSODVPLQ H[FUHWLRQ XX ,QIHUWLOLW\5HFXUUHQWPLVFDUULDJHV
into the bile

In :LOVRQGLVHDVHEHFDXVHRIPXWDWLRQLQATP7B gene,
SDWLHQWVEHFRPHGH¿FLHQWRIDGHQRVLQHWULSKRVSKDWDVH
(ATP) protein which results in -
XX ,PSDLUHGLQFRUSRUDWLRQRIFRSSHU &X LQWR
ceruloplasmin by the liver and thus decreased secretion
RIceruloplasmin into blood
XX 'HFUHDVHGH[FUHWLRQRIFRSSHULQWRELOH

The net results are

XX 5HGXFWLRQRIceruloplasmin in blood
.) .D\VHU)OHLVFKHU ULQJ
XX $FFXPXODWLRQRIIUHH&XLQKHSDWRF\WHVDQG&X Courtesy: Dr Farzana Sharmeen
LQGXFHGWR[LFLQMXU\WRKHSDWRF\WHV
Wilson disease

XX 6SLOOLQJRYHURIIUHH&XIURPOLYHULQWRFLUFXODWLRQ Diagnosis
XX &XLQGXFHGWR[LFLQMXU\WR5%& KDHPRO\VLV EDVDO %DVHGRQ&) VXSSRUWVIURPWKHUHOHYDQWLQYHVWLJDWLRQV
JDQJOLDFRUQHDNLGQH\ERQHMRLQWV SDUDWK\URLGV
XX &RQFRPLWDQWLQFUHDVHLQXULQDU\&XH[FUHWLRQ
 Step on to Paediatrics 275

Investigations Treatment
Parameters Results A. Supportive
XX Haemoglobin Decreased
XX Copper Chelators
TT 'SHQLFLOODPLQHPJNJGD\WZLFHGDLO\EHIRUH
< 20 mg/dl meal. Start with lower dose and increase over 1 to 2
XX S. ceruloplasmin
QRUPDOPJGO weeks to the desired dose
TT Trientine hydrochloride 20 mg/kg/day
!ȝJGD\
XX 24 hours urinary Copper TT Tetrathiomolybdate, is being tested as an alternate
QRUPDOȝJGD\
therapy
XX SGPT, S. Bilirubin, May be raised XX Others supportive agents
XX Prothrombin time TT Zinc acetate: 25 mg, orally, 3 times a day may reduce

Reveals change in copper absorption. Zinc should not be given at the

XX 05,RIEUDLQ
basal ganglia same time as copper chelators
TT 3\ULGR[LQHPJGD\LVJLYHQGDLO\GXULQJWKHUDS\
XX D- penicillamine challenge ,IXULQDU\&RSSHU with Penicillamine to prevent optic neuritis
test H[FHHGV!ȝJ TT Both the copper chelators and Zinc will be continued
XX Patient will take in 24 hours then it is IRUOLIH
3HQLFLOODPLQH PJ 
VXJJHVWLYHRIWilson XX Diet
KRXUO\IRUKRXUVDQG
disease (done only TT $OORZGLHWGH¿FLHQWLQFRSSHUHJPLON PLON
during this period all urine
KDVWREHFROOHFWHGLQDMDU when 24 hours urinary SURGXFWVJUHHQOHDI\YHJHDEOHVVXJDUFROGGULQNV
for Copper estimation &XLVȝJGD\ lemon juice, tomato juice
TT Avoid diet rich in copper e.g.meat, chicken, honey,

!ȝJJPRIGU\ MDPFKLOOLHJDUDPPDVDODSXOVHVZKHDWÀRXU
XX Liver biopsy to measure ZHLJKWRIOLYHULV chocolates, dried nuts, mushroom
hepatic coppper content FRQILUPDWRU\ QRUPDO
ȝJJPGU\ZHLJKW %6SHFL¿FWUHDWPHQWLiver transplantation.
Prognosis
7KHSURJQRVLVIRUXQWUHDWHG:LOVRQGLVHDVHLVSRRU

Wilson disease
276 Step on to Paediatrics

References
1. Molla MR. Physical *URZWK 'HYHORSPHQW&RQFLVH7H[WERRNRI3HGLDWULFVndHGµ
2. Hutchinson JH et al. Practical Pediatric Problems. 6th ed. Singapore: PG Asian Economy Edition; 1989.
 6RNRO5-HWDO/LYHU 3DQFUHDV :LOVRQ'LVHDVH &XUUHQW'LDJQRVLVDQG7UHDWPHQW3HGLDWULFVrdHG
.HGLD6HWDO1HXURORJLF 0XVFXODUGLVRUGHUV &HUHEUDOSDOV\ &XUUHQW'LDJQRVLV 7UHDWPHQW3HGLDWULFVrd ed; 2016:

 5REELQVDQG&RWUDQ3DWKRORJLF%DVLVRI'LVHDVHVth ed. 2010, Saunders, p863-64.

SELF ASSESSMENT
Short answer questions [SAQ]
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4. What do you mean by pseudohypertrophy? Where does this occur in DMD?
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 36
Accidents and Emergencies
Kerosene poisoning - - - - - - - - - - - - - 277
OPC poisoning- - - - - - - - - - - - - - 278
Foreign body aspiration (FBA) - - - - - - - - - - - 279
Burn - - - - - - - - - - - - - - - 280
Snake bite- - - - - - - - - - - - - - 283
Drowning - - - - - - - - - - - - - - - 285
Dog bite- - - - - - - - - - - - - - - 287

Children are the frequent victims of various accidents KEROSENE POISONING

and these pose them to life-threatening emergencies. The
common accidents & emergencies (A&E) of children are– XX Commonest childhood poisoning (37% of all poisoning)
XX At risk children: Age 1-5 years, due to their natural
XX Accidental ingestion of poisons, household curiosity to explore
substances, drugs etc. XX Easy access to children due to it’s availability in most
XX Drowning poor households and wrong storage in beverage bottles
XX Foreign body aspiration in the airway XX Ingestion occurs more during summer months
Burn & scald
Pathogenesis
XX

XX 5RDGWUDI¿FDFFLGHQWV
The principal concern of kerosene oil poisoning is
XX Snake, dog/insect biting
its aspiration into lungs that may occur during initial
XX Electrocution
ingestion or during vomiting. Following aspiration, it
XX Injury by sharp objects & domestic animals
FDXVHVLQÀDPPDWLRQWROXQJVSDUHQFK\PD(chemical
pneumonitis) which may progress to atelectasis,
In this chapter, accidental poisoning, foreign body pneumothorax or pleural effusion and which interferes
aspiration, drowning, burn, snake and dog bite will be with gaseous exchange and hypoxia. This ultimately
discussed. affects CNS and other vital organs.
Fatal dose: 30 ml and fatal period is 24 hours.
Accidental Poisoning
Accidental ingestion of poisonous agents is the most Clinical Manifestations
common way of poisoning among children. Of the The child may–
different agents, the following substances are commonly Be asymptomatic, just only have H/o kerosene ingestion
XX
Kerosene poisoning
associated with accidental poisoning. XX Cry excessively because of pain and irritation in the
throat
XX Kerosene XX Have sensation of choking, nausea or vomiting
XX Household products e.g.bleach, cosmetics, toiletries, XX Have characteristic odour in breaths & vomitus
detergents, disinfectants, petroleum distillates etc. XX Have features of pneumonia e.g. cough, breathlessness,
XX Drugs, of other family members wheeze, fever
XX Organophosphorus compounds (OPC) XX Have colicky abdominal pain, diarrhoea
XX Have arrhythmias, congestive cardiac failure
XX Rarely, seizure and coma
277
 278 Step on to Paediatrics

Physical Examination XX Observe for at least 24 hours to note evidence of

XX General condition & vital signs are usually normal respiratory or other complications (CNS) as an initial
XX Sometime, high fever may be present asymptomatic child may develop full-blown picture of
kerosene oil poisoning after 24 hours of ingestion
XX Features of pneumonia may be present e.g. fast
EUHDWKLQJFKHDVWLQGUDZLQJQDVDOÀDULQJFUHSVHWF
XX Give Antibiotics, when there is suspicion of secondary
pneumonia
XX Pupils are usually normal but may be either constricted
or dilated, if coma supervenes
Gastric lavage is contraindicated as it is associated with
Diagnosis aspiration of kerosene into the lungs.
Based on C/F and supports from relevant investigations.

Investigations
XX X-Ray chest
ORGANOPHOSPHORUS COMPOUND
TT Early stage: Fine, punctuate mottling present in
(OPC) POISONING
perihilar areas

Pathogensis
Organophosphorus compounds causes neurotoxicity
through inhibition of acetylcholinesterase: the enzyme that
breaks Acetylcholine. So, acetylcholine is not metabolized.
As a result, there is persistent cholinergic discharge at the
neuromuscular junctions.

Clinical Manifestations
XX Smell of OPC are usually felt
XX Clinical features appear within few hour of exposure,
and the typical features are–

XX Profuse sweating
XX Increased salivation
XX Blurring of vision
XX Muscle twitching
XX Constricted pupils
XX Convulsion
XX Flaccid paralysis &
deep coma in the late
XX Muscle cramp
stage of the disease
XX Diarrhoea or vomiting XX Variable
XX Headache haemodynamic status
XX Pulmonary congestion
Patchy opacities in lungs

Investigations
TT /DWHUVWDJH3DWFK\LOOGH¿QHGRSDFLWLHVPD\GHYHORS XX RBC cholinesterase level. A decrease in <25% of
in both lungs particularly the lower lobes
QRUPDOLQGLFDWHVLJQL¿FDQWH[SRVXUH
TT Sometimes there may be evidence of pneumatocoele

and later pneumothorax Treatment

XX CBC: Neutrophilic leukocytosis, but may be normal XX Hospitalize immediately
XX Counsel parents about the nature & fate of OPC
Treatment
poisoning
OPC poisoning

Mainly supportive and includes– XX Remove all contaminated clothes and wash the body
XX Care of airway & breathing (see page 254 ) thoroughly with soapy water
XX IV saline, if patient is dyspnoeic or unable to tolerate XX Give gastric lavage, if patient arrives within 30 minutes
oral or NG feed of ingestion
XX Provide O2 inhalation, if there is respiratory distress/low XX Assess vital signs quickly e.g. pulse, BP, capillary
SPO2 UH¿OOLQJWLPHSXSLOVHWFHYHU\KRXUV
 Step on to Paediatrics 279

XX Clear the airway and support breathing (ABC) XX When in the Supra-glottic airway (larynx & trachea),
XX Keep the patient in lateral position to avoid aspiration LWWULJJHUVSURWHFWLYHUHÀH[HVDQGODU\QJRVSDVPDQGLQ
XX ,QIXVH,9ÀXLGWRPDLQWDLQQRUPDOKDHPRG\QDPLF about 90% cases, it is coughed out
status, nutritional support and to administer drugs XX When small objects cross the glottis and lodge in the
XX O2 inhalation:1-2 liters/minute lower airway (infra-glottic airway), it induces cough
XX Inj $WURSLQH DPS PJ ,WLVVWDUWHGDWDGRVHRI and variable respiratory distress of variable intensity. In
0.05 mg/kg IV and repeated every 10-15 minutes to a 80-90% cases, it is lodged into right principal bronchus
maximum of 2-5 mg till the pupils are dilated (i.e. full In the airway, when it causes partial obstruction (Ball-
atropinization) Valve effect),DLUFDQHQWHUGXULQJLQVSLUDWLRQEXW¿QG
GLI¿FXOWLHVWRFRPHRXWGXULQJH[SLUDWLRQDQGXOWLPDWHO\
Signs of atropinization gives rise to XQLODWHUDOK\SHULQÀDWLRQ On the otherhand,
XX Mydriasis (dilated XX Dry mouth and nose when FB completely blocks the air passage (Stop-valve
pupil) XX Anhydrosis (absence of effect), air cannot enter distal to obstruction and ultimately
XX Tachycardia sweating) the obstructed lungs collapse.
XX Flushing XX Bronchodilatation
Clinical Manifestations
XX Sudden onset of coughing, chocking or wheezing in
Then, gradually taper the dose of atropine and maintain for
a previously well child with a history that the child
at least 2-3 days, based on the size of the pupils. Atropine running with food in the mouth or playing with seeds,
antagonizes the muscarinic parasympathetic effects of small coins or toys
OPC but does not affect the nicotinic receptor and it does XX Inability to vocalize, presence of cyanosis (complete
not improve muscular weakness. obstruction)
XX Give Inj. Pralidoxime (Cholinesterase reactivator): XX Presence of stridor (partial obstruction)
30 mg/kg diluted, and infused IV over 5-30 minutes) in
addition to Atropine. It is most useful if given within 48 Diagnosis
KRXUVRIH[SRVXUH,WPD\EHUHSHDWHGHYHU\KRXUV Based on clinical features and supportive investigation.
as needed
XX Give Antibiotics to prevent pneumonia and other Investigations
infections XX X-Ray Chest (frontal & lateral view). Features are–
XX Put catheter before starting atropine, as it constricts the TT Normal in about 80% of laryngotracheal lodging

sphincters TT 8QLODWHUDOK\SHULQÀDWLRQZKHQ)%ORGJHGLQ

XX Monitor the patient as needed to note the signs of principal bronchus with ball valve effect. However,
atropinization & other vital parameters ELODWHUDOK\SHULQÀDWLRQRFFXUVZKHQ)%ORGJHGLQ
XX Provide other supportive care– trachea
TT Maintenance of hygiene (including oral hygiene)

TT Care of bowel and bladder

TT Orophyaryngeal & nasopharyngeal suction when

needed

FOREIGN BODY ASPIRATION (FBA)

The second leading cause of accidental death next to
GURZQLQJDPRQJFKLOGUHQEHWZHHQPRQWKVWR\HDUVRI
age. FBA is commonly seen with small, round foods such 8QLODWHUDOK\SHULQÀDWLRQRIOHIWOXQJDQGDPHWDOLF
as nuts and seeds, berries, corn/popcorn, beans etc. IRULHJQERG\LQOHIWSULQFLSDOEURQFKXV
Snake bite

Pathogenesis XX 2WKHU¿QGLQJVDUHIHDWXUHVRIFROODSVHSQHXPRQLWLV
TT In about 20% cases, FB is visible
After aspiration, FB can lodge anywhere along the
respiratory tract and produce variable features. XX CT scan of chest: A helpful diagnostic tool
 280 Step on to Paediatrics

Treatment
XX Back blow/Heimlich maneuver to expel the FB out
BURN
%XUQLVDJOREDOSXEOLFKHDOWKSUREOHPSRVLQJDVLJQL¿FDQW
mortality and morbidity. In Bangladesh, it is common
among all age groups and children are particularly
vulnerable.
XX Burn: A dry heat injury caused by the application of
ÀDPHor heated solid substances to the body resulting in
coagulation necrosis of the tissues.
XX Scald:
A moist
heat injury
caused
by the
application
of a hot
If this maneuver is failed, then– liquid, at
or near its
XX 5HIHUWKHFKLOGWRUHPRYHWKH)%E\HLWKHU¿EUHRSWLFor
boiling
rigid bronchoscopy (the gold standard)
point or in
XX Surgery in complicated cases its gaseous
form (such
Prevention
as steam), to the body.
XX Do not let young children to play with toys, small
enough to put in their mouths. Apart from dry & moist heats, burn can also results from
XX Keep small objects HJPHGLFLQHVQXWVHWF out of reach electricity, chemicals (e.g. acid, alkali), frost bite, friction,
of small children irradiation, thunder, coal tar, bitumen etc.
XX Educate doctors regarding the possibility of FBA when
sudden onset of coughing and choking in a well child

Pathogenesis
BURN

Damage of cells
Secretion of stress hormones,
suppression of anabolic hormones & Ĺ6XUIDFHWRPDVVUDWLRLQ
5HOHDVHRILQÀDPPDWRU\ activation of neural mechanisms children, less insulating fat &
mediators, cytokines & burn toxin lower muscle mass

YDVRGLODWDWLRQĹFDSLOODU\SHUPHDELOLW\
Tachycardia, hyperthermia &
protein wasting Hypothermia, Hypoglycemia
ĹDOEXPLQORVV ĻFROORLGDO
ĹÀXLGORVV
osmotic pressure

Shock Small circulating volume

([WUDYDVDWLRQRIÀXLGLQWKH
interstitial spaces
Burn

• Oedema Small circulating 'HOD\LQÀXLGUHVXVFLWDWLRQ

‡+\SRYROHPLDCĻ&23 volume in children
 Step on to Paediatrics 281

Types of burn injuries, based on depth of tissues/skin involved

XX Partial thicness burn e.g. 6XSHU¿FLDO 6XSHU¿FLDOGHUPDO Deep dermal burns
O O O

XX Full thickness burn: involve all layers of skin & other deep structures

Superficial Deep Full

Superficial dermal dermal thickness

Epidermis

Dermis

Subcutaneous

Burn injuries: Types, causes, characteristics and outline of management

Pain sensation
Types Affected areas Causes Characteristics Dressing by
& Healing
TT 6XSHU¿FLDO Epidermis only, no Sunlight, TT Dry, erythema TT Very TT Ointment
burn dermis ÀDVK0LQRU TT Brisk capillary Painful TT Hydrocolloid
scald UH¿OO TT Heals by TT Collagen sheet
5-7 days
TT 6XSHU¿FLDO Epidermis and Hot liquid TT Moist, blister, TT Painful TT Hydrocolloid
dermal burn deep upto papillary (scald) reddened with TT Heals TT Collagen sheet
dermis broken blister by10-14 TT Amniotic membrane
TT Brisk CRT days
TT Deep Epidermis, papillary Hot liquid/ TT Moist, white TT Pain, less TT Silver sulphadiazine
dermal burn dermis and deep scald / slough red TT Heals by cream
upto reticular dermis PLQRUÀDPH mottled 21-28 days TT Hydrocolloid,
contract TT Sluggish CRT TT Early excision &
grafting
TT Full All layers of skin Severe TT Dry, charred, TT Painless, TT Silver sulphadiazine
thickness/ and deeper tissues VFDOGÀDPH whitish Absent TT Never cream
deep burn e.g. muscles, bones, electric burn CRT heals TT Excision &
tendons are affected reconstruction
Burn
 282 Step on to Paediatrics

Burn wound assessment TT Infuse: The measured amount continuously for 24

hours
Percentage of burn TT After 24 hours, Infuse 50% of the measured
UHVXVFLWDWLRQÀXLGV0DLQWHQDQFHÀXLG
18% 17% TT After 48 hours, titrate according to the input-output
chart
II. Give Analgesics, LIVHYHUHSDLQ
TT Morphine (0.1-0.2mg/kg/dose), IV or
Front Front
18% 18%
TT Diclofenac or Ibuprofen or Paracetamol, oral/rectal
9% 9% 9% 9% TT Add H2 blocker
Back Back
III. Give Antibiotics
18% 18%
TT 2nd and 3rd generation Cephalosporin, IV in adequate
doses
14% 14% 14.5% 14.5% IV. Monitor urine output
TT Insert Indwelling catheter for burns of >10%, all
electric and genital burns for meticulous assessment
of urine output, which should be: 0.5-1 ml/Kg BW/
Age 0-1 year Age 2 year hour orPOKRXU
V. Ensure wound care
Rule of 9
TT Clean the burnt area with normal saline and cover &
XX Age 0-1 years: Head & Neck region: 18%; Trunk
dress with materials as mentioned in the table above
(front & back): 18%+18%; Upper limbs: 9%+9%;
Lower limbs: 14% + 14%.
TT ,IVXFKPDWHULDOVDUHQRWDYDLODEOH, then cover
the area with a thick layer of Silver sulphadiazine
XX For each year thereafter: Take1% from the head & neck
cream and further bandage by sterile rolls, and to be
and add it to the lower limbs (0.5% each)
changed every 24 hours
XX At 10 years, it attains the adult’s measurement

Investigations
XX Blood: CBC, CRP, Grouping & Rh typing
XX Blood: S. electrolytes, albumin, creatinine, glucose
XX X-Ray chest and Others, as indicated

Management
,,QIXVH,9ÀXLG
TT Indications: Children >10% and Infant>5% burn
TT Rationing: Initially to Resuscitate and thereafter as
0DLQWHQDQFHÀXLG 3KRWRJUDSK6XSHU¿FLDOGHUPDOEXUQLQDPRQWKVROGFKLOG
¿UVWSKRWR DQGDIWHUGD\VIROORZLQJGUHVVLQJZLWKK\GURFROORLG
TT Fluids are infused simultaneously under 2 headings–
O 5HVXVFLWDWLRQÀXLG 0DLQWHQDQFHÀXLG
O
VI. Ensure Feeding & Nutrition
For Resuscitation TT Provide high protein & high calorie diets, rich in
TT Fluid Type: Ringer’s/Hartmann’s solution vitamins & minerals and plenty of liquids
TT Amount to be infused (calculation by Parkland TT Feeding may be given through NG tube, particularly,
formula): 3-4 ml × BW (Kg) × % of burn of TBSA in facial burn, any severe burn, inhalation burn,
TT +RZWRLQIXVH*LYHòRIWRWDODPRXQWZLWKLQ¿UVW electric burn or having any complications
KRXUVDQGWKHUHVWòE\QH[WKRXUV VII. Start Managing the Scars early
For Maintenance (according to page 319) LPPHGLDWHO\IROORZLQJKHDOLQJ
TT Fluid type: 5% dextrose in 0.45% Saline
TT Massage the area with vaseline, coconut oil or any
TT $PRXQWWREHLQIXVHG)RU¿UVWNJ%:#PO lubricants, silicon based ointment etc.
Burn

NJKUVIRUQH[WNJ#PONJKUVIRU
TT Apply Sunscreen lotion (SPF 35+) to prevent
IXUWKHUNJ%:#PONJKUV abnormal pigmentation
 Step on to Paediatrics 283

VIII. Prepare for Rehabilitation Snake venom

TT In acute phase, Splints and proper positioning are ,WLVPRGL¿HGVDOLYDFRPSULVHGRISURWHLQVDQGGLIIHUHQW
used to minimize joint deformities & contractures enzymes. These enzymes determine the toxicities.
TT Start passive & active range of motion early
TT Ensure gradual rigorous therapies like stretching, Pathogenesis & Clinical manifestation
range of motion and strengthening exercise Whenever a poisonous snake bites, the clinical features
solely depends on the toxins present in the venom as
IX. Manage post burn complications by early surgical
mentioned in the following table.
interventions & physiotherapy for cases with–
TT Non-healing ulcer, unstable scar, hypertrophic scar, Toxins, Snake and Clinical manifestations
keloid, contractures etc and Types of
Proper counseling for cases with post burn psychosis Snake Clinical manifestations
TT
venom
TT Counsel the family about complication, prognosis TT Generalized muscle weakness as
etc. manifested by
'' Lethargy
What to do at community?
'' Ptosis
XX (QVXUHUHVFXHUVDIHW\¿UVWWRKHOSVDYHWKHYLFWLP
XX Encourage STOP-DROP-ROLL method to estinguish
¿UHRQWKHYLFWLP
XX Remove the
victim from
the source of
burn
Remove all
Cobra and Coral snakes
XX

cloths to Bilateral ptosis

reduce contact
Neurotoxin

burn TT Paralysis of eye ball muscles

XX Ensure airway, TT Broken neck sign
breathing,
circulation
XX First Aid:
COOL-
COVER-
CALL
TT Cooling all burns with running tap water for10 min

Do not apply ice, cold water, toothpaste, ointments, Broken neck sign
butter or any other “home remedies”. &RXUWHV\3URI0$)DL]
TT Cover the burnt area with a clean cloth
TT 'LI¿FXOWLHVLQVSHHFK
TT Call for medical attention and hospitalize
TT 'LI¿FXOWLHVLQRSHQLQJRIPRXWK
TT Protrusion of tongue
TT Shallow respiration
Haemolysis
Haemo-

TT
Vipers
toxins

TT Haemorrhage and hypovolemic

SNAKE BITE shock
TT Severe bodyache
Incidence
Sea snakes
Myotoxins
& Nephro

TT Black urine, because of

toxins

XX Global: 5.5 million/year; Deaths: 1,00,000/year myoglobinuria from muscle

Drowning

XX %DQJODGHVK\HDU'HDWKV\HDU breakdown
Of the 3000 known species of snakes, only 200 are TT Scanty urine, anuria (AKI)
poisonous.
 284 Step on to Paediatrics

Management Further Treatment

XX Antibiotics, parenteral
I. At Community XX Tetanus prophylaxis
XX Reassure the victim who may be very anxious XX Administration of polyvalent antivenom (effective
XX Immobilize the bitten limb with splint and sling as against Cobra, Krait, Russel viper & Saw scaled viper)
practiced in fracture of long bone
and frequent monitoring for its toxicities and response
TT If bite is in lower limb, not allow walking

TT If bite is in upper limb, do not allow moving the limb

XX Dose: 10 vials irrespective of age and sex
XX Ideally pressure immobilization method (by simple
XX Preparation: Each vial is diluted with 10 ml distilled
crepe bandage or any long strips of clothes (e.g.
water. Then all 10 diluted vials (100 ml) are further
gamcha, lungi) can be helpful.
GLOXWHGZLWKPORI,9ÀXLGe.g. DA/DNS/NS
(total 200 ml)
XX $GPLQLVWUDWLRQWKURXJK,9GULSRYHUKRXU #
drops/min)

Indications for using polyvalent antivenom

Source: Internet XX Neurotoxic signs

XX Rapid extension of local swelling
XX Acute renal failure
3UHVVXUHLPPRELOL]DWLRQ XX Acute circulatory failure
XX Bleeding abnormalities
XX Transfer quickly to the nearest health facility/hospital XX Hemoglobinuria/myoglobinuria
TT During transfer, do not allow anything by mouth and

keep the bitten part immobilized Other Treatment

II. At Hospital XX Neostigmine-atropine combination (for neurotoxic
XX Assess the Vital parameters quickly e.g. respiration, features only)
F\DQRVLVSXOVH%3FDSLOODU\UH¿OOLQJWLPH
XX Inj. Atropine 15 µgm/kg IV followed by Inj.
XX Start Resuscitation e.g. maintenance of– Neostigmine 50-100 µgm/kg SC, 4 hourly, until
TT Airway (clearing airway) See page 254
neurotoxic features are overcome
TT Breathing (Bag & Mask ventilation or endotracheal
XX Fresh blood transfusion for patients with coagulopathy
LQWXEDWLRQDQGDUWL¿FLDOYHQWLODWLRQ
XX Care of the bitten part–
TT Wash with antiseptic solution
TT &LUFXODWLRQ ,9FU\VWDOOLQHÀXLGe.g. DNS, NS,
TT In case of local necrosis & gangrene surgical
Hartmann solution etc.)
XX Assess the case in details clinically debridement and skin grafting may be needed
XX Identify the species of the snake (if brought) Treatment of non venomous snake bite

Investigations
XX Reassurance
XX 20 minutes whole blood
XX Tetanus prophylaxis
clotting test (WBCT)
XX Observation for 24 hours
Fresh water drowning

XX ECG
Source: Internet

XX Complete blood counts

XX Blood urea, S creatinine
XX S. CPK
XX Urine R/M/E
%ORRGLQOHIWWHVWWXEHGLG
XX Immuno-diagnosis by ELISA QRWFORWDIWHUPLQXWHV
 Step on to Paediatrics 285

DROWNING
Drowning is a process Pathophysiological events of drowning
that results in respiratory
impairment from
submersion/immersion
in a liquid medium. In
drowning, a liquid-air
interface develops at
the entrance of victim’s
airway, which prevents the
individual from breathing
oxygen. Outcome of
drowning includes death,
morbidity or complete
recovery.

Incidence
In Bangladesh, 20% of all
deaths are from drowning
and is more among under 5
children.

Fresh water drowning

Drowning in fresh water
leads to the rapid passage
of large quantities of
water from the lungs to
the blood (as fresh water
is hypotonic compared
to the blood). This
leads to haemodilution
and hyponatraemia. ,
The diluted hypotonic
blood causes diffusion
of water in the cells,
(mainly in RBC) causing
haemolysis, hyperkalaemia
and, in severe cases,
haemoglobinuria with
glomerular damage.
Severe hypoxia (due
to haemolysis) results
in severe anoxic brain
Drowning

GDPDJHDQGDWULDO¿EULOODWLRQ(due to hyperkalaemia) leading to immediate death.

 286 Step on to Paediatrics

Salt water drowning The clinical presentation, complications and outcome of the
Drowning in sea water leads to rapid transition of patients depend upon–
large quantities of water by osmosis (as salt water is XX Submersion time–
hypertonic compared to the blood) from intravascular TT Submersion duration <5 min - associated with

space to the lung parenchyma. The net results are– favourable outcome
TT Pulmonary oedema TT Submersion duration >10 min - highly associated with

TT Increased blood osmolality & crenation of RBC poor outcome

TT Hypovolaemia XX Water temperature
All these events cause– XX Water tonicity (fresh water/salt water)
TT Hypoxaemia
XX Degree of water contamination
TT Cardiac arrest
XX Associated injuries (specially cervical spine & head)
TT Cerebral anoxia and death
XX Type and timing of rescue and resuscitation efforts
XX Response to initial resuscitation

Clinical Manifestations Investigations

XX Anxious appearance of victim
XX &%&FRDJXODWLRQSUR¿OH0D\EHDOWHUHG
XX Feartures, related to associated
XX Arterial blood gas (ABG) analysis: Acidosis
complication– XX S electrolytes: Hypo or hypernatraemia, hyperkalaemia
TT Altered vital signs e.g, hypothermia, XX Random blood suger (RBS): Decreased
tachycardia, bradycardia XX SGPT, SGOT: May be raised
Fresh water drowning

TT Tachypnoea, dyspnoea (from pulmonary XX BUN, S creatinine: May be altered

oedema) XX Chest X-Ray: To assess any–
TT Altered level of consciousness, TT Evidence of aspiration, pulmonary oedema or segmental

QHXURORJLFDOGH¿FLW IURPFHUHEUDO atelectasis suggesting foreign body(s) e.g. silt or sand aspiration
oedema, cerebral hypoxia, stroke) TT Displacement of endotracheal (ET) tube

TT Acidotic breathing (metabolic acidosis) XX X-Ray cervical spine or CT scan of neck: When neck trauma is
TT Apnoea, Asystole (cardiac arrest)
suspected
TT Renal failure, & Death XX ECG: To evaluate cardiac arrythmia
 Step on to Paediatrics 287

Management XX Initiate IV infusion of normal saline or Ringer’s lactate

(10-20 ml/kg) in case of poor perfusion for volume
I. At Community expansion
Basic life support at the scene of event is the most XX Keep the child warm by warm saline infusion, wrapping
important determinant of outcome. with blankets etc
XX Rescue the patient from water as soon as possible
XX Antibiotic: Not indicated unless the patient was
XX Remove wet cloth & wrap the victim in warm blankets submerged in contaminated water or sewage
XX Assess vital signs e.g. pulse, BP, respiration
XX Follow up: SPO2, BP, blood sugar & temperature
XX Open the airway & remove visible debris, if present in
XX 2EVHUYHWKHSDWLHQWIRUKRXUVEHIRUHGLVFKDUJH
the oropharynx with a ¿QJHUVZHHSmaneuver Complications
XX Initiate rescue breathing immediately (mouth to mouth/ XX Cardiac arrest, bradycardia
mouth to nose), if required
Prognosis
XX ,UUHYHUVLEOHEUDLQGDPDJHRFFXUVDIWHUPLQXWHVRI
submersion
XX Most children who survive are rescued within 2 minutes
of submersion and who die are rescued after 10 minutes
of submersion
XX Patients who are alert or mildly obtunded at
presentation have an excellent chance of full recovery
XX Of hospitalized victims–
TT 15% die

TT 20% survive with severe neurologic sequelae

Prevention
XX Appropriate barriers must be built around ponds
XX Parents should supervise their children around water
XX Start chest compressions and Bag & Mask ventilation
&35 LIGH¿QLWHSXOVHLVQRWIHOWZLWKLQVHFRQGV
XX Children should be taught safe conduct around water
and during boating

DOG BITES
XX &KLOGUHQ ER\V!JLUOV RIDJHVEHWZHHQ\HDUVDUH
attacked more
XX Give O2ZLWKIDFHPDVN#/PLQDVVRRQDV XX Injuries are of 3 types e.g. abrasions, puncture wounds
available and lacerations.
XX Arrange for quick transfer to hospital

II. At Hospital
XX Give O2ZLWKIDFHPDVN#/PLQ
XX Support Respiration: Intubate and start mechanical
Salt water drowning
Source: Internet

/AMBU ventilation when the patient has any of the

following signs–

XX Poor respiratory effort XX Severe acidosis

XX Altered sensorium XX Severe dyspnoea XX The major concern dog bite is about acquaring rabies
XX Severe hypoxaemia
with 100% mortality
 288 Step on to Paediatrics

Diagnosis Treatment
Mainly clinical. Whenever, a child is brought with h/o dog XX Clean the wound properly
bites, the following questions should be asked. XX Give Antibiotics to avoid secendary infection
XX What is the type of the animal? Domestic/wild
XX Give inj Teavax and TIG, if tetanus vaccination status is
XX Was it provoked/unprovoked attack? uncertain
XX What is the tetanus immunization status?
XX Give Anti-Rabies vaccine (ARV): Cell culture vaccines
HJ3XUL¿HG9HUR&HOO5DELHV9DFFLQH 3XUL¿HG&KLFN
XX What is the status of the wound/underlying structure?
Embryo Cell Vaccine.
XX Is there any H/O drug allergy TT Dose: 0.1ml/dose, Intradermally

After clinical assessment, further evaluation includes– TT Sites:

TT X-Ray of the affected part and sending ³³ For adults: At each deltoid muscles (2 sites)

TT Wound swab; For culture & sensitivity ³³ For children (<2yrs): At antero-lateral thigh,

TT Total doses: 4 ; On Day 0, Day 3, Day 7 and Day 28

Category of dog bite injury
XX Give Rabies Immunoglobulin (RIG): In Category III
Category Characteristics Treatment injury only
I Touching or feeding No treatment
Pre exposure prophylaxis
XX

animals, licks on the except XX Indication: Laboratory workers and health care
skin cleaning
providers who take care of infected animals (mainly
II Nibbling of uncovered XX Immediate dog) and human
skin, minor scratches vaccination XX Anti-Rabies Vaccine Intradermally.
or abrasions without only TT Dose: 0.1ml/dose in a single site

bleeding, licks on TT Total doses: 3, On Day 0, Day 7 and Day28

broken skin
III Single or multiple XX Immediate
transdermal bites or vaccination
scratches, contamination XX Administration
of mucous membrane of anti-rabies
with saliva from licks; Immunoglobu
exposure to bat bites or
scratches

References
1. Utpal KS, Layland FC. Poisoning in children. 3rdHG1HZ'HOKL-D\SHH%URWKHUV
2. National guideline for management of snake bites, DGHS, Bangladesh, 2000.
3. Caglar D, Quan L. Drowning and Submersion Injury. Nelson Textbook of Pediatrics, 20th(G
4. National Guideline for Dog/Animal Bite Management, DGHS, Bangladesh, June 2014.
5. Chowdhury GMA et al. Management of respiratory foreign body-12 years’ experience with 382 cases. Bangladesh J Child
+HDOWK
 $KPHG7HWDO(SLGHPLRORJ\RI+RVSLWDOL]HG%XUQ3DWLHQWVLQ%DQJODGHVK5HSRUW%DQJ-3ODVW6XUJ  
7. Herdon D (2012). Total Burn Care. 4th(GLWLRQ6DXQGHUV,6%1
Dog bite

8. Sheridan RL (2012). Burns. 1st(GLWLRQ/RQGRQ0DQVRQ3XEOLVKLQJ/WG,6%1

9. Training manual of Emergency Management of Severe Burns by Australia and New Zealand Burn Association.
10. Ahmed Tet al. Epidemiology of Hospitalized Burn Patients in Bangladesh: 2013 Report. Bang J Plast Surg 2014;5(2): 3-8.
 Step on to Paediatrics 289

11. 2013 Population & Housing Census: Preliminary Results. Bangladesh Bureau of Statistics. Archived from the original (PDF)
on 15 January 2013. Retrieved 12 March 2014.
12. Herdon D (2012). Total Burn Care. 4th(GLWLRQ6DXQGHUV,6%1
13. Sheridan RL (2012). Burns. 1st(GLWLRQ/RQGRQ0DQVRQ3XEOLVKLQJ/WG,6%1
14. Training manual of Emergency Management of Severe Burns by Australia and New Zealand Burn Association.

SELF ASSESSMENT
Short answer questions [SAQ]
1. Write down the basic pathophysiology of OPC poisoning.
2. What agents are commonly involved in accidental poisoning in children?
 1DPH¿YHFRPPRQDFFLGHQWVDQGHPHUJHQFLHVLQFKLOGUHQ
4. Write down the pathological events of drowning.
5. Write down the management of Snake bite.
 :ULWHGRZQWKHLPSRUWDQWFRPSOLFDWLRQVDQGWUHDWPHQWRIDFKLOGZLWKNHURVHQHSRLVRQLQJ

Multiple choice questions [MCQ]

1. Agents commonly associated with childhood poisoning are–
___ a) corrosive agents ___ b) alcohol ___ c) kerosene
___ d) drugs ___ e) datura
2. The following antidotes are reccomended in OPC poisoning–
___ a) Atropine ___ b) Pralidoxime ___ c) Obidoxime
___ d) Naceylcysteine ___ e) Flumazenil
3. The pathognomonic features of organophosphate poisoning include–
___ a) miosis ___ b) dry mouth ___ c) fasciculation
___ d) bronchospasm ___ e) Central stimulation of respiratory center
4. First line management of snake bite in the community includes–
___ a) assurance ___ b) antivenom ___ c) tight tourniquet
___ d) quick referral to hospital ___ e) immobilization of affected limb
5. Cardinal features of OPC poisoning include–
___ a) Miosis ___ b) Fasciculation ___ c) Bronchospasm
___ d) Diarrhoea ___ e) Dry mouth
 $QDSK\ODFWLFVKRFN±
___ a) Can be triggered by bee string ___ b) Is a type III immune response
___ c) Is characterized by vasodilatation ___ d) Is due to neurogenic vasomotor disturbance
Self assessment

___ e) best treated with anti-histamine

 37
Parasitic Infestations
Amoebiasis - - - - - - - - - - - - - - 290
Giardiasis - - - - - - - - - - - - - - 292
Ascariasis - - - - - - - - - - - - - - 292
Enterobiasis- - - - - - - - - - - - - - 293
Ancylostomiasis - - - - - - - - - - - - - 293

Intestinal infestation of parasites is quite common among XX +RXVHÀLHVDQGFRFNURDFKHVSDVVLQJIURPIDHFHVWR

children in a country like Bangladesh. In this chapter, the unprotected food
following common intestinal parasitic diseases will be
discussed.
Pathogenesis

XX Amoebiasis XX Enterobiasis
XX Giardiasis XX Ankylostomiasis
XX Ascariasis

AMOEBIASIS

Source: Internet
Causative parasite: (QWDPRHEDKLVWRO\WLFD

/LIHF\FOHRI(KLVWRO\WLFD

Life cycle at a glance

XX +RVW0DQLVWKHRQO\KRVW GH¿QLWLYH
XX Infective from: Mature quadrinucleate cyst
XX Route of infection: Faecal – oral
XX Pathogenic form: Trophozoite
Site of lesion: Large intestine
Source: Internet

XX

XX Diagnostic stage: Cyst & trophozoite

Amoebiasis

Transmission
XX Faecal-oral route i.e. ingestion of Entamoeba cyst
XX Faecal contamination of drinking water, vegetables and
foods
XX Eating of uncooked vegetables and fruits which have
been fertilized with infected human feces
290

XX Handling of food by infected individual (cyst carriers)

 Step on to Paediatrics 291

Amoebic Colitis XX Others

TT Chest X-Ray:
XX Gradual onset of colicky abdominal pain, tenderness &
fever An elevated right
XX 'LDUUKRHDPRWLRQVGD\DQGIUHTXHQWO\DVVRFLDWHG hemidiaphragm
with tenesmus (painful sudden bowel evacuation) and a right-sided
XX Stool: Blood stained and contain a fair amount of pleural effusion
mucous may be seen
TT Ultrasonogram
XX Occasionally, there is severe diarrhoea resulting in
dehydration and electrolyte disturbances /CT scan of
abdomen & 86*VKRZLQJDEVFHVVFDYLW\

Amoebic Liver Abscess hepatobiliary

The most common extraintestinal amoebiasis. It results system : Shows
position and size
from spread of the organisms from the intestine to the liver
of liver abscess
via the portal vein.
XX High grade fever
XX Pain: Constant, dull aching pain located in right upper
abdomen or epigastrium
XX 1RQVSHFL¿FV\PSWRPVe.g. nausea, vomiting,
abdominal distention, diarrhoea, and constipation
XX Jaundice is usually absent Complications &7RIDEGRPHQVKRZLQJDEVFHVVFDYLW\
XX Intestinal
Investigations TT Fulminant colitis with perforation
XX Stool R/M/E: Shows trophozoites containing ingested TT Toxic megacolon

RBCs TT Chronic nondysenteric colitis

TT Amoeboma

TT Perianal ulceration

XX Hepatic: Rupture of liver abscess may lead to–

TT Granuloma cutis

TT Haemoptysis of anchovy sauce pus

TT Empyema thoracis

TT Generalized peritonitis

TT Fatal purulent pericarditis

Source: Internet

XX Metastatic lesion
TT Pulmonary amoebiasis

TT Cerebral amoebiasis

TT Cutaneous amoebiasis

TT Splenic abscess

,QJHVWHG5%&VLQWURSKR]RLWHV
Treatment
XX CBC: Leukocytosis, mild anaemia, high ESR XX Metronidazole: 35-50 mg/kg/day, 8 hourly for 10 days
(N.B. Metronidazole can be used in severe infection or
if patient is unable to take orally.)
or
XX Tinidazole: 50 mg/kg/day once daily for 3-5 days or
XX Nitazoxanide: 7·5 mg/kg/dose, 12 hourly for 3 days.
Very effective in intestinal amoebiasis
Giardiasis

Followed by either–
XX Paromomycin: 25-35 mg/kg/day, 8 hourly for 7 days or
XX Diloxanide furoate: 20 mg/kg/day, 8 hourly for 10 days
 292 Step on to Paediatrics

GIARDIASIS Treatment
XX The following are the drug of choice
Causative parasite: *LDUGLDLQWHVWLQDOLV TT Tinidazole (>3 years): 50 mg/kg/day, Single dose
Transmission: Faecal–Oral route through ingestion of TT Nitazoxanide

foods contaminated with cyst. ³³ 12-48 months: 100 mg, 12 hourly for 3 days

³³ 4-12 years: 200 mg, 12 hourly for 3 days

Life cycle ³³ >12 years : 500 mg, 12 hourly for 3 days

Cyst of giardia produce TT Metronidazole: 15 mg/kg/day, 8 hourly for 5-7 days

trophozoites that colonize the

lumen of duodenum and proximal
jejunum where they attach to
the brush border of the intestinal
ASCARIASIS
epithelium and multiply by binary
¿VVLRQ Causative parasite: $VFDULVOXPEULFRLGHV
7KHSDUDVLWHVFDXVHLQÀDPPDWLRQ
and partial villous atrophy there. This ultimately leads to
Transmission:
malabsorption of foods and discomfort and malnutrition. Faecal-Oral route
through ingestion of
Life cycle at a glance foods contaminated
with mature ova
XX +RVW0DQLVWKHRQO\KRVW GH¿QLWLYH containing developing
XX Infective form: Cysts embryos.
XX Route of infection: Faecal – oral
XX Pathogenic form: Trophozoites
XX Site of lesion: Small intestine Life cycle
Life cycle starts with ingestion of eggs. After ingestion,
Clinical Manifestations larvae are liberated from the eggs which penetrate the gut
XX Asymptomatic wall to enter into portal vein and then into liver and right
XX Recurrent attacks of– heart. From there, larvae enter into pulmonary artery
TT Nausea, vomiting orOHWKDUJ\ÀDWXOHQFHEORDWLQJ and penetrate into the alveoli and then crawl up through
TT Abdominal discomfort or pain and sometimes
bronchi and then coughed up and swallowed to Re-enter
abdominal distension, weight loss again into small intestine to grow up as adult worm.
TT Acute diarrhoea
Life cycle at a glance
XX Fever & vomiting are unusual

Complications
XX +RVW0DQLVWKHRQO\KRVW GH¿QLWLYH
XX Malabsorption syndrome
XX Infective from: Embryonated egg
XX Reiter’s syndrome
XX Route of infection: Faecal – oral
XX Reactive arthropathy
XX Pathogenic from: Adult & larva
XX Liver granuloma
XX Site of lesion: Small intestine
XX 'H¿FLHQF\RI9LW$%12
XX Lactose intolrance Clinical Manifestations
XX 1RQVSHFL¿FV\PSWRPVHJ
Diagnosis TT Nausea, colicky abdominal pain, irregular motions
XX Basically clinical and
XX Sometimes–
Ascariasis

TT Worms may pass through vomitus or in the stools

XX ,GHQWL¿FDWLRQRIF\VWVor trophozoites of parasite in
TT Patients may present with urticarial rash, cough,
stool
XX Giardia antigen by ELISA respiratory distress /|IÀHU¶VV\QGURPH
 Step on to Paediatrics 293

Complications Clinical Manifestations

XX 0DODEVRUSWLRQ QXWULWLRQDOGH¿FLHQF\ XX Perianal pruritus especially at night is the commonest
XX Intestinal obstruction (ascariasis crisis) symptom
XX Appendicitis XX GIT symptoms like abdominal pain, nausea, vomiting,
XX Pancreatitis diarrhoea
XX Acute cholecystitis XX Sometimes adult worms are found moving over the
XX Allergic reactions (urticaria) stool

Diagnosis Complications
XX Loss of appetite
Based on–
XX Weight loss
XX Clinical suspicion XX Restlessness & irritability
XX Stool examination: Ova of the parasite or adult worms XX Vulvovaginitis, urethritis
XX CBC: May show eosinophilia XX Appendicitis (rare)
Treatment
Diagnosis
XX Anthelmintics: Options are
TT Albendazole: < 2 years – 200 mg and >2 years – 400
Based on–
mg as single dose or XX Clinical presentation
TT Levamisole: 3 mg/kg as single dose or XX Stool exam: Presence of adult worms on naked eye
TT Pyrantel pamoate: 10 mg/kg as single dose XX Perianal skin swabs: Detection of ova
TT Mebendazole: 100 mg 12 hourly for 3 days
Treatment
XX Mebendazole, a single dose (100 mg), PO for all ages.
All the family members should be treated simultaneously.
Repeated after 2 weeks with a cure rates of 90-100%
XX Good nutritional support
Alternative regimens include
XX Albendazole (400 mg), Single oral dose for all ages,
repeated in 2 weeks or
ENTEROBIASIS XX Pyrantel Pamoate (11mg/kg, max.1gm) PO, Single dose

Causative parasite: (QWHURELXVYHUPLFXODULV

Transmission
Faecal-Oral
route. The gravid ANCYLOSTOMIASIS
female worm lays
ova around the Causative parasites: $QF\ORVWRPDGXRGHQDOH or Necator
anus, especially DPHULFDQXV
at night. The ova
Transmission
are then carried to
the mouth by the Transmission occurs
¿QJHUVDQGVRUH through penetration
infestation takes place. of skin by the
¿ODULIRUPODUYDH
Life cycle at a glance When child walks
bare foot on the
XX +RVW0DQLVWKHRQO\KRVW GH¿QLWLYH contaminated soil,
Infective from: Embryonated egg
Enterobiasis

XX
WKH¿ODULIRUPODUYDH
XX Route of infection: Faecal-Oral, retrograde through penetrate directly through the skin, commonly through the
anus, autoinfection from hand to mouth thin skin between toes, dorsum of feet and inner side of
XX Pathogenic from: Adult female & sticky eggs sole.
XX Site of lesion: Caecum
 294 Step on to Paediatrics

Life cycle Investigations

Larvae from soil, after penetration through skin enter into XX CBC with PBF: Low Hb, microcytic hypochromic
lymphatics and then into blood stream. From blood, they anaemia and eosinophilia
enter into alveoli and then into bronchi and trachea. From XX S albumin: Low
trachea, larvae enter into oesophagus and then into small XX X-Ray chest: Done when patients present with
intestine to grow as adult worm. In the intestine, they suck respiratory symptoms
EORRGDQGFDXVHEORRGORVVUHVXOWLQJLQLURQGH¿FLHQF\ Treatment
anaemia. XX Anthelmintics–
Life cycle at a glance TT Albendazole:<2 years (200 mg) and >2 years (400
mg) as single dose or
TT Levamisole: 3 mg/kg as single dose or
XX +RVW0DQLVWKHRQO\KRVW GH¿QLWLYH
TT Pyrantel pamoate:11 mg/kg, orally, OD for3days or
XX Infective from: Filariform larva
TT Mebendazole: 100 mg 12 hourly for 3 days
XX Route of infection: Penetration through skin
XX Pathogenic from: Adult & larva
XX Site of lesion: Small intestine All the family members should be treated simultaneously.

XX Suppoert the child with good nutrition

XX Correct anaemia oral iron. Consider Blood transfusion
Clinical Manifestations in severe anaemia
XX Symptoms related to skin e.g.Hook worm dermatitis
(ground itch)
XX GIT symptoms e.g. Loose stools, vomiting or upper
Prevention of parasitic diseases

abdominal pain
XX Maintenance of proper hand hygiene
XX Respiratory symptoms e.g. Paroxysmal cough with
XX Improving education about practice of sanitary
blood stained sputum condition and sewage facility
XX Features of anaemia and oedematous swelling
XX 3XUL¿FDWLRQRISXEOLFZDWHUVXSSO\E\FKORULQDWLRQ
particularly in untreated patients VHGLPHQWDWLRQDQG¿OWUDWLRQ
XX Discontinuing the practice of using human feces as
Complications fertilizer
XX Anaemia secondary to blood loss XX Regular washing and deworming the pets
XX Pulmonary eosinophilia /|IÀHU¶VV\QGURPH XX Regular inspection of meat at slaughter house
XX Pruritus XX Use of insect repellent while at work and use of
XX Cutaneous larva migrans insecticide treated mosquito net during sleeping
XX Gastrointestinal bleeding XX Regular deworming of children

Diagnosis
Based on clinical features and demonstration of eggs in
stool.
Ancylostomiasis
 Step on to Paediatrics 295

References
1. Messacar K, et al. Infections: Parasitic & Mycotic. In Current Pediatric Diagnisis & Tratmemnt, 23rdHGS
2. Chatterjee KD. Parasitology in relation to Clinical Medicine, 12th ed. India 1980.
3. Hossain MA, et al. Medical Parasitology-Basic and Clinical. 2nd ed. Mymensingh: Ittadi Book Center; 2008.
4. Maurice E, Salvana T, Salata RA. Amebiasis. In: Kliegman RM, Stanton BF, Geme III JWS, Schor NF, Behrman RE. Editors.
Nelson Textbook of Pediatrics, 20th(GLWLRQ1HZ'HOKL(OVHYLHU
5HHG6/$PHELDVLVDQGLQIHFWLRQZLWKIUHHOLYLQJDPHEDV+DUULVRQ¶V3ULQFLSOHVRI,QWHUQDO0HGLFLQHth ed. New York:
McGraw-Hill Medical Publishing Division; 2005. p. 1214-1218.

SELF ASSESSMENT
Short answer questions [SAQ]
1. What are the clinical features of amoebic liver abscess?
2. How will you investigate a case of amoebic liver abscess?
3. Write down the complications & treatment plan of amoebic liver abscess
4. Write down the clinical features & treatment plan of giardiasis

Multiple choice questions [MCQ]

1. Parasites enter the body through faecal-oral route are–
___ a) G. Intestinalis ___ b) (9HUPLFXODULV ___ c) $'XRGHQDOH
___ d) 1$PHULFDQXV ___ e) $/XPEULFRLGHV
2. Microcytic hypochromic anaemia commonly occurs in–
___ a) ancylostomiasis ___ b) giardiasis ___ c) enterobiasis
___ d) ascariasis ___ e) amoebiasis
 /|IÀHU¶VV\QGURPHLVDVVRFLDWHGZLWK±
___ a) ancylostomiasis ___ b) ascariasis ___ c) giardiasis
___ d) enterobiasis ___ e) amoebiasis
4. Complications commonly associated with ascariasis are–
___ a) haemorrhage from gut ___ b) vulvo-vaginitis ___ c) intestinal obstruction
___ d) ground itch ___ e) urethritis
5. The following are antihelmentics–
___ a) Metronidazole ___ b) Tinidazole ___ c) Albendazole
___ d) Mebendazole ___ e) Pyrantel pamoate
Self assessment
 38
Common Surgical Problems of Children
Cleft lip and/or Cleft palate- - - - - - - - - - - 296
Oesophageal atresia with or without tracheoesophageal fistula - - - - - 297
Congenital diaphragmatic hernia - - - - - - - - - - 298
Eventration of diaphragm - - - - - - - - - - - 298
Infantile hypertrophic pyloric stenosis- - - - - - - - - 300
Duodenal atresia - - - - - - - - - - - - - 301
Intussusception - - - - - - - - - - - - - 302
Hirschsprung disease - - - - - - - - - - - - 303
Anorectal malformations - - - - - - - - - - - - 304
Undescended testis - - - - - - - - - - - - 305
Posterior uretheral valve - - - - - - - - - - - - 306
Hydrocephalus - - - - - - - - - - - - - 307
Other surgical problems - - - - - - - - - - - - 308

Apart from medical problems, childrens also suffer from CLEFT PALATE
surgical problems, commonly from congenital and a few
from acquired ones. In this chapter, common congenital A congenital defect
surgical problems are discussed. The common acquired of hard palate that
surgical problems are already discussed in chapter 13. results from failure
of fusion of the
palatine processes
of the developing
maxilla.

CLEFT LIP When cleft plate

is associated with
A congenital micognathia and
defect in the glossoptosis, it is
upper lip and called Pierre Robin
sequence.
Cleft lip, cleft palate

results from
failure of
union between
The major concerns of both the clefts are–
medial nasal
and maxillary XX )HHGLQJGLI¿FXOW\
processes XX Aspiration pneumonia
(from which XX Middle ear infection
upper lip is XX Failure to thrive
developed). It
may be either
unilateral or
296

bilateral.
 Step on to Paediatrics 297

Treatment Cardinal Features

Medical XX History of maternal polyhydramnios
XX Feeding
TT Isolated cleft lip: Help the baby to ‘latch on’ i.e
XX Excessive drooling and secretions from mouth after
birth
attach to the nipple at the beginning of the feeding
TT Combined cleft lip & cleft palate: Feeding by long
XX &KRNLQJRQDWWHPSWHGIHHGLQJLQGLFDWHV¿VWXORXV
connections with trachea
handled spoon in upright position
XX Respiratory distress as a consequence of aspiration
XX Treatment of Respiratory tract infection and middle ear
of saliva
infection promptly with antibiotics
XX Failure to pass a nasogastric/orogastic tube to the
Surgery stomach
There is a conventional µ5XOHRI¶ applied for surgical
correction of cleft lip and palate

Weight Age Haemoglobin Investigations

Cleft lip 10 lb (~4.5 kg) 10 weeks 10 gm/dl XX X-Ray chest and abdomen shows–
TT Presence of coiled nasogastric tube in the upper
10
Cleft palate 10 kg 10 gm/dl pouch. Along with it, if gas shadow is found in
months
stomach & intestine, it means a tracheoesophageal
¿VWXODLVSUHVHQWWRWKHGLVWDORHVRSKDJXV,Q
oesophageal atresia without tracheoesophageal
¿VWXODQRJDVLVVHHQLQVWRPDFK
OESOPHAGEAL ATRESIA WITH OR
WITHOUT TRACHEOESOPHAGEAL
FISTULA
The commonest malformation of upper gut
Types
3UR[LPDO
oesophagus
Most common

Trachea

'LVWDO
Source: Internet

oesophagus

$WUHVLDZLWKGLVWDO ,VRODWHG
¿VWXOD  oesophageal
DWUHVLD 
Oesophageal atresia

2HVRSKDJHDODWUHVLDZLWKWUDFKHRHVRSKDJHDO¿VWXOH
SUHVHQFHRIJDVVKDGRZLQJXW

$WUHVLDZLWKGRXEOH ,VRODWHGWUDFKHRRHVRSKDJHDO $WUHVLDZLWKSUR[LPDO

¿VWXOD  ¿VWXOD +W\SH   ¿VWXOD 
 298 Step on to Paediatrics

/HIW%URQFKXV

5LJKW%URQFKXV /HIW/XQJ

5LJKW/XQJ

Source: Internet
6PDOO
intestine
'LDSKUDJP PRYHVLQWR
FKHVWFDYLW\

This results in–

XX Respiratory distress since birth due to compression

of the lung on the affected side
XX Shifting of the heart and mediastinum to the side
opposite to herniation

The rapidity and severity of presentation is related to–

2HVRSKDJHDODWUHVLDZLWKRXWWUDFKHRHVRSKDJHDO¿VWXOD
TT Degree of pulmonary hypoplasia resulting from lung
QRJDVVKDGRZLQJXW compression by the intrathoracic abdominal contents
in utero
Treatment TT Degree of associated pulmonary hypertension
Associated congenital heart defects
Medical
TT

TT Affected infants are prone to develop pneumothorax

XX Counsel the parents about the nature of the anomaly,
treatment options and prognosis during attempt at ventilation of the hypoplastic lungs
XX Keep the baby warm by keeping under overhead
warmer
XX Keep the baby, Nothing per oral Cardinal Features
XX *LYHPDLQWHQDQFH,9ÀXLG'$%DE\VDOLQH
XX Place a soft NG tube in upper pouch on low intermittent Severe respiratory distress and cyanosis since birth
suction to drain secretions and to prevent aspiration
XX The head of the bed should be elevated to prevent refux
RIJDVWULFFRQWHQWVWKURXJKWKHGLVWDO¿VWXODLQWROXQJV Signs
XX Give IV Ampicillin plus Gentamicin, if aspiration is
XX Flaring of alae nasi, cyanosis of lips, toung
suspected
XX Chest
TT Inspection: Severe chest indrawing, fast breathing
XX Consult Paediatric surgeon immediately
Eventration of Diaphragm

TT Auscultation of lungs on the affected side of chest

Surgery: 7KHGH¿QLWLYHWUHDWPHQW ³³ Breath sounds: Poor or diminished

³³ Additional sounds: Bowel sounds may be heard

TT Auscultation of heart

³³ Heart sounds: Displaced to the normal side

CONGENITAL DIAPHRAGMATIC ³³ Tachycardia

HERNIA (CDH) XX $EGRPHQ6FDSKRLGVKDSHGLQGLFDWHVVLJQL¿FDQW

visceral herniation to the chest
A congenital defect of the diaphragm through which the
coils of intestine from the abdominal cavity herniate up
into the chest.
 Step on to Paediatrics 299

Investigations Treatment
XX Chest X-Ray (plain & Contrast): Shows bowel loops in
the chest with mediastinal shift to opposite side Medical
XX Counsel the parents about the nature of the anomaly,
treatment options and prognosis
XX Keep the baby warm by either keeping inside incubator
or under overhead warmer
XX Keep the baby nothing per oral (NPO)
XX Maintain an upright position so that head and chest is
higher than abdomen and feet
XX Give O2 through a nasal cannula (not by mask) to
avoid aerophagia (as it may distend the bowel loops
which further compresses the lungs)
XX ,IDUWL¿FLDOYHQWLODWLRQLVQHHGHGavoid bag mask
ventilation and immediately intubate the baby
XX Insert NG tube for gastric decompression and thereby to
prevent bowel distension and further lung compression
XX *LYHPDLQWHQDQFH,9ÀXLG '$%DE\VDOLQH
XX Give IV Ampicillin plus Gentamicin
XX If baby is in shock (weak pulse, CRT >3 sec) give–
TT Normal Saline,10-20 ml/kg over 30 min
&RLOVRILQWHVWLQHLQWKHOHIWVLGHRIFKHVWZLWKVKLIWLQJ
RIPHGLDVWLQXP OHIWGRPHDEVHQW  TT Inotropic agents such as Dopamine (5-10 µgm/

kg/min) or Dobutamine (10-15 µgm/kg/min) after

XX S Electrolytes: May be altered volume correction
XX Arterial Blood Gas: May show respiratory and/or XX Monitor SPO23XOVH%3DQGFDSLOODU\UH¿OOWLPH
metabolic acidosis XX Consult Paediatric surgeon immediately
XX Prepare the patient with pre-operative measures

Surgery: 7KHGH¿QLWHWUHDWPHQW

Congenital diaphragmatic hernia

EVENTRATION OF DIAPHRAGM
Eventration is another congenital malformation of
diaphragm with similar clinico-pathological consequences
as that of congenital diaphragmatic hernia. Here, the dome
of diaphragm remains abnormally elevated because of it’s
incomplete muscularisation. The abnormally elevated
diaphragm may compress the ipsilateral lungs with
respiratory distress and causes shifting of mediastinum
towards the normal (opposite) side.

&RQWUDVW;UD\RIXSSHU*,VKRZLQJFRLOVRILQWHVWLQHLQOHIWKHPLWKRUD[
 300 Step on to Paediatrics

Cardinal Features
XX Projectile non bilious vomiting, almost after every feed
usually begins between 2-4 weeks of age, but may start
as late as 12 weeks. In about 10% of cases, vomiting
may start at birth
XX The baby always remains hungry and sucks vigorously
after the episodes of vomiting

XX The baby may be dehydrated due to repeated vomiting

XX The upper abdomen may be distended after feeding, and
prominent gastric peristaltic waves are seen passing from
left to right of
the abdomen and
more obvious after
feeding
XX The enlarged
pylorus, described
as an “olive mass”,
of 5-15 mm in
longest dimension
$EQRUPDOO\HOHYDWHGLQWDFWOHIWGRPHRIGLDSKUDJP may be felt on
ZLWKVKLIWLQJRIPHGLDVWLQXPWRULJKWFKHVW deep palpation in 2OLYHVKDSHGPDVVPRYLQJIURPOHIWWRULJKW
the right upper
The main difference between these two conditions abdomen, specially after vomiting
is that the dome of diaphragm remains intact in Investigations
eventration, unlike that of hernia. XX Ultrasonography of abdomen: Diagnostic features are–
TT Pyloric muscle thickness >4 mm
TT Diameter of pylorus 10-14 mm
INFANTILE HYPERTROPHIC TT Pyloric channel length 15-19 mm
PYLORIC STENOSIS (IHPS)
XX Barium meal X-Ray of upper gut: Shows an elongated
It is a progressive gastric outlet obstruction occurring pylorus with contrast material coursing through the
in infants younger than 12 weeks. It results from mucosal interstices of the canal, forming the double-track
Infantile hypertrophic pyloric stenosis

postnatal muscular hypertrophy & hyperplasia of the sign/string sign (large arrowheads), with an additional
pylorus. central channel along the distal portion (small arrowhead).
Mass impression on the gastric antrum (arrow), best seen
during peristaltic activity, is termed the shoulder sign
'UDZLQJ1DELOD7DEDVVXP

Source: Internet

1DUURZHG
VWHQRVHG
pyloric sphincter

Aetiology: Unknown
 Step on to Paediatrics 301

XX CBC: Elevated Hb and haematocrit from dehydration Investigations

XX S electrolytes: Hypochloraemic alkalosis with XX Plain X-Ray abdomen erect posture: Shows “double
hypokalaemia is the classic metabolic abnormality. bubble shadow”
Hyponatraemia also present. XX Contrast X-Ray of upper GIT: No dye passed beyond
XX S Bilirubin: Mild unconjugated hyperbilirubinaemia duodenum
Treatment
Medical
XX Counsel the parents about the disease and its outcome
XX Keep the infant NPO and decompress stomach by NG
suction
XX Correct dehydration & electrolyte imbalance before
surgical intervention
TT If severely dehydrated: Infuse Normal Saline bolus

#PONJRYHUPLQXWHV7KHQ±
³³ Continue Baby saline (5% dextrose in

0.225%NaCl): 1.25-2 times, the normal

maintenance requirment, until the baby is well
hydrated (as assessed by good urine output)
³³ $GGPORI,QM.&OSHUPORI,9ÀXLGRQFH

a good urine output is achieved

Surgery
Ramstedt pyloromyotomy is the treatment of choice.
'RXEOHEXEEOHVKDGRZ

DUODENAL ATRESIA
Congenital
occlusion of
duodenal lumen
'UDZLQJ1DELOD7DEDVVXP

due to failure of the 6WRPDFK

primitive solid gut
tube to canalize. The
occlusion may be
complete or partial. 'XRGHQDO
atresia

Cardinal Features
Recurrent attacks of vomiting (mostly bilious) within
hours of birth.
Duodenal atresia

Signs 1RG\HEH\RQGGXRGHQXP
XX Dehyration, because of repeated vomiting
XX Abdomen: XX S electrolytes: Dyselectrolytemia e.g. hyponatraemia,
TT May be scaphoid shaped
hypokalaemia, hypochloraemia and metabolic alkalosis
TT Sometines, epigastric fullness (due to dilation of the

stomach and proximal duodenum)

 302 Step on to Paediatrics

Treatment Cardinal Features

Medical Signs
XX Counsel parents about the disease and its outcome XX Intermittent, severe colicky abdominal pain
XX Keep the infant NPO with screaming and drawing up of the knees in a
XX Decompress stomach by NG suction previously well child
XX *LYH,9ÀXLG '$or 10% Baby saline) XX The child appears calm and relieved in between
XX Correct hypokalaemia, if necessary attacks
XX Give antibiotics (Ampicillin+Gentamicin), if indicated XX Vomiting and diarrhoea occur soon afterward in 90%
XX Consult Paediatric surgeon immediately of cases
XX Stool looks like UHGFXUUDQWMHOO\. This is a mixture
Surgery of mucous, sloughed mucosa and blood
XX Duodenoduodenostomy, either open or laparoscopic
Abdomen
XX Inspection: Distended
XX Palpation: A tender sausage-shaped mass is felt in upper
INTUSSUSCEPTION mid abdomen
XX Auscultation: Bowel sound may be absent
The most common cause of bowel obstruction during the XX Digital rectal examination: The presence of bloody
¿UVW\HDUVRIOLIHPRVWO\RFFXUULQJDURXQGPRQWKV PXFXVRQWKH¿QJHUDVLWLVZLWKGUDZQDIWHUUHFWDO
when complementary foods are introduced. examination supports the diagnosis of intussusception
Intussusception is the invagination of one segment of
intestine into another segment. It can occur anywhere
along the small and large bowel, most commonly at ileo-
caecal valve, where ileum invaginates into the caecum
(ileo-colic).

Aetiology& Risk factors

Unknown, (in 85% of cases). However, the Risk factors
are – Small bowel polyp, Meckel diverticulum, viral
enteritis, hypertrophy of Peyer patches, lymphoma etc.
6WRROORRNVOLNHUHGFXUUDQWMHOO\
Pathology
The proximal portion of bowel (the intussusceptum), while Investigations
invaginates into the distal bowel (the intussuscipiens), it XX Plain X-Ray abdomen: Small bowel dilatation
pulls it’s mesentery
along with it.
This causes constriction
of mesenteric blood
vessels, obstruction
in venous return
with engorgement
Source: Internet

(oedema) of the
intussusceptum. This
Intussusception

leads to it’s necrosis,

bleeding, perforation
,QWXVVXVFHSWXP,OHXP
and peritonitis. On LQYDJLQDWHVLQWRFDHFXP
rare occasions, the
advancing intestine may be prolapsed through the anus.
;UD\DEGRPHQVKRZLQJGLVWHQGHGERZHOORRSV
 Step on to Paediatrics 303

XX Air or barium contrast enema: Shows intussusception in XX Give Potassium correction if necessary
the caecum XX Consult Paediatric surgeon immediately
XX Non-operative reduction with barium or water-soluble
)LOOLQJGHIHFW contrast, or air (pneumatic reduction). It should not be
attempted if signs of strangulated bowel, perforation or
toxicity are present

Surgery
In ill patients with evidence of bowel perforation or when
hydrostatic or pneumatic reduction has been unsuccessful.

Source: Internet
HIRSCHSPRUNG DISEASE (HD)
(CONGENITAL AGANGLIONIC
MEGACOLON)
&RQWUDVW;UD\DEGRPHQVKRZLQJ¿OOLQJGHIHFWDWFDHFXP
The most common cause of lower intestinal obstruction in
XX USG of whole abdomen: Classic doughnut or target neonates (80%) and among older children.
appearance of an intussusceptum inside an
intussuscipiens
Aetiology & Risk factors
XX Down syndrome
XX Familial
'RXJKQXW XX Boys are 4 times more at risk than girls
appearance
Pathogenesis
HD results from an absence of ganglion cells in the
mucosal (Meissner plexus) and muscle layers (Auerbach
plexus) of large gut. The absence of ganglion cells result
in failure of the colonic muscles to relax in front of an
Source: Internet

advancing bolus and give rise to colonic obstruction.

The normal colon proximal to the aganglionic segment
gets dilated with increased intraluminal pressure. In
addition, the mucosa of the dilated colon become thin and
LQÀDPPHGFDXVLQJGLDUUKRHDEOHHGLQJDQGSURWHLQORVV
(enterocolitis)
86*DEGRPHQVKRZLQJGRXJKQXWVLJQ

Types
Treatment XX Aganglionosis at recto-sigmoid area (80%): Short
Medical segment
Hirschsprung disease

XX Counsel parents about the disease, its consequences,

XX Aganglionosis extends proximal to sigmoid colon (15-
treatment etc. 20%): Long segment
XX Keep the baby NPO
XX Aganglionosis affects the entire large gut (5%): Total
segment
XX *LYHDSSURSULDWH,9ÀXLGHJEDE\VDOLQH
XX Insert an NG tube & decompress stomach
XX Give IV Ampicillin plus Gentamicin
 304 Step on to Paediatrics

Clinical Manifestations seen in neonates since the normal proximal bowel has
not had time to become dilated. Retention of barium for
Neonates Older infants and children 24-48 hours is not diagnostic of HD in ilder children
XX +LVWRU\RIGLI¿FXOWLHVLQ as it typically
XX Delayed passage of
passage of stools, since 1st occurs in
meconium beyond
few weeks of life retentive
WKH¿UVWKRXUV
of life
XX Chronic constipation constipation as
refractory to usual well.
XX Repeated vomiting
treatment
XX Abdominal distension XX Rectal biopsy: C
XX Abdominal distention with Reveals
XX If a soft rubber palpable dilated loops of
catheter is passed absence of
colon the ganglion
through the anal B
XX Rectal examination cells in the
opening it’s tip
commonly reveals an submucosal
is stained with $
empty rectum and forceful (Meissner)
meconium on
expulsion of faecal and myenteric
withdrawal
material upon withdrawal (Auerbach)
XX Infants may also RI¿QJHU
present with plexus and
$&RQVWULFWHG]RQHB7UDQVLWLRQ]RQH
XX Gripping of the examining hypertrophied
enterocolitis, sepsis, C'LODWHGSUR[LPDOFRORQ
¿QJHU anal grip) may be nerve trunks
and perforation
felt due to spastic zone
Treatment
Investigation Medical
XX Plain X-Ray abdomen: Shows dilated proximal colon TT Counsel parents about the disease and outcome
and absence of gas in the pelvic colon If the child presents with features of obstruction–
TT Keep the baby NPO
TT *LYHPDLQWHQDQFH,9ÀXLGe.g. Baby saline
TT Give Potassium correction, if necessary
TT Give IV antibiotics, e.g. Ampicillin plus Gentamicin
TT Insert an NG tube & decompress stomach
TT Give rectal irrigations with normal saline 3-4 times
daily
TT Consult Paediatric Surgeon immediately

Surgery
7KHGH¿QLWLYHWUHDWPHQW

ANORECTAL MALFORMATIONS
Hirschsprung disease

Anorectal malformations include a spectrum of

developmental anomalies of the lowest portion of the
intestinal and urogenital tracts. Most patients present
with imperforate anus2WKHUVSUHVHQWZLWKD¿VWXORXV
'LVWHQGHGERZHOORRSVDQGQRJDVVKDGRZLQWKHSHOYLFFDYLW\ connection either with urethra (in males) or with vestibule
(in females) and presents with history of passage of
XX Barium enema: Shows a transition zone between meconium through urethra (coloured urine), through
normal dilated proximal colon and a smaller-caliber vagina or through some abnormal openings in the
constricted distal colon. Transition zone may not be perineum.
 Step on to Paediatrics 305

IMPERFORATE ANUS UNDESCENDED TESTIS

(CRYPTORCHIDISM)
Clinical Manifestations
Cryptorchidism literally means hidden testis. It may be
XX H/o failure to pass
meconium by 24 unilateral or bilateral. When a boy is seen with single or
hours after birth no testicle in the scrotum, one should think of the
XX Absence of anal following possibilities–
opening or visible XX Testis is incompletely descended and remains anywhere
anal pit in its normal pathway of descent e.g. inguinal canal,
XX Abdominal VXSHU¿FLDODQG
distention, may be deep inguinal
in advanced cases ring or in the
abdomen
$EVHQWDQDORUL¿FH XX Testis is in
ectopic position
Investigations e.g. femoral and
XX Invertogram at perineal areas
24 hours: The XX Agenesis of testis
baby is held
XX Testicular
upside down
retraction, due
and X-Ray is
to a hyperactive
focused from
cremasteric (FWRSLFWHVLV LQWKHSHULQHXP
a lateral side.
This reveals the UHÀH[
level of the gas
Aetiology & Risk factor
shadow (rectal XX Unknown but may be related to genetic, hormonal or
pouch) whether
mechanical factors
below the level
of coccyx or not.
XX Prematurity
Pouch above the Clinical Manifestations
tip of coccyx are XX The scrotum
regarded as high
on the side of
variety anomalies nondescent will
XX USG of be seen empty
abdomen: ,QYHUWRJUDPVKRZLQJJDVVKDGRZ UHFWDO
SRXFK EHORZWKHOHYHORIFRFF\[ and not as well
To evaluate developed as
associated urinary tract abnormalities the contralateral
normal side
Treatment XX Screen the
perinium to
Medical search for any
TT Counsel parents about the disease and its outcome ectopic testis
Anorectal malformations

If the child presents with features of obstruction XX Any associated +\SRSODVWLFVFURWXPZLWKXQGHVFHQGHGWHVWHV

TT Keep the baby NPO pathology e.g.
TT *LYHPDLQWHQDQFH,9ÀXLGe.g.10% DA/Baby saline inguinal hernia
TT Insert an NG tube & decompress stomach Complications
TT Give IV Antibiotics, e.g. Ampicillin plus Gentamicin XX Infertility
TT ,GHQWL¿\ WUHDWDVVRFLDWHGFRPRUELGLWLHVSURPSWO\ XX Testicular malignancy
TT Consult Paediatric surgeon immediately XX Associated hernia
Surgery
XX Torsion of the cryptorchid testis

7KHGH¿QLWLYHWUHDWPHQW
 306 Step on to Paediatrics

Investigations
XX Ultrasound of abdomen: To search the absent testicle VUR GRADING
XX MRI or CT scan of abdomen: For intra-abdominal testes 7KH,QWHUQDWLRQDO&ODVVL¿FDWLRQ6\VWHPIRU985
XX Laparoscopy: Diagnostic FRPSULVHVWKHIROORZLQJ¿YHJUDGHV

Treatment *UDGH, 5HÀX[LQWRQRQGLODWHGXUHWHU

*UDGH,, 5HÀX[LQWRUHQDOSHOYLVDQGFDO\FHVZLWKRXW
Medical dilation
TT Hormonal therapy with hCG or LH-releasing
hormones (LHRH): Controversial *UDGH,,, 5HÀX[ZLWKPLOGWRPRGHUDWHGLODWLRQDQG
minimal blunting of fornices
Surgery *UDGH,9 5HÀX[ZLWKPRGHUDWHXUHWHUDOWRUWXRVLW\DQG
TT 2UFKLRSH[\VKRXOGEHSHUIRUPHGEHWZHHQ
dilation of pelvis and calyces
months of age or soon after diagnosis
*UDGH9 5HÀX[ZLWKJURVVGLODWLRQRIXUHWHUSHOYLV
and calyces, loss of papillary impressions,
and ureteral tortuosity

POSTERIOR URETHERAL VALVE Clinical Manifestations

The most common cause of severe obstructive uropathy Neonates: Distended bladder, palpable kidneys, vomiting,
among the boys. SRRUXULQDU\VWUHDPIDLOXUHWRWKULYHUHQDOLQVXI¿FLHQF\
Older children: Vomiting, poor urinary stream, urinary
Pathogenesis UHWHQVLRQEODGGHUGLVWHQVLRQUHQDOLQVXI¿FLHQF\
3HUVLVWHQFHRIDEQRUPDOFRQJHQLWDOOHDÀHWVLQWKHSURVWDWLF XX )HDWXUHVRIUHQDOLQVXI¿FLHQF\HJSDOOHUYRPLWLQJHWF
part of the urethra causes narrowing of the bladder outlet
ZLWKFRQVHTXHQWREVWUXFWLRQRIXULQHÀRZ7KLVFDXVHV Diagnosis
increased pressure in the organs proximal to the site of %DVHGRQFOLQLFDOIHDWXUHVDQG¿QGLQJVIURPWKHUHOHYDQW
obstruction e.g. urinary bladder, ureters, renal pelvis investigations.
resulting in their dilatation and enlargement. If not
UHOHLYHGLWZLOOJLYHULVHWRYHVLFRXUHWHULFUHÀX[ 985  Investigations
hydroureter, K\GURQHSKURVLVDQGUHQDOLQVXI¿FLHQF\ XX Ultrasonogram
Undescended testis, Posterior uretheral valve

of genito-urinary
system
Lt Kidney Rt Kidney
XX Voiding
cystourethrogram
XX Assessment of
renal function

&RXUWHV\3URI*0XLQXGGLQ
Lt ureter Rt ureter

Ureter opening to Urinary bladder

bladder and oneway
valves

posterior urethral valve causing

both side obsrruction
9RLGLQJF\VWRXUHWKURJUDP$3YLHZVKRZLQJ
Treatment JURVVGLODWDWLRQRIXUHWHUVDQGUHQDOSHOYLV
3RVWHULRUXUHWKUDOYDOYH
Surgery
Transurethral ablation of the valves.
 Step on to Paediatrics 307

HYDROCEPHALUS Investigations
Ultrasonogram/CT scan of brain.
It is the enlargement of head size from ventriculomegaly
due to accumulation of CSF either from overproduction or
impaired circulation and absorption.

Types
XX Noncommunicating (Obstructive): Stenosis of
aqueduct of Sylvius and pressure from CNS tumors
over the CSF pathway
XX Communicating: Results from obliteration of
subarachnoid cistern or malfunctioning of arachnoid
villi and occurs in meningitis, leukaemia and
overproduction of CSF as in choroid plexus papilloma

Clinical Manifestations
XX Progressive enlargement of head size, frontal bossing
XX Delayed closure of anterior fontanelle and/or widely
split cranial sutures
XX “Sunsetting” of eyes (due to pressure on superior
colliculus causing eyes to rotate downward
XX Sometimes, there may be signs of raised intracranial
pressure e.g. vomiting, headache, convulsion
TT OFC > 95th centile

&7VFDQRIEUDLQVKRZLQJELODWHUDOO\HQODUJHGODWHUDOYHQWULFOHV

+\GURFHSKDOXV

8OWUDVRQRJUDPRIEUDLQVKRZLQJELODWHUDOO\HQODUJHGODWHUDOYHQWULFOHV
Hydrocephalus

Diagnosis
%DVHGRQFOLQLFDOIHDWXUHVDQG¿QGLQJVIURPWKHUHOHYDQW
investigations. Treatment
Surgery
Ventriculo-peritoneal shunt.
 308 Step on to Paediatrics

SUMMARY OF OTHER SURGICAL PROBLEMS IN CHILDREN

Other varietes of
XX 6SLQDEL¿GDRFFXOWD%RQ\GHIHFWZLWKRXWDQ\KHUQLDWLRQRIPHQLQJHV
XX Meningocele: Protrusion of the meninges
XX Myelomeningocele: Protrusion of the meninges along with portion
of spinal cord through a bone defect in the vertebral column. The
PHQLQJHVFRYHUHGVDFLVXVXDOO\¿OOHGZLWKCSF
Clinical presentation:
XX Paraplegia
6SLQDOGHIHFW XX Continuus dribbling of urine & saliva

XX Too short frenulum lingula resulting in reduced mobility of tongue

Source: Internet

causing feeding and speech problem

XX Treatment : Frenulotomy

7RQJXHWLH $QN\ORJORVVLD

XX Swelling at the level of umbilicus due to protrusion of intestinal coils

through weak periumbilical muscles
XX Danger: Strangulation of gut
XX Most cases usually disappear by 1–1½ years of age. Others require
surgical repair
8PELOLFDOKHUQLD
Summary of other surgical

&RXUWHV\3URI0G
$VKUDI8O+XT.D]DO

XX Full thickness defect in abdominal wall resulting in protrusion of

intra-abdominal viscera to the exterior
XX Protruded organs are not covered by peritoneum
XX Treatment: Surgery

Gastroschisis

XX A midline abdominal wall defect through which intra-abdominal

viscera herniate into the base of the umbilical cord
XX In contrast to gastroschisis, protruded organs are covered by a
membrane and contained within the peritoneal sac
problems

XX Treatment: Surgery
2PSKDORFRHOH

2PSKDORFRHOH
 Step on to Paediatrics 309

XX A whole or a part of the extrahepatic bile ducts is absolutely atretic

XX Usually presents with jaundice (direct hyperbilirubinaemia), pale
stool and hepatomegaly
XX 7UHDWPHQW6XUJHU\ 0RGL¿HG.DVDL3RUWRHQWHURVWRP\ VKRXOGEH
done as early as possible)
$FKLOGZLWKELOLDU\DWUHVLDZLWKOLYHU
IDLOXUH DVFLWLV)77 MDXQGLFH

&RXUWHV\3URI$+DQLI7DEOX
XX Presents with history of passing of few drops of blood after the
passage of stool
XX Bleeding is painless and not smeared on stool
XX Treatment: Polypectomy

5HFWDOSRO\S

XX Urethral opening is ectopically located on the ventrum of the penis

proximal to the tip of the glans penis or as far down the scrotum or
perineum
XX The penis is more likely to have associated ventral shortening and
curvature, called chordee
XX 2OGHUFKLOGUHQKDYHGLI¿FXOW\LQPLFWXULWLRQDVWKHXULQHµVSUD\¶
backwards
+\SRVSDGLDV
XX Treatment: Surgery
&RXUWHV\3URI0G$VKUDI8O+XT.D]DO

XX Malformation of the penis in which the urethra ends in an opening on

the upper aspect (the dorsum) of the penis
XX 7KLVPD\OHDGWREDFNZDUGÀRZRIXULQHLQWRWKHNLGQH\UHSHDWHG
UTI and urinary incontinence

Summary of other surgical problems

XX Treatment: Surgery

(SLVSDGLDV
XX Inability to retract the foreskin of the penis
XX Treatment
TT Nonsurgical
&RXUWHV\3URI$+DQLI7DEOX

³³ Application of topical steroid creams such as betamethasone,

mometasone furoate and cortisone: Steroids work by reducing

WKHERG\ VLQÀDPPDWRU\DQGLPPXQHUHVSRQVHVDQGDOVRE\
thinning the skin
³³ Stretching of the foreskin can be accomplished manually

TT Surgical

3KLPRVLV ³³ Circumcision

³³ Minor operations to relieve foreskin tightness

 310 Step on to Paediatrics

&RXUWHV\3URI$+DQLI7DEOX
XX Entrapment of a retracted foreskin behind the coronal sulcus results
in impairment of venous return from the glans with consequent
worsening venous engorgement of glans
XX Furthermore this causes compromised arterial supply & painful
swelling of the glans that may eventually lead to gangrene or
autoamputation of the distal penis
XX Treatment: Surgery

3DUDSKLPRVLV

XX $FROOHFWLRQRIÀXLGZLWKLQWKHSURFHVVXVYDJLQDOLVWKDWSURGXFHV
swelling in the scrotum
&RXUWHV\3URI$+DQLI7DEOX

XX Presents with irreducible swelling in the scrotum

XX 7UDQVLOOXPLQDWLRQWHVWRIWKHVFURWXPLVSRVLWLYHGLVSOD\LQJÀXLGLQ
the tunica vaginalis
XX Usually spontaneous resolution by 18 months, otherwise surgery.
(herniotomy)

+\GURFRHOH
&RXUWHV\3URI$+DQLI7DEOX

XX It results from persistent patency of the processus vaginalis

XX Presents with reducible swelling in the groin or scrotum that increase
in size on crying or after activity
XX Treatment: Herniotomy as soon as diagnosed
Summary of other surgical problems

Inguinal hernia

XX Congenital deformity involving one foot or both where the affected

foot appears rotated internally at the ankle (inverted and adducted)
XX Serial plaster cast with gentle manipulation of the foot towards the
corrected position before the cast is applied and changed every 1-2
weeks
XX Treatment: Surgery (If nonoperative treatment is unsuccessful)

7DOLSHVHTXLQRYDURXV
 Step on to Paediatrics 311

References
1. Hoffenberg EJ et al. Gastro-intestinal tract. In: Current Pediatric Diagnosis and treatment, 23rdHG
2. Kliegman RM et al, Nelson Textbook of Pediatrics, 20th(GLWLRQ1HZ'HOKL(OVHYLHU
2. Smith D et al. The newborn infant. In Current Pediatric diagnosis and Treatment, 23rdHG
3. Khan MR, Rahman ME. Essence of Pediatrics. 4th ed. 2011. Chapter 23 , Common Surgical Problems; p.444-454.
4. Kabir ARML. Pediatric Practice on Parents Presentation, 1st ed. Dhaka: Asian Colour Printing; 2011.
5. Raine JE, Cunnington AJ, Walker JM. 100 Cases in Paediatrics. London: Hodder Arnold; 2009.

SELF ASSESSMENT
Short answer questions [SAQ]
1. How will you manage a case of cleft lip & cleft palate?
2. What is eventration?
3. Write down the difference between eventration & congenital diaphragmatic hernia
4. Write down the clinical features of congenital diaphragmatic hernia
5. How will you treat a neonate with congenital diaphragmatic hernia?
 :ULWHGRZQWKHFOLQLFDOIHDWXUHV LQYHVWLJDWLRQVRILQIDQWLOHS\ORULFVWHQRVLV
7. Write down the clinical manifestation of Hirschsprung disease
8. How will you evaluate a neonate with imperforated anas?

Self assessment
 39
Fluid, Electrolyte and Acid-base
Homeostasis
Body fluid- - - - - - - - - - - - - - 312
Daily fluid requirement - - - - - - - - - - - - 312
Fluid replacement- - - - - - - - - - - - - 312
S Electrolytes & Dyselectrolytaemia
¼¼ Hyponatraemia - - - - - - - - - - - - - 314
¼¼ Hypernatraemia - - - - - - - - - - - - - 314
¼¼ Hypokalaemia - - - - - - - - - - - - - 315
¼¼ Hyperkalaemia- - - - - - - - - - - - - 316
Acid–base homeostasis - - - - - - - - - - - - 318
Plasma Anion Gap - - - - - - - - - - - - - 319

BODY FLUID as well as intracellular space is controlled by –

Our body is composed of both solids and water. Only XX Oncotic pressure: Exerted by Serum albumin
WRWDOERG\ZDWHU 7%: DORQHFRQVWLWXWHVDERXW XX Osmotic pressure: Exerted by S. electrolytes mainly by
of total body weight and the remaining 40% by the Na+
solids e.g. protein (18%), mineral (7%) and fat (15%). Daily fluid requirement

Contribution of tbw to body Equal to Daily Routine loss through urine (50%), skin (30%),
weight in different stages of life airways (15%) and stool (5%). To replenish this loss, one
KDVWRGULQNVLPLODUDPRXQWRIÀXLGGDLO\ZKLFKLVRWKHUZLVH
Foetus 85%
called 0DLQWHQDQFHÀXLG.
Neonate 75%(Term), Higher (Preterm) 0DLQWHQDQFHÀXLG+RZPXFKGDLO\"
Infant  XX Neonates
TT $JH'D\PONJGD\ 7HUP PONJGD\
1st year-Puberty 
(Preterm)
TT Thereafter, daily increment#PONJGD\ 7HUP 
'LVWULEXWLRQRIWRWDOERG\ÀXLG
ml/kg/day (Preterm) upto 1st Week of life
XX Two-third: Intra-cellular
XX One-third: Extracellular, as follows– NB,QSUHWHUPEDELHV¶DPRXQWRIIOXLGFDQEHUDLVHGXSWR
PONJGD\E\GD\VRIDJH
Extracellular Fluid XX Infants & Children
TT For 1st 10 kg body weight: 100 ml/kg/day
Intracellular Fluid 20% of body weight (BW)
(40% of BW) Interstitial fluid (15% of BW) TT For Next 10 kg body weight: Add 50 ml/kg/day

Plasma (5% of BW) TT Everything over 20 kg body weight: Add 20 ml/kg/day

Body fluid

to a maximum of 2400 ml/day

7UDQVFHOOXODUÀXLG is the portion of total Example:0DLQWHQDQFHÀXLGUHTXLUHPHQWIRUDNJFKLOG
body water contained within epithelial lined will be as follows–
spaces. It is about 2.5% of the total body water. TT For 1st 10kg: (100×10) ml/day +
([DPSOHVRIWKLVÀXLGDUHFHUHEURVSLQDOÀXLG TT For 2nd 10kg(50×10) ml/day +
RFXODUÀXLGMRLQWÀXLGDQGXULQHLQEODGGHU TT For Weight >20kg (20×8) ml/day
312

7KHGLVWULEXWLRQRIÀXLGDFURVVWKHSODVPDLQWHUVWLWLXP
Total POGD\ POGD\
 Step on to Paediatrics 313

5HFRPPHQGHG$JHVSHFL¿F0DLQWHQDQFHÀXLG Then plan for replacement of 5HPDLQLQJÀXLGGH¿FLW

(RD)ZKLFKLVHTXDOWR  7RWDOÀXLGGH¿FLW±WKHDPRXQW
Birth to
48 hours- > 10 administered as a bolus in Phase I). This, along with the
Age 24-48 1-10 years
1 year years amount allocated next 24 hours will be given in another 2
hours
phases–
5-10% 5-10% Phase II (8 hours): The 1st half of the total amount
5-10% TT

Dextrose Dextrose will be replaced during this period

Choice dextrose
in 0.225% in 0.45%
of 10% DA in 0.9% TT Phase III (16 hours): The 2nd half of the total
NaCl NaCl
Fluid NaCl DPRXQWRIÀXLGZLOOEHJLYHQLQWKHQH[WKRXUV
(Baby (Junior
(DNS)
saline) saline) Example: A 22 kg child is hospitalized with severe
dehydration due to acute diarrhoea. He is estimated to
)OXLGGH¿FLWand Ongoing loss: These are additional have 10% weight loss. His S Na+ is 140 meq/l. He has no
losses apart from daily routine loss through– ongoing losses.
TT Gastro-intestinal tract e.g.diarrhoea, vomiting, naso-
gastric suction 4+RZWRFDOFXODWH UHSODFHÀXLGLQDFKLOG"
TT Third space loss e.g. burn, trauma, sepsis, abdominal D 7RWDOÀXLGGH¿FLW RINJ  /PO
surgery
E 0DLQWHQDQFHÀXLG
TT Urine e.g. diabetes mellitus, diabetes insipidus etc. TT First 10 kg of BW: 10×100 ml = 1000 ml/day
)OXLG'H¿FLW+RZWRDVVHVV"
TT Second 10 kg of BW: 10×50 ml = 500 ml/day
TT Remainder 2 kg of BW: 2×20 ml = 40 ml/day
)OXLGGH¿FLWLVDVVHVVHGRQWKHEDVLVRIH[LVWLQJGHJUHH
of dehydration and expressed as percentage loss of body The total amount of maintenance ÀXLGPOZKLFK
weight as follows– VKRXOGEHUHSODFHGE\QH[WKRXUV#POKRXU
Degree of Percentage loss The total amount [a+b LHGHILFLWPDLQWDLQDQFH] has to
Dehydration of Body weight be given over next 24 hours as follows:
Mild 3-5%
i) Phase I: Two Bolus amount (as the child does not
Moderate >5-10%
respond to a single bolus)
Severe >10-15%
1st bolus: 10 ml/kg = 10×22 = 220 ml
2nd bolus: 10 ml/kg =10×22 = 220 ml
Fluid replacement: How? So, total bolus amount given is 440 ml of Normal saline.
By considering– 5HPDLQLQJGH¿FLW 5'  ± PO PO
XX 5HSODFHPHQWRIDQ\H[LVWLQJÀXLGGH¿FLWby any of
WKHIROORZLQJÀXLGVe.g. ORS, Normal saline, DNS, ii) Phase II: 5HSODFHPHQWE\¿UVWKRXUV±
Baby saline, Cholera saline, Hartman, depending on the a. 1stòRI5' LHPO
DHWLRORJ\RIÀXLGORVVHOHFWURO\WHSUR¿OHDQGVHYHULW\RI
dehydration, and E0DLQWHQDQFHÀXLG POîKRXUVLHPO
XX Continue providing theGDLO\DJHVSHFL¿FPDLQWHQDQFH Total   PO#GURSVPLQXWH
ÀXLGHYHQO\RYHUKRXUV
iii) Phase III:5HSODFHPHQWE\QH[WKRXUVRI
0HWKRGVRIÀXLGUHSODFHPHQW
Fluid replacement

a. 2ndòRI5' LHPO
7KHUHDUHGLIIHUHQWZD\VWRUHSODFHWKHÀXLG$VLPSOH
E0DLQWHQDQFHÀXLG POîKRXUVLHPO
method is discussed below.
Total   PO#GURSVPLQ
Phase I: Infuse immediate bolus amount #PONJRI
QRUPDOVDOLQHWRUHSODFHDQ\H[LVWLQJÀXLGGH¿FLW,WPD\
be repeated until haemodynamic status is stable and urine
output is adequate.
 314 Step on to Paediatrics

SERUM ELECTROLYTES & Q. How to correct Na+GH¿FLW"

DYSELECTROLYTAEMIA Na+ Requirement (mEq) = (Desired Na+- Observed Na+)
î%: .J î+ Daily maintenance dose of Na+ (2-3
(OHFWURO\WHVDUHWKHPLQHUDOVSUHVHQWLQWKHERG\ÀXLGWKDW mEq/kg/day) for next 2 days.
dissociate into ions, carrying electric charges and exert
WKHLUHIIHFWVWRPDLQWDLQERG\ÀXLGGLVWULEXWLRQDFLGEDVH Example: S. Na+ level of a 7 day old baby (weight 1.5 kg)
balance, muscle and nervous system functions and other is 122 mEq/L.
important processes. TT Existing Na+ GH¿FLW   îî P(T
TT Maintenance Na+ =3×1.5×2 days = 9 mEq
Common electrolytes in blood
Cations Anions
XX Total Na+ Requirements =11.7+9 = 20.7 (appro.21mEq)
and this amount has to be replaced over next 48 hours
Name Serum level Name Serum level XX Fluid requirement during this 48 hours =1.5×150×2 =
Na+ 135-145 mmol/L Cl- PPRO/ 450 ml

K+ 3.5-5.5 mmol/L HCO3- 22-30 mmol/L Therefore, total 21 mEq Na+ has to be replaced through
Ca++ 8.4-10.2 mg/dl PO4-- 2.9-5.4 mg/dl PODSSURSULDWH,9ÀXLGRYHUKRXUV
TT $SSURSLDWHÀXLGKHUH1D&ODVLWFRQWDLQV
Mg++ 1.5-2.4 mg/dl SO4-- 2.4-4.1 mg/dl mEq Na+/L or 22 mEq in 450 ml (see chart on p 324)
TT Rate of infusion: 9 microdrops/min as at this rate Na+
,QRXUERG\QRUPDOO\HOHFWURO\WHVDQGÀXLGUHPDLQLQD correction will be 11 mEq/day
state of equilibrium. But in disease process, this balance
is altered and the patients suffer from dyselectrolytaemia, Important notes
dehydration orÀXLGRYHUORDG7KHHOHFWURO\WHLPEDODQFHV
mostly encountered in clinical practices are abnormalities
XX Avoid rapid correction because it may cause central
related to Na+ (hypo or hypernatraemia) as well as pontine myelinolysis
abnormalities in K+ (hypo or hyperkalaemia).
XX Daily Na+correction should not be >12 mEq /L
XX Daily maintenance Na+ should also be added, during
The different types of dyselectrolytaemia, their aetiology WKHGH¿FLWFRUUHFWLRQ
and their way of corrections are discussed below. XX In severe hyponatraemia (S. Na+<120 mEq /L), 3%
NaCl may be used

HYPONATRAEMIA (S. Na+ <135 mEq/L)

Aetiology HYPERNATRAEMIA (S. Na+ >145 mEq/L)

XX Water overload, SIADH, Sepsis
XX Excess Na+ loss through stool, as in diarrhoea Aetiology
XX Congenital adrenal hyperplasia XX Ingestion of excess Na+ through improperly mixed
XX Hypoaldosteronism formula milk or ORS, NaHCO3, seawater
Pathogenesis
XX Persistent fever
XX ,QIXVLRQRIK\SHUWRQLF,9ÀXLG
In hyponatremia, cells of the body are swollen and if this
XX :DWHUGH¿FLW
Hyponatraemia

occur in the brain, serious neurological consequences (e.g.

TT Increased insensible loss as occurs in preterm infants,
permanent disability and death) can occur.
babies under radiant warmer, phototherapy
TT 'HFUHDVHGÀXLGLQWDNHLQKRWKXPLGHQYLURQPHQW
Clinical manifestation
XX Nausea, irritability, malaise, lethargy XX Endocrinopathies e.g. hyperaldosteronism, diabetes
XX Dehydration insipidus
XX Headache, coma, Seizures when S Na+ falls <120mEq/L
 Step on to Paediatrics 315

Pathogenesis XX After restoration of intravascular volume–

TT Select, half strength NS (0.45% NaCl) as the
In hypernatraemia, high S Na+GUDZVÀXLGIURPLQVLGHWKH
maintenance ÀXLG
cells, causing the cells to become crenated. This cellular
TT Determine, the duration of correction of high Na+
changes can occur in any organs of the body. When
level to normal, based on the existing S Na+ level e.g.
RFFXUVLQQHXURQVWKLVLQWUDFHOOXODUWRH[WUDFHOOXODUÀXLG
shift causes decrease in brain volume and the shunken TT [Na] 145-157 mEq/L 24 hour
brain tends to move away from the skull and meninges.
This predisposes tearing of intracerebral and the bridging TT [Na] 158-170 mEq/L 48 hour
vessels with intracranial e.g. subarachnoid, subdural, TT [Na] 171-183 mEq/L 72 hour
and parenchymal hemorrhages and patients present with
seizures, coma or other neurological manifestations.
TT >1D@P(T/ 84 hour

To combat this osmotic dysequilibrium, the neurons

TT &DOFXODWHWKHDPRXQWRIPDLQWHQDQFHÀXLGWREH
automatically generate intracellular idiogenic osmoles
infused for the projected duration as shown above.
WRSUHYHQWÀXLGVKLIWLQJIURPLQWUDFHOOXODUVSDFH7KLV
Allocate extra 20-30% greater than the calculated
information is very important to consider during Na+
amount and adjust the rate of infusion accordingly
correction. If correction is done rapidly, there will be a XX Assess, clinical status, particularly hydration and S Na+
KLJKFKDQFHRIVKLIWLQJRIÀXLGIURPWKHH[WUDFHOOXODUWR OHYHORIWKHSDWLHQWDQGDGMXVWÀXLGPDQDJHPHQW,I±
intracellular space of neurons and this will cause brain TT Signs of volume depletion again from ongoing loss,

swelling, central pontine myelinolysis (CPM) seizures $GPLQLVWHU16EROXV#PONJ

or coma. Therefore, hypernatraemia should be corrected TT S Na+ decreases too rapidly, then either– a) increase

VORZO\ P(TGD\#P(TKRXU  Na+FRQFHQWUDWLRQRI,9ÀXLGor b) decrease rate of

Severity ,9ÀXLGLQIXVLRQ
TT S Na+ decreases too slowly, then– a) decrease Na
XX Mild: >145-155 mEq/L
XX Moderate: >155-175 mEq/L FRQFHQWUDWLRQRI,9ÀXLGor b) increase rate of IV
ÀXLGLQIXVLRQ
XX Severe : >175 mEq/L
TT Replace ongoing losses as those occur

HYPOKALAEMIA (S K+ level<3.5 mmol/L)

Aetiology
XX PEM
1RUPDOQHXURQ &UHQDWHGQHXURQLQ
VHYHUHK\SHUQDWUHPLD XX Diarrhoea, nasogastric loss, persistent vomiting
XX Long-term use of diuretics (thiazides), laxatives,
Clinical Manifestation steroids, digoxin, amphotericin B, mineralocorticoids
XX Irritability, restlessness, lethargy, high pitched cry XX Intrinsic renal disease e.g. Bartter syndrome
XX Variable degree of dehydration XX Cushing syndrome, DKA
XX Doughy feeling of skin
XX Sometimes, apnoea, convulsions, coma
Pathogenesis
Potassium is an important electrolyte for nerve and muscle
Management cell function, specially cardiac muscles.
Hypernatraemia

The goal is to bring S Na+ level slowly towards normal In low K+, muscles and nerves cannot function properly
value. The steps of management are as follows– and patients presents with weakness and cardiac symptom
XX Restore intravascular volume with Normal Saline (NS)
#PONJERG\ZHLJKW5HSHDWDGGLWLRQDOEROXVHV# Clinical Manifestation
10-20 ml/kg, if signs of dehydration e.g. hypotension, XX Skeletal muscle e.g. weakness, fatigue, cramp,
tachycardia, poor perfusion still exists K\SRUHÀH[LDSDUDO\VLV
 316 Step on to Paediatrics

XX Smooth muscle e.g. decreased peristalsis, constipation, HYPERKALAEMIA (S K+ level>5.5 mmol/L)

ileus, urinary retention
XX Heart muscle: palpitation, arrythmias e.g. ectopic beats,
atrial & ventricular tachycardia/arrest Aetiology
XX Haemolysis, rhabdomyolysis
Investigations: ECG changes XX Renal failure e.g. acute or chronic
XX 0LQHUDORFRUWLFRLGGH¿FLHQF\$GGLVRQ¶VGLVHDVH

Pathogenesis
Both hypo and hyperkalemia can lead to abnormal heart
rhythm and the important clinical effect is related to
electrical rhythm of heart.

Clinical Manifestation
XX $V\PSWRPDWLFQRQVSHFL¿F±ZHDNQHVVIDWLJXH
XX Cardiac arrhythmia
XX Muscle weakness, tinglings, paraesthesias
XX Paralysis, tetany
XX Palpitation or chest pain

Investigations: ECG changes

Management
+RZWRFRUUHFW.GH¿FLW"
XX Required K+(mmol): (Desired – Existing K+ levels) ×
BW (Kg) × 0.3

Easy way to correct hypokalaemia

S K+ level Amount of Inj. KCl to be
(mmol/L) added in with 100 ml IV fluid
3.5-4.5 1 ml = 2 mmol
3.0-3.5 1.5 ml = 3 mmol
Hypokalaemia, Hyperkalaemia

2.5-3.0 2 ml = 4 mmol
2.0-2.5 PO PPRO
KCl drip 0.5-1mmol /kg/hour
<2
under close cardiac monitoring
Important notes
XX Oral correction should be continued for 5-7 days after
acute phase management
Management
XX IV correction should be given when strictly needed and I. Mild hyperkalaemia 6.!PPRO/
provided that the patient is not in renal failure XX Restrict/avoid intake of extra potassium through
XX Correction of concomitant hypocalcaemia and acidosis SRWDVVLXPULFKÀXLGor foods e.g. fruits or drugs
should be delayed till potassium level improves as this
will further lower down S. Potassium
 Step on to Paediatrics 317

II. Moderate to severe hyperkalaemia (S K+!PPRO/

TT Myocardial cell membrane XX Calcium gluconate (10%)
stabilization Dose: 0.5-1 ml/kg, IV, slowly over 5-10 minutes
XX Insulin (short acting)
'RVHXQLWNJ,9ZLWK'$#PONJRYHUPLQXWHV
TT Redistribution of XX Salbutamol nebulization
extracellular K+ into cells Dose: 2.5 mg (<25 kg) or 5 mg (>25 kg) with normal saline (2 ml)
XX Sodium bicarbonate
Dose: 1-2 mmol/kg, IV over 10-15 min
XX Sodium polystyrene sulfonate resin (Kayexalate)
TT Oral: 1 month-18 years

TT Enhance elimination of K+ Dose: 125-250 mg/kg (max.15 g) in 15-30 mL 70% sorbitol, 3-4/day
from the body through gut TT Rectal: Neonate
Dose: 125-250 mg/kg, dilute each gm resin in 5-10 ml methylcellulose or water,
UHSHDWHGDVQHFHVVDU\HYHU\KRXUV
XX Renal replacement therapy
TT Other ways to eliminate K+ TT Peritoneal dialysis
from body (refractory cases)
TT Haemodialysis

(OHFWURO\WHV LRQLFFRQFHQWUDWLRQDQGWRQLFLW\RIFRPPRQO\XVHGRUDODQG,9ÀXLGV
Ca
7\SHVRIÀXLGV Na+ K+ Cl- HCO3- Glucose Acetate Lactate Tonicity
++
Low osmolality ORS 75 20  20 75 -- -- -- Hypotonic

ReSoMal 45 40 70 7 125 -- -- -- Hypotonic

Plasma 140 45 100  2.3 -- -- Isotonic

0.9% Saline/Normal Saline 154 -- 154 -- -- -- -- -- Isotonic

0.45% Saline /Junior Saline 77 -- 77 -- -- -- -- -- Hypotonic

0.3% Saline 51 -- 51 -- -- -- -- -- Hypotonic

0.225% Saline 42 -- 42 -- -- -- -- -- Hypotonic

5% Dextrose in 0.9% Saline 154 -- 154 -- 5 -- -- -- Hypertonic

5% Dextrose in .45% Saline 77 -- 77 -- 5 -- -- -- Hypertonic

D5 0.225% Saline 42 -- 42 -- 5 -- -- -- Hypertonic

D10 0.225% Saline 42 -- 42 -- 10 -- -- -- Hypertonic

3% Saline 514 -- 514 -- -- -- -- -- Hypertonic

Cholera Saline 133 13 98 -- -- -- 48 -- Hypertonic

Hyperkalaemia

Hartman’s Solution 131 5 111 -- -- 2 -- 29 Isotonic

Ringer’s Lactate 130 4 109 -- -- 1.5 -- 28 Isotonic

D5 in Lactated Ringer’s 130 4 109 -- 5 1.5 -- 28 Hypertonic

 318 Step on to Paediatrics

ACID-BASE BALANCE HCO3- in urine. As HCO3- normally buffers H+ in the

H[WUDFHOOXODUÀXLG (&) WKLVH[FHVVXULQDU\+&23- loss
Acid-base balance i.e. maintaining arterial blood pH indirectly conserves H+ in the ECF and ultimately brings
between 7.38-7.42 is very important to ensure normal body’s pH back to normal.
functioning of pH-sensitive enzyme systems in our
body. It is regulated by the interactions between the Normal Arterial Blood Gas and interpretation
lungs, kidneys and chemical buffer systems
Analyte Normal Range Interpretation
(e.g.carbonic acid-bicarbonate buffer system,
hemoglobin, phosphate, ammonium) present in our The pH indicates if a patient
body. Over 50% of the blood’s buffering capacity is pH 7.35-7.45 is acidaemic (pH < 7.35) or
provided by the Carbonic acid-Bicarbonate buffer alkalaemic (pH > 7.45)
system, 30% by haemoglobin and the remainder by
A low PaO2 indicates that the
phosphates and ammonium. 80-100 mmHg
PaO2 patient is not oxygenating
or 9.3-13.3 kPa
Whenever, Retain HCO3̄ properly, and is hypoxaemic
there is Lose HCO3̄ Lose H+ A high PaCO2 (respiratory
disturbances acidosis) indicates
in acid-base RENAL 35-45 mmHg
PaCO2 underventilation, a low PaCO2
balance, the orN3D
Alkalinization $FLGL¿FDWLRQ indicates (respiratory alkalosis)
Chemical of urine of urine
hyper or over ventilation
buffers [HCO3̄ ]
S+Į A low HCO3íindicates metabolic
principally the Pco2
Decrease Increase HCO3 í
 PPRO/ acidosis, a high HCO3í indicates
Carbonic acid-
Pco2 Pco2 metabolic alkalosis
Bicarbonate
buffer system
The 4 major types of Acid-Base disorders
initially come Hyperventilate Hypoventilate
into action HCO3- pCO2
to correct the LUNG Conditions pH Causes
(mEq/L) mmHg
imbalance. 9LDSXOPRQDU\DQGUHQDO
FRPSHQVDWRU\PHFKDQLVPV Normal 7.4 24 40
Subsequently,
the Pulmonary and Renal compensatory mechanisms
TT Aspirin poisoning
Metabolic
augment the process towards further correction. The <7.4 <22 TT DKA, RTA
acidosis
¿QDOVWDELOL]DWLRQRIDFLGEDVHEDODQFHRIFRXUVH
TT Diarrhoea
depends on elimination of primary cause. TT Prolonged
The pulmonary regulation is accomplished by vomiting
maintaing appropriate CO2 concentration in the extra- Metabolic TT NaHCO3
>7.4 !
FHOOXODUÀXLG (&) E\DGMXVWLQJWKHUDWH GHSWKRI alkalosis ingestion
respiration.
TT Cushing’s disease
TT Conn’s disease
The renal regulation is accomplished by–
TT CNS Depression
'' UHDEVRUSWLRQRI¿OWHUHG+&23 primarily in the
Acid–base homeostasis

proximal tubule, and

TT Airway
Obstruction
'' excretion of H+ or HCO3- in the distal tubules to Respiratory
match the net input of acid or base <7.4 >45 TT Pneumonia
acidosis TT Pulmonary edema
)RUH[DPSOH when body is in acidosis, the kidneys
TT Pneumothorax
then do 2 things i) excrete acidic urine i.e, secrete H+
TT Myopathy
LQWRWXEXODUOXPHQLL UHDEVRUEDOOWKH¿OWHUHG+&23-
which are added back to the ECF and balances the TT Hyperventilation
acids (H+) and bases (HCO3-) towards normal. Respiratory as in anxiety
>7.4 <35
alkalosis TT Mech Ventilation
On the otherhand, when the body is in alkalosis, TT Salicylates/Sepsis
the kidneys excrete alkaline urine i.e. excrete excess
 Step on to Paediatrics 319

Anion Gap (AG) Mechanism

'H¿QDWLRQ,WLVWKHGLIIHUHQFHEHWZHHQWKHPHDVXUHG NAGMA results from direct loss of NaHCO3 from
cations (Na+) and the measured anions (Cl- & HCO3-). It is diseases of gut e.g. acute diarrhoea, where fall of serum
principally affected by changes in unmeasured anions in Na+ and a reduction of ECF volume will stimulate renal
the blood. In clinical practice, the plasma anion gap helps retention of Na+ and Cl-. Thereby the lost HCO3- (i.e.
us to evaluate patients with metabolic acidosis, in relation anions) being replaced by the anions of retained Cl- and
to their aetiology. Sometimes, In some diseases, patients thus electrical neutrality is maintained. That is why
have metabolic acidosis with normal anion gap (Non anion hyperchloraemic metabolic acidosis is an alternate term
gap metabolic acidosis NAGMA). On the otherhand, for NAGMA. It can also occurs by the use of drugs which
some patients have metabolic acidosis with high anion gap inhibit renal reabsortion of HCO3- e.g. acetazolamide,
(High anion gap metabolic acidosis HAGMA). amiloride, PG inhibitors
It is determined by this formula: (Na+- (Cl-+HCO3-) and a In HAGMA, as already mentioned that there is an
Normal anion gap is 4-11. increament in unmeasured anions. The aetiology behind
In our body, the number of serum anions must be equal HAGMA, can be expressed by the mnemonics GOLD
to the number of serum cations to maintain electrical MARK.
neutrality, as described in the diagram below. G = Glycols
Normal plasma Acidosis (no gao) Acidosis (gao) O = Oxoproline (toxic metaboletes of paracetamol)

UC UC UC
L = L-Lactate e.g. lactic acidosis
UC UC UA
D = D-Lactate (exagonous LA produced by gut bacteria)

HCO3– M = Methanol (alcohol)

HCO3–
HCO3– A = Aspirin (Salicylate)
R = Renal failure (uraemia)
Na+ Na+ Na+
K = Ketones ( deabetic, alcoholic, starvation)
CI– CI– CI–

Normal anion High Anaion

gap MA gap MA
UC = unmeasured cation; UA = Unmeasured anion (NAGMA) (HAGMA)

HCO3- Ļ Ļ
Characteristics
From the above diagram, it is clear that- Cl- Ĺ No change
In NAGMA, there is fall in serum HCO3-
Unmeasured
(hypobicarbonataemia) and this fall is matched by an No change Ĺ
Anions
equivalent increament in serum Cl- (hyperchloraemia) to
maintain the electrical neutrality of blood. Here, there is
no increament in unmeasured anions.
Acid–base homeostasis

In HAGMA, there is increament in unmeasured anions

e.g. ketoacids, e.g. beta hydroxyl butyrate and acetoacetate
other acids, phosphates, urea along with fall in serum
HCO3- (hypobicarbonataemia). Here, no change in serum
Cl-
 320 Step on to Paediatrics

References
 *UHHQEDXP/$3DWKRSK\VLRORJ\RIERG\ÀXLGVDQGÀXLGWKHUDS\1HOVRQ7H[WERRNRI3HGLDWULFVth Edition. New Delhi:
(OVHYLHU
2. Ford DM, et al. Fluid, electrolyte, & acid-base disorders & theray. In: Current Pediatric diagnosis & Treatment, 23rdHG

3. Khan MR, Rahman ME. Essence of Pediatrics. 4th ed. New Delhi: Elsevier; 2011. Chapter 11, Fluid Electrolyte and Acid-Base
disturbances: 212-18.
4. Kabir ARML. Pediatric Practice on Parents Presentation, 1st ed. Dhaka: Asian Colour Printing; 2011.
5. Barrett KE et al. Ganong’s Review of Medical Physiology. 21st ed: McGraw-Hill Medical Publishing Division; 2003.

SELF ASSESSMENT
Short answer questions [SAQ]
 +RZFDQ\RXFDOFXODWHGDLO\ÀXLGUHTXLUHPHQW"&DOFXODWHWKHÀXLGUHTXLUHPHQWRIDFKLOGZHLJKLQJNJ
2. What are the causes of hyponatraemia? Write down the principles of management of hyponatraemia.
3. Write down the causes and clinical features of hyperkalaemia.
 1DPHWKHLPSRUWDQWFDXVHVRIK\SRNDODHPLD+RZFDQ\RXFRUUHFWWKHGH¿FLHQF\RISRWDVVLXPRIDEDE\ZHLJKLQJNJ
(Serum K+ 2.4 mmol/L)?
5. Write down the composition of cholera saline.
 :ULWHGRZQWKHQRUPDOYDOXHRI$%*

Multiple choice questions [MCQ]

 :KLOHDVVHVVLQJGDLO\ÀXLGUHTXLUHPHQWWKHIROORZLQJVKRXOGEHWDNHQLQWRFRQVLGHUDWLRQ±
___ a) urinary loss ___ b) respiratory loss ___ c) sweating ___ d) loss with diarrhoea ___ e) loss with vomiting
2. Major cations of plasma
___ a) Sodium ___ b) Potassium ___ c) Magnesium ___ d) Calcium ___ e) Ammonium
 0DMRUFRPSRQHQWVRIÀXLGFRPSDUWPHQWVDUH±
___ a) intracellular ___ b) interstitial ___ c) plasma ___ d) peritoneal ___ e) transcellular
 7KHIROORZLQJDUHH[DPSOHVRIWUDQVFXOOXODUÀXLG±
___ a) &6)  BBBE RFXODUÀXLG BBBF MRLQWÀXLG BBBG SODVPD BBBH SHULWRQHDOÀXLG
5. Causes of hypernatraemia–
___ a) diabetes insipidus ___ b) pancreatitis ___ c) diarrhoea ___ d) diuretics ___ e) hyperaldosteronism
 7KH(&*FKDQJHVLQK\SHUNDOLHPLD±
___ a) ST elevation ___ b) narrow QRS complex ___ c) tall R wave
___ d) prolonged PR interval ___ e) T inversion
7. Treatment options of hyperkalaemia includes–
___ a) Sodi-bicarb ___ b) Insulin ___ c) 10% DA ___ d) dialysis ___ e) Calcium gluconate
8. The following statement regarding acid-base homeostasis is true–
___ a) normal pH of blood is 7.0 ___ b) a low HCO3 indicates alkalosis
Self assessment

___ c) hyperventilation causes low PCO2 ___ d) pH is proportionate to H+ content of the body
___ e) acid imbalances are controlled by kidney alone
 40
Instruments & Procedures in Paediatrics
Lumber puncture needle - - - - - - - - - - - - 321
Salah bone marrow aspiration needle - - - - - - - - - 322
AMBU bag - - - - - - - - - - - - - - 323
Tongue depressor - - - - - - - - - - - - - 323
Three-way stop cock - - - - - - - - - - - - 323
Umbilical catheterization- - - - - - - - - - - - 323
Exchange transfusion - - - - - - - - - - - - 324
Small volume blood transfusion - - - - - - - - - - - 325
Nasogastric/oro gastric tube- - - - - - - - - - - 325
Nebulization & Peak Flow Meter - - - - - - - - - - 326
Capillary blood collection for glucose monitoring - - - - - - - 327
Oxygen therapy- - - - - - - - - - - - - 327

Lumber puncture needle XX Back of the patient should be right at the edge of the
XX Parts table, its transverse axis i.e. a line passing through the
posterior superior iliac spine should be vertical
TT Trocar (stilette) with knob
Trocar XX An expert assistant
TT Cannula
is needed to hold the
Use: Lumber puncture patient in position
XX After positioning, site
Cannula
of lumber puncture is
Lumber puncture LGHQWL¿HGE\th lumber
vertebra, which is in the
Site

same plane with iliac

Usually done in 3rd intervertebral space (between 3rd & 4th crest
lumber vertebra). XX Physician should wear
mask, gown and gloves
Procedure XX After putting skin wash
XX Take consent draping, LP is done with

Lumber puncture needle

from the all aseptic precautions
parents before by putting thumb of left
doing the hand on the spine and
procedure introducing the needle
XX Patient should E\ULJKWKDQG¿UPO\
be lying on through the skin in the
his side on mid-line between the
D¿UPWDEOH spines
with the XX Direction of the needle
knees and should be forward and
chin as nearly slightly towards the head
apposed as XX As the dura is pierced
possible there is a sense of
(restrained position) pressure release
321
 322 Step on to Paediatrics

XX As the needle enters subarachnoid space, CSF comes Salah bone marrow aspiration needle
out
XX After withdrawal of LP needle a sterile dressing should Cannula

be applied
XX 3DWLHQWVKRXOGOLHÀDWIRUKRXUVZLWKRXWSLOORZDQG
should be given drink immediately after the maneuver Parts
XX Trocar (stilette) with knob
During LP, spinal needle traverses through the XX Cannula
following layers XX Adjustable guard
1. Skin Trocar
2. Facia and SC fat
3. Surpaspinous ligament
4. Interspinous ligament Bone marrow aspiration
5. Ligamentum flavum
Sites
 (SLGXUDOVSDFHDQGIDW HSLGXUDODQHVWKHVLD XX Children <2years: Medial aspect of upper end of tibia
needle stops here) XX Children >2years: Posterior iliac crest, spinous process
7. Dura mater
of vertebrae, manubrium sterni (rare)
8. Subdural space, and
9. Arachnoid mater Procedure
XX First take written consent from the parents or legal
Indications gurdian before doing the procedure
XX Diagnostic
XX Fix the guard of the aspiration needle about ½ the depth
TT Suspicion of meningitis (pyogenic, tubercular, viral),
of bone
encephalitis
XX Then ask the patient to lie down in prone position for
TT Systemic diseases e.g. multiple sclerosis, SLE
iliac crest site or on his back for manubrium sterni
TT Suspicion of GBS, sub-arachnoid haemorrhage,
XX Wear mask, gown
and gloves
multiple sclerosis
TT Evaluation for CNS leukaemia
XX After putting
skin wash and
TT For diagnosis e,g. myelography, cysternography
draping, inject 2%
XX Therapeutic xylocaine at the
TT Intrathecal chemotherapy, as in leukaemia
site of puncture and
TT Relief of pseudotumor cerebri
LQ¿OWUDWHXSWRWKH
TT Spinal anaesthesia periosteum
XX Then push the
Contraindications aspiration needle
through the skin vertically down by screwing method
XX Raised ICP due to mass lesion of brain or spinal cord
until bone is penetrated
Bone marrow aspiration needle

with high risk for transtentorial or cerebellar tonsillar

herniation (e.g. posterior fossa tumor, midline shift) XX A sudden loss of resistance indicates that the needle
XX Critically ill patient entered in the marrow space
XX Skin infection at site of LP
XX Now remove the stilette and attach a syringe to the
XX Thrombocytopenia <20X109/L cannula
XX Aspirate marrow by negative suction
XX Then withdraw the needle, press the puncture site and
Complications seal with a sterile swab
XX 7KHQSUHSDUH¿OPRQJODVVVOLGHDQGSUHVHUYHWKHUHVWRI
XX Headache XX Haemorrhage
the aspirate in EDTA
XX Local pain XX Introduction of infection
XX Brain stem herniation XX Injury to vertebral disc
 Step on to Paediatrics 323

Indications Contraindications
XX Diaphragmatic hernia
Diagnostic XX 7UDFKHRRHVRSKDJHDO¿VWXOD H[FHSWKLJKYDULHW\
Haematological disorders e.g. leukaemia, ITP, non
Tongue
XX
depressor
Hodgkin lymphoma, myeloproliferative disorders,
plasma cell disorders, megaloblastic anaemia, A tool, used to depress the tongue allowing the
multiple myeloma examination of mouth and throat.
XX Infectious diseases e.g. Kala-azar, TB, PUO Types: Metallic, Plastic, Wooden
XX Storage diseases e.g. Gaucher disease, Niemann-
Pick disease Uses
To observe the throat and oral cavity clearly to note any
XX Infectious diseases e.g. Kala-azar, TB, PUO sign of -
XX Storage diseases e.g. Gaucher disease, Niemann disease XX Faucal diphtheria
XX Therapeutic: Bone marrow transplantation XX Tonsillitis
XX Pharyngitis
Contraindications XX Retropharyngeal abscess
XX Local skin infection or recent irradiation therapy at the XX Koplick’s spot
sampling site XX Oral thrush
XX Known case of haemophilia, thrombocytopenia XX Palatal palsy
XX Bone marrow disorders e.g. osteomyelitis, osteogenesis XX Cleft palate, and also to
imperfecta
XX Remove any foreign body from
XX While using anticoagulants
posterior part of tongue
Complications
XX Shock e.g. vaso-vagal/haemorrhagic
XX Local suction pain Three-way stop cock
XX Introduction of infection e.g. osteomyelitis Uses
XX Haemorrhage XX To facilitate administration of drugs orÀXLGVWKURXJK
XX Overpuncture (injury to deep structures) e.g.great multiple channels in a single IV access
vessels XX Exchange Transfusion

AMBU (artificial manual breathing unit)

6HOILQÀDWLQJEDJKDYLQJWKHIROORZLQJSDUWV
 Mouth piece/mask
 AMBU bag proper

 O2 connector
 O reservoir
2

 Pop-up valve AMBU, Tongue depressor

Indications
XX Resuscitation of neonates
as in-
 Perinatal asphyxia  RDS Umbilical vein catheterization
7KLVSURFHGXUHLVGRQHLQWKH¿UVWIHZGD\VRIOLIHIRU±
 Apnoea e.g. sepsis, IVH
XX Infusion of a very sick newborn e.g. preterm VLBW
XX Respiratory failure from any cause, e.g.
baby, whose peripheral veins are not accessable
 GBS  Pneumonia  Head injury XX Exchange transfusion (ET)
 Severe acute asthma  Poisoning
 324 Step on to Paediatrics

Procedure b) ABO incompatibility: O group of homologous rhesus

XX Clean the cord and surrounding skin with an antiseptic type or mother’s group should be used
solution. Then tie a suture around the base of the cord 5HI$EVDU1.DZVHU&$HWDO%-&+  

Procedure
XX The whole procedure
is done in an isolated
room with strict
aseptic precautions. An
assistant is needed to
help, monitor and tally
the volume of blood
exchanged
6WHSVLQXPELOLFDOYHLQFDWKHWHUL]DWLRQ
XX Umbilical
XX Cut the cord, 1-2 cm from the base with a sterile scalpel catheterization is done
(A), Identify the umbilical vein (single, larger, thin ¿UVW
walled vessel) and umbilical arteries (two thicker XX 2 three way stop cocks
walled vessels). Hold the cord near the vein with sterile are attached end-to-end
forcep to make 4 ways
XX Hold near end of the catheter with sterile forceps and 'LVWDO
DGYDQFHLWLQWRWKHYHLQ LWVKRXOGSDVVHDVLO\ IRU outlet
cms (B)
3UR[LPDO
XX Check that catheter is not kinked and that blood draws 3DWLHQW¶V outlet
back easily; if not (when any block), pull back the HQG
2SHUDWRU¶V
catheter partly and re-introduce HQG
XX Secure with 2 sutures into the cord leaving 5 cm long
suture ends. Tape suture and catheter (C) ([FKDQJHWUDQVIXVLRQ

After removing the catheter, apply pressure to the XX One way is connected with distal end of umbilical
Umbilical vein catheterization, Exchange transfusion

umbilical stump for 5-10 minutes catheter and another (opposite) end is connected to 20
ml disposable syringe
Exchange transfusion (ET) XX Distal sideway from the operator is connected to donor
blood set
Indications
XX Proximal sideway is connected to a saline set leading
XX Severe hyperbilirubinaemia secondary to haemolytic
to an empty saline bag into which patient’s blood is
disease of newborn e.g. Rh or ABO incompatibility
expelled out and discarded
XX Sepsis, DIC
XX 2QHURXQGVKRXOGEHPDGHWRFRQ¿UPWKHIXQFWLRQLQJ
XX Polycythaemia (partial exchange transfusion)
of the ET set up. Then exchange is done by push-pull
XX Metabolic disorder causing severe acidosis technique
XX 6HYHUHÀXLGHOHFWURO\WHLPEDODQFH XX The amount of blood is removed that is tolerated by the
infant. This is usually-
Aims of ET in Haemolytic TT For <1500 gms: 5 ml.  For 2500 gms: 10 ml.
Disease of Newborn TT For <3500 gms 15 ml.  >3500 gms: 20 ml.
XX To reduce hyperbilirubinaemia
XX To correct anaemia XX 7KHGH¿QHGDPRXQWRIEORRGLVZLWKGUDZQ¿UVWIURP
XX To remove damaged and antibody coated RBCs the patient slowly and steadily, it is then expelled out
XX 7RUHPRYHXQ¿[HGDQWLERGLHV through proximal sideway outlet, by keeping the inlet
closed
Selection of Blood in ET XX Then 15 ml of donor’s blood is drawn from the
a) Rh-incompatibility: Rh-negative blood of same group suspended bag through distal sideway outlet, keeping
as infant or O blood group compatible with serum of the proximal one closed and this drawn blood is pushed
mother and infant slowly to the infant
 Step on to Paediatrics 325

XX To prevent metabolic acidosis it was a common practice Indications

to inject Inj. Sodi-bi-carb (8.4%) 1ml after each 100ml
When transfusion of small amount of blood is required for
of blood exchange, which is not indicated now a days.
critically ill small infants, for their overall welbeing, as in–
If the baby is symptomatically hypocalcaemic 1ml
of Ca-gluconate can be given very slow I/V under  Severe anaemia  Severe sepsis
monitoring of heart rate
XX During ET, baby has to be kept warm and preferably Procedure
done in open warmer. An intake output chart along with
XX First do blood grouping of both donor and recipient and
monitoring of heart rate, respiratory rate, temperature, cross-matching
colour any important events has to be noted XX Wash hands thoroughly and then put on gloves
XX At the end of procedure blood sample is sent for post XX Wash the donor’s antecubital area with iodine and spirit
exchange estimation of - throughly and cover the area with a sterile sheet
TT Serum bilirubin  Serum electrolytes XX Calculate the amount of blood to be transfused to the
TT Serum calcium  Blood glucose level baby
TT Haemoglobin
XX Draw anticoagulant in the 50cc syringe from the
XX Serum bilirubin level has to be checked routinely transfusion bag (3ml for each 20 ml blood, e.g. 3ml
DQWLFRDJXODQWIRUPOGRQRU¶VEORRG/LNHZLVHPO
XX If no further ET is required umbilical catheter is
anticoagulant for 34 ml blood and so on..
withdrawn and a dry sterile dressing is applied to the
umbilicus
XX After taking requisite amount of anti-coagulant in the
50 cc syringe, empty the blood bag of the remaining
XX After ET, phototherapy may be continued
anticoagulant
Complications XX Now draw the calculated amount of blood from the
GRQRUSXQFWXULQJWKHDQWHFXELWDOYHLQE\*EXWWHUÀ\
XX During Exchange needle in the 50cc syringe and then transfer into the
Air embolus
 Volume imbalance
 Acidosis
 empty blood bag
Arrhythmias
 Respiratory distress
 XX Finally, transfuse this blood to the infant following the
Hyperkalaemia
 Anaemia/Polycythaemia
 standard procedure
Fluctuating BP and cerebral blood flow
Complications


XX After Exchange

Infection Hypoglycaemia
  Hypernatraemia

Usual hazards of blood transfusion.
Thrombocytopenia
 Polycythaemia or anaemia


Coagulopathy or neutropenia
 Necrotising


enyerocolitis Blood borne infections


Nasogastric (ng) tube insertion
Graft versus host disease

Insertion involves the placement of a tube into stomach
via nose. The main purposes are to-
Small volume blood transfusion TT 'HÀDWH
stomach in
Requirements acute abdomen
XX 50 cc syringe  Blood bag with anticoagulant TT Feed the
XX Blood transfusion set %XWWHUÀ\QLGGOH * preterm, very
LBW, sick or
neurologically
Exchange transfusion

unstable babies
TT check patency
or obstruction
of oesophagus,
when suspicion
of esophageal atresia
TT assess feed tolerance in preterm, LBW babies
TT collect gastric lavage for AFB in tuberculosis
TT check blood in gastric contents as occurs in NEC
 326 Step on to Paediatrics

Procedure Procedure
XX Wash hands properly XX Clean all the parts before use
XX Hold the tip of the tube against the child’s nose, XX $W¿UVWDWWDFKWKHDLUWXEHWRWKHDLURXWOHWRIWKH
measure the distance from the nose to the ear lobe, then machine
from there to the xiphisternum (epigastrium) XX Fit the air tube with mixing chamber and mask
XX Take measured amount of drugs into the mixing
chamber by syringe & mix with normal saline to make
a total volume of 3 ml
XX Connect the electrical line and turn on the switch
XX /RRNZKHWKHU¿QHPLVW ZHWDHURVRO LVFRPLQJRXW
through the mask adequately
XX Place the child in upright position & facilitate to take
slow deep breaths through mouth
XX Mark the tube at this point
XX Put the mask to the face of the child covering nose and
XX +ROGWKHFKLOG¿UPO\/XEULFDWHWKHWLSRIWKHFDWKHWHU
mouth adequately (not so tightly)
ZLWKOLTXLGSDUDI¿QDQGSDVVLWWKURXJKQRVWULOSXVKLQJ
slowly until it enters into the stomach without any
XX &RQWLQXHQHEXOL]DWLRQXQWLO¿QHPLVWLVQRORQJHU
UHVLVWDQFH:KHQWKHPHDVXUHGGLVWDQFHLVUHDFKHG¿[ present
the tube with tape at the nose XX Clean the machine after use & store the drugs in right
XX Aspirate a small amount of stomach contents with place
DV\ULQJHWRFRQ¿UPWKDWWKHWXEHLVLQSODFH,IQR
Drugs with dose
aspirate is obtained, inject air down the tube and listen XX Salbutamol (5 mg/ml ): 0.15 mg(0.03 ml)/kg/dose to
with a stethoscope over the abdomen
a maximum 5 mg (1 ml)/ Salbutamol (2.5 mg/2.5ml ):
XX If any doubt about the insertion, withdraw it and insert
0.15 mg (0.15ml)/kg/dose.
again XX Ipratropium bromide: 250 µgm/dose

Peak Flow Meter

Orogastric tube insertion
It is a small hand-held device used to monitor a person’s
Insertion involves the placement of a tube into stomach
ability to breath-out air. It measures a person’s strength
via oropharynx for the purposes mentioned in NG tube
RIDLUÀRZWKURXJKWKHEURQFKLDQGWKXVWKHGHJUHHRI
feeding insertion.
obstruction in the airways.
Nebulization 3HDNH[SLUDWRU\ÀRZUDWH 3()5
Mobile blood transfusion, Nasogastric tube

Parts It is the maximum speed of expiration of a person, as

XX Motor or pump PHDVXUHGZLWKDSHDNÀRZPHWHU,I3()5LVKLJKHU
XX Air inlet, air airway is well, but if lower, airway is contricted.
outlet
Parts
XX Filter XX Mouth piece Indicator/Cursor Measuring scale
XX Air tube
XX Mask Uses
XX Mixing chamber XX To assess the status of a patient with asthma & COPD
or cup XX 7RDVVHVVWKHHI¿FDF\RIPDQDJHPHQWLQDVWKPD&23'
XX T piece or mouth
piece
 Step on to Paediatrics 327

How to use?
1. Place the
Procedure
indicator at
1. Keep the Glucometer & strip ready with appropriate
the base of the
code number
numbered scale
2. Stand up or 2. Wash hands and put on gloves
sit in upright 3. Advice the patient to sit or lie down
posture
4. Select appropriate puncture site
3. Take a deep
breath 5. Warm the puncture site
4. Place the  &OHDQWKHSXQFWXUHVLWHZLWKGLVLQIDFWDQWDQGDOORZLWWR
meter in mouth air dry to provide effective disinfection
and close 7. Puncture the skin with the disposable lancing device
lips around
the mouth  :LSHDZD\WKH¿UVWGURSRIEORRGZLWKDGU\JDX]HSDG
piece. Do not  6TXHH]HJHQWO\WKHSXQFWXUHVLWHWRDOORZIUHHÀRZRI
SXWWRQJXHLQVLGHWKHKROH GRQRWSXW¿QJHURYHU blood
measuring scale
10. Touch the test strip on to the blood drop and allow it
5. Blow out as hard and fast as can
WRÀRZLQWRWKHWHVWVWULSLQFDSLOODU\DFWLRQ
 :ULWHGRZQWKHQXPEHU\RXJHW
When adequate amount of blood is drawn, Glucometer
 5HSHDWWKHVWHSVWRWZRPRUHWLPHV
will automatically produce a beep sound and starts to
8. Write down the highest of the three numbers achieved function. Usually reading will appear within 10-15
Peak Flow Meter usually not applicable for <5 years of age. seconds
XX Dispose the used materials (gloves, gauze etc.) properly
Capillary blood glucose monitoring
in a container approved for their disposal
Instruments XX Remove gloves, wash hands before proceeding to the
XX Lancing device next patient
XX Gloves
XX Gauze
XX Alcohol as antiseptic Oxygen therapy is life saving
Bandages and micropore
Delivery system
XX

tape XX Nasal canula/ nasal prong

XX Glucometer and strip XX Masks e.g. simple mask, partial re-breather mask, non
re-breather mask, ventury mask
XX Oxygen hood
Puncture sites Oxygen tent
Nebulization, Peak flow meter
XX

XX Finger stick (for XX AMBU bag

older child): XX T-piece
Palmar surface
of the distal Indications
segment of the XX Central cyanosis
PLGGOH¿QJHU XX Grunting
ideally of the XX )HHGLQJGLI¿FXOW\GXHWRUHVSLUDWRU\GLVWUHVV
non-dominant
XX Severe lower chest wall indrawing
hand
XX Head nodding
XX Heel stick (for neonate and infant): Lateral or medial
plantar surface of the heel
XX 5HVSLUDWRU\UDWH•PLQ

Amount of blood needed: 1 drop

 328 Step on to Paediatrics

Ways to give oxygen XX Face mask: Oxygen delivery, 5 L/min.

XX Nasal prong: These are short tubes inserted & placed
just inside into the nostrils and secure with a piece of
tape on it

Oxygen delivery: 1-2 L/min.

+XPLGL¿FDWLRQQRWUHTXLUHG
XX Nasal catheter:7KLVLVD
FR catheter, which is passed
XX Head box: Oxygen delivery, 7 - 10 L/min.
to the back of the nasal
cavity. The catheter is placed
at a distance equal to that
from the side of the nostrils
to the inner margin of the
eyebrow
Oxygen delivery:/PLQ+XPLGL¿FDWLRQQRWUHTXLUHG
XX Nasopharyngeal catheter:7KLVLVD)5FDWKHWHU
which is passed to the pharynx just below the level of
uvula. The catheter is placed at a distance equal to that
from side of the nostrils to the front of ear
Capillary blood glucose mvonitoring, Oxygen therapy

Side effects
XX Fatigue
XX Nasal dryness/bloody nose
XX Morning headache

Oxygen delivery:/PLQ+XPLGL¿FDWLRQLVUHTXLUHG
 41
Model OSPE for Practice
In this chapter few model OSPE stations are given related to the given OSPE stations. They can also be
comprising of X-rays, instruments, photographs, clinical acquainted with other OSPEs from different other clinical
& laboratory data and case scenarios. Students are advised problems in light of these examples to prepare themselves
to go through these and think of other possible questions optimally for examination.

OSPE station: 1
Instruction to the student
Please look at the X-ray and answer the questions given below -
1. Name 3 findings in this X-ray.
2. What is the probable diagnosis?
3. Name 2 other radiological features you expect in this disease?
4. What is the basic pathology of the disease?
5. Write 2 common way of presentation.

OSPE station: 2
Instruction to the student
Please look at the X-ray and answer the following questions -
1. Write 3 important findings on this X-ray.
2. What is the likely diagnosis?
3. Write two important investigations to reach a diagnosis.
4. Name the major biochemical change in the blood that determine the pathological
consequence of the disease.
5. Outline the principal of management.
 :KDWLVWKHVSHFLILFWUHDWPHQWRIWKLVFRQGLWLRQ"
OSPE station: 3

CXR of a 7 years old boy with fever, cough & breathlessness
Instruction to the student
Please look at the X-ray and answer the following questions -
1. Write down 2 important findings in this X-ray.
2. What is your radiological diagnosis?
3. Mention 2 important diseases that may give rise to these findings.
4. Write the findings on chest examination that you expect here
Model OSPE

5. What investigations will you do to confirm the diagnosis?

OSPE station: 4
Instruction to the student
Please look at the X-ray and answer the following questions -
1. Mention 3 findings that you see in this X-ray.
2. What is your radiological diagnosis?
3. Mention 3 important information that you may need in history.
329

4. Name 5 relevant investigations that will help you to reach the diagnosis.
 330 Step on to Paediatrics

OSPE station: 5
Instruction to the student
Please look at the X-ray and answer the questions given below -
1. Write down the findings present in this chest X-ray.
2. What is your radiological diagnosis?
3. Mention 3 important organisms responsible for this change.
4. Write the findings on chest examination that you expect in this patient.
5. Name 3 important complications those may occur if it remains untreated.
OSPE station: 6
This is an X-ray of a 12 months old boy presented with blue lips since birth and
growth failure.
Instruction to the student
Please look at the X-ray and answer the following questions -
1. What do you see in this chest X-ray ?
2. What is your radiological diagnosis?
3. What the cardiac anomalies that is present in this disease?
4. Write 3 important complications of this disease.
OSPE station: 7
This is an X-ray of a 7 months old child admitted with cough, wheeze &
breathlessness.
Instruction to the student
Please look at the x ray and answer the following questions -
1. Mention 3 important findings present in this chest X-ray.
2. What is your radiological diagnosis?
3. Name the most important organism responsible for this disease.
4. What is the mainstay of treatment of this illness?
OSPE station: 8
Instruction to the student
Please look at the photograph and answer the questions -
1. What do you see in the photograph?
2. What is the most likely diagnosis?
3. What organism is responsible for the disease?
4. Write down the systemic complication related to this skin lesion.
5. Write down two drugs used to treat this skin lesion.
OSPE station: 9
7KLVLVWKHNDU\RW\SHRIDPRQWKROGEDE\IURPD\HDUVROGPRWKHU7KLVEDE\
ZDVQRWJURZLQJSURSHUO\IDFLQJGLI¿FXOWLHVWRIHHGDQGKDGDV\VWROLFPXUPXURQ
precordial examination.
Instruction to the student
Model OSPE

Please look at the photograph and answer the questions -

1. Write comment on the above karyotype.
2. What is your diagnosis?
3. Write 5 important clinical features of this baby.
4. Write 3 important cardiac defects associated with this condition.
 Step on to Paediatrics 331

OSPE station: 10
This photograph is taken from a 6 years old child presented with general-
ized oedema and scanty urine.
Instruction to the student
Please look at the photograph and answer the questions -
1. What is your provisional diagnosis?
2. Name 4 important investigations with findings that will help to reach the diagnosis.
3. Name 5 important complications that may develop in this disease.
4. Write the treatment of this disease.

OSPE station: 11
Instruction to the student
Please look at the photograph and answer the questions -
1. Mention 3 important features evident in this photo.
2. Mention 4 questions that you need to ask the mother to reach a diagnosis.
3. What investigation will you do to diagnose this child?
4. What complications can arise if this patient remains untreated?
5. What is the treatment of the disease and for how long?
OSPE station: 12
7KLVSKRWRJUDSKLVIURP\HDUVROGER\ZKRSUHVHQWHGZLWKJXPEOHHGLQJDQG
purpuric spots following an episode of viral infection 14 days back. O/E he was
mildly anaemic and had no organomegaly.
Instruction to the student
Please look at the photograph and answer the questions -
1. What is your likely diagnosis?
2. Write down 2 important investigations with expected findings to reach the
diagnosis.
3. Write down the treatment options for this disease.
OSPE station: 13
This is a photograph of a 2 years boy from a very poor family weighing 5kg who was
admitted with skin change and bipedal oedema.
Instruction to the student
Please look at the photograph and answer the questions -
1. Why these changes happen to the child?
2. What changes in the eyes can occur in this child?
3. Summerize the skin abnormalities you can see.
4. Write down the expected anthropometric findings in this child?
5. Outline the steps of management of this case.
OSPE station: 14
Instruction to the student
Model OSPE

Please look at the instrument provided and answer the question -

1. Identify the instrument.
2. Write down indications of its use.
3. Mention 4 contraindications of its use.
 332 Step on to Paediatrics

OSPE station: 15
Instruction to the student
Please look at the instrument provided and answer the questions -
1. Identify the instrument.
2. Write 4 important indications of its use.
3. Mention the sites for doing the procedure by this instrument.
OSPE station: 16
Instruction to the student
Please look at the instrument provided and answer the questions -
1. Identify the instrument.
2. Mention 2 important clinical use of it in paediatric patients.
3. Mention 5 important differential diagnoses of white patches in throat.
OSPE station: 17
A 7 years old girl presented with fever, swelling of knee and ankle joints one after another for 5 days & chest pain for
last 2 days. Her lab reports showed Hb 11gm/dl, TC of WBC 15,000/cmm, neutrophil 78%, lymphocyte 18%, monocyte
(65PPCRP 24 mg/L and $62WLWUH,8/
Instruction to the student
Go through the scenario and answer the following questions-
1. What abnormalities are present in the data?
2. What is your likely diagnosis?
3. Name 4 other investigations you think relevant to this case.
4. What immediate measure will you take in this case?
5. What long term complications can develop if this patient is not managed properly?
OSPE station: 18
$\HDUVROGER\SUHVHQWHGZLWKLUUHJXODUIHYHUDQRUH[LDDQGRFFDVVLRQDOJXPEOHHGLQJIRUODVWPRQWK+LV&%&
VKRZHG+EJPGO7&RI:%&FPPQHXWURSKLOO\PSKRF\WHDQGDW\SLFDOFHOOVSODWHOHWFRXQW
FPP
Instruction to the student
Go through the scenario and answer the following questions-
1. Summerise the abnormalities in the Haemogram.
2. What is your likely diagnosis?
3. What findings do you expect in physical examination and in the peripheral blood film?
4. How will you confirm the diagnosis?
5. Name the different steps of treatment of the disease.
OSPE station: 19
A 14 months old child presented with high fever and vomiting for 2 days and few attacks of generalized convulsions
prior to hospitalization. His &6)ZDVKD]\DQGKDGJOXFRVHPJGOSURWHLQPJGOFKORULGHPHTOFHOOV
cmm mostly neutrophil.
Instruction to the student
Go through the scenario and answer the following questions-
Model OSPE

1. Comment on the case scenario.

2. What is the diagnosis?
3. Name 2 common organisms responsible for this problem.
4. Outline the treatment plan for this child.
5. Name 4 complications that may occur, if not properly treated.
 Step on to Paediatrics 333

OSPE station: 20
Lab reports of an 8 years old boy who presented with polyuria and short stature revealed Hb 7g/dl, platelet count
FPP6FUHDWLQLQH—PRO/%ORRGXUHDPPRO/6.PPRO/6&DPPRO/LQFUHDVHG6
PO4 and blood pH 7.2.
Instruction to the student
Go through the scenario and answer the following questions -
1. What abnormalities do you see in the lab data?
2. What is your probable diagnosis?
3. Name 4 important clinical presentations of this patient.
4. Outline 5 principles of management.
5. What is the specific treatment for this patient?
OSPE station: 21
A 20 hours old baby presented with jaundice of face, trunk and palm.
Instruction to the student
Go through the scenario and answer the following questions -
1. Enumerate 2 possible important causes of this jaundice.
2. Write 5 investigations which will help to explain the aetio-pathogenesis.
3. Write down 2 options of treatment required for this baby.
4. What can happen if this baby remains untreated?
OSPE station: 22
A 3 years old boy who had been suffering from recurrent cough and wheeze suddenly developed severe respiratory
distress. On examination you noted profuse rhonchi in both lungs.
Instruction to students
Go through the scenario and answer the following questions-
1. What is your diagnosis?
2. Name 5 important parameters to be used to assess the severity of the condition.
3. Outline 5 immediate steps of managing the situation.
4. What informations do you think important to classify the disease?
OSPE station: 23
A 9 months old child weighing 7 kg is admitted with frequent, loose watery stool & vomiting for last 2 days.
Instruction to students
Go through the scenario and answer the following questions-
1. What clinical parameters will you consider to assess the dehydration of this child?
2. Name 3 important organisms responsible for this diarrhoea.
3. Write 2 investigations important for this case.
4. Outline the management of this child if he is severely dehydrated.
5. What fluid can be used to rehydrate this child?
 1DPHLPSRUWDQWFRPSOLFDWLRQVWKRVHFDQDULVHLIKHLVQRWSURSHUO\UHK\GUDWHG"
OSPE station: 24
$PRQWKVROGJLUOLVDGPLWWHGZLWKORZJUDGHIHYHUUXQQ\QRVHEDUNLQJFRXJKVWULGRUDQGEUHDWKLQJGLI¿FXO\
Model OSPE

Instruction to students
Go through the scenario and answer the following questions-
1. What is your likely diagnosis?
2. Write down 3 important organisms responsible for this illness.
3. What simple investigation will help to diagnose the case?
4. Write 4 important options of treatment.
 334 Step on to Paediatrics

OSPE station: 25
Please go through the following CSF data of a 18-month old child who presented with fever and recurrent attacks of
generalized convulsions and answer the attached questions -
a. Pressure: High
b. Appearance: Hazy
c. WBC: 320/cmm
d. Protein: 97 mg/dl
e. Glucose: 40 wgl/dl
I&KORULGHPPRO/
1. What abnormality do you see here?
2. What is the likely diagnosis?
3. What organism, commonly associated with?
4. Write the name of the drugs, effective here

OSPE station: 26
Instruction to students
Go through the scenario given below and answer the questions -
A 7-year old boy is admitted with puffy face & history of scanty high coloured urine. His laboratory reports are given
below-
a. Urine R/M/E shows RBC, RBC cast, Mild proteinuria
b. Blood biochemistry shows S.Na+ : 130 mmol/L, K+PPRO/&,PPRO/6&UHDWLQLQHPJGO

1. What is your inference from the laboratory data?

2. Write down the diagnosis?
3. Name one drug which is required immediately.
4. Name 3 complications of this disease.

OSPE station: 27
Instruction to students
*RWKURXJKWKHJLYHQFOLQLFKDHPDWRORJLFDOSUR¿OHRID\HDUROGER\ZKRSUHVHQWHGZLWKJXPEOHHGLQJDQGDQVZHUWKH
following questions -
a. HP : 10gm/dl,
b. WBC : 9000/cmm
c. 40,000/cmm
d. PBF : Non-specific
e. BT : 10 minute
I &7PLQXWH
1. What is the likely diagnosis?
2. What investigations will help you to confirm the diagnosis?
3. What are the treatment options?
Model OSPE
Annexure
Recipe/Composition of
(a) F-75 and F-1 00 . . . . . . . . . . . 327
(b) Oral Rehydration Salt [ors] . . . . . . . . . 328
(c) ReSoMal . . . . . . . . . . . . . 328
(d) Electrolyte-mineral solution . . . . . . . . . 328
Bilirubin charts
XX For babies < 35 weeks, < 1000g . . . . . . . . . 329
XX For babies < 35 weeks, 1000-1499g . . . . . . . . 330
XX For babies < 35 weeks, 1500-1999g . . . . . . . . 331
XX For babies < 35 weeks, > 1999g . . . . . . . . . 332
XX For babies at 35-37 + 6 weeks . . . . . . . . . 333
XX For babies at 38 + 0 weeks or older . . . . . . . . 334
Growth charts
XX Weight-for-age percentile: Boys, birth to 36 months . . . . . 335
XX Weight-for-age percentile: Boys, 2 to 20 years . . . . . . 336
XX Length-for-age percentile: Boys, birth to 36 months . . . . . 337
XX Stature-for-age percentile: Boys, 2 to 20 years . . . . . . 338
XX Head circumference-for-age percentile: Boys, birth to 36 months . . 339
XX Weight-for-length percentile: Boys, birth to 36 months . . . . . 340
XX Weight-for-stature percentile: Boys, 2 to 20 years . . . . . 341
XX BMI-for-age percentile: Boys, 2 to 20 years . . . . . . . 342
XX Weight-for-age percentile: Girls, birth to 36 months . . . . . 343
XX Weight-for-age percentile: Girls, 2 to 20 years . . . . . . 344
XX Length-for-age percentile: Girls, birth to 36 months . . . . . 345
XX Stature-for-age percentile: Girls, 2 to 20 years . . . . . . 346
XX Head circumference-for-age percentile: Girls, birth to 36 months . . 347
Annexure

XX Weight-for-length percentile: Girls, birth to 36 months . . . . . 348

XX Weight-for-stature percentile: Girls, 2 to 20 years . . . . . . 349
XX BMI-for-age percentile: Girls, 2 to 20 years . . . . . . . 350
335
 336 Step on to Paediatrics

Recipe/Composition of
(a) F-75 and F-100
Amount for F-75 Amount for F-100

Type of milk Ingredients

Dried skimmed milk 25 g 80 g

Sugar 70 g 50 g

&HUHDOÀRXU 35 g --

Dried skimmed Vegetable oil 30 g (or 35 ml) J or 70 ml)

milk
Electrolyte Mineral mix 20 ml 20 ml

Water: make up to 1000 ml 1000 ml

Dried whole milk 35 g 110 g

Sugar 70 g 70 g

&HUHDOÀRXU 35 g --

Dried whole Vegetable oil 20 g (or 20 ml) 30 g (or 35 ml)

milk
Electrolyte Mineral mix 20 ml 20 ml

Water: make up to 1000 ml 1000 ml

Respiratory Tract, F-75 and F-1000

Full-cream cow’s milk 300 ml 880 ml

Sugar 70 g 75 g

&HUHDOÀRXU 35 g --
Full-cream
cow’s milk Vegetable oil 20 g (or 20 ml) 20 g (or 20 ml)

Electrolyte Mineral mix 20 ml 20 ml

Water: make up to 1000 ml 1000 ml

(b) Oral Re-hydration Salt [ORS]

 Step on to Paediatrics 337

WHO ORS Na+ K+ Cl-

WHO ORS Fluid source
Composition (Low (mmol/L) (mmol/L) (mmol/L)
(Old) g/L
osmolarity) g/L
Glucose 13.5 20 Stomach 20-80 5-20 100-150

NaCl  3.5 Small intestine 100-140 5-15 90-120

Trisodium citrate 2.9 2.9 Ileostomy 45-135 5-15 20-120

KCl 1.5 1.5 Diarrhoeal
10-90 10-80 10-110
stool
Molar contents mmol/L mmol/L
Glucose 75 111 (e) Electrolyte-mineral solution
Na 75 90
Molar content
K 20 20 Ingredients Quantity (g)
of 20 ml
Cl  80 Potassium Chloride 224 24 mmol
Citrate 10 10 Tri-potassium Citrate 81 2 mmolv
Total osmolarity 245 mmol/L 311 mmol/L Magnesium Chloride  3 mmol

(c) ReSoMal Oral Re-hydration solution Zinc Acetate 8.2 ȝPRO

Copper Sulphate 1.4 ȝPRO
Ingredients Amount
Water: make up to 2500 ml
Water (boiled and cooled) 850 ml
WHO-ORS (New low osmolarity
One 500 ml packet
formulation)
Sugar 20 g :HLJKWEDQGWDEOHIRUµ1(:¶8SFRPLQJ
Electrolyte-mineral solution PO FDCs for TB

G (OHFWURO\WHFRQWHQWRIYDULRXVERG\ÀXLGV

Number of Tables
Weight Bands (Kg) Intensive Phase Countinuation Phase
RHZ (mg) E (mg) RH (mg)
75/50/150 per tablet 100 per tablet 75/50 per tablet
4-7 1 1 1 Composition of ORS, ReSoMal
8-11 2 2 2
12-15 3 3 3
 4 4 4
25+ Use adult dosages and preparations
Bilirubin chart 1 338 Step on to Paediatrics
Step on to Paediatrics 339

Bilirubin chart 2
Bilirubin chart 3 340 Step on to Paediatrics
Step on to Paediatrics 341

Bilirubin chart 4
Bilirubin chart 5 342 Step on to Paediatrics
 1. American Academy of Pediatrics Subcommittee on Hyperbilirubinaemia, 2. Clinical Practice Guideline: Management of hyperbilirubinaemia in the newborn
infant 35 orPRUHZHHNVRIJHVWDWLRQ3HGLDWULFV+RUQ$HWDOPhototherapy and exchange transfusion for neonatal hyperbilirubinaemia:
Step on to Paediatrics

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Morris BH et al. Aggressive vs conservative phototherapy for infants with extremely low birth weight. New England Journal of Medicine. 2008; 359(18):1885-
343

4XHHQVODQG0DWHUQLW\DQG1HRQDWDO&OLQLFDO*XLGHOLQH01951HRQDWDOMDXQGLFH

Bilirubin chart 6
Growth chart 1 344 Step on to Paediatrics
Step on to Paediatrics 345

Growth chart 2
 346 Step on to Paediatrics

cm in in

42 42
105
41 97th 41
95th
40 90th 40
100
39 75th 39

38 50th 38
95
37 25th 37

36 10th 36
90 5th
35 3rd 35

34 34
85
33 33

32 32
80
31 31

30 30
75
29 29

28 28
70
27 27

26 26
65
25 25

24 24
60
23 23

22 22
55
21 21

20 20
50
19 19
Growth chart 3

18 18
45
17 17
cm in in
Birth 3 6 9 12 15 18 21 24 27 30 33 36
Age (months)
Step on to Paediatrics 347

Growth chart 4
Growth chart 5 348 Step on to Paediatrics
Step on to Paediatrics 349

Growth chart 6
Growth chart 9 350 Step on to Paediatrics
Step on to Paediatrics 351

Growth chart 10
Growth chart 11 352 Step on to Paediatrics
Step on to Paediatrics 353

Growth chart 12
Growth chart 13 354 Step on to Paediatrics
Step on to Paediatrics 355

Growth chart 14
Growth chart 15 356 Step on to Paediatrics
Step on to Paediatrics 357

Growth chart 16
358 Index
Step on to Paediatrics 359

Index
Index 360 Step on to Paediatrics
Step on to Paediatrics 361

Index
Index 362 Step on to Paediatrics
Step on to Paediatrics 363

Index
Index 364 Step on to Paediatrics