2023 Manual of MSK US A Self Study Protocol Medical Ambosscom

Mark H.
Greenberg
Alvin Lee Day
Suliman Alradawi
2023
Manual of
Musculoskeletal
Ultrasound
A Self-Study, Protocol-Based Approach
Manual of Musculoskeletal Ultrasound
Mark H. Greenberg • Alvin Lee Day
Suliman Alradawi
Manual of Musculoskeletal
Ultrasound
A Self-Study, Protocol-Based Approach
Mark H. Greenberg Alvin Lee Day
Division of Rheumatology Division of Rheumatology
Department of Internal Medicine Columbia VA Health Care System
University of South Carolina School of Department of Internal Medicine
Medicine, Columbia, SC University of South Carolina School of
USA Medicine, Columbia, SC
USA
Suliman Alradawi
Department of Medicine, Division of
Rheumatology
Advocate Christ Medical Center, Advocate
Medical Group, Chicago, IL
USA
ISBN 978-3-031-37415-9 ISBN 978-3-031-37416-6 (eBook)

https://doi.org/10.1007/978-3-031-37416-6
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To my wife, ultrasound model, partner and
best friend, Brenda.
Thank you for your constant support,
patience, humor, and sacrifice in creating
this book.
—MHG
To my wife, Stani, who filters my ideas,
champions my endeavors, and centers
our home.
—ALD
To my father, Tayssir, who made me a curious
lifelong learner. To my mother, Sameera, who
always supported any project I set my mind
to achieve without hesitation. To my siblings,
Kenan, Shahlan, and Tala, who inspire me to
be a better version of myself every day. To my
best friend and colleague, Dr. Amisha Shah,
whose encouragement and optimism helped
inspire the creation of this work.
—SA
Foreword
Doctors Greenberg, Day, and Alradawi have created a first-of-its-kind book on

learning how to perform musculoskeletal ultrasound. Despite musculoskeletal ultra-
sound holding great potential for many clinicians across a broad spectrum of spe-
cialties and subspecialties, it is presently underutilized. A primary reason for this
underutilization is the difficulty level and time needed to learn a new clinical skill
set that involves a wide variety of anatomical structures and clinical pathologies.
This situation has been compounded by the limited availability of qualified instruc-
tors in musculoskeletal ultrasound.
The authors have expertly addressed these issues with a learning approach that is
simple, straightforward, clinically-oriented, protocol-based, and self-directed. The
development of this approach draws on their extensive experience in the clinical
application of musculoskeletal ultrasound and the many lessons learned from teach-
ing a wide variety of learners over the years. Once the basic terminology and prin-
ciples of ultrasound scanning are presented in the first chapter, learners can readily
make great use of the book by selecting anatomical regions, structures, and scan-
ning protocols most relevant to their learning and clinical practice needs.
Chapters are based on standard approaches to specific musculoskeletal regions
such as the anterior, posterior, medial, and lateral areas of the knee. Each chapter
begins with a chapter abstract followed by sections covering the reasons to perform
the particular ultrasound study, questions to be answered by the study, basic regional
physical and sonographic anatomy, relevant clinical comments including discussion
of pathology, as well as potential pitfalls. The chapter ends with easy-to-follow
step-by-step protocols for scanning and checklists for simplicity and consistency
then a list of references. The diagnostic strength of using the ultrasound protocols
for identifying specific pathology is also indicated when relevant.
Emphasis is placed on learning to capture normal clinically relevant ultrasound
images of the major musculoskeletal regions of the body and identifying important
anatomical structures involved in common musculoskeletal pathology in that region.
Learners are greatly aided in acquiring the critical knowledge base for scanning so
many anatomical structures involved in musculoskeletal pathologies with the use of
vii
viii Foreword
catchy mnemonics, simple yet memorable illustrations, cartoon images, and high-
quality normal ultrasound images with relevant structures identified.
For those new to ultrasound a thorough appreciation of the normal is essential in
learning to recognize and understand clinical pathology. The authors discuss essen-
tial aspects of common pathology and tips and tricks to recognize and remember
them but do not present pathological ultrasound images. Instead, they provide
extensive definitive references on pathology to supplement the content of each
chapter.
This book will be of great value to those new to ultrasound, those with consider-
able experience performing ultrasound but new to musculoskeletal ultrasound, and
those wanting to expand their musculoskeletal ultrasound knowledge and skill. The
authors have not only delivered a powerful and exciting new way to learn musculo-
skeletal ultrasound but are also introducing a new approach to ultrasound education
in general. Their contribution deserves special recognition for advancing ultrasound
education and the role it can play in ultimately advancing patient care.
Professor of Medicine and Past Dean Richard A. Hoppmann, MD,

University of South Carolina School of Medicine FACP, FAIUM
Columbia, SC, USA
Preface
While teaching musculoskeletal ultrasound, we observed that students learned best

when imaging defined structures guided by commonsense instructions.
This experience led to our writing various protocols with logical instructions for
each step, including probe movements.
After achieving the ability to capture normal images, the next step was to remind
the reader why we were doing a particular examination, that is, what pathology to
look for in an image.
Each chapter starts with the clinical questions we want an ultrasound examina-
tion to answer and basic anatomy. With so much anatomy to learn, we liberally used
simple illustrations, whimsical cartoons, and often corny mnemonics to aid in
recollection.
We discuss pathologic entities discernible on ultrasound, pitfalls to avoid, and
imaging tricks of the trade.
Our goal is to guide the reader to proficiency in musculoskeletal ultrasound with-
out an instructor being present.
Columbia, SC, USA Mark H. Greenberg

Columbia, SC, USA Alvin Lee Day
Chicago, IL, USA Suliman Alradawi
ix
Contents
1 Introduction/Getting Started�� 1

Why Learn Musculoskeletal Ultrasound?�� 1
Why a Protocol-Driven Approach?�� 1
The Goals of This Manual �� 2
Tools�� 2
Technique�� 6
Tissues�� 9
Sonographic Pathology by Structure �� 15
Artifacts: Friend or Foe?�� 19
Organization of the Manual �� 21
References�� 23
2 Volar Wrist�� 27
Basic Anatomy �� 27
Clinical Comments�� 29
Pitfalls�� 31
Method �� 32
References�� 42
3
Dorsal Wrist (Radial, Dorsal, Ulnar) �� 45
Necessary Basic Anatomy�� 46
Pitfalls�� 55
Method �� 56
References�� 73
4 Fingers�� 77
Necessary Basic Anatomy (Fig. 4.1)�� 78
Pitfalls�� 92
Method �� 93
References�� 106
xi
xii Contents
5 Hand Arthropathies �� 109

Necessary Anatomy �� 109
Pitfalls�� 128
Method �� 130
6 Anterior Elbow�� 147
Anatomy�� 147
Pitfalls�� 155
Method �� 155
7 Posterior Elbow�� 167
Anatomy�� 167
Pitfalls�� 170
Method �� 171
8 Lateral Elbow �� 177
Anatomy�� 177
Pitfalls�� 182
Method �� 182
9 Medial Elbow�� 189
Pitfalls�� 194
Method �� 195
10 Shoulder�� 207
Pitfalls�� 227
Method �� 228
11 Anterior Ankle�� 255
Basic Anatomy (Fig. 11.1) �� 255
Pitfalls�� 267
Method �� 267
Contents xiii
12 Posterior Ankle and Heel�� 279

Bony Anatomy �� 280
Pitfalls�� 288
Method �� 289
13 Lateral Ankle�� 299
Pitfalls�� 309
Method �� 310
14 Medial Ankle�� 323
Basic Bone Anatomy (Fig. 14.1)�� 323
Pitfalls�� 332
Method �� 333
15 Forefoot and Toes �� 347
Pitfalls�� 360
Method �� 361
16 Anterior Knee�� 373
Pitfalls�� 379
Method �� 380
17 Posterior Knee�� 391
Necessary Basic Anatomy: Posterior Knee�� 392
Ligament Damage�� 395
Nerve Damage�� 396
Blood Vessel Pathology�� 396
Fabella Pathology�� 396
Cartilage Damage�� 397
Meniscal Damage�� 397
Pitfalls�� 397
Method �� 397
xiv Contents
18 Lateral Knee �� 409

Anterolateral Ligament�� 412
Lateral Collateral Ligament �� 412
Lateral Meniscus�� 413
Biceps Femoris Tendon�� 414
Common Peroneal Nerve �� 414
Pitfalls�� 414
Method �� 415
19 Medial Knee�� 425
Basic Anatomy (Fig. 19.1) �� 426
Pes Anserine Tendons and Bursa �� 426
Medial Collateral Ligament Bursitis�� 429
Medial Meniscus�� 429
Pes Anserine Tendons and Bursitis�� 430
Snapping Pes Anserine Tendons�� 430
Infrapatellar Branch of the Saphenous Nerve Damage�� 431
Pitfalls�� 431
Method �� 432
20 Anterior Hip �� 439
Ligaments�� 441
Neurovascular Bundle�� 442
Anterior Hip (Joint) Recess �� 442
Hip Joint�� 443
Iliopsoas Muscle, Tendon, and Bursa�� 443
Tensor Fascia Lata and Sartorius �� 443
Rectus Femoris�� 443
Joint Effusion and Synovitis�� 444
Iliopsoas Bursitis�� 444
Labrum Abnormalities �� 445
Postsurgical Hip �� 445
Tendon and Muscle Abnormalities�� 446
Snapping Hip Syndrome�� 446
Calcific Tendinosis�� 447
Diabetic Muscle Infarction�� 447
Meralgia Paresthetica�� 448
Contents xv
Inguinal Lymph Nodes�� 448

Pitfalls�� 449
Method �� 449
21 Posterior Hip�� 461
Anatomy�� 461
Piriformis Syndrome�� 465
Ischiogluteal Bursitis �� 465
Pitfalls�� 465
Method �� 466
22 Lateral Hip �� 473
Tendinosis and Tendon Tears �� 478
Snapping Iliotibial Band and External Lateral Snapping
Hip Syndrome �� 478
Morel-Lavallee Lesion �� 479
Tensor Fascia Latae Tendinopathy�� 479
Bursal Abnormalities �� 480
Proximal Iliotibial Band Syndrome �� 480
Pitfalls�� 480
Method �� 481
23 Medial Hip�� 489
Tendinosis and Partial-Thickness Tears �� 491
Muscle Strain �� 492
Adductor Insertion Avulsion Syndrome�� 492
Other Sources of Pain�� 492
Method �� 492
24 Crystalline Disease �� 497
Gout�� 498
Calcium Pyrophosphate Deposition Disease �� 500
Sonographic Overlap �� 501
Pitfalls�� 502
Method �� 502
xvi Contents
25 Enthesopathy�� 513
Special Clinical Consideration: Inflammatory Arthritis
Differentiation�� 517
Pitfalls�� 517
Method �� 518
Index�� 533
Contributors
Suliman Alradawi (Illustrator) Department of Medicine, Division of

Rheumatology, Advocate Christ Medical Center, Advocate Medical Group,
Chicago, IL, USA
Alvin Lee Day Division of Rheumatology, Columbia VA Health Care System,
Department of Internal Medicine, University of South Carolina School of Medicine,
Columbia, SC, USA
Mark H. Greenberg Division of Rheumatology, Department of Internal Medicine,
University of South Carolina School of Medicine, Columbia, SC, USA
xvii
Chapter 1
Introduction/Getting Started
Musculoskeletal ultrasound (MSUS) has grown by leaps and bounds over the past
decade due to technological advances and the need for inexpensive point-of-care
imaging. The modality is indispensable in physiatry, orthopedics, podiatry, and
rheumatology. However, gaining operational proficiency can be challenging.
Why Learn Musculoskeletal Ultrasound?
Health care professionals who have achieved competence in MSUS will attest to the
difference in their practices. Orthopedic surgeons use MSUS to understand the
function and structure of injured joints and surrounding soft tissues to better plan,
or even avoid, surgery. Podiatrists can now instantly confirm soft tissue diagnoses
involving the heel and ankle. Physiatrists and sports medicine specialists use sonog-
raphy for rapid and precise injury assessment, thus formulating effective rehabilita-
tion and accurate return-to-activity timetables. Ultrasound is integral to the field of
regenerative medicine. Rheumatologists employ MSUS to define structural, func-
tional, and inflammatory conditions to inform better therapeutic decisions.
Why a Protocol-Driven Approach?
Protocol-driven examinations improve the efficiency of ultrasound (US) examina-

tions [1]. We prefer protocols since we less frequently perform certain investiga-
tions, and consistently obtaining a set of standard views ensures that all necessary
images are acquired.
The contents do not represent the views of the U.S. Department of Veterans Affairs or the United
States Government.
© The Author(s), under exclusive license to Springer Nature 1
Switzerland AG 2023
M. H. Greenberg et al., Manual of Musculoskeletal Ultrasound,
https://doi.org/10.1007/978-3-031-37416-6_1
2 1 Introduction/Getting Started
The Goals of This Manual
This Manual demonstrates MSUS protocols that evaluate conditions commonly

found in clinical practice. We show image acquisition methods in the illustrations
along with the goal image. Readers may freely use these protocols in their clinical
practice. We designed the order of image acquisition and hints intended to prevent
the examination from grinding to a halt.
We also attempt to demystify the US and smooth the way from “Point A” to
“Point B,” enabling the US student to examine a normal joint. It is challenging to
recognize pathology if one cannot capture and appreciate the image of normal struc-
tures. While we demonstrate some pathological conditions, this book does not focus
on pathology. Many excellent books will serve that purpose; we have listed but a
few [2–5].
Before appreciating pathology, the practitioner of MSUS needs to understand the
echogenic appearance of different tissue structures and the basic anatomy and func-
tion of the region-of-interest (ROI). The next step is to learn to acquire these normal
images logically and consistently. We have employed the hints that our medical
students, residents, and fellows have found useful when learning US.
The last step is to understand the context. What can an US exam tell us in a par-
ticular clinical circumstance? What questions can be answered by using US? In
which situations is the US diagnostically strong, weak, or somewhere in between?
What are the common pitfalls and normal variants?
Many excellent US books meticulously describe normal and abnormal sonoanat-
omy, but our focus is on clinical utility and image acquisition. The authors acknowl-
edge that learning sonoanatomy is daunting. We employ various mnemonic devices,
including cartoon images, acronyms, word associations, phrases, and connections to
prior knowledge. The illustrations aspire to be simple yet memorable visualizations
of key concepts.
Tools
The Ultrasound Machine
A basic understanding of the control buttons and knobs of your US machine is nec-
essary to acquire optimal images. Thankfully, the controls are comparable on most
devices, although some variations exist. Learning a vehicle’s controls is the first step
to driving. We suggest reviewing the reference below, in addition to your US
machine‘s “quick-start” guide for further information [6]. Below is a brief descrip-
tion of a typical US machine controls:
Depth/frequency: This controls the depth of penetration of the US beam, deter-
mined by the individual transducer’s frequency range. The image depth is noted
Tools 3
in centimeters on the ultrasound viewscreen. Lower frequencies achieve higher

depth scans but at the cost of less resolution, thus fewer details.
Gain: This controls the number of incoming echoes processed by the US machine.
The higher the gain, the brighter the image, with the downside of increased
noise, artifacts, and decreased contrast in fine detail. Some devices have time–
gain controls (TGC) to adjust the returning ultrasound beam at specific depths.
By changing the TGC, you can focus on enhancing the echotexture of a spe-
cific structure at a particular depth. However, a common mistake is adjusting
the gain to focus on a particular depth when changing the frequency is
required.
Color flow Doppler: This button activates color flow Doppler (CF), which detects
tissue movement and direction.
Power Doppler: This button activates power Doppler (PD), which detects the
strength of tissue movement, making it more sensitive to tissue (blood) flow.
Pulse repetition frequency: This knob works with Doppler imaging. The lower the
pulse repetition frequency (PRF), the more Doppler signals are seen on the
image, at the risk of increased noise and artifacts.
Freeze frame, image recording, cine: The freeze-frame button locks in the image
so that you can save/record. Likewise, a video clip is helpful for dynamic US
studies and documenting ultrasound-guided procedures. The sonographer can
usually prolong the video clip duration to capture more extended studies. Video
clip capture controls differ somewhat in each machine.
Distance measurements: Caliper buttons allow measurements between two points.
Measuring the cross-sectional area (CSA) of the object requires measuring the
height and width and letting the machine calculate the size. Alternatively, many
devices permit the sonographer to directly outline the structure’s circumference
to calculate a CSA.
Presets: These are buttons with standard settings to make it simpler to achieve the
settings needed to evaluate specific structures. For example, a preset for a hand
will have a higher frequency than for a hip. Presets do not work on every person
since you may have a thin individual in whom you can use a higher frequency to
look at the hip.
Probe (Transducer)
The probe is commonly corded and interfaces the patient to the US machine. The
probe emits sound waves to a target, receives the reflected waves, and transmits
them to the US machine and viewscreen. Probes used for MSUS are often linear or
curvilinear and have varied footprint sizes. Each probe has a predetermined fre-
quency range.
Terms
Terms are jargon used to communicate in the US world.

B mode scanning is “brightness” mode, which demonstrates a grayscale image.
Attenuation is the weakening of the returning ultrasound beam with a loss of
resolution.
Echotexture is the appearance of structures and tissues in US images [7].
Echogenicity (Fig. 1.1) describes a tissue’s ability to reflect or transmit US waves
compared to surrounding tissues and its subsequent appearance on the US screen
[8]. Images can be hyperechoic (bright white), hypoechoic (gray), or anechoic
(black). Heterogeneous is a mixture of light and dark. Isoechoic describes that
the structure has a similar echogenic appearance to adjacent tissue, sometimes
making it difficult to discern. We recognize body structures and tissues by their
different sonographic features. Recognizable structures include bone, blood ves-
sels, nerves, tendons, ligaments, muscles, cartilage, synovial tissue, and
ligaments.
Anisotropy (Figs. 1.2a, b, and 1.3) is described as distortion and loss of clarity of
an US image when the US wave does not fall upon a structure at precisely 90°
[9]. The image will appear artifactually hypoechoic. Minute changes in the angle
of the US wave (insonation angle) may cause a structure to “disappear.”
Structures that are affected include ligaments, nerves, and particularly tendons.
Anisotropy and the degree of anisotropy can also help identify these structures.
The frequency of the US wave dictates image quality. The higher the frequency, the
more detail is revealed, albeit at the expense of diminished depth penetration [8].
The goal is to visualize the ROI with the highest frequency probe possible to
maximize sonographic detail. For MSUS, we typically employ higher-frequency
probes (10–22 MHz).
Longitudinal axis (LAX) is a notation for a longitudinal probe direction in which
images are parallel to or line up with the extremity. Many call this the long-axis
view [8].
Transverse axis (TAX) is a notation for the transverse orientation of the image.
This cross-sectional view is alternatively referred to as the short-axis view [8].
Hyperechoic Isoechoic Hypoechoic Anechoic
Fig. 1.1 Echogenicity

Tools 5
a b
Fig. 1.2 Anisotropy is created when the angle of the probe is not perpendicular and some or all of
the reflected ultrasound waves do not return to the probe. (a) No anisotropy since the returning
ultrasound wave is fully acquired by the probe. (b) Anisotropy is produced since the returning
ultrasound wave is not detected by the probe
Fig. 1.3 Tendon in

longitudinal view. Note the
hyperechoic echotexture
due to the parallel fibrils.
Anisotropy is appreciated
distally
Note that the classic definition of LAX or TAX probe orientation is with respect to
an extremity’s axis. Sometimes we may buck tradition by describing the probe‘s
orientation with respect to a particular structure rather than the extremity in
which the structure resides. When this does occur, we describe it in the text. An
example would be when evaluating the subscapularis tendon, a structure oriented

90° to the proximal upper extremity.
Grayscale ultrasound is an US image of tissues comprised of black, white, and
shades of gray [10]. Grayscale is the standard image in MSUS to which we may
add Doppler imaging.
Doppler imaging uses the Doppler effect to detect blood flow through a vessel [11].
Color flow Doppler tells us the direction of blood flow [11]. A helpful mne-
monic is “BART”: Blue Away, Red Toward.
Power Doppler appears as a single color, most commonly red or orange. It
does not tell the direction of blood flow and is considered by some to be more
sensitive than CF in detecting slow flow rates in small vessels [12]. PD is
helpful for detecting increased blood flow, which indicates neovascularization
or inflammation. To minimize PD artifact while not sacrificing sensitivity, we
often need to adjust the PRF downward from factory settings to show minimal
to no PD activity over uninvolved bones [13]. Steadying the hand that holds
the probe will further minimize artifacts.
Technique
This section describes how to use your US probe to obtain optimal images. The
technique is critical. The examiner should hold the probe comfortably with at least
one finger touching the patient for stability. Wrap the probe cord around the wrist or
behind the neck to avoid a distracting tug (Fig. 1.4).
Both the patient and the examiner must be comfortable [14]. The view screen
should be at eye level, directly in front of the examiner, to avoid head twisting. The
probe direction or orientation is up to the examiner. The probe has a fin or dot, called
Fig. 1.4 Avoiding cord tugs

Technique 7
a b
Fig. 1.5 Angling movements. (a) Heel-toe and (b) tilting
the probe marker, which corresponds to the dot on the viewscreen. Orient the probe
in whichever direction facilitates easy recognition of the structures in the
ROI. Routine probe movements are listed below. Of note, the terminology for these
maneuvers may differ among sources.
Angling Movements
1. Heel-toe (Fig. 1.5a) means that the probe footprint remains stationary, but the
transducer is angled about its long axis [10].
2. Tilting (Fig. 1.5b), alternatively called toggling, fanning, or rocking, means that
the probe footprint remains stationary, but the transducer is angled about its short
axis [15].
Dynamic Movements
1. Longitudinal slide (Fig. 1.6a) or LAX slide means to move the probe along the
long axis of the probe.
2. Transverse slide (Fig. 1.6b) or TAX slide is like the LAX slide, but the direction
of movement is along the short axis.
3. Rotation (Fig. 1.7) is when the probe is slowly spun to various degrees, with the
axis of rotation being the center of the transducer [15]. A rotation variant keeps
a b
Fig. 1.6 Dynamic movements. (a) Longitudinal slide and (b) transverse slide
Fig. 1.7 Dynamic

movement. Rotation
Tissues 9
one end of the probe stationary and then rotates the other end in one direction
and then the other. We find this maneuver invaluable to regain visualization of
narrow longitudinal objects such as injection needles. Rotation is critical for
obtaining orthogonal views of an ROI to confirm pathology [16]. Orthogonal
views depict the shape of an object in two perpendicular dimensions to create a
three-dimensional mental image of the object.
4. Compression occurs when the examiner firmly presses the transducer against
the surface of the ROI. With this maneuver, veins collapse, but arteries do not.
Also, compression will displace free fluid in a bursa or joint recess, but thick-
ened synovial tissue will not shift much. Be mindful that compression may inad-
vertently reduce PD activity in an image.
5. Floating the probe maintains a thick layer of US gel between the skin surface
and transducer to enhance the resolution of superficial structures.
Sonopalpation
Sonopalpation is a technique in which the examiner uses the transducer to delineate

pathology. One type of sonopalpation is compression, described above. There are
other types as well:
1. Pain-localizing sonopalpation is when the sonographer uses compression to
detect the point of maximal tenderness by reproducing pain. Once localized, the
examiner can sonographically interrogate the painful area for signs of pathology.
2. Dynamic sonopalpation is when the examiner holds the transducer in a fixed
position. The body part is moved passively or actively to determine the abnormal
movement of a ROI.
3. Combined pain-localizing and dynamic sonopalpation occurs when a maneu-
ver will reproduce or exacerbate pain while the examiner directly observes the
pathologic mechanism.
Tissues
Echogenic Features of Normal Tissues
Bone, being hyperechoic, is the most straightforward structure to visualize since it

reflects sound waves in total, rendering only the bony surface visible [17]
(Fig. 1.8).
Tendons (Fig. 1.9a, b) are hyperechoic due to their longitudinal, parallel fibrils [18].
In a longitudinal view, healthy tendons exhibit a “brush-like” pattern. However,
the fibrils appear as numerous hyperechoic dots and dashes in a cross-
sectional view.
Fig. 1.8 Bone
a b
Fig. 1.9 (a) Tendon in longitudinal view illustrating hyperechoic echotexture due to the parallel
fibrils. (b) Tendon in transverse view. Hyperechoic echotexture produces “dots and dashes”
Fig. 1.10 Ligament

(orange arrows) in
longitudinal view showing
similar, but less
conspicuous echotexture as
compared to tendon
Ligaments (Fig. 1.10) also have parallel longitudinal fibrils but are less hyperechoic
than tendons in longitudinal and transverse views. Therefore, the echotexture of
ligaments is less striking on US. Ligaments may be more difficult to view due to
anisotropy from their varying attachment points.
Tissues 11
Arteries and veins are anechoic to hypoechoic due to the blood inside (Fig. 1.11a)
[19]. Color flow Doppler detects the direction of flow in arteries and veins and
serves to delineate one from another (Fig. 1.11b). Power Doppler detects blood
flow in arteries and veins (Fig. 1.11c). Probe compression is a practical means to
differentiate veins from arteries, as veins will compress with probe compression
(Fig. 1.11d).
Nerves (Fig. 1.12a, b) appear as a mixture of hyperechoic and hypoechoic areas,
which convey a “honeycomb” appearance in TAX [20]. Alternatively, a normal
nerve in TAX may demonstrate several wavy hyperechoic lines, not entirely
parallel to each other. “Tram tracks” are often used to describe the sonographic
appearance of normal nerves in LAX. The outer hyperechoic epineurium pro-
duces two parallel lines that resemble tram tracks [21]. Linear hypoechoic nerve
fascicles alternate with hyperechoic connective tissue within the nerve itself, cre-
ating lines that parallel the epineurium. Nerves are more echogenic than muscles
but less echogenic than tendons. Nerves also exhibit anisotropy, but not quite as
much as tendons [22].
Muscle (Fig. 1.13a, b) is hypoechoic with hyperechoic fibroadipose perimysium
interspersed within the muscle tissue [23]. In the longitudinal view, the perimy-
a b
c
d
Fig. 1.11 (a) Transverse view of the common carotid artery and internal jugular vein, grayscale.
(b) Transverse view of the common carotid artery and internal jugular vein, color flow Doppler.
Vein is red, artery is blue. (c) Transverse view of the common carotid artery and internal jugular
vein, power Doppler. (d) Transverse view of the common carotid artery and internal jugular vein,
power Doppler, probe compression. The vein is compressed, whereas the lumen of the artery
remains patent
a b
Fig. 1.12 (a) Nerve in transverse axis. Note the honeycomb appearance in cross section. (b) Nerve
in long axis. Note the tram-tracks appearance
a b
Fig. 1.13 (a) Muscle in long axis. Note the hypoechoic texture with interspersed hyperechoic
perimysia. Pennate pattern. (b) Muscle in short axis. Note the hyperechoic perimysia. “Starry
night” pattern. Alternatively, an “uncooked steak” appearance
Tissues 13
a b
Fig. 1.14 (a) Fibrocartilage: hyperechoic triangular-shaped knee meniscus. (b) Hyaline cartilage:
hypoechoic to anechoic, distal femoral cartilage
Fig. 1.15 Hyaline

cartilage interface reflex
sia run lengthways, producing a pennate pattern, like a bird’s feather. In cross
section, longitudinal and speckled areas invoke a classic “starry night”
appearance.
Cartilage (Fig. 1.14a, b) is hyperechoic or anechoic, depending on the type.
Fibrocartilage is hyperechoic, whereas hyaline cartilage is hypoechoic to
anechoic [24]. The surface of normal cartilage may have a thin, smooth, hyper-
echoic interface reflection signal when the US wave is perpendicular (Fig. 1.15).
Synovial tissue (Fig. 1.16) is hypoechoic intra-articular tissue that will not condense
or shift with probe pressure [25].
Tenosynovium (Fig. 1.17) is a thin sheath encasing a tendon [26]. This sheath is
composed of synovial cells and may not be apparent unless pathology is pres-
ent [27].
The paratenon, considered a “false tendon synovial sheath,” is separate from yet
still surrounds the tendon [28, 29]. A paratenon is a loose collection of areolar
connective tissue which supplies blood to a tendon. Tendons with paratenons
include the Achilles tendon and the extensor tendons of the fingers [28, 30].
Fig. 1.16 Synovial tissue
Fig. 1.17 Tenosynovium
Fig. 1.18 Longitudinal

view of anterior knee,
suprapatellar bursa. The
bursa is connected to the
knee joint and normally
contains a small
(physiologic) amount of
synovial fluid
Synovial fluid (Fig. 1.18) is liquid located within a joint capsule, bursa, or tenosy-
novial sheath. It is anechoic and will shift (displace) with probe compression
[31]. A bursa is a sac that contains synovial fluid [24]. There may be a slight
hyperechoic coating surrounding anechoic synovial fluid. Some bursae typically
have a small amount of physiologic synovial fluid, while others are not visual-
ized unless distended by a pathologic amount of synovial fluid [32].
Sonographic Pathology by Structure 15
Sonographic Pathology by Structure
The examiner confirms pathology with images in two perpendicular, or orthogonal,

planes. Images of pathology, with a few exceptions, are beyond the scope of this
Manual. Please refer to other books which contain many pathologic US images [2–5].
The international network called OMERACT (Outcomes Measures in Rheumatology)
has been vital in establishing uniform ultrasound definitions of pathology [16].
Bone
Erosion: An intra-articular discontinuity of the bone surface visible in two perpen-

dicular planes [16].
Osteophyte: Appears as a step-up bony prominence [16].
New bone growth most often occurs in spondyloarthritis, in which extraneous bone
called an enthesophyte might develop at the insertion of tendons or ligaments
on bone.
Acute fracture may demonstrate discontinuity of the bone cortex with possible
step-off deformity [33].
Arteries
Halo sign is a homogeneous, hypoechoic wall thickening of an artery, appearing as

a dark halo surrounding a sharply defined arterial lumen, which may signify giant
cell arteritis. The halo remains visible even with probe compression [16].
Veins
Venous thrombosis may be evident with vein resistance to compression by the

transducer, best noted on CF. Echogenic material may be seen wholly or partially
occluding the vessel [19].
Nerves
Entrapment: Nerves tend to enlarge proximal to compressions, as may occur when

constricted within tight fibro-osseous canals such as the cubital tunnel and the
carpal tunnel [34]. There may be focal or diffuse swelling of the nerve, with loss
of the normal nerve echotexture.
A true neuroma following nerve injury results from a disorganized attempt to

regenerate, culminating in a morass of nerve and scar tissue [34]. The unaffected
portion of the nerve is continuous with the hypoechoic neuroma.
Cartilage
Fibrocartilage is usually hyperechoic. A hypoechoic cleft may represent a tear.

Fibrocartilage may also exhibit hyperechoic deposits of varied sizes and shapes,
raising suspicion of calcium pyrophosphate crystal deposition disease
(CPPD) [16].
Hyaline cartilage is ordinarily anechoic or slightly hypoechoic. Like fibrocartilage,
it may exhibit the same hyperechoic deposits of CPPD [16].
Osteoarthritic hyaline cartilage damage may be evident by thinning or loss of
anechoic cartilage producing irregularity and loss of sharp margins [16]. Early
signs of osteoarthritic cartilage may be a loss of clarity in the cartilage and a loss
of sharpness at the outer border of the cartilage [35]. A subtle sign of hyaline
cartilage surface damage may be the lack of a slight hyperechoic reflection.
Monosodium urate (MSU) crystals may form a thick layer superficial to the hya-
line cartilage covering joint surfaces [36]. This hyperechoic, continuous, or dis-
continuous layer persists despite changing the angle of the probe (insonation
angle) and is called the double contour sign (DCS). The MSU layer is often so
thick that its width rivals the thickness of the bony cortex. Sonographic visualiza-
tion of a DCS by itself is not unequivocally diagnostic for gout but is simply
evidence for MSU deposition on the cartilage surface.
Tendons and Ligaments
Tendon damage often appears as a focal tendon defect (loss of fibers) [16]. The
sonographer should position joints to enhance tendon tension to help visualize
and grade tendon tears.
Complete tears may display two stumps, perhaps retracted from the ROI [37]. An
absent tendon should prompt a thorough search for tendon stubs.
A partial-thickness tear presents as a focal anechoic region with loss of fibrillar
pattern but the preservation of overall tendon continuity [38]. Be mindful of
anisotropy mimicking a partial-thickness tear.
Full-thickness tears will exhibit features of partial-thickness tears, but an actual
tendon gap is noted [38]. Understand that a full-thickness tear does not mean that
there is a complete tear of the tendon, only that the tear has traversed the breadth
of the tendon. Of course, a full-thickness tear may eventually progress to a com-
plete tear.
Sonographic Pathology by Structure 17
Tendinosis, a degenerative process, is the preferred term over tendonitis or tendi-

nopathy. In tendinosis, there may be a partial loss of fibrillar pattern, edema,
hypoechoic areas, small anechoic clefts due to intrasubstance tearing, or perhaps
calcium deposits [39]. Note that PD activity may be present with tendinosis, but
realize that this may be neovascularization as a response to tendon injury rather
than a sign of inflammation.
Tenosynovitis is tenosynovial hypertrophy signified by abnormal anechoic or
hypoechoic tissue within the synovial sheath. Tendon sheaths develop tenosyno-
vitis due to an external or internal source of irritation, which may also occur with
tendinosis. There may be hyperemia on Doppler imaging and perhaps synovial
fluid within the sheath [16].
Paratenonitis manifests as hypoechoic edematous changes adjacent to a tendon
[29, 40]. The paratenon superficial to the extensor tendons of the fingers may
also exhibit anechoic fluid collections [30]. There may be neovascularization on
Doppler imaging [27].
Calcium pyrophosphate deposition crystals in tendons are hyperechoic, often
linear formations that move along within the tendon during a dynamic assess-
ment [16].
Monosodium urate crystals may also be present within tendons, represented as
aggregates, hyperechoic areas, or tophi [41].
Ligament damage is analogous to that of tendons, as ligaments may also show
tears, CPPD fragments, and degeneration. The ligament may enlarge and become
hypoechoic in areas or may show loss of fibrillar echotexture with or without
tears [39]. If the ligament appears to be intact, stress testing the ligament in com-
parison with the normal contralateral side may demonstrate the laxity of the
damaged ligament. The US examiner may find it difficult to discern the retracted
stumps of a complete ligament tear as opposed to those of complete tendon tears.
Enthesitis: The enthesis is where a tendon or ligament attaches to the bone. The
sonographer delineates enthesitis as a hypoechoic or thickened insertion within
2 mm from the bony cortex [16]. Additionally, there may be bony erosion or
calcifications/enthesophytes as a sign of structural damage. If active enthesitis is
present, there may be a Doppler signal.
Muscle
Muscle strain or tear may be associated with swelling and loss of continuity of the
perimysial hyperechoic fibers.
Muscle hematomas, initially hypoechoic, later become hyperechoic as the hema-
toma transitions to granulation tissue [42].
The sonographer detects muscle atrophy by noting a loss of muscle mass compared
with the contralateral unaffected muscle [43]. The atrophic muscle may eventu-
ally demonstrate increased echogenicity.
Other Pathologic Findings
Excessive synovial fluid is indicated by detecting overabundant, commonly

anechoic material within the joint capsule. This material is displaceable and
compressible but does not exhibit a Doppler signal [31].
Hyperechoic deposits of CPPD may be present in the synovial fluid. The exam-
iner may mobilize these deposits by joint movement and probe pressure [16].
MSU aggregates and even tophi may also be present within the syno-
vial fluid.
Synovitis is synovial hypertrophy, defined as abnormal hypoechoic synovial tissue
within the joint capsule that cannot be displaced, is poorly compressible, and
may exhibit Doppler signal [16].
Loose bodies may appear as hyperechoic, rounded forms within the synovial
fluid [44].
Cartilage interface sign: Hyaline cartilage may typically exhibit a slight hyper-
echoic superficial surface that may be exaggerated when an adjacent overly-
ing hypoechoic torn tendon touches the cartilage surface. This
hyperechogenicity is further augmented if the tear is associated with anechoic
fluid, which rests upon the cartilage surface. This phenomenon may be seen
with articular-sided supraspinatus tendon tears that extend to the carti-
lage [45].
Bursitis or bursal inflammation may result from an external source of irritation,
such as excessive pressure on the bursa. Likewise, the inflammatory instigator
may come from within, such as infection, crystal disease, or inflammatory
arthropathy [46]. The excess synovial fluid may cause bursal distension.
Ganglion cysts may arise from a joint or tendon sheath and may be degenerative
due to prior trauma or simply idiopathic [47]. They may appear as well-defined
cysts or as multiloculated structures. Ganglia are noncompressible and contain
hypoechoic to anechoic mucinous fluid.
Monosodium urate crystal deposition upon the surface of hyaline cartilage which
produces DCS, has been detailed above. These deposits may also occur within
synovial tissue or tendons in the form of aggregates, or tophi. MSU aggregates
may appear as heterogeneous, hyperechoic foci exhibiting substantial reflectivity
of sound waves even with changes in insonation angle [16]. Aggregates may
form circumscribed tophi that are inhomogeneous, hyperechoic, or hypoechoic,
perhaps surrounded by a slight anechoic halo. MSU aggregates and tophi may
occasionally generate a posterior acoustic shadow and can be present in many
locations.
Calcium deposits may occur within synovial fluid, tendons, ligaments, or cartilage
and appear as hyperechoic structures varying from tiny specks to large blocks.
Calcium can be abnormally deposited due to a metabolic issue, an autoimmune
disease, dystrophic calcification due to tears, or a degenerative process [48]. The
latter is called dystrophic calcification.
Artifacts: Friend or Foe? 19
Artifacts: Friend or Foe?
Artifacts are the desert mirages of US. They are parts of images that do not genu-
inely exist but result from the technology used to create them. In this case, US
waves strike a target and are reflected to the transducer for graphic interpretation by
the machine. Remember that what you see on the US screen is the machine’s virtual
construct, not necessarily the truth. So, when we use US, we substitute virtual real-
ity for actual reality. In MSUS, artifacts can be both confounding and convenient.
There are many different artifacts. Below are the more common ones.
Anisotropy has been described in the Terms section above. See Figs. 1.2a, b,
and 1.3.
Reverberation occurs when the US wave is perpendicular to two parallel, highly
reflective surfaces [49]. The wave acts like a ping-pong ball, bouncing back and
forth between the two surfaces; the transducer registers a portion of the wave
with each ricochet. The US machine interprets the returning US waves as multi-
ple parallel structures deep to the object(s). Wave reflection is dependent on the
difference in acoustic impedance between objects, and the larger the difference,
the more reflection occurs. The tissue’s density and the speed of sound within the
particular tissue determine the acoustic impedance [49].
Needle visualization exploits the reverberation artifact (Fig. 1.19). The two highly
reflective surfaces on each side of the needle encourage the US beam to bounce
back and forth within the entire needle, with some US waves returning to the
transducer with each rebound. This scenario produces a reverberation artifact at
integer multiples of the needle’s width. This artifact occurs in solid and hollow
needles and is not dependent on the presence of an inner lumen [50].
A subset of reverberation artifacts is the comet-tail artifact [51]. The objects pro-
ducing this artifact are tiny in length and depth, and the two reflective surfaces are
very close to each other. This type of reverberation trails off in a triangular pattern
like a comet’s tail. However, separate reverberation lines are difficult to resolve
due to the narrow depth of the object. The B-line artifact in abnormal lungs is a
typical example. Still, the comet-tail artifact can also occur with small foreign
bodies, adenomyomatosis of the gallbladder, or thyroid colloid nodules [52, 53].
Mirror-image artifacts occur when a target object is near a deeper strong reflector
[49, 54]. The US wave bounces off a robust reflective surface (such as the bony
cortex); however, part of the US wave impacts the deepest side of the target
object and is reflected to the strong reflector and then finally back to the trans-
ducer. The transducer detects the returning errant US wave, oblivious to its
meandering path, and then constructs an image. The time differences in echoes
returning to the transducer between the object and the strong reflector produce a
mirror image of the target object, which deceptively appears deep to the reflect-
ing surface. The deeper appearing mirror image is typically not as intense as the
original in grayscale. Mirror images can also occur with CF or PD (Fig. 1.20).
Acoustic shadowing, also called posterior acoustic shadowing, occurs when the
US wave is reflected, absorbed, or refracted by an object, resulting in an anechoic
Fig. 1.19 Reverberation of a therapeutic needle in a practice gel phantom
Fig. 1.20 Mirror-image artifact due to the strong reflector of the trachea (air). The color flow
Doppler signal is mirrored on the other side of the trachea
or hypoechoic area deep to the object [51]. Acoustic shadowing most commonly
occurs with bones. The object becomes a de facto soundwave umbrella, resulting
in a hypoechoic or even anechoic shadow deep to the object.
Acoustic enhancement, also called posterior acoustic enhancement, occurs when
a fluid-filled structure such as a cyst or bursa demonstrates increased echo-
genicity deep to the target structure, since US waves are less attenuated by the
fluid than the surrounding soft tissues. The US machine misinterprets these
relatively stronger soundwaves as an area beyond the target that has enhanced
echogenicity [49]. Acoustic enhancement is helpful to verify that the structure in
question is, in fact, fluid-filled. Figure 1.21 reveals acoustic enhancement deep to
a normal fluid-filled bladder. Additionally, turning on CF can determine that the
fluid-filled structure is neither an artery nor a vein.
Interface reflex (Fig. 1.15) occurs over hyaline cartilage. It is a thin, bright hyper-
echoic line along the edge of a smooth superficial cartilage surface, present only
if the probe is precisely perpendicular to the surface [55]. The interface reflex
(IR) should not be confused with gout’s DCS. An IR may also be confused with
a CIS but should be easily distinguishable since there would be no evidence of an
Artifacts: Friend or Foe? 21
Fig. 1.21 Acoustic

enhancement deep to a
normal fluid-filled bladder
overlying tendon tear with an IR. The IR helps gauge the smoothness of the outer
surface of cartilage, indicating which segments of cartilage are intact.
Organization of the Manual
We have divided his book into various examination sections designed to evaluate
specific conditions. For instance, the volar wrist is often examined separately from
the rest of the wrist when assessing for carpal tunnel syndrome. Most protocols are
region-specific; however, protocols for enthesopathy and crystal arthropathy involve
multiple body areas.
Limited Versus Complete Protocols
The MSUS protocols developed for this Manual explore ROIs of common clinical
conditions. Limited protocols, typically 2–5 images, detect the presence of a sono-
graphic finding. Complete protocols offer more detail regarding the joint space and
additional structures in a region. Limited protocols can be pulled from the complete
protocols as needed.
Finished Reports
Finished reports should contain standard information that often includes:

1. Report Title: Limited or Complete Exam, Area Examined (e.g., volar wrist) or
Specialty Examination (e.g., enthesopathy)
2. Ultrasonographer’s name
3. Impression
4. Examination side of the body
5. Indication for the examination
6. Study for diagnosis, prognosis, or treatment monitoring
7. Prior treatment failures
8. Technique and equipment used
9. Image Key or List of Images
10. Findings
The “Impression” appears toward the report’s top since most readers want to
know the results. The “Image Key” lists the images of the protocol in chronological
order. If the examiner desires additional views, they can insert these views into the
image list. Finally, “Findings” will contain the raw data noted on the exam. We find
it helpful to create a template with a detailed routine examination of the ROI; the
sonographer can later make changes to reflect pathology/variations found in the
individual patient. This section also reminds us of the structures that need to be
evaluated in ROI. We find this format helpful when first learning diagnostic US and
doing examinations that we perform less frequently. A practice guideline for docu-
mentation of ultrasound reports is available [56].
Additional Suggestions
Regarding the US machine, you do not need to purchase the most expensive machine
available. Manufacture-reconditioned/warranted machines are often acceptable if
new machines are too expensive. For ergonomics, obtain a height-adjustable exami-
nation table with a removable armrest. While you are learning, set aside dedicated
time for practice. You may not want to charge patients until you feel confident that
the US report is meaningful. Make sure images are retrievable and backed up
if needed.
When studying US, write down your questions as they occur. Seek the answers
in a textbook or journal article, ask a mentor, or save your list to ask an instructor at
a course. Always pick up the probe. It never hurts. Incorporating MSUS into your
practice improves patient care and practitioner satisfaction.
The goal of this Manual is to acquire quality US images of normal structures. It
is then up to the examiner to apply the same protocol steps when seeking pathology.
We hope to make the notoriously steep learning curve of MSUS a bit gentler.
Become adept at producing the images in this Manual. Try the protocols on yourself
and different normal subjects to gain confidence and speed. You always have a will-
ing test subject—yourself!
As you embark on learning this exciting modality, remember that MSUS is not
done in a vacuum. Before a sonographic evaluation, a focused history and physical
exam will help guide the US exam and suggest new diagnostic considerations.
However, it is essential to keep in mind that abnormalities found by US may not be
References 23
the cause of the complaint. The practitioner must place US findings into proper
clinical context. Finally, and most importantly, MSUS requires direct interaction
between clinician and patient. This laying on of hands is beneficial in many ways.
Acknowledgment While writing this Manual, we encountered several commonly used descrip-
tive terms (e.g., tram-tracking, Popeye’s sign, etc.) that have become part of the MSUS lexicon.
Every effort has been made to track down the first usage of these terms to acknowledge their prov-
enance and recognize their creator. Sometimes, however, we can not find the origin of these widely
used terms. We do not assume credit for or imply authorship of these terms and would like to rec-
ognize the unheralded creators of these wonderfully evocative terms and expressions.
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Chapter 2
Volar Wrist
Reasons to Do the Study

1. Carpal tunnel syndrome diagnosis and cause
2. Compression of the ulnar nerve in Guyon’s canal
3. Wrist pain
4. Soft tissue swelling
5. Evaluation of the flexor tendons for tears, tendinosis, and tenosynovitis
6. Evaluation for possible tenosynovitis
7. Evaluation for inflammatory arthritis
Questions to Be Answered
1. Is there a structural or inflammatory cause for wrist pain?
2. Is there sonographic evidence of median or ulnar nerve compression? If so, what
is the structure(s) causing this?
3. What is the true nature of an abnormal physical examination finding, and is this
causing the discomfort?
4. What is the next step in alleviating the problem (e.g., splinting, injection, medi-
cation, surgery, or a combination)?
Basic Anatomy
1. Bones
2. Soft tissue structures (Fig. 2.1a, b)
States Government.

Switzerland AG 2023
28 2 Volar Wrist
S, scaphoid; FCR, flexor carpi radialis; FPL, flexor pollicis longus; FR, flexor renaculum; MN,
median nerve; PL, palmaris longus; UA, ulnar artery; UN, ulnar nerve; P, pisiform
b
S, scaphoid; FCR, flexor carpi radialis; FPL, flexor pollicis longus; FR, flexor renaculum; MN,
median nerve; PL, palmaris longus; UA, ulnar artery; UN, ulnar nerve; P, pisiform
Fig. 2.1 (a) Carpal tunnel schematic. (b) Carpal tunnel schematic cartoon. S scaphoid, FCR flexor
carpi radialis, FPL flexor pollicis longus, FR flexor retinaculum, MN median nerve, PL palmaris
longus, UA ulnar artery, UN ulnar nerve, P pisiform
Clinical Comments 29
Clinical Comments
Ultrasound (US) can detect compression of the median nerve (MN) in the carpal
tunnel (CT) and the ulnar nerve (UN) in the wrist and hand. It can also detect the
presence of pertinent wrist variants, such as a persistent median artery (PMA), a
bifid MN, and accessory muscles. Calcium and monosodium urate deposits, tenosy-
novitis, tendon pathology, soft tissue swelling, and hyperemia are readily apparent.
Carpal Tunnel Syndrome
Carpal tunnel syndrome (CTS) is a dysfunction of the MN within the CT due to

injury, compression, or other causes. The CT is a passageway at the wrist through
which multiple tendons and the MN traverse to reach the hand. The roof is the flexor
retinaculum (FR), or transverse carpal ligament, while the carpal bones form the
floor and edges. Patients may complain of numbness, tingling, or weakness of the
first three digits of the hand [1].
US can detect a sonographic appearance of the MN consistent with CTS to help
corroborate a clinical diagnosis. However, the US exam cannot “rule in” or “rule
out” CTS. To make the diagnosis, the patient must have the clinical symptoms of the
syndrome, irrespective of the sonographic appearance [2]. Ultrasound can detect
MN compression as nerve swelling just proximal to the constriction point in the
fibro-osseous canal; the swollen nerve is called a “pseudoneuroma” [3].
For the diagnosis of CTS, electrophysiologic studies (EPS) remain the tests of
choice but may be normal in 10–25% of patients with clinical CTS [4, 5]. However,
US may confirm CTS in approximately 30% of patients with a clinical diagnosis of
carpal tunnel syndrome but normal EPS [6]. Bear in mind that US and EPS are
complementary [2]. The two different studies approach the diagnosis of CTS from
different viewpoints and thus are not always in agreement. Ultrasound demonstrates
structural changes, while EPS describes nerve function. If compression of the MN
is causing clinical CTS, US and EPS may frequently agree. However, EPS is better
suited for evaluating noncompressive causes of mononeuropathy in either the MN
or UN [2].
Ultrasound is a potent tool for evaluating CTS but does have limitations. A
patient who does not meet sonographic criteria for CTS may still have the condition.
Further, US cannot verify CT surgical release adequacy [7].
To evaluate for CTS using US, compare the amount of swelling of a constricted
MN to a more proximal (presumably normal-sized) portion of the MN in the fore-
arm (Fig. 2.2). The examiner identifies the MN by its deep location proximal to the
CT in the protocol. Next, the sonographer compares the cross-sectional area (CSA)
30 2 Volar Wrist
Step 1 starts at the Step 2 is to move Step 3 verifies the Step 4 is to return
ulnar aspect over probe to the median nerve to the wrist and
the pisiform middle of the wrist which lies deep measure the-now
to get beer between the verified-median
visualizaon of the muscles ~12 cm nerve
median nerve proximally
candidate
Fig. 2.2 Summary of the four steps to locate the median nerve and determine enlargement
of the MN at the wrist and the point ~12 cm proximal to the wrist by dividing the
CSA of the MN at the wrist by the CSA ~12 cm proximal. This quotient is the
wrist:forearm ratio (WFR). A WFR value greater than 1.4 strongly implies that the
patient has MN compression within the CT [8]. Alternatively, if the CSA at the wrist
is >2 mm2 more than the MN at the point ~12 cm proximal to the wrist, this is 97%
sensitive and 100% specific for CTS [9].
Other signs of CTS are:
1. Notch sign: a distinct area of compression of the MN, often seen in the
longitudinal-axis (LAX) view [10].
2. Bulging or bowing outward of the FR [11].
3. Compressed or flattened MN [11].
4. Morphologic changes of the MN, including loss of distinct nerve echotexture,
swelling of the MN, or thickening of the perineurium [12].
In some cases, MN enlargement proximal to the compression may not be the
most salient feature. The examiner may observe MN compression from a thickened
FR, flexor tenosynovitis, a ganglion cyst, or an anomalous muscle. The width of the
midline FR, from proximal to distal, is about 14.4 ± 1.9 mm [13]. The FR thickness
is usually 1–1.5 mm [11]. However, the FR may be more than 30% thicker in
patients with CTS [14]. A thickened FR may point to repetitive action as a cause of
CTS. Be on the alert for a thickened FR, flexor tenosynovial hypertrophy, a gan-
glion cyst, anomalous muscles, MN displacement, and two variants: a bifid MN
and a PMA.
The examiner may begin with a limited protocol to determine if there is, in fact,
sonographic evidence for MN compression. If needed, the examiner performs a
complete volar wrist evaluation to include the UN since the deep motor branch
Pitfalls 31
(DMB) of the UN innervates the adductor pollicis and the flexor pollicis brevis
muscles [15]. Thus, compromise of the UN may cause thumb weakness, mim-
icking CTS.
After structural evaluation, look for a safe area to place an injection, should this
be necessary. We perform CT injections using US to improve efficacy and safety [2,
16, 17]. When injecting the CT, be aware that the recurrent median nerve (RMN) is
a branch of the MN that variably branches off the radial aspect of the nerve, some-
times within the CT. An 18 MHz high-frequency probe is crucial for detecting this
small nerve branch [18].
This protocol focuses on the soft tissues of the volar wrist. If your examination
does not elucidate the cause of volar wrist pain, proceed to evaluate the carpal
bones, the distal ulna, and the radius. We can better evaluate ligamentous tears with
dorsal wrist views. Other modalities such as radiographs, computerized tomogra-
phy, and magnetic resonance imaging will better delineate bony abnormalities than
the US examination.
Ulnar Nerve Damage
Ulnar neuropathy may cause paresthesia of the fifth and the ulnar aspect of the
fourth fingers [19]. The DMB of the UN supplies the hypothenar muscles, interos-
sei, adductor pollicis, and flexor pollicis brevis [15]. Therefore, compromise of the
DMB may mimic median neuropathy by causing thumb weakness.
If the UN or one or both branches are compressed, there may be a loss of the
normal echotexture. There are no specific sonographic criteria for UN dysfunction,
but a helpful suggestion is to compare the maximal CSA of the affected nerve to a
more proximal, normal portion of the UN [20].
If a nerve branch is compromised, determine what structure is responsible. The
most common structure compressing the UN is a ganglion cyst [21]. Remember that
Guyon’s Canal is superficial to the FR and is separate from the CT. Note if a
hypoechoic or anechoic structure, such as a ganglion cyst, is present, perhaps com-
pressing the UN. If so, look for the root or stalk of the ganglion. Power Doppler
(PD) or color flow Doppler (CF) may help delineate an ulnar artery aneurysm or
pseudoaneurysm, which likewise might compress the UN.
Pitfalls
1. To avoid mistaking a flexor tendon for the MN, move the probe ~12 cm proxi-
mally up the forearm, and the true MN will arc in a radial direction and move
deep to rest on the pronator quadratus muscle. Reversing the course of the
probe will bring the image of the MN back into the CT, thus identifying
the MN [7].
32 2 Volar Wrist
2. It is difficult for the US to determine if a CT release has been successful. The FR

appearance will vary, and the MN size will not predict clinical outcomes [7,
22, 23].
3. An anechoic or hypoechoic rim surrounding a flexor tendon in the transverse
axis (TAX) may be due to normal variant distal extension of a muscle, tenosyno-
vial hypertrophy, or frank tenosynovitis. Power Doppler activity in the tendon
sheath indicates more active tenosynovitis. Rotating the probe to LAX will
determine whether or not this is simply normal tapering of the muscle as the
tendon is formed [7].
4. When tracing the nerve to calculate the CSA, measure inside the hyperechoic
epineurium [7].
5. Learn the sonographic criteria for the diagnosis of CTS based on measurement
of the CSA to determine MN swelling:
(a) CSA of MN at the CT >12 mm2 [7, 24].
(b) CSA >2 mm2 in the CT compared with the CSA over the pronator quadratus
(>4 mm2 for bifid MN) [7, 9].
(c) The WFR method of comparing the ratio of the CSAs of the swollen distal
MN to the unaffected, more proximal MN [8]. Again, a WFR value greater
than 1.4 strongly implies that the patient has MN compression
within the CT.
Method
Begin the steps for identifying the MN and determining the presence of sonographic
criteria for CTS (Fig. 2.2).
rotocol Image 1: Volar Wrist, Ulnar Aspect, Transverse

P
(Fig. 2.3)
Begin with the patient’s arm resting with the palm up and the wrist in a neutral posi-
tion. The patient is facing the examiner. Place the probe on the volar wrist crease in
TAX toward the ulnar aspect of the wrist to look for the rounded bony structure of
the pisiform bone. See the pulsation of the UA. If this is not apparent, turn on PD to
delineate the UA.
Deep to the UA, note the proximal edge of the FR, which is the hyperechoic,
fibrillar band-like structure that stretches horizontally from the scaphoid bone and
reaches the base of the pisiform bone. The FR may appear hypoechoic depending
on the angle of insonation. The FR is located just deep to the pulsating UA. The FR
is both the floor of Guyon’s canal and the roof of the carpal tunnel.
Method 33
Fig. 2.3 Protocol Image 1:

Volar wrist, ulnar aspect,
transverse
Fig. 2.4 Protocol Image 2: Volar wrist, mid-wrist, transverse
Protocol Image 2: Volar Wrist, Mid-Wrist, Transverse (Fig. 2.4)
Next, keep the probe in TAX orientation and perform an LAX slide in the radial
direction. You will see several ovoid structures as you seek the MN. Tilt the trans-
ducer in either direction to better delineate these structures. Select one deep to the
FR and consider it the “median nerve candidate,” since we want to verify that this is
the MN. The structure should have an elliptical and honeycomb appearance and
exhibit moderate anisotropy. It may look more like parallel wavy lines than a hon-
eycomb. A surrounding hyperechoic epineurium is a piece of additional evidence
that the structure is a nerve.
34 2 Volar Wrist
Fig. 2.5 Protocol Image 3: Forearm, 12 cm proximal to wrist crease, transverse
rotocol Image 3: Forearm, 12 cm Proximal to Wrist Crease,

P
Transverse (Fig. 2.5)
Verify the MN identity by performing a proximal TAX slide of approximately

12 cm to see if your prime MN candidate dives deeper as you move the probe. In
this location, the MN lies superficial to the pronator quadratus muscle and has a
more circular or even triangular appearance. The MN is hyperechoic relative to the
surrounding muscle.
rotocol Image 4: Median Nerve, 12 cm Proximal to Wrist

P
Crease, Transverse, Cross-Sectional Area Measurement
(Fig. 2.6)
Center the MN and freeze the image. Select the measure function and trace the inner
circumference within the epineurium [7]. The MN, roughly 12 cm proximal to the
wrist, will not be constricted in this location [9]. The typical CSA is 4–9 mm2. An
alternative to free measurement is the preset elliptical measurement function. The
Method 35

Median nerve, 12 cm
proximal to wrist crease,
transverse, cross-sectional
area measurement
maximal height and width of the MN are measured, enabling the US machine to
calculate the CSA.
rotocol Image 5: Proximal Carpal Tunnel, Transverse

P
(Fig. 2.7)
Move the probe distally in a TAX slide to follow the MN back to the wrist crease. It
will become more superficial and ovoid as it eventually nestles beneath the FR. Look
at the MN at the proximal edge of the FR. Capture the image of the verified MN that
has the largest CSA and well-defined edges. Look for loss of normal MN echotex-
ture, FR thickening, MN compression or flattening under the FR, and hyperechoic
swelling or thickening of the epineurium surrounding the MN. Note if there is a
variant split (bifid) MN (Fig. 2.8). Look at the surrounding flexor tendons to see if
there is swelling of the tendon or its surrounding sheath (the tenosynovium). Inspect
for other structures within the CT that might compress or displace the MN, such as
a ganglion cyst.
You can also check the flexor pollicis longus (FPL) in the CT radial to the
MN. When you think that a particular tendon might be the FPL, manually flex and
extend the thumb to verify its identity. Likewise, look for the flexor carpi radialis
(FCR), which is superficial to the CT. Manually flex and extend the wrist to verify
that this is the correct tendon. The region near the FCR and the radial artery is a
common area for ganglion cysts, which often originate from the radiocarpal joint
capsule. The FCR itself may develop tenosynovitis with inflammatory arthritis. The
FCR tendon may exhibit tendinosis or tendon tears associated with osteoarthritis of
the scaphoid-trapezium-trapezoid (triscaphe) joint [7].
Look for variants within the CT, including an extension of the flexor digitorum
superficialis muscle, an encroaching lumbrical muscle, or a palmaris longus (PL)
36 2 Volar Wrist
Fig. 2.7 Protocol Image 5: Proximal carpal tunnel, transverse
Fig. 2.8 Bifid median

nerve
tendon within the CT. Oddly, the PL can sometimes be “reversed” where the muscle
is distal to the tendon [25].
rotocol Image 6: Median Nerve, Proximal Carpal Tunnel,

P
Transverse, Cross-Sectional Area Measurement (Fig. 2.9)
Measure the largest CSA at the wrist. Be sure to measure within the hyperechoic
epineurium surrounding the MN. Compare the MN CSA at the wrist to the MN
~12 cm proximal to the wrist by dividing the CSA of the MN at the wrist by the
Method 37

Median nerve, proximal
carpal tunnel, transverse,
cross-sectional area
measurement
CSA ~12 cm proximal. This quotient is the WFR. A WFR value greater than 1.4
strongly implies that the patient has MN compression within the CT [8]. Alternatively,
if the CSA at the wrist is >2 mm2 more than the MN at the point ~12 cm proximal
to the wrist, this is 97% sensitive and 100% specific for CTS [9].
rotocol Image 7: Proximal Carpal Tunnel, Transverse + Power

P
Doppler (Fig. 2.10)
Turn on PD to determine if there is a PMA or evidence of active tenosynovitis. Scan

at the edge of the CT and throughout the entire CT. Do not forget to lower the pulse
repetition frequency (PRF) to enhance the detection of active tenosynovitis.
However, avoid dropping the PRF so much that extraneous PD artifacts emerge.
When using PD, remember to use a light touch and plenty of transmission gel. Only
the UA or the radial artery will exhibit PD activity in most cases.
If you are considering a carpal tunnel injection, an option is to check PD or CF
to look for blood vessels that might complicate the procedure. From this informa-
tion, determine if and from what approach you would like to inject the carpal tunnel,
bearing in mind that there is a radial branch of the MN (recurrent or thenar branch
of the MN), which may not be apparent on US [26]. This smaller nerve sometimes
resides within the CT and argues for injecting via the ulnar aspect.
38 2 Volar Wrist
Fig. 2.10 Protocol Image 7: Proximal carpal tunnel, transverse + power Doppler
rotocol Image 8: Median Nerve, Longitudinal ± Power Doppler

P
(Fig. 2.11)
Next, center the probe over the MN and rotate the probe 90° to look at the MN in
LAX. Observe any compression and FR thickening. A trick is to center the probe on
the MN in TAX so that when you rotate the probe, you see an ovoid MN expanding
out and becoming a longitudinal structure. The MN has the typical “train or tram
tracks” of a nerve, best observed proximally, where the MN assumes a more normal
appearance.
Follow the nerve down into the CT, performing a heel-to-toe maneuver if needed
to keep the probe parallel to the MN. Constriction of the MN may produce a “dumb-
bell sign” in this view. Placing a rolled-up towel under the metacarpals will prevent
wrist hyperextension [20]. Try to follow the MN distally.
Deep to the flexor tendons, note the hyperechoic volar aspects of the distal radius,
lunate, and capitate bones. An additional image might be the MN in LAX with PD
to look for tenosynovitis of the flexor tendons or aneurysms present in the CT. The
above steps comprise the limited evaluation of the CT, which rapidly determines if
there is evidence for MN compression.
Method 39
Fig. 2.11 Protocol Image

8: Median nerve,
longitudinal ± power
Doppler

9: Proximal Guyon’s canal,
transverse + power
Doppler
rotocol Image 9: Proximal Guyon’s Canal, Transverse + Power

P
Doppler (Fig. 2.12)
To complete the full volar wrist soft tissue examination, identify the UN in Guyon’s
canal by again placing the probe in TAX at the level of the pisiform, as was done in
Protocol Image 1. Identify the UA with the help of the PD and the rounded hyper-
echoic pisiform bone that delineates the proximal portion of Guyon’s canal.
40 2 Volar Wrist
Protocol Image 10: Proximal Guyon’s Canal, Transverse
Turn off the PD to improve resolution. The UN abuts the UA on its ulnar aspect.
Again, note that the FR is both the floor of Guyon’s canal, and the roof
of the CT.
Protocol Image 11: Distal Guyon’s Canal, Transverse (Fig. 2.13)
Move the probe in TAX more distally (TAX slide). The pisiform will disappear, and
then the deeper hyperechoic hook of the hamate will appear. The two branches of
the UN are evaluated at this level. The UN’s superficial sensory (SSB) and DMB
may be seen, having separated off from the central UN. The SSB may be superficial
to the hamate at about the same depth as the UA. The DMB may be seen just on the
ulnar aspect of the hook of the hamate. The separation of the two branches distally
may be challenging to discern.
Repetitively moving the probe from proximally to distally may enhance appre-
ciation of the split. One or both tiny nerve branches may be hypoechoic as you move
the probe due to anisotropy. Once each component is identified, correct for anisot-
ropy by tilting the probe. The DMB may be located slightly more ulnar than the
SSB; alternatively, the two branches may stack up vertically [27].

11: Distal Guyon’s canal,
transverse
Method 41

12: Ulnar artery at Guyon’s
canal, longitudinal + power
Doppler
rotocol Image 12: Ulnar Artery at Guyon’s Canal,

P
Longitudinal + Power Doppler (Fig. 2.14)
Center the probe on the UA in TAX. Turn the transducer 90° to visualize the UA in
LAX. Alternatively, visualize what you believe is the UN in LAX, turn on the PD,
and then perform a very slight TAX slide in the radial direction to visualize part of
the pulsating UA.
rotocol Image 13: Ulnar Nerve at Guyon’s Canal, Longitudinal

P
(Fig. 2.15)
Once you visualize the UA, turn off the PD and move the probe slightly in an ulnar
direction to capture and verify the identity of the UN in LAX. If normal, the nerve
should exhibit “train or tram tracks” echotexture. You may be able to discern the
more distal splitting of the UN into its superficial and deep branches.
42 2 Volar Wrist

13: Ulnar nerve at Guyon’s
canal, longitudinal
Complete Volar Wrist Ultrasonic Examination Checklist

□ Protocol Image 1: Volar wrist, ulnar aspect, transverse
□ Protocol Image 2: Volar wrist, mid-wrist, transverse
□ Protocol Image 3: Forearm, 12 cm proximal to wrist crease, transverse
□ Protocol Image 4: Median nerve, 12 cm proximal to wrist crease, transverse,
cross-sectional area measurement
□ Protocol Image 5: Proximal carpal tunnel, transverse
□ Protocol Image 6: Median nerve, proximal carpal tunnel, transverse, cross-
sectional area measurement
□ Protocol Image 7: Proximal carpal tunnel, transverse + power Doppler
□ Protocol Image 8: Median nerve, longitudinal ± power Doppler
□ Protocol Image 9: Proximal Guyon’s canal, transverse + power Doppler
□ Protocol Image 10: Proximal Guyon’s canal, transverse
□ Protocol Image 11: Distal Guyon’s canal, transverse
□ Protocol Image 12: Ulnar artery at Guyon’s canal, longitudinal + power Doppler
□ Protocol Image 13: Ulnar nerve at Guyon’s canal, longitudinal
References
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of carpal tunnel syndrome. Ultrasound versus electromyography. Radiol Clin N Am.
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Chapter 3
Dorsal Wrist (Radial, Dorsal, Ulnar)

1. Wrist pain or stiffness
2. Possible de Quervain’s tenosynovitis
3. First extensor compartment tenosynovitis, tendinosis, tears
4. Proximal compartment syndrome
5. Evaluation of soft tissue swelling or masses
6. Pain or weakness after trauma
7. Loss of finger extension capability
8. Paresthesia on the hand dorsum
Questions We Want Answered
1. What is the cause of wrist pain?
2. Is tenosynovitis present, and if so, what is the cause?
3. Is there an underlying inflammatory condition affecting the hand, and is it a
systemic process such as spondyloarthropathy, rheumatoid arthritis, or crystal
disease?
4. If there is an inflammatory condition, is it eroding cartilage or bone?
5. Is there a structural, functional, or repetitive injury problem causing the
hand pain?
6. What is causing soft tissue swelling?
7. What is this lump on the hand dorsum?
8. Are the tendons, ligaments, and cartilage surfaces normal in appearance?
9. Is there evidence for tendon compartment intersection syndromes?
10. Is there evidence for a triangular fibrocartilage complex tear?
11. Is there any evidence for calcium deposition in the triangular fibrocartilage that
might indicate calcium pyrophosphate deposition disease?
States Government.

Switzerland AG 2023
46 3 Dorsal Wrist (Radial, Dorsal, Ulnar)
12. Is there evidence for a ganglion? If so, is the origin a joint or tendon sheath?
13. Is there evidence for radial nerve compression?
Necessary Basic Anatomy
Carpal Bones (Fig. 3.1a, b)
1. Proximal carpal bones (radial to ulnar)

(a) Scaphoid: Boat-like
(b) Lunate: Crescent-shaped, like the moon
(c) Triquetrum: Triangular
(d) Pisiform: Pea-shaped
2. Distal carpal bones (ulnar to radial)
(a) Hamate: Bone with a hook (palmar directed)
(b) Capitate: Head
(c) Trapezoid: Like the trapezium but smaller in size
(d) Trapezium: Like a table
a b
Fig. 3.1 (a) Basic anatomy. (b) Basic anatomy cartoons

Necessary Basic Anatomy 47
A mnemonic for the carpal bones, starting at the proximal row on the radial
side and moving in a circular direction:
Straight Line To Pinky, Half Circle To Thumb
Joints of the Wrist (Fig. 3.2)
1. Radiocarpal joint (RCJ): This is the junction of the distal radius and two of the
carpal bones, the scaphoid and lunate. The RCJ is best seen in longitudinal
(LAX) on ultrasound (US).
2. Intercarpal (midcarpal) joint: Formed between the proximal and distal rows of
carpal bones, it is also best seen in LAX on US.
3. Distal radioulnar joint (DRUJ): Located between the two distal bones of the
forearm, its best view on US is in transverse (TAX).
Lister’s Tubercle (Fig. 3.2)
Lister’s tubercle (LT) is a palpable bony prominence on the dorsum of the distal
radius [1]. It is well-delineated on US and an invaluable sonographic landmark
between the second and third extensor compartments. Along the ulnar aspect of LT
runs the third extensor compartment (EC), which contains the extensor pollicis
Fig. 3.2 Wrist joints and

Lister’s tubercle
longus (EPL). Lister’s tubercle acts as a pulley for the EPL since this tendon angles
back toward the first digit [2].
Extensor Compartments (Fig. 3.3a)
The primary soft tissue structures of the dorsal wrist are the various extensor and
abductor tendons of the six wrist compartments. The dorsal (extensor) wrist tendons
are separated into six fibro-osseous compartments (radial to ulnar) [3]:
1. Abductor pollicis longus (APL) and extensor pollicis brevis (EPB)
2. Extensor carpi radialis longus and brevis (ECRL and ECRB)
3. Extensor pollicis longus (EPL)
4. Extensor digitorum (ED) and extensor indicis (EI)
5. Extensor digiti minimi (EDM)
6. Extensor carpi ulnaris (ECU)
A story about an apple helps us remember the hand extensor compartments and
tendons (Fig. 3.3b).
a b
Fig. 3.3 (a) Extensor compartments (b) Extensor compartment cartoons

1. Extensor compartment #1: Eve, having taken a bite of the APL (abductor pol-
licis longus), is confronted by a short policeman (extensor pollicis brevis). He
informs her that she and Adam must leave the Garden of Eden.
2. Extensor compartment #2: They drive their car to earth along a long and then
a brief route (extensor carpi radialis longus and brevis).
3. Extensor compartment #3: Wearing no clothes, Adam and Eve are immedi-
ately arrested by a tall policeman (extensor pollicis longus).
4. Extensor compartment #4: They are given an extensive sentence of commu-
nity service for indecent exposure (extensor digitorum communis and indicis).
5. Extensor compartment #5: Nine months later, Eve bears a son whom they like
to call Adam’s mini-me (extensor digiti minimi).
6. Extensor compartment #6: Adam becomes an Uber driver to support his grow-
ing family (extensor carpi ulnaris).
The first EC is the most radial. The APL is most ventral, that is, closer to the
radial aspect of the palm. Logically, the APL abducts the thumb, and EPB extends
the thumb. You can manually move the thumb (or another finger) to verify the ten-
don’s identity at any point in the US exam.
In the first EC tunnel, the floor is the bony groove of the radial styloid. Variations
include a vertical septum splitting the first EC into separate sub-compartments, one
containing the APL, the other the EPB. Another variation is that the APL may be a
single tendon or consist of multiple tendon slips. We also find the mnemonic “The
second EC is double-crossed” to be helpful. The second EC is crossed twice: ini-
tially by the first EC proximal to the wrist and again by the third EC as it moves
obliquely to the thumb distal to the wrist. The ECU tendon is found in the ulnar
groove and is technically not located over the wrist dorsum.
Soft Tissue Structures
1. Extensor retinaculum (ER): Located superficially to the extensor tendons, it

forms the roof of the extensor tendons.
2. Scapholunate ligament (SLL): The SLL is located between the scaphoid and
lunate carpal bones and is a triangular structure that is mechanically important as
a wrist stabilizer [4]. Sonographically detectable tears may occur here. The SLL
is best evaluated from the dorsal approach in TAX but can also be assessed from
the volar aspect.
3. Triangular fibrocartilage complex (TFCC): The triangular fibrocartilage runs
from the ulnar side of the distal radius to the base of the ulnar styloid [5]. It sepa-
rates the RCJ from the DRUJ. There are multiple components to the TFCC, but
the chief sonographic components are the articular disc (AD) and the meniscal
homologue (MH) (Fig. 3.4). The AD appears triangular on US, with the deep
portion tapering in part due to attenuation from structures that lie superficially.
The MH seems to be almost ovoid-shaped. It may be difficult to discern the nor-
mal AD and MH from the surrounding ligaments on US.
Fig. 3.4 Triangular

fibrocartilage complex
simplified schematic
Superficial Radial Nerve
Ultrasound enables the identification of the superficial radial nerve (SRN) at the
level of the distal radius [6]. More proximally, at the level of the distal forearm, the
SRN is close to the cephalic vein [6, 7]. A high-frequency probe of at least 17 MHz
may be needed to follow the small branches of the SRN.
Clinical Comments
Always start with hand or wrist radiographs. Include clenched fist views if you sus-
pect an SLL tear. As always, radiographs give the lay of the land before the US exam
and will provide essential clues such as joint space narrowing, fracture, osteonecro-
sis, TFCC calcium deposits, and bone alignment abnormalities. Joint space narrow-
ing implies cartilage erosion or thinning that the examiner should detect on US.
de Quervain’s Tenosynovitis
de Quervain’s stenosing tenosynovitis (dQT), in which the first EC tendon sheath

and the covering ER become irritated and inflamed, often has a mechanical origin
due to overuse [8]. Repetitively lifting a baby may produce dQT, termed baby wrist
[9]. Symptoms include pain at the distal radius radiating to the forearm or thumb,
local swelling, sensitivity to pressure, and crepitus [10, 11]. Finkelstein’s test is
when the examiner places the thumb in the fist and flexes the wrist in an ulnar direc-
tion. This maneuver reproduces the symptoms of dQT and is the clinical examina-
tion of choice [12].
Ultrasound may reveal thickening of the tenosynovial sheath and overlying ER,
tendinopathy, or fluid within the tendon sheath. The normal ER is barely visible, so
thickening is a significant sign. Other sonographic findings include a hypoechoic
peritendinous halo sign (due to edema) and, if in the acute phase, power Doppler
(PD) activity in the affected soft tissues [13].
Due to tendinopathy, the affected tendon(s) may have changed shape from oval
to more circular in the TAX view [8]. Dynamic US in LAX view may reveal tendon
obstruction under the thickened ER impeding smooth tendon gliding. If a variant
vertical septum exists between the two tendons, then only one tendon may be
involved with dQT, more commonly the EPB.
The first EC may also develop tenosynovitis associated with inflammatory
arthropathies such as rheumatoid arthritis, psoriatic arthritis, other spondyloarthrop-
athies, sarcoidosis, or chronic crystal arthropathy. Tenosynovitis may present as an
effusion within the synovial sheath or a thickened tendon sheath. Probe pressure
may cause fluid displacement, helping to differentiate an effusion from tenosyno-
vial thickening. If a septum exists within the compartment, then corticosteroids may
need to be injected into each separate tendon sheath to treat the condition effec-
tively. Ultrasound-guided needle injection helps target the affected tendon sheath
accurately [14].
Intersection Syndromes
Remember that the first EC crosses the second EC close to the wrist. This can cause
the proximal intersection syndrome (PIS), which is different from the distal inter-
section syndrome (DIS), which happens when the third EC crosses the second EC
farther from the wrist (Fig. 3.5). In each intersection syndrome, the compartments
develop inflammation as they cross paths.
Proximal intersection syndrome: Proximal intersection syndrome results from
overuse, producing pain and swelling at the distal forearm. Proximal intersec-
tion syndrome is also known as crossover syndrome, peritendinitis crepitans,
or oarsman’s wrist [8]. Pain occurs approximately 4–8 cm proximal to the wrist
on the dorsal forearm, where the first and second extensor compartments cross
[8, 11, 15]. Ultrasound findings at the site of PIS can include edema, loss of the
hyperechoic plane dividing the two different compartments, tenosynovial effu-
sion, tendinosis, hypervascularity on Doppler, and sometimes ganglion cysts
[8, 11]. The cause and pathologic mechanisms of PIS are not well understood.
Fig. 3.5 Intersection

syndrome locations
Distal intersection syndrome: This occurs just distal to LT where the third EC
crosses over the second EC [8]. Repeated flexion and extension of the wrist pro-
duce irritation between the two tendons. Ultrasound reveals tenosynovial effu-
sion of the EPL proximal and distal to the intersection. With EPL tenosynovitis,
consider other causes of impingement, such as underlying osteophytes, scaphoid
or distal radius fractures, or surgical hardware [8].
Fourth Compartment
Fourth compartment tenosynovitis may occur with inflammatory arthropathy and

infectious disease [16]. Ultrasound reveals tenosynovial and retinacular thickening
with PD activity [8]. Tenosynovitis may also arise with hardware impingement,
such as after radial fracture repair due to an impinging screw tip. The hyperechoic
screw tip with reverberation is often clearly seen. Such impingement may cause a
complete tear of the tendon in the fourth EC; retraction may result in the nonvisual-
ization of a tendon within its sheath. Another cause of tenosynovitis in the fourth EC
occurs when the EI muscle has not yet formed into a tendon [17]. The anomalous
muscle may cause compression within the fourth EC.
Fifth Compartment
Anatomic variation of the EDM may be associated with tenosynovitis. Further,

DRUJ arthritis may also cause EDM tenosynovitis due to the contiguity of the two
structures [8, 18].
Sixth Compartment
Although the ER covers the ECU tendon, an additional, deeper subsheath secures the
ECU tendon within the groove of the ulnar head [16, 19]. Repetitive stress on the
tendon may lead to stenosing tenosynovitis of the subsheath. In such cases, US reveals
thickening of the ER, fibrosis, and reactive tenosynovial effusion. Attenuation or tear-
ing of the subsheath may result in ECU tendon instability or even dislocation out of
the ulnar groove [19]. Such ECU tendon dislocation differs from the normal partial
subluxation of the ECU tendon with forearm supination. Tears of the subsheath occur
with a recurrent injury in racquet sports, abrupt twisting, and severe DRUJ arthropa-
thy. Tendonitis of the ECU may mimic TFCC injury. Tenosynovitis of the ECU may
also be an early sign of rheumatoid arthritis and may predict erosion progression [20].
Scapholunate Ligament Tear
The SLL is an important wrist stabilizer [21]. Tears of the SLL may occur with
sports-related injuries and, if unrecognized, may result in enduring wrist instability
and arthritis termed scapholunate advanced collapse [22, 23]. An MRI or CT arthro-
gram is the gold standard for evaluating SLL tears [22]. The SLL is best seen on the
wrist dorsum on US and is identifiable as a hyperechoic fibrillar structure [24].
However, the normal dorsal SLL may be invisible to US. In one US study, the nor-
mal dorsal SLL was completely visible in 48%, partly visible in 30%, and barely
visible or invisible in 23% [25]. Sprains may reveal a hypoechoic and thickened
ligament. With a complete tear, the SLL may not be visible, although, again, the
lack of visualization of the SLL may be usual for some individuals.
Ulnar deviation of the wrist creates tension on the SLL and may demonstrate
widening (dissociation) of the scapholunate interval in the presence of a complete
SLL tear [26]. Some advocate a clenched fist dynamic maneuver as more reliable
[27]. The normal distance between the scaphoid and the lunate bones is 2.9–4.5 mm
[28]. Sonography may be a reasonable screen for SLL tears [29]. The sonographic
finding of a normal, intact SLL essentially excludes scapholunate dissociation. If an
SLL tear is clinically suspected, dynamic sonography may reveal the diagnosis and
preclude the need for an MR arthrogram [29]. If you suspect a SLL tear, use US to
compare with the contralateral wrist. Stress US or radiographs (patient grips an
object firmly or makes a fist with maximal ulnar deviation) compared with neutral
views may show a gap (>4 mm on radiographs) between the two bones with an SLL
tear. This finding is known as the Terry Thomas sign, named after the comedian with
the large gap between his teeth [30].
Again, sonographic evaluation of the SLL is still considered inferior to MR or
CT evaluation [31]. Scapholunate ligament degeneration may occur with inflamma-
tory arthropathy, particularly calcium pyrophosphate deposition disease (CPPD)
and rheumatoid arthritis and is associated with intercarpal synovitis. Sonographic
detection of hyperechoic calcium crystals in the SLL is supportive evidence for
CPPD [32].
Triangular Fibrocartilage Complex Injury/Calcium Deposition
The TFCC, composed of cartilage and ligaments, stabilizes the ulnar aspect of the
wrist during rotational movements. This wide variety of wrist movements separates
humans from lower primates [33]. Causes of TFCC injuries include falling onto a
hyperextended wrist, using a bat or racquet, or a power drill injury torquing the
wrist. Damage to the TFCC presents with ulnar-sided wrist pain after an injury.
While a high-resolution US may be a suitable screen for TFCC tears, magnetic reso-
nance arthrogram imaging is the most accurate diagnostic tool [29]. Nonetheless,
TFCC lesions may still be challenging to diagnose, even with MR imaging [34].
On US, the AD typically has an elongated-to-triangular shape and lies just distal
to the ulnar head. It has a homogenous hypoechoic or slightly hyperechoic echotex-
ture. A tear manifests as a hypoechoic to anechoic fissure in the structure. Patients
with active rheumatoid arthritis in the wrist who demonstrate high PD scores are
prone to TFCC tears [35]. The TFCC is vital to evaluate in rheumatology since there
may be conspicuous calcium deposition in the AD and perhaps the MH. Such chon-
drocalcinosis is a solid clue to CPPD presence. In one study of patients with CPPD,
there was substantial agreement in the finding of chondrocalcinosis of the TFCC
comparing US and CT [32].
Ganglia
Ganglia are the most common masses of the wrist and hand [36]. These are cysts filled
with thick fluid and lined with a fibrous capsule [37]. They may be round, soft, firm,
painless, or tender on clinical examination. A ganglion has no synovial lining and hence
differs from a synovial cyst, in which the synovial membrane herniates through a joint
capsule. Many clinicians use the terms ganglion, ganglion cyst, and synovial cyst inter-
changeably. However, US cannot reliably differentiate between the two [38]. Ganglia
may be caused by trauma, arthritis of any cause, tendon injury, or tenosynovitis.
Ganglia may connect to joints, tendon sheaths, ligaments, joint capsules, or bur-
sae. Clinically undetectable (occult) ganglia are frequently detected by US [37].
Most ganglia occur at the wrist from either the dorsal capsule near the SLL or the
radial aspect of the volar wrist between the radial artery and the flexor carpi radialis;
Pitfalls 55
it is debatable which of these two locations is most common [39]. Other ganglia
locations include the ulnar aspect of the wrist associated with the triangular fibro-
cartilage complex tear. Ganglia sonographically appear hypoechoic to anechoic, are
well-defined, and may show septa [37]. Increased posterior through-transmission
may be noted [40]. There may be Doppler activity, which may or may not correlate
with symptoms [37]. The differential diagnosis for ganglia includes tenosynovial
giant cell tumor, epidermoid cyst, lipoma, tenosynovitis, rheumatoid nodule, gouty
tophus, tendon xanthoma, and synovial sarcoma [41]. If you detect a mass that may
be a ganglion, then look for a stalk and attempt to follow it down to its point of
origin. A stalk’s presence helps confirm the diagnosis while determining the under-
lying structural issue responsible for the ganglia.
Tenosynovitis
Tenosynovitis may clinically appear as a mass if there is significant hypertrophy

[37]. Ultrasound reveals a tendon surrounded by anechoic fluid or hypoechoic and
hypertrophied synovium (see Chap. 5).
Superficial Radial Nerve
The superficial branch of the radial nerve (SRN), a purely sensory nerve, becomes
superficial about 9 cm proximal to the styloid process of the radius [11, 42]. The
nerve bifurcates to supply the first and second webspaces and the dorsolateral
thumb. The practitioner should suspect SRN injury with a radius fracture or hard-
ware, fracture fixation pins, penetrating trauma, handcuffs, compression from tight
jewelry or a cast, and cephalic vein cannulation [11, 43, 44]. Additionally, the SRN
may be compressed between the brachioradialis muscle and the ECRL tendons,
known as Wartenberg’s Syndrome [7, 45]. Damage to the SRN produces lateral
wrist and thumb pain, numbness, and paresthesia similar to dQT symptoms [11].
Further, Wartenberg’s Syndrome may also be associated with dQT. A positive
Tinel’s test over the affected nerve may help to clinically discriminate between these
pathologic entities [44]. Ultrasound reveals a local thickening of the nerve, particu-
larly when compared with the contralateral side [11]. Ultrasound will distinguish
Wartenberg’s syndrome from dQT or trapeziometacarpal joint arthritis [7].
Pitfalls
1. Before performing an US exam for dorsal wrist pain, always mark the location
of the pain since this is useful in making the diagnosis.
2. When looking at the TFCC, do not mistake the MH for the AD, the latter being
thinner and abutting the ulnar head.
3. The examiner should delineate a dorsal ganglion cyst from a distended RCJ
recess [46].
4. If you detect a mass that may be a ganglion, look for a stalk and attempt to fol-
low it down to its point of origin to confirm the diagnosis. You may also be able
to determine the underlying structural issue responsible for the ganglia.
5. When examining the dorsal wrist in LAX, do not mistake the anisotropy of the
more superficial ER for true tenosynovitis or tenosynovial fluid. Such misiden-
tification of tissue for synovitis is called pseudotenosynovitis [46].
6. Another cause of pseudotenosynovitis in the LAX view of a tendon is the nor-
mal hypoechoic muscle tapering at the musculotendinous junction, mimicking
a thickened tenosynovium [46]. Avoid this pitfall by verifying what appears to
be tenosynovitis in two orthogonal planes.
7. Do not neglect to evaluate the tendon sheath of the ECU for inflammatory teno-
synovitis since this is a high-yield area when considering rheumatoid arthritis
[46–48].
8. Scapholunate ligament tears can be challenging to diagnose. With a complete tear,
the SLL may not be visible, but remember that nonvisualization of the SLL may
be expected in some individuals. Stress-view radiographs and US may be helpful.
9. Do not mistake the hypoechoic synovium superficial to the scaphoid and lunate
bones for an intact SLL in the TAX view [49].
10. A hypoechoic septum may exist between the APL and the EPB in the first
EC. Remember this if you contemplate injecting the first compartment, since
both sub-compartments may need to be separately injected.
11. In the first EC, accessory APL or EPB tendons may confuse the situation and
are essential to recognize since they may have separate tendon sheaths. If pres-
ent, accessory tendons may predispose to dQT and complicate potential surgi-
cal decompression. One trick is to look at the surrounding area and manually
abduct and extend the thumb to see if there are extra tendons present.
12. Locating the SRN may require a higher-frequency probe than 12 MHz, typi-
cally at least 17 MHz [6, 7].
13. Note that the SRN is ventral to the APL, so if you plan to inject the first EC or
the fascial plane between the first EC and the second EC, avoid a ventral
approach, which might injure the radial nerve and artery.
14. Tendonitis of the ECU may clinically mimic TFCC injury.
Method
The patient is seated opposite you, the wrist is neutral, and the forearm is halfway
between supination and pronation. The sonographer lines the thumb dorsum up with
the forearm. A rolled towel under the wrist may give added support. Ask the patient
to momentarily abduct the thumb to identify the anatomic snuff box, defined by two
extensor compartments at the base of the thumb on the radial aspect. In pen, draw
one line on each of the two tendons of the snuff box—the one closest to the palm is
the first EC, and the other one is the third EC.
Method 57
Next, palpate the dorsal distal radius and mark off the slight bony ridge, LT. Use
at least a 12 MHz linear probe for the examination, but be mindful that locating the
SRN may require a higher-frequency probe, perhaps 17 MHz or higher [6, 7]. Use
PD to find arteries and evaluate hyperemia.
rotocol Image 1: First Extensor Compartment at Scaphoid,

P
Transverse + Power Doppler (Fig. 3.6)
Center the probe over the first EC in TAX and find the radial styloid. It is bony,
superficial, and almost pointed. Perform a slight TAX slide distally until you see a
drop-off of bone (the radioscaphoid joint) and, continuing distally, see the deeper
bony scaphoid. Turn on the PD to see the large radial artery (RA) that should be
central and deep to the APL and EPB. Center the probe over the RA. The first EC is
superficial to the RA in this location. The APL is closer to the palm and may be
divided into three slips. The cephalic vein, detected on Color Flow, is at the same
level as the RA but is more dorsal.
Fig. 3.6 Protocol Image 1: First extensor compartment at scaphoid, transverse + power Doppler
Fig. 3.7 Protocol Image 2: First extensor compartment at scaphoid, transverse
rotocol Image 2: First Extensor Compartment at Scaphoid,

P
Turn PD off to focus on the APL. The APL is often divided into three slips and is
ventral to the EPB. The RA is central to and deep to the APL, whereas the SRN is
superficial to the APL. The nerve may not be well-visualized. The cephalic vein is
more dorsal and closer to the EPB. The APL and EPB may have accessory tendons
that predispose them to tenosynovitis of the first EC. Note that Protocol Images 1
and 2 are distal to the ER.
rotocol Image 3: First Extensor Compartment at Distal Radius,

P
Do a TAX slide proximally back to the bony distal radius to see the scaphoid
bone disappear and the distal radius reappear. Stop here. The thin hypoechoic
line superficial to the tendons of the first EC is the ER. The slender ER may be
Method 59
Fig. 3.8 Protocol Image 3: First extensor compartment at distal radius, transverse
challenging to visualize unless pathologically thickened, such as occurs

with dQT.
The three slips of the APL have merged into a single tendon. Many people will
have a hypoechoic septum between the APL and EPB. The septum may have a
slight associated bone elevation on the radius, a clue to its presence. The APL is
closer to the palm and is larger than the EPB. The two tendons are usually ovoid-
shaped, but they may be more rounded if tendinosis is present.
de Quervain’s tenosynovitis affects the tendon sheath and overlying ER. There
may be anechoic fluid in the tendon sheath, tendinosis, and ER thickening.
Remember, dQT is due to entrapment deep to the ER, often associated with overac-
tivity of thumb movement. Make sure that you are aware of the location of both the
RA and SRN before injecting. The SRN is next to the APL, closer to the palm (more
ventral), and outside the tendon sheath. Damage to the SRN may cause pain that can
mimic dQT.
Once you visualize the SRN in TAX, follow the nerve proximally or distally to
look for an area of damage or compression. The RA is now in a ventral/ulnar posi-
tion deep to the first EC. Accessory APL or EPB tendons may confuse the situation
and are very important to recognize since they may have separate tendon sheaths.
One trick is to look at the surrounding area and manually abduct and extend the
thumb to see if there are extra tendons present.
Fig. 3.9 Protocol Image 4: First extensor compartment at distal radius, transverse + power Doppler
rotocol Image 4: First Extensor Compartment at Distal Radius,

P
Transverse + Power Doppler (Fig. 3.9)
Next, turn on the PD to look at the RA and assess for PD activity that indicates pos-
sible acute tenosynovitis.
rotocol Image 5: First and Second Extensor Compartments at

P
Proximal Intersection, Transverse (Fig. 3.10)
Turn the PD off, then move the probe in TAX proximally, observing the APL as it
moves in an ulnar direction over the deeper second EC tendons. The crossing of the
first and second ECs, about 3–5 cm proximal to the wrist crease, is the potential
location for PIS. This intersection is more proximal to the site of dQT. The contents
of the first EC may look more muscular than tendon-like at this location since it is
Method 61
Fig. 3.10 Protocol Image 5: First and second extensor compartments at proximal intersection,
transverse
near the myotendinous junction. The second EC contents are typically formed ten-
dons at this location. If you have difficulty discriminating the first from the second
EC, tilt the probe to use anisotropy to your advantage.
If there is pain over the intersection of the first and second ECs, look for a thick-
ened fascia between the two compartments and possible tendinosis. Sonopalpatory
pain may be precipitated or aggravated by actively resisting the patient’s wrist

extension. Always compare what you think might be an abnormal US finding with
the normal contralateral limb.
rotocol Image 5a (Optional): First and Second Extensor

P
Compartments at Proximal Intersection,
Transverse + Power Doppler
Turn the PD on to look for inflammation and RA variants or branches. Make sure
that you are aware of the location of the RA and the SRN before injecting.
rotocol Image 6: Second Extensor Compartment at Distal

P
Radius, Transverse (Fig. 3.11)
Next, have the patient place the palm down and slightly flex the wrist downward
over the edge of the exam table. Do a TAX slide distally to the wrist crease to visual-
ize the first EC once again at the distal radius (Protocol Image 3). Then perform a
slight LAX slide in the ulnar direction to visualize LT, which should appear as a
sharp bony peak at the distal radius. The second EC is nestled next to the radial
aspect of LT with the ECRB tendon abutting LT.
Fig. 3.11 Protocol Image 6: Second extensor compartment at distal radius, transverse
Method 63
rotocol Image 6a (Optional): Second Extensor Compartment at

P
Distal Radius, Transverse + Power Doppler
Turn on the PD to look for hyperemia of the tenosynovium of the second EC.
rotocol Image 7: Third Extensor Compartment at Distal

P
Radius, Transverse (Fig. 3.12)
With the PD off, move the probe slightly in an ulnar direction and center it on the
first oval structure on the ulnar side of LT. A single tendon, the EPL, inhabits the
third EC. Verify that you are looking at the EPL by extending the first digit.
Fig. 3.12 Protocol Image 7: Third extensor compartment at distal radius, transverse
Fig. 3.13 Protocol Image 8: Third extensor compartment at distal intersection, transverse
rotocol Image 8: Third Extensor Compartment at Distal

P
Intersection, Transverse (Fig. 3.13)
The thin EPL runs diagonally in a radial direction to the first digit; you may be able
to follow this in TAX or LAX to its insertion on the dorsum of the first digit, distal
phalanx. The third EC comprises the ulnar aspect of the anatomic snuff box. On its
way to its insertion, the EPL is superficial to the second EC as it crosses over. This
crossing may cause DIS. The EPL and ECRB share a joint opening with their ten-
don sheaths, and in DIS, both the second and third ECs will show tenosynovitis
[8]. You may find it challenging to visualize the EPL in LAX beyond the dis-
tal radius.
rotocol Image 8a (Optional): Third Extensor Compartment at

P
Distal Intersection, Transverse + Power Doppler
Turn on the PD to look for tenosynovitis if DIS is suspected.

Method 65
rotocol Image 9: Scapholunate Joint, Transverse ± Stress View

P
(Fig. 3.14)
Go back to the distal radius in TAX and center the probe over LT. Move the trans-
ducer distally, and the radius will drop out of view. Continue moving the TAX slide
distally until you see two bones with an intervening space. The scaphoid is radial,
and the lunate is on the ulnar aspect. You are now looking for the SLL that should
bridge these two carpal bones. You can see the ligament in about 50% of healthy
people. Therefore, you may normally see some or none of the SLL. If you visualize
it completely, that is strong evidence that no significant tears are present. If you
suspect an SLL tear, measure the distance between these two bones with and with-
out stress (the patient makes a fist and flexes the wrist in an ulnar direction). Compare
this distance with the contralateral side. Do not misidentify the hypoechoic synovium
superficial to the scapholunate joint as the SLL.
Fig. 3.14 Protocol Image 9: Scapholunate joint, transverse ± stress view

rotocol Image 10: Fourth and Fifth Extensor Compartments at

P
Distal Radius, Transverse (Fig. 3.15)
Next, with the wrist back in a neutral position, perform a slight TAX slide proxi-
mally back to LT and then an LAX slide in the ulnar direction. You will see the third
EC and the adjacent fourth and fifth ECs. You can verify the fifth EC identity since
it is superficial to the DRUJ. The fourth EC contains ED and EI, and the fifth EC
contains EDM. The second and fifth fingers each have a second extensor tendon, the
EI and EDM, respectively. Move the digits manually to verify which tendons are in
the fourth and fifth compartments. If necessary, add additional images for any ten-
don in LAX and TAX, with and without PD.
Fig. 3.15 Protocol Image 10: Fourth and fifth extensor compartments at distal radius, transverse
Method 67
Fig. 3.16 Protocol Image 11: Distal radioulnar joint at distal radius, transverse ± power Doppler
rotocol Image 11: Distal Radioulnar Joint at Distal Radius,

P
Transverse ± Power Doppler (Fig. 3.16)
Next, focus on the flat distal radius and a curved, semi-circular ulnar head. The fifth
EC sits at this junction, superficial to the joint space of the DRUJ. Perform a TAX
slide proximally and then distally to fully evaluate the DRUJ. Use PD if you are
looking for synovitis.
rotocol Image 12: Sixth Extensor Compartment at Distal Ulna,

P
Transverse + Dynamic Exam (Fig. 3.17)
Place a rolled towel beneath the wrist to elevate it, and place the wrist in a slight
radial deviation. Perform a LAX slide in an ulnar direction to center the probe over
the ulnar bone, then perform a TAX slide distally. You should see a curved semi-
circular bony structure, the ulnar groove for the ovoid ECU. Observe the ER, which
is superficial to the tendon. You may want to perform slight distal and proximal
TAX slides as you rotate the transducer around the distal ulna bone to inspect for
rheumatoid bone erosion [50]. Make sure to look at the tenosynovium surrounding
the ECU for thickening since tenosynovitis of this tendon sheath may be an early
sign of rheumatoid arthritis and may predict erosion progression [20].
Fig. 3.17 Protocol Image 12: Sixth extensor compartment at distal ulna, transverse + dynamic exam
The ECU location typically changes with pronation and supination. To dynami-
cally evaluate for ECU subluxation, the patient plants the elbow on the exam table,
forearm in a vertical position, palm facing away. Place the probe in TAX across the
distal ulna to visualize the ECU. Have the patient slowly rotate the palm inward to
a neutral position and then toward the patient. Slowly move the transducer along
with the rotating forearm by keeping the ECU in focus and observing its relation to
the underlying distal ulna. The ECU should move to a dorsal location but may dis-
locate out of the groove if the subsheath deep to the ER is damaged. When doing
dynamic testing, apply the probe lightly in TAX to avoid tethering the
ECU. Remember that many ordinary people will have some degree of asymptom-
atic ECU subluxation.
Method 69
Fig. 3.18 Protocol Image 13: Sixth extensor compartment at distal ulna, longitudinal
rotocol Image 13: Sixth Extensor Compartment at Distal Ulna,

P
Longitudinal (Fig. 3.18)
Go back to the initial position in Protocol Image 12, using a rolled towel beneath the
wrist. Pronate the forearm, center the ECU in the image in TAX, and then rotate the
probe 90° to look at the ECU in LAX. Then perform a TAX slide around the ulnar
styloid (toward the palm) to look at the entire tendon. Visualize the hyperechoic
lunate in a moderately deep location. This slide around the distal ulna may reveal an
ulnar styloid fracture or bone erosion not apparent on radiographs.
rotocol Image 14: Triangular Fibrocartilage Complex,

P
Longitudinal + Radial Deviation Wrist (Fig. 3.19)
With the probe still in LAX, have the patient radially flex the wrist to facilitate the
evaluation of the soft tissues of the TFCC. The proximal bone is the distal ulna, and
the triquetrum is the distal bone. The moderately deep, slightly curved bone is the
Fig. 3.19 Protocol Image 14: Triangular fibrocartilage complex, longitudinal, radial devia-
tion wrist
lunate. The deepest visible bone, however, is the distal radius. Abutting the distal
ulna is the AD, which appears as a hypoechoic (or slightly hyperechoic) elongated
triangle in a vertical orientation toward the radius. Deep to the ECU tendon and
between the AD and triquetrum is the location of the MH. A slight tilting of the
probe helps to delineate these structures. Look for calcium deposits in the AD, a
finding that may indicate CPPD. The AD and MH may be difficult to delineate in
the absence of calcification.
rotocol Image 15: Radiocarpal Joint at Scaphoid

P
and Trapezoid, Longitudinal ± Power Doppler (Fig. 3.20)
Next, remove the towel and place the wrist in a pronated, flat, and neutral position
directly on the examination table. Go back to the TAX view of the dorsal scaphoid
and lunate (Protocol Image 9). Move the probe in an LAX slide in a radial direction
to center it over the scaphoid. Rotate the probe 90° to LAX to see the scaphoid and
the more distal trapezoid in LAX. Turn on PD to look for joint recess synovitis
if needed.
Method 71
Fig. 3.20 Protocol Image 15: Radiocarpal joint at scaphoid and trapezoid, longitudinal ±
power Doppler
rotocol Image 16: Radiocarpal and Intercarpal Joints,

P
Longitudinal ± Power Doppler (Fig. 3.21)
Perform a slow TAX slide in the ulnar direction. The scaphoid disappears, and you
then see the lunate and, more distally, the capitate bone. Examine the dorsal recesses
and the extensor tendons, looking for crystal deposition and effusion in the recesses.
Turn on the PD if necessary to delineate synovitis. Be wary of feeder blood vessels
(located superficial to the joint recesses) mimicking PD activity (see Chap. 5 for
further information).
Complete Dorsal Wrist Ultrasonic Examination Checklist
□ Protocol Image 1: First extensor compartment at scaphoid, transverse + power
Doppler.
□ Protocol Image 2: First extensor compartment at scaphoid, transverse.
□ Protocol Image 3: First extensor compartment at distal radius, transverse.
□ Protocol Image 4: First extensor compartment at distal radius, transverse + power
Doppler.
□ Protocol Image 5: First and second extensor compartments at proximal intersec-
tion, transverse.
Fig. 3.21 Protocol Image 16: Radiocarpal and intercarpal joints, longitudinal ± power Doppler
□ Protocol Image 5a (optional): First and second extensor compartments at proxi-

mal intersection, transverse + power Doppler.
□ Protocol Image 6: Second extensor compartment at distal radius, transverse.
□ Protocol Image 6a (optional): Second extensor compartment at distal radius,
transverse + power Doppler.
□ Protocol Image 7: Third extensor compartment at distal radius, transverse.
□ Protocol Image 8: Third extensor compartment at distal intersection, transverse.
□ Protocol Image 8a (optional): Third extensor compartment at distal intersection,
transverse + power Doppler.
□ Protocol Image 9: Scapholunate joint, transverse ± stress view.
□ Protocol Image 10: Fourth and fifth extensor compartments at distal radius,
transverse.
□ Protocol Image 11: Distal radioulnar joint at distal radius, transverse ± power
Doppler.
□ Protocol Image 12: Sixth extensor compartment at distal ulna, transverse +
dynamic exam.
□ Protocol Image 13: Sixth extensor compartment at distal ulna, longitudinal.
□ Protocol Image 14: Triangular fibrocartilage complex, longitudinal, radial devia-
tion wrist.
□ Protocol Image 15: Radiocarpal joint at scaphoid and trapezoid, longitudinal ±
power Doppler.
□ Protocol Image 16: Radiocarpal and intercarpal joints, longitudinal ± power
Doppler.
References 73
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Chapter 4
Fingers

1. Finger pain, stiffness, or dysfunction.
2. Evaluation of soft tissue swelling or masses.
3. Pain or weakness after trauma.
4. Loss of finger extension or extension capability.
1. What is the cause of finger pain? Is it injury, a functional issue, an inflammatory
process, or a tumor?
2. Is synovitis, tenosynovitis, or enthesitis present, and if so, what is the cause?
3. Is there an underlying inflammatory condition affecting the hand, and if so, is it
a systemic process such as spondyloarthropathy, rheumatoid arthritis, or crystal
disease?
5. Is there a structural, functional, or repetitive injury problem?
7. What is this lump on the finger?
8. Are tendons/ligaments/cartilage normal in appearance?
9. Is there evidence for ganglion cysts, and if so, is the origin the joint or the ten-
don sheath?
10. What is causing a triggering finger?
11. What is the first carpometacarpal joint’s status?
States Government.

Switzerland AG 2023
78 4 Fingers
Fig. 4.1 Finger joints
Necessary Basic Anatomy (Fig. 4.1)
The remarkable dexterity of the human finger is directly related to its complex
anatomy.
Digits 2 Through 5
For digits 3 and 4, think of the number 3 [1]:

Three joints: metacarpophalangeal, proximal interphalangeal, and distal
interphalangeal
Three phalanges: proximal, middle, and distal
Three of the five annular pulleys (A1, A3, and A5) are over the flexor surfaces of the
three finger joints in each digit.
Three cruciate pulleys (C1–3) are poorly seen on US due to anisotropy
Three tendons: flexor digitorum superficialis (FDS), flexor digitorum profundus
(FDP), and the extensor tendon (ET)
Digits 2 and 5 each have an additional extensor tendon (the extensor indicis (EI)
and extensor digiti minimi (EDM), respectively).
Extensor Tendons (Fig. 4.2)
The extensor tendons run along the dorsal aspect of the finger. The ETs are incom-
pletely ensheathed in a tenosynovium, and a paratenon covers the portion of the ET
over the metacarpophalangeal joint (MCPJ) [2]. Distal to the MCPJ, the ET splits
into a central and two lateral slips (bands) [3]. The central slip inserts into the dorsal
Fig. 4.2 Extensor tendon

simplified
80 4 Fingers
aspect of the base of the middle phalanx, while the lateral slips insert into the dorsal
part of the distal phalangeal base.
Flexor Tendons (Fig. 4.3)
The two flexor tendons (FTs), one deep (FDS) and one shallow (FDP), are stacked
upon each other on the volar aspect of the MCPJ [1]. A tenosynovium surrounds the
FTs. The FDS splits in two at the proximal phalanx. Each segment of the FDS
moves along the side of the FDP and then inserts into the middle phalanx, deep into
the FDP. The FDP goes on to insert on the distal phalanx base.
Fig. 4.3 Flexor tendons

simplified
Finger Pulleys (Fig. 4.4)
The flexor tendon sheath is strapped down to the bone via the annular and cruciate
pulleys [3]. The pulley system prevents bowstringing of the FTs during finger flex-
ion. The Cl pulley is classically designated between the A2 and A3 annular pulleys.
Some authors delineate the cruciate pulley between the A1 and A2 pulleys as C1
and renumber the cruciate ligament system as C1–C4 [4]. For consistency, we have
chosen the original designation of three cruciate ligaments as C1–C3, with the C1
located between the A2 and A3 pulleys.
Annular pulleys A1–A4 are usually visible with high-frequency transducers [5].
These annular pulleys appear in longitudinal (LAX) view as elongated hyperechoic
structures; however, they may be hypoechoic depending on anisotropy. In the trans-
verse (TAX) view, each annular pulley is slightly hyperechoic at the most superficial
portion of the flexor tendon but becomes hypoechoic to anechoic as the pulley
drapes down along the edges of the flexor tendons [5]. The sonographer can visual-
ize the C1 cruciate pulley in LAX view nearly 50% of the time, appearing as a
thickened longitudinal hyperechoic structure. Annular pulley A5 and cruciate pul-
leys C2 and C3 are usually not visible sonographically [5].
Fig. 4.4 Volar finger

annular and cruciate
pulleys
82 4 Fingers
Volar Plates
All finger joints have thick fibrocartilage volar, or palmar, plates to limit finger
hyperextension [3]. In LAX view, these are seen as a hyperechoic triangular struc-
ture superficial to the articular cartilage. The volar plate over the metacarpal head is
the easiest to visualize.
Extensor Hood
The extensor hood (EH), a fibrous tissue that covers the ET, keeps the ET in place
at the MCPJ [1]. Sagittal bands from the EH travel along both sides of the MCPJ to
the volar plate, thus stabilizing the ET.
First Digit
Three pulleys: two annular and one oblique

Two phalanges: proximal and distal
Two joints: the first metacarpophalangeal and the interphalangeal
Two extensor tendons
Two flexor tendons
Two abductor tendons
One adductor pollicis tendon
One opponens pollicis tendon
Clinical Comments
Several pathologic entities occur in the fingers. Please refer to other chapters for
more information (Table 4.1).
Table 4.1 Common pathologies of the fingers by chapter

Introduction Hand arthropathies Crystalline disease
Fracture Synovitis Gout
Neuroma Erosions Calcium pyrophosphate deposition
disease
Dorsal wrist Tenosynovitis Hydroxyapatite deposition disease
De Quervain’s tenosynovitis Paratenonitis
Forefoot Enthesitis
Foreign bodies Tendon damage
Masses
Pathology by Location
It is clinically helpful to classify finger pathology according to dorsal, ventral, and

lateral locations.
Dorsal Aspect
Extensor Tendon Tears
Extensor tendon tears may result from open or closed injury [6]. The examiner
should describe the tear location and whether it is complete or partial thickness. For
partial-thickness tears, define the percentage of tendon involved; for complete ten-
don tears, describe the degree of tendon retraction and any associated avulsed bony
fragment [6]. Full-thickness tears present sonographically as tendon discontinuity,
and the stumps may show loss of normal fibrillar echotexture with evidence of ten-
dinopathy [6]. If retracted, there may be a complete absence of the tendon. Use
dynamic views to evaluate the gap between tendon stumps.
Partial-thickness tears sonographically appear as incomplete discontinuities or
focal losses of fibular echotexture [6]. If acute, there may be hypoechoic to anechoic
tendon abnormalities, perhaps with tendon swelling or a hematoma. Chronic partial-
thickness tears reveal hypoechogenicity with surrounding fibrosis [6]. Bony frag-
ments within the tendon are hyperechoic with posterior shadowing.
Mallet Finger
Also called baseball finger, this occurs when sudden, forceful extreme flexion of the
extended distal interphalangeal joint (DIPJ) injures the ET at its insertion on the
base of the distal phalanx [3]. For example, this injury may occur when a baseball
hits a fingertip. Patients present with pain, swelling, and a loss of ability to extend
the DIPJ [3]. Untreated, a swan neck deformity may ensue [6]. Ultrasound (US)
reveals the disrupted insertion of the ET on the distal phalanx and tendon swelling
[3, 6]. There may also be a retracted tendon in the form of a soft tissue mass, with a
detached avulsed bone fragment.
Central Slip Injury
The central slip of the ET at the base of the middle phalanx may be injured due to
sudden flexion of the proximal interphalangeal joint (PIPJ), direct trauma to the
dorsal surface of the middle phalanx, or volar dislocation of the PIPJ [6]. This injury
acutely presents with pain and swelling, along with a diminished ability to extend
the PIPJ. Some extension capability is initially retained at the PIPJ if the lateral slips
remain intact [3].
84 4 Fingers
The unaffected lateral slips eventually migrate in a volar direction, producing

PIPJ flexion and DIPJ extension and, ultimately, the boutonniere deformity [3].
Therefore, overlooking a central slip lesion may result in a permanent boutonniere
deformity [6]. To confirm the pathology, place the probe in LAX over the dorsal
PIPJ to look for a central ET defect and abnormal gliding of the central tendon slip
with finger flexion and extension.
Boxer’s Knuckle
Sagittal bands are part of the dorsal EH located at the MCPJ. The bands connect
the volar plate to the ET and prevent ET subluxation during movement [6].
Sagittal band disruption commonly occurs with direct trauma to the proximal
phalanx of the dorsal MCPJ, such as in boxing [3]. The resultant radial or ulnar
subluxation or dislocation of the ET adversely affects MCPJ extension [3, 6].
Ultrasound reveals a hypoechogenic abnormal sagittal band. The ET may be
normal or swell and lose fibrillar pattern [3]. Dynamic US in the TAX view
shows subluxation or dislocation of the ET between the metacarpal heads with
MCPJ flexion [6].
Paratenonitis
Extensor tendons of the fingers do not have an actual tenosynovial sheath; however,
a paratenon surrounds the portion of the ET dorsal to the MCPJ. Inflammatory con-
ditions, overuse, and trauma may cause paratenonitis [6].
Volar Aspect
Flexor Tendon Injury
Tendon sprain can result in tendinopathy and increased FT thickness, most reliably
evaluated near the A1 pulley [6, 7]. Comparison to the contralateral FT is useful.
Since the FDP inserts on the distal phalanx base and the FDS inserts on the middle
phalanx, it is relatively easy to differentiate the two tendons on both TAX and LAX
views [3]. Passively flexing and extending the PIPJ will activate both FTs, whereas
moving the DIPJ in isolation will actuate only the FDP. Dynamic US is standardly
done with active, passive, and resisted FT evaluations to delineate partial and com-
plete tears [3]. Ultrasound shows partial tears as hypoechoic fusiform swelling of
the tendon with focal loss of fibrillar echotexture. You may not find the tendon in a
complete tear, only stumps [3].
Jersey Finger
The distal FDP tendon insertion may be injured when the DIPJ is bent and then
forcefully hyperextended, such as in sports when a player grabs a jersey, and the
opponent accelerates away [6]. The fourth finger is most often affected. A complete
tear may cause the tendon to retract, leaving an empty tendon sheath. There may
also be a bone avulsion [6]. This injury results in an inability to flex the DIPJ.
Trigger Finger
Trigger finger is a form of stenosing tenosynovitis. It most commonly arises at the

A1 pulley, superficial to the palmar aspect of the MCPJ. As the patient bends the
finger, there is a brief blockage of the FT and subsequent painful snapping when it
is extended [8]. A thickened A1 pulley compresses the FT, provoking tendon
impingement, swelling, and tenosynovitis. The first, third, and fifth fingers are most
involved [8]. In most cases, trigger fingers are idiopathic or due to repetitive micro-
trauma. However, athletes who use rackets may be prone to direct pressure on the
A1 pulley. Other conditions that may predispose to trigger finger include trauma,
diabetes, rheumatoid arthritis (see below), amyloid, hypothyroidism, and acromeg-
aly [8]. Less typically, trigger finger may result from scarring, tumors, or peritendi-
nous ganglion cysts [8].
Hypoechoic thickening of the A1 pulley is best seen on the TAX view. An A1
pulley thickness greater than 0.62 mm is a cutoff value in healthy adults [9]. Along
with intermittent locking during extension, the trigger finger may present with a
palmar tender nodular area due to A1 pulley thickening [8]. Potential sonographic
findings with trigger fingers [3] are as follows:
(a) Diffuse hypoechoic thickening of the A1 pulley.
(b) Swollen, rounded appearance of the FT in TAX view.
(c) Real-time visualization of the locking/snapping of the flexor tendon at
the MCPJ.
Sometimes, it is just the FDS, contiguous to the A1 pulley, that will catch while
the FDP movement remains unhindered. A ganglion cyst uncommonly arises from
the FT sheath near the A1 pulley but may cause a trigger finger; ganglion removal
may be necessary to prevent the recurrence of the trigger finger [10]. Ultrasound can
evaluate trigger fingers and guide treatment decisions [11].
(See Chap. 5 for more information.)
Tenosynovitis
Flexor tenosynovitis may be due to trauma, inflammatory arthropathy, overuse, or

infection [6]. Ultrasound reveals acute changes such as tenosynovial effusion, dis-
tended tenosynovium, and hyperemia on power Doppler (PD). The FT may lose its
86 4 Fingers
normal fibrillar echotexture and become thickened [6]. In more chronic flexor teno-
synovitis, the synovial sheath may thicken, producing a “blurred image” of the ten-
don [6, 12]. Foreign bodies from penetrating trauma may also cause tenosynovitis
[6]. Chronic inflammatory arthropathy may be associated with small echogenic par-
ticles called rice bodies. Chronic overuse may produce a thickened pulley, leading to
stenosing tenosynovitis and trigger finger. Ultrasound provides needle injection
guidance and may assess the efficacy of treatment for the inflammatory condition [6].
Rock Climber Finger
Ultrasound reveals the normal annular pulley to be 0.3–0.5 mm in thickness [6]. In

LAX view, the pulley looks like a hyperechoic line on top of an oblong center that
is anechoic to hyperechoic and rests on the outer edge of the FDS tendon. On the
TAX view, the pulley appears hyperechoic at the volar aspect and hypoechoic at the
lateral aspect due to anisotropy [6].
In rock climbers, the combination of PIPJ flexion coupled with DIPJ hyperexten-
sion generates excessive stress on the pulley. This injury most commonly affects the
A2 pulley of the third and fourth digits [6]. Baseball players, bowlers, and patients
receiving multiple corticosteroid injections near the pulley may also develop an A2
pulley injury [4]. Rock climbers routinely have thickened annular pulleys [6]. The
pulley may be subject to strains or partial or complete tears, with the latter causing
FT bowstringing.
Measuring the tendon-to-bone distance (TBD) in LAX view between the FT and
bone is a sensitive method to detect milder degrees of bowstringing [6]. Compare
the volar tendon position at rest and dynamically in resisted flexion. The normal
TBD at the A2 pulley ligament is less than 2 mm [6]. There are various opinions on
what absolute TBD value is consistent with a complete A2 tear, but values greater
than 2 mm should heighten suspicion for an A2 injury [4]. Partial pulley tears pro-
duce minimal to no FT displacement. Still, the pulley may appear hypoechoic and
swollen on US, perhaps exhibiting hyperemia on PD with a more acute injury [6].
In addition to bowstringing, sonographic findings associated with A2 pulley inju-
ries include the frank absence of the pulley in LAX view, an FT sheath cyst, tenosy-
novial fluid, the presence of fibrous tissue, PIPJ or DIPJ effusion, or thickening of
the A2 pulley [4]. One literature review describes that US and MRI have similar
accuracy for diagnosing A2 pulley injuries; however, US offers a dynamic assess-
ment of the FT pulley system and easy side-to-side comparison [4].
Volar Plate Injuries (Fig. 4.5)
The volar plate is a fibrous structure located just superficially to the cartilage of the
volar PIPJ and MCPJ, abutting the FT. It sonographically appears as a hyperechoic,
curvilinear form covering the joint cartilage. A high-frequency transducer is neces-
sary to evaluate correctly. If suddenly hyperextended, the volar plate, particularly
Fig. 4.5 Volar plate injuries
the PIPJ plate, may sustain a substance tear or, more commonly, a bony avulsion of
the distal insertion on the middle phalanx with an intact volar plate [3]. Lateral
radiographs may suggest a bony avulsion; US confirms a hyperechoic cortical bony
fragment. A hypoechoic cleft within a swollen volar plate signifies a volar plate
substance tear [3]. A full-thickness tear through the volar plate is less common than
a bone avulsion at the distal insertion. If the avulsion fracture at the distal insertion
of the PIPJ volar plate is substantial and involves the collateral ligaments, the mid-
dle phalanx may become unstable and chronically dislocated [13].
88 4 Fingers
A full-thickness volar plate tear will appear as a hypoechoic discontinuity within

the volar plate on US [14]. The plate may retract with a full-thickness tear, demon-
strating an increased gap when the joint is stressed in hyperextension. Treatment
depends on the size of the bony avulsion and joint instability [15]. Ultrasound helps
gauge volar plate stability and assess edema resolution when treating
conservatively.
Dupuytren’s Disease
Also called palmar fibromatosis, Dupuytren’s disease occurs in up to 2% of the

population and appears as a thickening of the palmar aponeurosis [3, 16, 17]. This
fibrous tissue, usually occurring in older men, most often affects the third and fourth
fingers [17]. It can present as nodules, cords, or thick fibrous bands and may prog-
ress to involve the FTs causing flexion contractures that limit finger movement.
Ultrasound reveals a hypoechoic structure overlying and possibly adhering to the
FT. [17]. This nodular, hypoechoic lesion is located between the FT and the skin and
has sharp margins but no internal hyperemia on Doppler [3]. Dynamic finger move-
ments reveal adherence if present [3, 17].
Ganglion Cysts
These cysts contain mucoid material surrounded by fibrous tissue but lack a syno-
vial lining [3, 18]. Ganglia may also occur along the palmar aspects of the fingers
near the A1 pulleys, presenting as painful, firm masses [16]. Ultrasound reveals
small anechoic lesions adjacent to interphalangeal joints or tendon sheaths with
posterior acoustic enhancement [19]. Ganglion cysts often occur along the FTs in
the lateral and medial aspects. Still, they do not seem to directly affect the tendon
itself since dynamic US reveals no impedance of FT movement or position change
of the cyst [3].
Transection Neuromas
Small caliber palmar digital nerves are prone to injury during finger laceration [20].
High-frequency US helps diagnose traumatic digital nerve injuries. The TAX view
may reveal a loss of nerve continuity that can be confirmed in the LAX view [20].
An injured nerve may eventually form a posttraumatic neuroma. These may occur
as a stump neuroma or a neuroma-in-continuity and appear as a hypoechoic, well-
defined mass lacking internal vascularity [20].
Glomus Tumor
Glomus tumors are rare benign vascular tumors that occur most commonly on the
fingertips and under the fingernail [21]. These are extremely painful nodules and are
often temperature-sensitive [3]. The US appearance is that of a small solid mass
beneath the fingernail with homogeneous hypoechogenicity and perhaps erosion of
underlying phalangeal bone. Doppler activity may reveal a mass with hyperemia,
but a lack of Doppler activity does not rule out the presence of this lesion [16, 21,
22]. While there are no specific sonographic findings for glomus tumors, excruciat-
ing pain with a hypervascular mass beneath the fingernail is diagnostically useful
[3, 23]. MRI remains the best diagnostic test to differentiate the mass from other
soft tissue tumors [3, 24].
Tenosynovial Giant Cell Tumors
Giant cell tumor (GCT) is a localized form of pigmented villonodular synovitis,

which affects the tendon sheath and is often nodular [16]. These slow-growing, firm
masses are common soft tissue tumors of the hand and wrist, primarily affecting the
distal fingers’ volar aspect. On US, a tenosynovial GCT is homogeneous, hypoechoic,
well-defined, in close contact with a tendon, and has a variable Doppler appearance
[16]. These tumors have internal echoes and lack posterior acoustic enhancement [3].
In addition, these masses may be lobulated, do not move with tendon movement, and
produce pressure erosions of the bony cortex. Pathologic verification is required [16].
Lateral Aspects
The volar plate and collateral ligaments stabilize the MCPJs and PIPJs [3]. With
high-frequency transducers, we can evaluate the collateral ligaments of the inter-
phalangeal joints. The MCPJ collateral ligaments are sonographically inaccessible
in the LAX view except for the first MCPJ, the radial aspect of the second MCPJ,
and the ulnar part of the fifth MCPJ [3]. The anisotropic collateral ligaments appear
on US as hyperechoic to hypoechoic bands traversing the joint.
Ulnar Collateral Ligament Injuries (Fig. 4.6)
The first digit ulnar collateral ligament (UCL) at the MCPJ, integral for joint func-
tion and stability, may be injured with sudden hyperabduction and hyperextension
[25, 26]. This injury typically occurs during a fall while gripping a ski pole, but
years ago it resulted from a repetitive injury from strangling wounded rabbits
(“gamekeeper’s thumb”). Immediate imaging is necessary to determine if surgery is
needed since delay may result in chronic pain, osteoarthritis, and decreased hand
90 4 Fingers
Fig. 4.6 Ulnar collateral ligament tears
function [26]. MRI is the gold standard for characterizing UCL tears, but US has
also proven highly accurate [27]. A UCL tear may range from a simple sprain to
partial and full-thickness tears [26].
A partially torn UCL appears on US as hypoechoic and thickened [3].
Nondisplaced complete UCL tears have a stump near the proximal or distal inser-
tion of the ligament, which remains in anatomic alignment. This nondisplaced UCL
is a gamekeeper’s or skier’s thumb [3]. However, when the proximal stump of a
completely torn UCL displaces out of anatomic alignment, it ceases to be called a
gamekeeper’s thumb. It is now characterized as a Stener lesion that will not heal
with conservative management [3, 26, 28].
The defining feature of a Stener lesion is that the rolled-up stump is either at the
proximal edge or superficial to the adductor aponeurosis. The US appearance of a
Stener lesion demonstrates the proximal UCL stump to be a hypoechoic mass adja-
cent to the metacarpal neck and head; the hyperechoic adductor aponeurosis appears
to be leading into the mass [26, 27]. This appearance resembles a “yo-yo on a
string.” The yo-yo is the retracted proximal UCL stump, folded up upon itself, and
the string is the adductor aponeurosis [26]. It is noteworthy that the rolled-up UCL
remnant location is not always superficial to the adductor aponeurosis, yet is still
characterized as a Stener lesion [28].
Ultrasound may also detect bony avulsions since radiographs are not sensitive in
this regard [26]. A pitfall is that an injured adductor aponeurosis may mimic intact
UCL fibers. Gently passively flexing and extending the interphalangeal joint will
identify the aponeurosis by showing the movement of the adductor aponeurosis
gliding smoothly over the MCPJ [28].
Ulnar Digital Neuroma
Traumatic irritation of the ulnar digital nerve of the first digit may occur in bowlers
and less commonly in baseball players, massage therapists, and jewelers [29]. This
repetitive trauma produces a painful soft tissue nodule along the ulnar/volar aspect
of the thumb in the web space between the first two digits. In addition, paresthesia
may extend along the medial aspect of the thumb, and Tinel’s sign might be positive
[29]. Ultrasound may successfully detect a neuroma when MRI fails, although, his-
torically, MRI has been the imaging modality of choice.
First Carpometacarpal Osteoarthritis
First carpometacarpal joint osteoarthritis commonly causes pain and disability, par-
ticularly in older populations. In a study of 93 participants, plain radiographs and
US comparably detected osteophytes, with US being more sensitive [30]. The
detection of erosions was also similar, although US may not depict some erosions
due to occluding osteophytes. Power Doppler activity in the first carpometacarpal
joint (CMCJ) correlated with increased severity of thumb base pain [30]. However,
pain and function are poorly associated with radiographic and US structural findings.
Rheumatoid Arthritis
Rheumatoid arthritis (RA) may affect fingers in myriad ways. Inflammation may
produce paratenonitis over the MCPJ, tenosynovitis of the flexor tendons, and syno-
vitis of the MCPJs and PIPJs [2]. Rheumatoid nodules may develop along tendon
sheaths and in subcutaneous tissue [31, 32]. Flexor and extensor tendon rupture may
occur due to chronic tenosynovitis causing secondary tendinopathy or from the abra-
sive effect of eroded bone or osteophytes. Synovitis of the MCPJs may loosen the
joint capsule and surrounding ligaments, resulting in ulnar drift, exacerbated by ten-
don subluxation or dislocation [31]. Likewise, the instability of PIPJs and DIPJs may
culminate in swan neck or boutonniere deformity. Rheumatoid arthritis increases the
predisposition to trigger fingers under the A1 pulley due to localized synovitis, teno-
synovitis, and rheumatoid nodules. Do not mistake the smooth groove-like curve
92 4 Fingers
proximal to the end of the dorsal metacarpal head as a bony erosion [28]. This “pseu-
doerosion” is the normal attachment point for the synovial membrane.
Pitfalls
1. When dynamically evaluating tendons with US, test passive, active, and resisted
movement.
2. Full-thickness tears may result in a loss of continuity or the absence of the ten-
don. The retracted tendon may form a soft tissue mass with a detached avulsed
bone fragment. Do not neglect to search for stumps.
3. Acute finger injuries need rapid evaluation to avoid permanent dysfunction or
deformity. Do not hesitate to obtain an MRI to confirm a sonographic diagnosis.
Timely referral to hand surgery is of paramount importance.
4. An extensor tendon central slip injury may present with a retained ability to
extend the PIPJ due to intact lateral slips of the extensor tendon. Do not incor-
rectly perceive this as a lack of damage to the central slip. Overlooking a central
slip injury may result in a permanent boutonniere deformity.
5. Direct injury to the MCPJs may disrupt the extensor hood sagittal band, causing
lateral subluxation of the extensor tendon. Do not neglect to perform dynamic
US in TAX view to diagnose tendon subluxation or dislocation.
6. With a volar finger laceration, suspect a traumatic digital nerve injury. Perform
careful US interrogation in TAX with confirmation in LAX view. Transected
nerves need to be promptly diagnosed with an immediate referral to a hand surgeon.
7. Do not neglect to assess the FDS and FDP in isolation. Passively flexing and
extending the middle and distal phalanges at the PIPJ activates both flexor ten-
dons, while bending the isolated DIPJ will move only the FDP.
8. A ganglion cyst arising from the flexor tendon sheath near the A1 pulley in the
presence of a trigger finger often requires the removal of the ganglion cyst to
prevent the recurrence of the trigger finger.
9. In any sudden hyperextension injury, examine the volar plate to look for evi-
dence of a substance tear or bony avulsion.
10. First MCPJ UCL injury diagnostic pitfalls:
(a) Do not mistake an injured abductor aponeurosis for intact UCL fibers.
Gentle passive extension and flexion of the interphalangeal joint will dem-
onstrate the gliding of an intact adductor aponeurosis. Overzealous joint
manipulation may convert a partial UCL tear into a complete one.
(b) The UCL remnant may be superficial to the adductor aponeurosis or located
at the proximal edge.
(c) Small bony avulsions noted on US but undetected radiographically may be
diagnostically helpful.
11. Beware of the dorsal metacarpal head “pseudoerosion,” which is a normal ana-
tomic indentation.
Method 93
Method
The patient faces the examiner with the pronated hand flat on a table or arm of the
chair. Start with the dorsal surface of the fingers. A rolled-up towel placed under the
fingers may help slightly bend the fingers to improve joint visualization. For the
volar aspect of the fingers, the hand is supinated, palm up, with extended fingers.
The examination for digits 2 through 5 is identical for each finger, although the
second and fifth digits offer additional radial and ulnar views. For the thumb, views
of the radial first CMCJ and the ulnar first MCPJ are most productive.
Use a linear probe with a frequency of at least 12 MHz. Evaluation of entheses
often requires a higher frequency, typically 16–22 MHz. Evaluate each joint for
fluid and synovitis at the dorsal recess. Pathologic conditions involving tendons are
confirmed with dynamic active, passive, and resisted maneuvers under US. Although
the protocol below only shows an individual digit, it is recommended that any digits
of interest be included.
rotocol Image 1: Dorsal Metacarpophalangeal Joint,

P
Extension + Flexion, Longitudinal ± Power Doppler (Fig. 4.7)
Place the transducer over the extended MCPJ in LAX. Perform TAX slides in radial
and ulnar directions to fully evaluate the cartilage and the synovial recess. Evaluate
the three margins of the joint recess: proximal, distal, and superficial. The superfi-
cial margin can be defined by passively flexing and extending the finger to identify
the moving extensor tendon, which borders the superior recess margin. Synovial
hypertrophy will expand these margins and is graded [1–3] (see Chap. 5). Look for
synovial fluid in the joint recess.
Examine the smoothness of the superficial surface of the cartilage covering the
metacarpal head (MCH). Look at the MCH itself and determine (a) if cartilage sur-
rounds the distal and dorsal portions of the MCH, (b) the constitution of the carti-
lage (focal or diffuse thinning, loss of sharpness of the superficial border), and (c) if
there is a normal hyperechoic interface reflex. A long-standing erosive process may
result in cartilage damage ranging from minimal to severe.
Passively flexing and extending the MCPJ will also enable a thorough inspection
of the cartilage covering the MCH. With a slightly flexed MCPJ, perform radial and
ulnar TAX slides to evaluate the cartilage more fully. Rock to probe as needed to
counter anisotropy, keeping the cartilage in focus. Remember, hyperechoic
synovium may have migrated into the area where cartilage previously existed.
If the radiographs indicate possible bone erosion, do a focused US examination
on that area to verify. Look at the bony surfaces of the MCH and the proximal pha-
lanx for irregularities. Do not mistake the normal smooth groove-like concavity
proximal to the MCH as a bony erosion since this is the proximal attachment site for
the synovial membrane [28]. If you suspect that there truly is erosion in this area,
look for contiguous synovial hypertrophy.
94 4 Fingers
Fig. 4.7 Protocol Image 1: Dorsal metacarpophalangeal joint, extension + flexion, longitudinal ±
power Doppler
Method 95
Remember to verify synovitis, cartilage erosion, and bone erosion in TAX view
(Protocol Image 2, below). The effusion may be present along with synovitis. The
synovitis may have receded in long-standing cartilage-erosive arthropathy, leaving
only residual cartilage or bone erosion. Turn on the PD for another image. Power
Doppler activity may be seen within the synovial tissue.
Also, examine the more superficial finger extensor tendon for absence, tendon
damage, or paratenonitis. Paratenonitis sonographically presents as hyperemia or
anechoic fluid along the extensor tendons [2]. It is most often associated with an
underlying inflammatory polyarthropathy. With paratenonitis, the underlying MCPJ
frequently has evidence of synovitis; however, paratenonitis may occur as an iso-
lated finding, perhaps due to joint deformity or overuse [2].
rotocol Image 2: Dorsal Metacarpophalangeal Joint,

P
Transverse, ± Power Doppler (Fig. 4.8)
Rotate the probe 90° to evaluate the slightly flexed MCPJ in TAX. Perform small
proximal and distal TAX slides to verify any pathology visualized in LAX. The PD
will delineate the dorsal digital arteries and may verify hyperemia noted on the
LAX view. The extensor tendon is ovoid and exhibits anisotropy. The TAX orienta-
tion offers another view of the cartilage covering the MCH but remembers to slightly
rock the probe to sharpen the view of the cartilage.

Dorsal
metacarpophalangeal joint,
transverse, ± power
Doppler
96 4 Fingers
Fig. 4.9 Protocol Image 3: Dorsal proximal phalanx, transverse ± power Doppler ± longitudinal
rotocol Image 3: Dorsal Proximal Phalanx, Transverse ±

P
Power Doppler ± Longitudinal (Fig. 4.9)
Still in TAX orientation, perform a distal TAX slide to see the hyperechoic cortex of
the proximal phalanx. Turn on the PD to see the dorsal digital arteries. Superficial
to the ET is the hypoechoic EH. If an abnormality is detected, rotate the probe 90°
to examine the ET and cortex in LAX.
rotocol Image 4: Dorsal Proximal Interphalangeal Joint,

P
Longitudinal ± Power Doppler ± Transverse (Fig. 4.10)
With the probe again in LAX orientation, center it over the PIPJ and perform TAX
slides in radial and ulnar directions to fully evaluate the cartilage and the synovial
recess. If you passively flex the joint, the cartilage may have better visibility.
Osteophytes may be the predominant finding, particularly in the older age group.
Method 97
Fig. 4.10 Protocol Image 4: Dorsal proximal interphalangeal joint, longitudinal ± power Doppler
± transverse
The dorsal recess may be enlarged and extend proximally in the presence of
synovitis. Such synovial hypertrophy may or may not have PD activity. Erosion of
bone may be evident with rheumatoid arthritis, psoriatic arthritis, and perhaps in
advanced gouty arthropathy. Verify any suspected bone erosion in the TAX view.
While in LAX orientation, turn on the PD for another image. Power Doppler activ-
ity may be positive within the synovial tissue. Verify abnormal findings in TAX by
rotating the probe.
rotocol Image 4a (Optional): Dorsal Middle Phalanx,

P
Transverse ± Longitudinal
Rotate the probe to TAX orientation and perform a TAX slide to see the hyperechoic
cortex of the middle phalanx. The central slip of the ET may be discernible in the
LAX view.
98 4 Fingers
Fig. 4.11 Protocol Image 5: Dorsal distal interphalangeal joint, longitudinal ± transverse
rotocol Image 5: Dorsal Distal Interphalangeal Joint,

P
Longitudinal ± Transverse (Fig. 4.11)
With the probe in LAX orientation, perform an LAX slide distally and center the
transducer over the DIPJ. Passive flexion of the joint may better expose the carti-
lage. Bony osteophytes may be evident. Abnormal findings should be verified in
TAX by rotating the probe.
rotocol Image 6: Dorsal Distal Phalanx Extensor Tendon

P
Insertion Longitudinal + Power Doppler (Fig. 4.12)
Examine for enthesopathy and enthesitis by looking for PD activity along the inser-
tion of the ET on the distal phalanx. This hyperechoic bone lies deep into the rever-
berating fingernail. Use copious transmission gel and the highest frequency probe
available.
Method 99
Fig. 4.12 Protocol Image 6: Dorsal distal phalanx extensor tendon insertion longitudinal +
power Doppler
rotocol Image 7: Volar Metacarpophalangeal Joint, Dynamic

P
Flexion, Longitudinal, ± Power Doppler ± Transverse (Fig. 4.13)
The patient places the hand palm side up with fingers extended on the examining
surface. Place the probe in LAX over the palmar surface of the MCPJ. For each
joint, perform a TAX slide in an ulnar direction and then a radial direction to fully
evaluate. Look for synovitis, tenosynovitis, cartilage erosion, and bone erosion.
Manually flex the finger to visualize the flexor tendons and surrounding tenosy-
novium. Isolated DIPJ passive flexion will activate only the FDP. The volar plate is
superficial to the joint cartilage, and the anisotropic A1 pulley is superficial to the
FDS. With a trigger finger, the superficial layer may be the only layer that becomes
snagged beneath a thickened A1 pulley. Turn on the PD to look for a signal.
When examining the volar MCPJ for synovitis, note that the synovial recess
extends proximally and should also warrant Doppler analysis (35). If there is suspi-
cion of a volar plate tear, look for a hyperechoic bony avulsion, a hypoechoic cleft,
or swelling of the volar plate. The gap of a complete volar plate tear may widen with
gentle passive hyperextension of the joint during a dynamic US examination. Turn
the probe 90° to look at the MCPJ in TAX to verify the pathology depicted on the
LAX view and gain another perspective on the A1 pulley. When looking for A1 pul-
ley thickening, compare the A1 pulley thickness to that of the same contralateral,
non-triggering finger.
100 4 Fingers
Fig. 4.13 Protocol Image 7: Volar metacarpophalangeal joint, dynamic flexion, longitudinal, ±
power Doppler ± transverse
rotocol Image 8: Volar Proximal Phalanx, Longitudinal ±

P
With the probe back in LAX, perform an LAX slide distally to visualize the hyper-
echoic cortex of the proximal phalanx (PP). Perform slight TAX slides in radial and
ulnar directions to encompass a full volar view of this bone. Look for a step-off
deformity that may indicate a fracture. In LAX view, the A2 pulley appears as an
oblong anechoic to hypoechoic structure resting on the superficial hyperechoic edge
of the FDS tendon. The pulley is normally 0.3–0.5 mm thick and covered by a thin
hyperechoic line on US [6].
To evaluate for bowstringing indicative of an A2 pulley tear, use a small-footprint
transducer. Place the PIPJ at least 40° of flexion and the DIPJ at 10° of flexion [2].
The examiner resists active flexion of the finger by applying fingertip-to-fingertip
resistance. Measure the TBD. Values greater than 2 mm may indicate an A2 pulley
tear [2]. Compare the volar tendon position at rest and dynamically in resisted
flexion.
Other signs of an A2 pulley injury are the absence of the pulley in LAX view,
tenosynovial fluid in the flexor tendon sheath, irregular thickening of the A2 pulley,
Method 101
Fig. 4.14 Protocol Image 8: Volar proximal phalanx, longitudinal ± transverse
a cyst in the flexor tendon sheath, scar tissue, and effusion of the PIPJ [2]. Partial
pulley tears produce minimal to no tendon displacement. Still, the pulley may
appear hypoechoic and swollen on US, perhaps exhibiting hyperemia on PD with a
more acute injury.
Rotate the probe 90° for the TAX view. In this view, the pulley appears to be
slightly hyperechoic at the volar aspect and hypoechoic at the lateral aspect. The
TAX view of the proximal phalanx demonstrates the FDS splitting, with each slip
moving away from the deeper, more central FDP.
rotocol Image 9: Volar Proximal Interphalangeal Joint,

P
Next, move the probe, in LAX, to the PIPJ. Perform TAX slides in the ulnar and
radial directions to fully evaluate the joint, synovial recess, and flexor tendon.
The A3 pulley is superficial to the PIPJ. Turn the probe 90° to TAX to verify
pathology.
102 4 Fingers
Fig. 4.15 Protocol Image 9: Volar proximal interphalangeal joint, longitudinal ± transverse
rotocol Image 9a (Optional): Volar Middle Phalanx,

P
Longitudinal ± Transverse
With the probe back in LAX, perform an LAX slide distally to visualize the hyper-
echoic cortex of the proximal phalanx. Perform slight TAX slides in radial and ulnar
directions to encompass a full volar view of this bone. Look for a step-off deformity
that may indicate a fracture. Depending upon the angle of the probe, the anisotropic
A4 pulley may be appreciated superficially to the FDS. Rotating the probe 90°
affords a TAX view of the flexor tendons, which have reversed their relative posi-
tions. The FDS, now deep into the FDP, inserts into the middle phalanx.
rotocol Image 10: Volar Distal Interphalangeal Joint,

P
Next, move the probe in LAX to the DIPJ. Perform small TAX slides in the ulnar
and radial directions to fully evaluate the joint, synovial recess, and flexor tendon.
The A5 pulley is superficial to the DIPJ, although it may not be visible.
Method 103
Fig. 4.16 Protocol Image 10: Volar distal interphalangeal joint, longitudinal ± transverse
rotocol Image 10a (Optional): Flexor Tendon Enthesis,

P
Longitudinal + Power Doppler
For this view, it is best to use a small footprint probe with a frequency of at least
18 MHz. Extend the finger against a flat surface and place the probe in LAX orienta-
tion. Move the transducer distally to the FDP insertion on the distal phalanx. Small
TAX slides in the ulnar and radial directions enhance the search for PD activity
indicative of active enthesitis. Remember, a light touch and abundant transmission
gel are mandatory.
rotocol Image 11: Ulnar Aspect of the First

P
Metacarpophalangeal Joint, Longitudinal ± Transverse
(Fig. 4.17)
The pronated hand is placed upon a curved bolster with the first and second fingers
draped on opposite sides, thus abducting the thumb. Place a high-frequency probe
in LAX along the ulnar aspect of the thumb base, focusing on the bony discontinu-
ity, which is the first MCPJ. To identify the UCL, first identify the hyperechoic bony
surfaces of the distal MC and proximal phalanx [27]. The normal UCL is a homo-
geneous fibrillar structure spanning the joint in this coronal view. The UCL may
104 4 Fingers
Fig. 4.17 Protocol Image 11: Ulnar aspect of the 1st metacarpophalangeal joint, longitudinal ±
transverse
appear hypoechoic, particularly the proximal portion. Rock the probe to look for
fibrillar echotexture. The adductor aponeurosis is superficial to the UCL; it is an
oblong, thin longitudinal structure that is hypoechoic to hyperechoic depending on
the degree of anisotropy.
Gently and passively flex the first interphalangeal joint to dynamically confirm
the identity and integrity of the adductor aponeurosis, which normally glides over
the MCPJ [27]. If the joint moves excessively compared with the contralateral joint
or the UCL shows partial or complete disruption, this may be a gamekeeper’s thumb.
With a complete UCL tear, the ligament remnant may displace off the joint in a
rolled-up ball proximal to the MCPJ, now termed a Stener lesion. With a Stener
lesion, the UCL remnant may be located superficial to the adductor aponeurosis.
Verify any sonographic findings in the TAX view.
rotocol Image 12: Radial Aspect of the First Carpometacarpal

P
Joint, Longitudinal ± Power Doppler (Fig. 4.18)
The hand is relaxed and prone, with the first digit placed along the edge of the
examination table. The transducer is placed in LAX along the thumbs; base dorsum,
with the long axis of the transducer aligned with the thumb. Identify the
Method 105
Fig. 4.18 Protocol Image 12: Radial aspect of the first carpometacarpal joint, longitudinal ±
power Doppler
hyperechoic longitudinal bony surface of the first metacarpal and look for the gap
between the first metacarpal base and the hyperechoic trapezium; this is the first
CMCJ. The joint space proximal to the first CMCJ is the scaphotrapeziotrapezoid,
or triscaphe, joint.
Gently grasp the thumb with your free hand and bend the first CMCJ. The first
CMCJ moves, but the intercarpal joint does not. Since the first CMCJ is frequently
affected by osteoarthritis, the joint may be narrowed, and osteophytes may hamper
clear-cut identification of the joint. Move the probe in a TAX slide in each direction
to obtain a more expansive view of the joint. The entire radial aspect of this joint is
sonographically visible. Turn on the PD to look for hyperemia.
Complete Fingers Ultrasonic Examination Checklist
□ Protocol Image 1: Dorsal metacarpophalangeal joint, extension + flexion, longi-
tudinal ± power Doppler.
□ Protocol Image 2: Dorsal metacarpophalangeal joint, transverse, ± power
Doppler.
□ Protocol Image 3: Dorsal proximal phalanx, transverse ± power Doppler ±
longitudinal.
□ Protocol Image 4: Dorsal proximal interphalangeal joint, longitudinal ± power
Doppler ± transverse.
□ Protocol Image 4a (optional): Dorsal middle phalanx, transverse ± longitudinal.
□ Protocol Image 5: Dorsal distal interphalangeal joint, longitudinal ± transverse.
106 4 Fingers
□ Protocol Image 6: Dorsal distal phalanx extensor tendon insertion longitudinal +

power Doppler.
□ Protocol Image 7: Volar metacarpophalangeal joint, dynamic flexion, longitudi-
nal, ± power Doppler ± transverse.
□ Protocol Image 8: Volar proximal phalanx, longitudinal ± transverse.
□ Protocol Image 9: Volar proximal interphalangeal joint, longitudinal ± transverse.
□ Protocol Image 9a (optional): Volar middle phalanx, longitudinal ± transverse.
□ Protocol Image 10: Volar distal interphalangeal joint, longitudinal ± transverse.
□ Protocol Image 10a (optional): Flexor tendon enthesis, longitudinal + power
Doppler.
□ Protocol Image 11: Ulnar aspect of the first metacarpophalangeal joint, longitu-
dinal ± transverse.
□ Protocol Image 12: Radial aspect of the first carpometacarpal joint, longitudinal
± power Doppler.
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Chapter 5
Hand Arthropathies

1. Hand pain
2. Hand stiffness
3. Hand swelling, diffuse, or localized
1. What is the cause of hand pain?
2. Is there an underlying inflammatory condition affecting the hand, and if so, is it
a systemic process such as spondyloarthropathy, rheumatoid arthritis, or crystal
disease?
4. Is there a structural, functional, or repetitive injury causing the hand pain?
7. What is this lump in the hand?
Necessary Anatomy
Joints
The joint capsule is the outer covering of the synovial recess; the capsule contains a
superficial fibrous layer and an inner synovial lining [1]. The joint capsule, ordinar-
ily thin and slightly hyperechoic on ultrasound (US), may or may not be easily
discernable. The synovial recess is typically hypoechoic, and we focus on the syno-
vial recess for synovitis grading.
States Government.

Switzerland AG 2023
110 5 Hand Arthropathies
Clinical Comments
The eye may be “the window to the soul,” but the hand is the window to the diagno-
sis. Ultrasound is superb for detecting subclinical synovitis, tenosynovitis, enthesi-
tis, cartilage and bone erosion, crystal deposition, and bony deformity [2–9].
Additionally, US elucidates the presence of ganglion cysts, soft tissue masses, and
the tendons’ functional abnormalities. The pattern of involvement may lead to a
diagnosis [10]. Diagnostically, US combined with radiographs, clinical evaluation,
and laboratory data enables clinicians to address the most significant challenges in
evaluating polyarthropathy:
1. Differentiating inflammatory from noninflammatory diseases.
2. Delineating the precise inflammatory disease.
The task is daunting when obesity obscures synovitis, in mild or early-onset disease,
and when serologies are negative [10]. Diagnosing early seronegative rheumatoid
arthritis (RA) and psoriatic arthritis (PsA) has been facilitated by US [11, 12]. Other
patients have a history compatible with an inflammatory condition but an unimpres-
sive physical examination. For all these patients, ultrasonic visualization of pathol-
ogy is invaluable.
So, where does US fit into the algorithm of polyarthropathy evaluation? The
answer is beyond the scope of this text but is superbly discussed elsewhere [10]. At
our institution, we evaluate the dorsal wrist, volar wrist, hand, and, if necessary, fin-
ger entheses for diagnostic purposes. We follow a standard protocol but also focus on
areas of pain and physical examination abnormalities. Our protocol is constantly
evolving to reflect changes in technology and concepts in this developing area. At
this point, US is not recommended to guide the treatment intensity in RA [13, 14].
However, for the individual patient with polyarthritis, US can be beneficial for:
Diagnosis: Ultrasound detects synovitis, cartilage, and bone erosion, tenosynovitis,
power Doppler (PD) activity, enthesitis, and crystal disease.
Treatment: Ultrasound can detect persistent subclinical active synovitis in patients
who are not improving clinically.
Prognosis: Ultrasound can assess the presence of bone and cartilage erosion.
Disease progression: Ultrasound can gauge the rate of progression of cartilage and
bone erosion.
Synovitis
Synovitis and Ultrasound
OMERACT definitions [15]:

Grayscale (GS): Hypoechoic abnormal hypertrophied synovial tissue within the
capsule that is not displaceable and poorly compressible; effusion does not need
to be present.
Power Doppler: Power Doppler activity may or may not be present; PD does not
need to be present to diagnose synovitis.
Ultrasound is superior to clinical examination for the detection of subclinical
synovitis [4, 16, 17]. In RA, US is superior to plain radiographs and comparable to
MRI for the detection of synovitis [16, 18]. Disease activity response to treatment
in RA is also reflected in changes in synovitis on US [18–23]. Power Doppler find-
ings of the hand and wrist have shown excellent correlation with other clinical mea-
surements of disease activity in RA [24, 25]. Notably, most RA patients in clinical
remission may continue to have joint synovitis that is undetected by all clinical
parameters [26]. The presence and activity of synovitis correlate directly with the
progression of joint erosion.
Since US informs about the presence and persistence of synovitis, and such
activity seems to correlate with response to treatment and potential for structural
damage, it would seem logical that US might be a reasonable means to guide the
treatment intensity of RA patients. However, two studies did not demonstrate
improved patient outcomes when using PD activity in joints to guide treatment
intensity [13, 14]. Another study using US findings to guide early RA treatment
intensity did not reduce MRI inflammation or result in less structural damage [27].
Perhaps future studies of longer duration may better clarify whether US has a role
in treatment guidance. We find US invaluable for detecting synovitis as a diagnostic
tool. For an individual patient, we perform US when we suspect disease activity that
is not clinically apparent to help decide whether to alter treatment [14]. We do not
use it routinely to guide treatment intensity, however.
Ultrasonic Grading of Synovitis
There is no standardized scoring system or even agreement about which joints to

evaluate. We describe several scoring systems for synovitis, erosion of cartilage and
bone, tenosynovitis, and enthesitis. Over the years, several synovitis scoring sys-
tems have been described [28]. This discussion pertains to individual joint synovitis
scoring. Composite multiple-joint scoring to derive a total score is a separate issue
beyond the scope of this Manual [29].
The EULAR-OMERACT individual joint scoring system has shown moderate to
good reliability in the metacarpophalangeal (MCPJ) [30]. We use this scoring sys-
tem in our practice. Although most methods have been validated for RA, some rheu-
matologists apply them for practical purposes to PsA. The US findings of synovitis,
effusion, and erosion detection are similar in these two diseases [31]. Scoring sys-
tems propose rules to encourage reliable readings among sonographers, character-
ize disease severity, and monitor treatment efficacy in multi-institutional studies.
However, in our institution, we simply note the presence and degree of synovitis.
We grade (score) each synovial joint recess for synovial thickening on GS (grade
0–3) and PD (grade 0–3) [11, 32, 33]. Recognizing the lack of synovitis (grade 0) or
severe synovitis (grade 3) is relatively easy. If we are uncertain whether the joint has
a grade 1 or grade 2 score, we sometimes score it as grade 1–2. To avoid observer
interpretation drift, we compare previous and current images. In our clinic, a hand
synovitis examination consists of the dorsal radiocarpal joint (RCJ) and the inter-
carpal (or midcarpal) joint (ICJ), the dorsal MCPJs of digits 2, 3, and 5, the dorsal
proximal interphalangeal joints (PIPJs) of digits 2 and 3, and the dorsal distal ulna
(DU). We add an evaluation of the triangular fibrocartilage complex (TFCC) when
considering calcium pyrophosphate deposition disease (CPPD). For finger enthesi-
tis evaluation, we examine the distal dorsal entheses of the extensor tendons in dig-
its 2 and 3. Other symptomatic or grossly anomalous sites are similarly evaluated.
If considering tenosynovitis, we examine the extensor tendons at the wrist, the
extensor carpi ulnaris (ECU), and the flexor tendons of the volar wrist and MCPJs.
We also grade any PD activity near the DU, which may indicate active synovitis [11,
34]. This protocol is subject to change based on validity testing and the clinical util-
ity of future novel scoring systems.
Grayscale Synovitis Grading (Table 5.1)
Synovitis of the dorsal MCPJ (independent of an effusion) is scored by GS as [30,

33] follows:
0: Absence of hypoechoic areas within the joint
1: Minimal (hypoechoic synovial hypertrophy [SH] up to the level of the imagi-
nary horizontal line connecting the (superficial) bone surfaces between the meta-
carpal head and the proximal phalanx)
2: Moderate (hypoechoic SH extending above the horizontal joint line but with the
upper surface of the SH being flat or concave)
3: Severe or marked (hypoechoic SH extending beyond the joint line with the upper
surface of the SH being convex)
The EULAR-OMERACT ultrasound task force excluded synovial fluid when scor-
ing synovitis, recognizing that effusion, albeit a proxy measure of inflammation, did
not add additional information regarding synovitis definition and severity [33]. In
actual practice, you will observe structures that may appear as hypoechoic or even
anechoic fluid but may be synovitis. Probe compression within a closed space, such
as a joint capsule, may not differentiate synovial fluid from synovitis. Thus, we
include the presence and extent of such structure in our report if there is no other
clear-cut evidence of synovitis.
Table 5.1 Summary of grayscale synovitis scoring [30, 33]

Summary of grayscale synovitis scoring
0 = Absence (no enlargement of the recess)
1 = Mild (minimal effusion or synovial hypertrophy)
2 = Moderate (moderate effusion/hypertrophy; the joint capsule bulges beyond the normal
confines)
3 = Severe or marked (extensive effusion/hypertrophy)
Table 5.2 Summary of power Doppler synovitis scoring [30, 33]

Summary of power Doppler synovitis scoring
0 = Absence (no intra-articular color signal)
1 = Mild (up to three color signals, two single and one confluent signal, or two confluent signals
in the intra-articular area)
2 = Moderate (greater than grade 1 to <50% of the intra-articular area filled with color signals)
3 = Marked (>50% of the intra-articular area filled with color signals)
Power Doppler Grading (Table 5.2)
Synovitis is scored by PD activity within the GS-defined synovium as [11, 33]

follows:
0: Absence (no intra-articular color signal)
1: Mild (up to three color signals, two single and one confluent signal, or two con-
fluent signals in the intra-articular area)
2: Moderate (greater than grade 1 but ≤50% of the intra-articular area filled with
color signals)
3: Marked (>50% of the intra-articular area filled with color signals)
Combined Scoring System
Combining the GS and the PD scoring has been proposed as another approach to
quantifying synovitis sonographically [33].
Summary of combined synovitis scoring scale:
0: Normal (no SH on GS + no PD signal)
1: Minimal (grade 1 SH on GS + ≤ grade 1 PD signal)
2: Moderate (grade 2 SH on GS + ≤ grade 2 PD—or—grade 1 SH on GS + grade 2
PD signal)
3: Severe (grade 3 SH on GS + ≤ grade 3 PD—or—grade 1 or 2 SH on GS + grade
3 PD signal)
Practical Synovitis Grading of Specific Joints in the Wrist and Hand
The joint capsule is graded for synovial proliferation by GS and neovascularization

by PD [11, 33]. We recommend the atlas-based approach for synovitis grading; the
sonographer directly compares the US image with various examples of GS and PD
synovitis [34].
Fig. 5.1 Dorsal

metacarpophalangeal joint
synovitis in grayscale and
power Doppler
Dorsal Metacarpophalangeal Joint Synovitis (Fig. 5.1)
Synovial hypertrophy in the dorsal recess will expand superficially to or beyond

an imaginary line between the superficial metacarpal (MC) head and the proxi-
mal phalanx; further hypertrophy occurs in a proximal and distal direction [33].
Other joints follow a similar pattern. Please refer to the atlas for specific exam-
ples [34].
Dorsal Radiocarpal and Intercarpal Joint Synovitis (Fig. 5.2)
We evaluate these two joints in longitudinal (LAX) to define GS synovitis based on

joint capsule distension and synovial swelling superficial to an imaginary line (beta-
line) between the superficial distal radius and the proximal superficial capitate
(Fig. 5.3) [35]. Furthermore, we score the RCJ and the ICJ separately for both the
GS activity and PD activity. However, be aware that many experts score these two
joints together. In the wrist, GS reflects SH as hypoechoic; we are interested in PD
activity only within the area of SH as defined by GS [11]. Since we are seeking PD
activity within the joint recess, PD activity superficial to the joint recess may simply
represent normal vasculature rather than actual neovascular change within the joint
recess [35].
Fig. 5.2 Dorsal radiocarpal and intercarpal joint synovitis in grayscale and power Doppler
Fig. 5.3 Beta-line
Synovitis Grading Hints
1. Optimize the PD settings.

The goal is to increase Doppler signal detection sensitivity while minimizing
random electrical noise and vessel wall motion artifacts [36, 37].
(a) Turn up the gain until random noise is encountered, and then slowly lower it
until the noise mostly or entirely disappears [37, 38].
(b) Use the lowest pulse repetition frequency (PRF) that does not produce exces-
sive noise. The lower the PRF, the lower the linked wall filter, and thus the
higher the sensitivity to blood flow. Since our goal is to detect minimal blood
flow, we want to maximize sensitivity but not so much as to create excessive
random noise [37].
(c) Use the smallest Doppler box possible to encompass the region of inter-
est (ROI).
(d) Whenever possible, recalibrate Doppler settings for each patient. However,
use identical settings on the same US device when following the Doppler
activity of an individual patient longitudinally [37].
2. To verify sufficient PD sensitivity, place the probe on the distal finger pulp. The
power Doppler signal should register over one-third of the finger pulp [10].
3. Avoid excessive transducer pressure since this may compress the small artery
flow and falsely ablate the Doppler signal [36].
4. The ROI should have relaxed tissue since tense, stiff tissue will compress the
vascular structures, causing false-negative results [36].
5. Despite the above scoring definitions for GS and PD, we are sometimes still
on the fence about the grade. We can use an intermediate designation in
that case.
6. To avoid observer interpretation drift, directly compare images from various
timeframes to gauge any change.
7. In our experience, the joint with the highest diagnostic yield is the MCPJ.
Cartilage Erosion
OMERACT definition [15]:

Cartilage erosion on GS: loss of anechoic structure and/or thinning of the cartilage
layer, and irregularities and/or sharpness of at least one cartilage margin.
It is noted that the above definition, as defined by OMERACT, is for hyaline
cartilage regarding osteoarthritis (OA) damage. Ultrasound reliably detects MCPJ
cartilage pathology [39]. Evaluation of erosions can be done concurrently with
synovitis grading. A recently proposed grading system for cartilage erosion is a bit
different from other synovitis grading systems in that there are only three catego-
ries, namely, 0, 1, and 2 (Fig. 5.4) [40].
Grade 0 (normal) shows robust anechoic/hypoechoic cartilage of uniform thickness
and a sharp outer edge in two orthogonal (90°) views.
Grade 1 (minimal change) shows cartilage with some focal thinning in areas or
incomplete loss of cartilage.
Grade 2 shows cartilage thinning or complete loss of cartilage, either focally or
diffusely.
Fig. 5.4 Scoring cartilage erosion

This novel system is a pragmatic grading system since it is relatively easy to recog-
nize normal, unadulterated cartilage (grade 0) and severely damaged cartilage
(grade 2). Grade 1 lies somewhere in between those two extremes. Examining the
MCPJ using this grading system has shown good inter- and intra-reader reliability
[40]. Whichever system is used, it is most important to perform orthogonal views of
as many cartilage segments as possible.
A technique we use to evaluate the MC head cartilage more thoroughly is for the
examiner to gently grasp the patient’s prone hand from palm side to palm side. The
examiner places the fingertips under the volar aspect of the middle phalanges and,
with the opposite hand, gently holds the probe over the dorsal MCPJ. The MCPJ is
flexed and extended by the examiner to demonstrate a more considerable extent of
the cartilage dynamically. We look at the cartilage interface reflex to delineate the
superficial aspect and smoothness of each segment of cartilage perpendicular to the
transducer. This technique has not been validated to our knowledge.
Normative US-derived values of MC head cartilage thickness are available [41].
Males have thicker cartilage than females. Interestingly, about 18% of normal peo-
ple had low-grade cartilage changes. Be aware that some athletes (such as weight-
lifters) may have increased MC head thickness [42]. It is important to note that
cartilage damage at the MCPJs may occur at least as often in OA as it does in RA;
however, in OA, the cartilage damage is more often distributed equally at MCPJs 2
through 5, whereas RA-induced cartilage damage predominantly affects MCPJs 2
and 3 [43].
Bone Erosion (Fig. 5.5)

Bone erosion on GS: Intra- and/or extra-articular discontinuity of bone surface vis-
ible in two perpendicular planes.
Look for step-offs, divots, or gaps in areas of bone that are usually smooth and
uninterrupted [44]. In RA, bone erosion has diagnostic utility and is indicative of a
more severe disease [45]. Standard radiographs lack sensitivity compared to US for
detecting bone erosion [46, 47]. One study, using CT as the gold standard, deter-
mined the sensitivity of US and radiographs for detecting RA bone erosion was
43% and 19%, respectively [48].
The highest yielding areas for RA erosions are the lateral quadrants of the second
and fifth MC heads and the fifth metatarsal (MT) head; the US examination of these
areas found bone erosion in 60% of patients with early RA. A cutoff of ≥ 2.5 mm
for erosion size maximizes sensitivity and specificity for RA erosions [49].
Another study described US-detected erosions with a false positivity rate of up
to 29% due to the high sensitivity to cortical irregularity that can occur when osteo-
phytes produce false erosions (pseudoerosions) [50]. A second type of pseudoero-
sion on US may result from normal bone contours being misinterpreted as erosion,
such as in the dorsal MC heads, the lunate, triquetrum, and ulna [51].
Fig. 5.5 Bone erosion
Fig. 5.6 Tenosynovitis
Tenosynovitis (Fig. 5.6)
The tenosynovium is the synovial-lined sheath encasing a tendon that may become
inflamed due to repetitive trauma or systemic inflammation.
Tenosynovitis on GS: Tenosynovial hypertrophy is present when abnormal anechoic
and/or hypoechoic (relative to tendon fibers) tissue within the synovial sheath is
non-displaceable and poorly compressible, and seen in two perpendicular planes.
There is abnormal tendon sheath widening due to abnormal tenosynovial fluid
and/or hypertrophy.
Tenosynovitis on PD: The tissue within the tenosynovium may or may not exhibit
Doppler signals. However, consider the Doppler signal to be significant only in
the presence of peritendinous synovial sheath widening on GS and only if:
1. It is noted in two perpendicular planes.
2. It is present within the peritendinous synovial sheath.
3. It is not due to normal feeding vessels entering the synovial sheath from sur-
rounding tissues.
Tenosynovitis may also occur due to mechanical compression of the tendon and
tenosynovial sheath, known as stenosing tenosynovitis. The classic example of
tenosynovitis is de Quervain’s tenosynovitis (also called stenosing tenosynovitis) of
the first extensor compartment (EC) at the wrist. Ultrasound is beneficial for
diagnosing and treating this condition [52]. Another example of stenosing tenosy-
novitis is the trigger finger, involving the flexor tendons. Tenosynovitis may occur
with inflammatory arthropathies such as rheumatoid arthritis, spondyloarthropa-
thies, and sarcoidosis. Tenosynovitis may cause compression of the median nerve
within the carpal tunnel.
Ultrasound is more accurate than clinical examination when detecting flexor
tenosynovitis [53]. Ultrasound of the flexor tendon sheath has helped predict which
patients will develop persistent RA with polyarthritis [54]. In addition, extensor
tenosynovitis in RA correlates with increased disease activity [55]. OMERACT has
developed a reliable US scoring system for tenosynovitis in RA [56]. Both GS and
PD have four grades (0–3: normal, minimal, moderate, and severe). This scoring
system has been shown to reliably detect changes over time [54]. In a small multi-
center study, tenosynovitis score changes did show substantial responsiveness to
RA treatment, with a good correlation with the Disease Activity Score but not with
the Health Assessment Questionnaire—Disability Index [57]. The most involved
tendon sheath in this RA study was that of the ECU. It remains to be seen if tenosy-
novitis scores should guide treatment intensity in RA.
Paratenonitis
A paratenon, tissue lacking a proper synovial membrane, surrounds the finger

extensor tendons superficial to the dorsal MCP joints. Paratenonitis sonographically
presents as hyperemia or anechoic fluid along the extensor tendons [58]. It is most
often associated with an underlying inflammatory polyarthropathy such as RA. The
underlying joint frequently has evidence of synovitis on US; however, paratenonitis
may occur as an isolated finding, perhaps due to joint deformity or overuse.
Enthesitis
The enthesis (Fig. 5.7) is the insertional point for attachment of not only tendons but
also ligaments, fascia, muscles, or joint capsules [59].
Enthesitis on GS: Hypoechoic and/or thickened tendon insertion <2 mm from the
bony insertion; it may be accompanied by enthesophytes, calcifications, or bony
erosions.
Enthesitis on PD: Doppler signal <2 mm from the bony insertion.
For the hand, the prime location to examine the enthesis is at the tendon insertion
onto the bone in the distal phalanges. Sonographically accessible areas for enthesis
evaluation include the insertions of the flexor and extensor tendons on the phalanges
[60–62]. Enthesitis is predominantly the domain of spondyloarthropathy (SpA), in
particular PsA. Given that 15% of patients with PsA have no evidence of psoriasis
before the arthritis presentation [63], confirmation of enthesitis may be supportive
Fig. 5.7 Enthesis
evidence for the disease. In PsA, enthesitis reportedly occurs in 35–50% of patients
[64]. However, enthesitis may also occur in RA, gout, crystalline diseases, sarcoid-
osis, juvenile idiopathic arthritis, diffuse idiopathic skeletal hyperostosis, and OA,
albeit less frequently than with SpA.
In the latest classification system for SpA, enthesitis is a significant criterion for
diagnosing both peripheral and axial SpA. However, for this system, the presence or
absence of enthesitis was derived clinically, not sonographically [59]. Enthesitis is
clinically underdiagnosed by physical examination [59]. Ultrasound has emerged as
the preferred method for enthesitis detection due to its sensitivity, structural delinea-
tion, and functional evaluation [64, 65]. Ultrasound may reveal subclinical enthesitis.
A scoring system for enthesitis has been developed, using 0–3 grading [66]:
Grayscale grades:
0: Normal
1: Hypoechogenicity
2: Hypoechogenicity + thickening + calcifications or enthesophytes
3: Grade 2 features + erosions
Power Doppler grades:
0: No PD signal
1: <2 punctate signals
2: 2–4 punctate signals or 1 confluent signal
3: >4 punctate signals or >1 confluent signal
A Doppler signal within 2 mm of the bony cortex is arbitrarily accessed for scor-
ing, although enthesitis may generate PD even 5 mm from cortical bone [67]. When
evaluating for enthesitis, focus on the tendon’s insertional points, particularly the
extensor tendons of fingers. Look for loss of tendon echotexture, the presence of
bony enthesophytes, and power Doppler activity. If present, score the enthesitis as
described above.
For psoriatic arthritis, US gives important diagnostic clues [68]:
1. Enthesitis may occur at the insertion of the extensor tendon on the bony distal
phalanx. Nail abnormalities in PsA are related to enthesopathy beneath the nail
bed [69, 70].
2. Enthesitis may present at the insertion of the central slip of the extensor tendon
on the PIPJ.
3. Paratenonitis, that is, inflammation (hypoechoic swelling with or without PD),

especially surrounding both the extensor tendon and paratenon over the
MCPJ [71].
4. Dactylitis is a sausage digit that is hypoechoic with diffuse soft tissue swelling,
especially surrounding the flexor tendons [72, 73].
In our experience, sonographic evaluation of fingers for enthesopathy requires a high-
definition probe set at a minimum of 16 MHz to look at the extensor and flexor enthe-
ses of the fingers. Grade enthesitis according to the proposed scoring system and
scrutinize for PD activity. A gentle examiner’s touch is needed to preclude a reduction
in the Doppler signal. Likewise, the finger should be in a relaxed, flat, neutral position
since putting tension on the tendon at the enthesis might diminish PD activity [74]. If
sonography documents enthesitis with positive PD, place this information into the
appropriate clinical context. In summation, US may confirm a clinical impression of
enthesitis and detect subclinical enthesitis. Nonetheless, sonographic demonstration
of enthesitis supports a SpA diagnosis but is not pathognomonic.
Crystal Deposition
In the hand, we look for crystal deposition within the TFCC and the MC head carti-
lage. Perform US on any suspicious area noted on radiographs or any site described
by the patient as painful.
Gout
More commonly, gout starts in the lower extremity, such as the first metatarsopha-
langeal joint (MTPJ), and later involves the upper extremities. In the hand, gout may
lead to acute, subacute, or chronic inflammation of the dorsal MCPJ and PIPJs,
mimicking RA [74]. Alternatively, structural deformity from chronic tophi may be
the prominent clinical feature. In patients with gout, monosodium urate (MSU)
crystals may deposit on cartilage surfaces forming the sonographic double contour
sign (DCS). This thick hyperechoic line on the cartilage surface parallels the bony
cortex, giving the appearance of an inverse sandwich cookie. The DCS is the most
sensitive US sign of gout in the hand and wrist [75].
OMERACT definition of DCS [15]:
Grayscale: An abnormal hyperechoic band over the superficial margin of the articu-
lar hyaline cartilage, independent of the angle of insonation, which may be either
irregular or regular, continuous, or intermittent, and can be distinguished from
the cartilage interface sign.
Gout may also form tophi, which are MSU crystals surrounded by inflammatory
cells and connective tissue that resemble granulomas [76]. Tophi are appreci-
ated by US.
OMERACT definition of tophus [15]:

Grayscale: A circumscribed, inhomogeneous, hyperechoic, and/or hypoechoic
aggregation (which may have a posterior acoustic shadow) and may be sur-
rounded by a small anechoic rim (halo).
Gout tophi may be seen in any location, including synovial recesses, tendon
sheaths, and even the finger pads [77]. Tophi on radiographs may imitate erosions
from RA but appear as an asymmetric bony punched-out region with a narrow cor-
tex and overhanging bony edge. Severe joint and bone destruction may occur with
chronic tophaceous gout. Although gouty tophi may affect tendons, less commonly
will gout cause tenosynovitis [77].
Gout aggregates may also be appreciated by US.
OMERACT definition of gout aggregates [15] the following:
Grayscale: Heterogeneous hyperechoic foci that maintain their high degree of
reflectivity, even when the gain setting is minimized, or the insonation angle is
changed, and which occasionally may generate a posterior acoustic shadow.
Calcium Pyrophosphate Deposition Disease.
Acute CPPD may present in the hands as localized inflammation and pain, often
confused with a gouty flare, hence the name “pseudogout” [78].
OMERACT definitions [15]:
CPPD in fibrocartilage on GS: Hyperechoic deposits of variable shape, localized
within the fibrocartilage structure, that remain fixed or move along with the
fibrocartilage during a dynamic assessment.
CPPD in hyaline cartilage on GS: Hyperechoic deposits of variable size and shape,
without posterior shadowing, localized within the hyaline cartilage that remain
fixed and move along with the hyaline cartilage during a dynamic assessment.
CPPD in tendons on GS: Hyperechoic, linear structures generally without posterior
shadowing, localized within the tendon, that remain fixed and move along with
the tendon during a dynamic assessment.
In the hand, CPPD tends to involve the RCJ, the ICJ, and all the MCPJs, joints
not typically involved with OA. There may be concomitant osteophytes and wrist
tenosynovitis, but without the marginal erosions seen in RA [79]. Involvement of
the MCPJs may show clinical swelling, localized synovitis, and cartilage destruc-
tion, thus imitating RA (“pseudorheumatoid”) [80]. Suspect CPPD if the soft tissue
distal to the ulnar styloid is calcified on a radiograph [79]. However, most patients
with this radiographic finding have no symptoms [81]. Bony hooks on the radial
side of the MC head may occur with CPPD [82].
If findings in the hand and wrist suggest CPPD, US imaging of other areas, such
as the knee, may help confirm evidence of more diffuse calcium deposition. In one
study of CPPD patients, US demonstrated calcium deposition in femoral cartilage
at a rate of three to four times that of the wrist [83]. Although US is becoming more
recognized as a useful imaging modality for CPPD [84], distinguishing the DCS of
gout from chondrocalcinosis may be challenging [85].
Masses
A suggested approach to the evaluation of masses in the hand:

1. Assess the clinical setting, such as a history of polyarthropathy, lipomas in other
areas, penetrating trauma, repetitive movement history, precipitating/aggravat-
ing activities, and the presence of pain.
2. Capture sonographic orthogonal images of the mass, noting echotexture, shape,
compressibility, border definition, the presence of a stalk, Doppler activity, rela-
tion to adjacent structures, and the effect of nearby dynamic movement.
3. Based on the degree of confidence in the sonographic and clinical diagnosis,
choose to follow clinically, pursue further imaging, or refer to a hand surgeon.
4. Sonographic measurement in two dimensions may help determine size change
over time [86].
5. Note that a palpable mass may not be easily detectable on US if it is isoechoic
with the surrounding tissue.
Ganglion Cysts
Ganglion cysts are the most common masses of the wrist and hand [87]. These cysts
are filled with a thick fluid, lined with a fibrous capsule, and may be round, soft or
firm, painless, or tender on clinical examination [86]. Ganglia have no synovial lin-
ing and are hence different from synovial cysts. With a synovial cyst, the synovial
membrane herniates through a joint capsule. However, US cannot reliably differen-
tiate between the two [88]. Many clinicians use the terms ganglion, ganglion cyst,
and synovial cyst interchangeably.
Ganglion cysts may occur due to trauma, arthritis of any cause, tendon injury, or
tenosynovitis. They result from connective tissue herniation from joints, tendon
sheaths, ligaments, joint capsules, or bursae. We frequently find clinically undetect-
able (occult) ganglion cysts [86]. Most ganglion cysts occur at the wrist from either
the dorsal capsule near the scapholunate ligament or the radial aspect of the volar
wrist between the radial artery and the flexor carpi radialis. It is debatable which of
these two locations is the most common [89].
Sonographically, ganglion cysts appear hypoechoic or anechoic, are well-
defined, and may show septa [86]. Increased posterior enhancement may be noted
[90]. There may also be Doppler activity, which may or may not correlate with
symptoms [86]. The volar ganglion may occur within the carpal tunnel and com-
press the median nerve. Flexor tenosynovitis may mimic a volar ganglion cyst [86].
The differential diagnosis for any ganglion includes tenosynovial giant cell tumor,
epidermoid cyst, lipoma, tenosynovitis, rheumatoid nodule, gouty tophus, tendon

xanthoma, and synovial sarcoma [91]. If you detect a mass that may be a ganglion,
search for a stalk and follow it down to its point of origin to confirm the diagnosis
and the underlying structural issue responsible for the ganglia.
Accessory Muscles
Accessory muscles may mimic a tumor and compress nerves. The most common
accessory muscle of the wrist is the accessory abductor digiti minimi, present in
approximately 4% of healthy people [92]. This particular accessory muscle may
compress the ulnar nerve during contraction within Guyon’s canal [93]. The ulnar
nerve, usually round, may appear ovoid, especially with abduction of the fifth fin-
ger, if it is impinged by this accessory muscle [86].
Extensor digitorum brevis manus is present in about 2% of healthy adults and
inserts on the index and middle finger dorsal aspect; it appears to be a fusiform lump
alongside the extensor tendon mimicking a ganglion, extensor tenosynovitis, or a
soft tissue tumor [86]. A third pseudotumor due to a muscle variant is the inverted
palmaris longus, where the muscle belly is distal and the tendon is proximal. The
muscle belly is present in the volar wrist and may present as a mass [94, 95].
Traumatic Disorders
Tendon Tear
With a complete tendon tear, the ends of the retracted tendons may appear as local-
ized masses [86]. Ultrasound delineates these tendon stumps’ locations and helps
determine surgical repair procedures.
Foreign Bodies
Foreign bodies may appear as localized masses surrounded by either an abscess or

chronic, granulomatous tissue [86]. An abscess manifests as a heterogeneous,
poorly defined fluid collection with hypervascular changes noted on color Doppler.
A granuloma appears as a hypoechoic halo around a foreign body.
Hematomas
These appear as fluid collections within subcutaneous tissues and may demonstrate
a fluid-fluid level [86].
Tumors, Pseudotumors, Other Lumps, and Bumps
Tenosynovial Giant Cell Tumors
Schwannomas and Neurofibromas
Schwannomas and neurofibromas may affect nerves in the hand and wrist. These
are also well-defined hypoechoic masses contiguous with a nerve and may have
posterior acoustic enhancement [96]. You may see the nerve entering the tumor and
exiting distally. Differentiation between schwannomas and neurofibromas is chal-
lenging if based exclusively on US findings [86].
Hemangiomas
These may be intramuscular and appear as anechoic to hypoechoic lesions with

mixed internal echoes and vascular channels associated with hyperechoic fat
[86]. Doppler typically shows low flow without evidence of arteriovenous
shunting.
Lipomas
Lipomas are typically soft and painless masses. Echogenicity is variable and relates
to adjacent soft tissue [97]. Lipomas are well-demarcated, homogeneous, and most
commonly hyperechoic. Differentiating a lipoma from a liposarcoma can be diffi-
cult, and pathologic verification is required [86].
Pseudoaneurysms
Pseudoaneurysms are false aneurysms that develop when an artery is damaged by

blunt or penetrating trauma [98]. An example of chronic blunt trauma causing a
pseudoaneurysm includes hypothenar or thenar hammer syndrome. A sac forms
outside the artery wall as blood dissects from the vessel. Doppler reveals high flow
in the artery adjacent to the cystic mass. Pseudoaneurysms may involve the palmar
arch but rarely directly affect the fingers, although emboli can cause digital isch-
emia and gangrene [98, 99]. The best diagnostic procedure is an angiogram, but US
can be considered an initial modality for evaluation [99–101].
Rheumatoid Nodules
Rheumatoid nodules from RA may occur in any location. Most, but not all, patients
with RA nodules are seropositive [102]. The nodules, often adjacent to bone, sono-
graphically demonstrate slightly blurred edges with mixed hypoechoic echotexture
[103]. There may be a central hypoechoic area, perhaps due to central necrosis. The
nodules are compressible with no posterior shadowing and no Doppler activity.
Osteophytes
Osteoarthritis typically involves the interphalangeal finger joints and the first carpo-
metacarpal joint (CMCJ). Osteoarthritis less commonly affects the MCPJs and the
wrist. First CMCJ OA commonly causes pain and disability, particularly in older
populations. In a study of 93 participants, plain radiographs and US comparably
detected osteophytes, with US being more sensitive [104]. Erosion detection was
also similar, although US may not detect some erosions due to occluding osteo-
phytes. Power Doppler activity in the first CMCJ correlated with increased severity
of thumb base pain [104]. However, pain and function are poorly associated with
radiographic and US structural findings. An osteoarthritic osteophyte appears as a
step-up bony prominence on US [15]. Enthesophytes, new bone growth associated
with tendon insertions, most often occur in spondyloarthritis and may mimic osteo-
phytes on US. However, plain radiographs will often differentiate between an enthe-
sophyte and an osteophyte.
Glomus Tumor
Neuromas
Small-caliber palmar digital nerves are prone to injury during finger laceration
[105]. The injured nerve responds by forming a neuroma. High-frequency US helps
diagnose traumatic digital nerve injuries. The TAX view may reveal a loss of nerve
continuity confirmed in the LAX view [105]. The neuroma itself may appear as a
hypoechoic, well-defined mass, lacking internal vascularity at the end of a normal-
appearing nerve. Sonopalpation over the neuroma may reproduce pain.
Using Ultrasound to Aid in the Diagnosis of Arthropathy
Certain arthropathies tend to involve distinct areas of the hands, and sonographic
results should be placed in the proper clinical context.
Specific Conditions
Rheumatoid arthritis often involves the ECU tenosynovium and may cause ulnar
styloid bone erosion. Synovitis and cartilage erosion may also occur with RA at the
wrist, MCPJs, and PIPJs. Look for bone erosion along the radial aspect of the sec-
ond MC head and the ulnar aspect of the fifth MC head since these areas are ame-
nable to fuller US interrogation [10, 47, 106].
Spondyloarthropathy
Spondyloarthropathy (SpA), in particular PsA, may involve the finger and wrist
joints and cause enthesitis of the extensor tendon, the collateral ligaments, and the
palmar plate, paratenonitis, tenosynovitis, bone/cartilage erosion, and bone prolif-
eration [10].
Gout
Look for a double contour sign over cartilage, urate aggregates at tendons/liga-
ments, and tophi in any location. Tophi may cause bone erosion with their classic
overhanging edges. The wrist joint may be involved with gout. Again, gout typically
starts in the foot/ankle, so there is often evidence of lower extremity involvement by
the time it affects the hand [10].
Calcium Pyrophosphate Deposition Disease (CPPD)
Evaluate for calcification within cartilage, including the TFCC, the MCPJs, and the
scapholunate ligament. The wrist is the most commonly affected by CPPD in the
hand [10].
Lupus
Lupus may cause synovitis of the wrist, the MCPJs, and the PIPJs. The concept that
lupus arthritis is non-erosive has recently been questioned [17, 107, 108].
Osteoarthritis
Osteoarthritis may damage the MC head cartilage in all five MCPJs compared to
RA, which tends to affect the hyaline cartilage covering MC heads 2 and 3.
Osteoarthritis-associated synovitis may be seen on GS and color Doppler at the first
CMCJ and interphalangeal joints [109]. Osteophytes may easily be seen at the first
CMCJ, the PIPJs, and the DIPJs.
Specific Ultrasound Findings
1. Flexor tenosynovitis within the carpal tunnel may produce carpal tunnel
syndrome.
2. Osteoarthritis may have a degree of synovitis and sometimes even PD activity,
which can be confused with a true systemic inflammatory arthropathy.
3. Differentiating seronegative RA from PsA can be challenging, particularly if
there is no history of psoriasis.
4. Hyperuricemia may be present in a patient with hand polyarthritis, but gout may
not be causing inflammation. Demonstrating a double contour sign in the hand
or elsewhere does not necessarily mean hand arthropathy symptoms are due
to gout.
5. If you detect synovitis of the wrist or MCPJs, look for specific high-yield US
findings, which will trigger a search for other sonographic diagnostic clues of
inflammatory arthropathy.
(a) Uncovering ECU tenosynovitis should heighten the suspicion of RA.
(b) The finding of calcium deposits at the TFCC, the scapholunate ligament, or
the hyaline cartilage of the MCPJs brings to mind the possibility of
CPPD. Immediate sonography of the distal femoral cartilage may confirm
chondrocalcinosis.
(c) If you come across a double contour sign or tophus in the hands, look for
evidence of uric acid deposition at the distal femoral cartilage, the tibiotalar
joint, and the first MTPJs.
(d) Discovering enthesitis at the distal extensor tendons of the fingers, although
not pathognomonic for PsA, should prompt a thorough evaluation of SpA.
Pitfalls
1. Do not neglect to recalibrate Doppler settings for each patient; use the lowest
gain and lowest PRF that do not produce excessive artifacts or noise.
2. Use identical settings on the same US device when following the Doppler activ-
ity of an individual patient longitudinally [37].
3. Verify sufficient PD sensitivity by placing the probe on the distal finger pulp.
The power Doppler signal should register over one-third of the finger pulp [10].
4. When evaluating PD activity, use minimal probe compression to avoid dampen-
ing blood flow [95].
5. Minimize the ROI box when using PD since this increases the frame rate and
helps detect hyperemia. In other words, use the smallest PD activity box pos-
sible [95].
Pitfalls 129
6. Do not be fooled by a feeder vessel entering the lunate mimicking PD activity

and thus synovitis [110].
7. Intra- and interobserver grading drift and disparities are overcome by compar-
ing current and prior images.
8. When examining the dorsal wrist in LAX, do not mistake the anisotropy of the
more superficial extensor retinaculum for tenosynovitis or tenosynovial
fluid [95].
9. Do not neglect to evaluate the tendon sheath of the ECU for inflammatory teno-
synovitis since this is a high-yield area when considering RA [95, 111, 112].
10. Confirm putative bone erosions with orthogonal views on US. If the presence
of an erosion affects treatment, then additional imaging modalities may be
necessary.
11. Be careful of the classic “pseudoerosion” of the metacarpal head, which is the
normal smooth concavity on the dorsal aspect of the distal metacarpal where
the bone shaft joins the metacarpal head [95]. If erosion is suspected, then the
presence of contiguous synovial hypertrophy would argue for actual erosion.
12. Interpreting the meaning of isolated SH on GS requires careful consideration of
the distribution of the synovitis and the patient history, physical examination,
laboratory tests, and radiographs [95]. Such synovitis may or may not indicate
underlying inflammatory arthritis.
13. Do not misinterpret a pulsating volar ganglion cyst adjacent to the radial artery
as a pseudoaneurysm [95].
14. Do not mistake a pseudoaneurysm for a soft tissue tumor.
15. The dorsal arch of the hand may have feeder vessels superficial to the synovium.
These vessels may mimic synovitis but are above the synovium [110]. Make
sure you look for PD activity within the boundaries of the synovium as
defined on GS.
16. Remember that the synovial recess reflection direction is distal for the radiocar-
pal and intercarpal joints and proximal for the radioulnar joint, the volar wrist,
the MCPJs, and the PIPJs.
17. Synovitis of the MCPJ is often due to RA but can also be due to PsA or crystal
disease. Occasionally, erosive OA, also known as inflammatory osteoarthritis,
may cause some degree of synovitis in the MCPJs.
18. Do not use US, including Doppler, to guide treatment intensity in RA; this may
result in overtreatment.
19. When examining the volar MCPJ for synovitis, note that the usual synovial
recess extends proximally and should be included with Doppler analysis.
20. Another cause of pseudotenosynovitis is the normal hypoechoic muscle taper-
ing at the musculotendinous junction. Avoid this pitfall by verifying what
appears to be tenosynovitis in two orthogonal planes.
21. Bone erosions ≥ 2.5 mm have maximal sensitivity and specificity for RA bone
erosions [49].
22. Always delineate a dorsal ganglion cyst from a distended radiocarpal joint
recess. The ganglion has minimal compressibility, whereas the distended recess
is more compressible.
Method
The patient faces you with the forearm pronated to expose the dorsal wrist. The
forearm rests on a flat surface; the wrist is in a neutral position. The fingers may be
placed on a slightly convex, curved surface to flex the finger joints and improve
visualization minimally. Use a linear probe with a frequency of at least 12 MHz.
Optimal evaluation of entheses often requires a higher frequency, at least 16 MHz.
The protocol below has the sonographer turning on and off the PD for each joint.
Some examiners prefer an alternative sequence of performing the entire examina-
tion using the GS and then repeating the whole examination with the PD.
rotocol Image 1: Dorsal Radiocarpal Joint, Intercarpal Joint,

P
Start with the probe in LAX along the dorsal radial aspect of the wrist to look for
the radiocarpal joint. Next, do a TAX slide in a slight ulnar direction and observe the
scaphoid’s disappearance and then the bony lunate’s emergence. You have located
the RCJ (radiolunate) and ICJ (lunocapitate). Move the probe in TAX slides in
Fig. 5.8 Protocol Image 1: Dorsal radiocarpal joint, intercarpal joint, longitudinal ± power Doppler
Method 131
either direction to sharply focus the bones and the dorsal synovial recesses. Record
the image.
The GS evaluation looks at the hypoechoic dorsal synovium, the curved, mild-
moderately hyperechoic joint capsule, and the hyperechoic bone. Observe for thick-
ening of the joint capsule, particularly of the RCJ, and evidence of GS synovial
hypertrophy. In addition, observe for effusion and ganglion cysts. Synovial hyper-
trophy, if present, should be graded as described in the Clinical Comments section.
Note the extensor tendon that is superficial to the joints. Do not mistake the anisot-
ropy of the extensor retinaculum for tenosynovitis or tenosynovial fluid.
Turn on the PD. Note that the PD signal that we focus on is within the joint
recess, deep into the joint capsule. See Clinical Comments for the grading (0–3)
system. Power Doppler activity superficial to the joint capsule may be due to normal
feeder vessels and does not reflect PD activity directly in the joints. However, note
if PD activity exists in the tenosynovium of the overlying extensor tendon.
rotocol Image 2: Dorsal Second Metacarpophalangeal Joint,

P
Lift the probe and place it over the second MCPJ in LAX. Perform slow TAX slides
in radial and ulnar directions to fully evaluate the cartilage and the synovial recess.
The radial aspect of this MCPJ is freely accessible and should be included in the
examination. Evaluate the three margins of the recess—proximal, distal, and super-
ficial. The superficial margin can be defined by passively flexing and extending the
finger at the MCPJ to identify the moving extensor tendon, which borders the supe-
rior recess margin. Synovial hypertrophy will expand these margins and can
be graded.
Examine the smoothness of the superficial surface of the cartilage covering the
MC head. Look at the MC head itself and determine (a) if cartilage surrounds the
distal and dorsal portions of the head; (b) the constitution of the cartilage (overall
thickness degree, uniformity, sharpness of the external border); (c) if there is a slight
hyperechoic reflective surface (interface reflex) indicating a smooth cartilage sur-
face; and (d) if there is focal or diffuse cartilage thinning, which would indicate
cartilage erosion. Passively flexing and extending the MCPJ will enable a thorough
inspection of the MC head’s cartilage. Remember that exuberant synovium may
have migrated into the area where cartilage previously existed.
Look at the bony surfaces of the MC head and the proximal phalanx for irregu-
larities, which may indicate bone erosion. If the radiographs suggest possible bone
erosion, do a focused US examination on that area to verify. An effusion may be
present along with synovitis. Prior synovitis may have receded in long-standing
cartilage-erosive arthropathy, leaving only residual cartilage or bone erosion. PD
activity may be noted within the synovial tissue. Remember to verify synovitis,
cartilage erosion, and bone erosion in TAX views; these can be saved as needed.
Fig. 5.9 Protocol Image 2: Dorsal 2nd metacarpophalangeal joint, longitudinal ± power Doppler
rotocol Image 3: Dorsal Second Proximal Interphalangeal

P
Place the probe over the second PIPJ in LAX. Perform slow TAX slides in radial and
ulnar directions to fully evaluate the cartilage and the synovial recess. Osteophytes
may be seen primarily in the older age group; the dorsal recess may be enlarged and
extended proximally. Synovial hypertrophy can be graded with or without PD activ-
ity. Erosion of bone may be seen in aggressive polyarthritis such as RA, PsA, and
perhaps in advanced gouty arthropathy. Again, verify suspected pathologies in the
TAX view. Power Doppler activity may be positive within the synovial tissue.
rotocol Image 3a (Optional): Dorsal Distal Second Phalanx

P
Extensor Tendon Insertion, Longitudinal ± Power Doppler
Examine for enthesopathy and enthesitis. Use the highest frequency probe available
(at least 16 MHz) and recall that while the extensor tendon inserts on the bony distal
phalanx, some fibers extend superficially to form the fingernail bed matrix.
Method 133
Fig. 5.10 Protocol Image 3: Dorsal 2nd proximal interphalangeal joint, longitudinal ±
power Doppler
rotocol Image 4: Dorsal Third Metacarpophalangeal Joint,

P
Longitudinal ± Power Doppler
Perform the same examination as per Protocol Image 2 above.
rotocol Image 5: Dorsal Third Proximal Interphalangeal Joint,

P
Perform the same examination as per Protocol Image 3 above.
rotocol Image 5a (Optional): Dorsal Distal Third Phalanx

P
Extensor Tendon Insertion, Longitudinal ± Power Doppler
Perform the same examination as per Protocol Image 3a above.

rotocol Image 6: Dorsal Fifth Metacarpophalangeal Joint,

P
Perform the same examination as per Protocol Image 2 or 4 above. The ulnar aspect
of the fifth MCPJ is easily accessible and should be included.
rotocol Image 7: Distal Ulna, Longitudinal ± Power Doppler

P
(Fig. 5.11)
Move the probe proximally to place it over the palpable protrusion of the dorsal
distal ulnar styloid in LAX. It will appear to be a hyperechoic, curved hill-like struc-
ture, generally covered with a rim of anechoic cartilage. Perform a TAX slide in an
ulnar direction to examine the cartilage covering the distal ulna. Confirm any pos-
sible erosions in TAX. Turn on PD to assess activity.
Fig. 5.11 Protocol Image 7: Distal ulna, longitudinal ± power Doppler

Method 135
rotocol Image 8: Ulnocarpal Joint, Longitudinal ± Power

P
Doppler (Fig. 5.12)
The patient turns the fingers radially to expose the ulnocarpal joint and extend the
ECU tendon. Place the probe in LAX along the ulnar aspect of the wrist, with one
end on the distal ulna and the other on the proximal carpal bone, specifically the
triquetrum. The lunate bone is the hyperechoic curved bone deep to and adjacent to
the triquetrum. You may see a flat, even deeper bone closer to the distal ulna; this is
the radius. Look at the TFCC articular disk and the more distal meniscal homolog.
Determine if calcium is embedded in the TFCC. Usually, the TFCC is barely visible
unless it contains some hyperechoic calcium. Also, look at the superficially located
ECU tendon and its synovial sheath. Confirm any possible pathology in TAX. Turn
on PD to assess activity.
Fig. 5.12 Protocol Image 8: Ulnocarpal joint, longitudinal ± power Doppler

Fig. 5.13 Protocol Image 9: Volar wrist, transverse ± power Doppler
rotocol Image 9: Volar Wrist, Transverse ± Power Doppler

P
(Fig. 5.13)
The patient supinates the forearm and rests the hand dorsum on the examination
surface, extending the fingers. Place the probe in TAX across the wrist. Identify the
median nerve and the flexor retinaculum. The flexor carpi radialis tendon, located
superficially to the carpal tunnel, has a surrounding tendon sheath. The flexor digi-
torum superficialis and deeper flexor digitorum profundus tendons are within the
CT. Also within the CT is the flexor pollicis longus tendon. A tenosynovium sur-
rounds these tendons. If there is an anechoic or hypoechoic rim surrounding part of
a tendon, it might be tenosynovitis. To verify, rotate the probe to LAX to ensure that
you are not simply seeing the normal myotendinous junction of the tendon. If the
tendon sheath is thickened, then turn on the PD.
rotocol Image 10: Volar Second Metacarpophalangeal Joint,

P
Examine the second MCPJ in LAX when looking for synovitis, tenosynovitis,
cartilage, and bone erosions. For each joint, perform a TAX slide in an ulnar
and then radial direction to fully evaluate the joint. Manually flex the finger to
Method 137
Fig. 5.14 Protocol Image 10: Volar second metacarpophalangeal joint, longitudinal ±
power Doppler
visualize the flexor tendon and surrounding tenosynovium. The A1 pulley and
volar plate may be visible superficially to the MCPJ. The volar plate is imme-
diately superficial to the joint cartilage, and the A1 pulley is just superficial to
the flexor tendon. Remember that the flexor tendon has a superficial (flexor
digitorum superficialis) and deep (flexor digitorum profundus) layer. The
superficial layer may be the only layer that becomes snagged beneath the A1
pulley with a trigger finger.
Turn on the PD to look for activity. When examining the volar MCPJ for synovi-
tis, keep in mind that the normal synovial recess extends proximally and should also
be included with Doppler analysis [113].
rotocol Image 11: Volar Second Proximal Interphalangeal

P
Next, move the probe, still in LAX, to the second PIPJ. Perform a TAX slide in
ulnar and radial directions to fully evaluate the joint, synovial recess, and
flexor tendon.
Fig. 5.15 Protocol Image 11: Volar second proximal interphalangeal joint, longitudinal ±
power Doppler
rotocol Image 12 (Optional): Volar Third

P
Metacarpophalangeal Joint, Longitudinal ± Power Doppler
Next, move the probe to the third MCPJ. Repeat the examination as per Protocol
Image 10.
rotocol Image 13 (Optional): Volar Third Proximal

P
Interphalangeal Joint, Longitudinal ± Power Doppler
Next, move the probe, still in LAX, to the third PIPJ. Repeat the evaluation as in
Protocol Image 11.
rotocol Image 14 (Optional): Flexor Tendon Enthesis,

P
Longitudinal + Power Doppler
For this view, it is best to use a high-frequency probe (at least 16 MHz). Remain in
LAX. For each of the fingers, move the transducer distally to examine the deep
flexor tendon insertion on the distal phalanx. Turn on PD.
Method 139
Complete Hand Arthropathies Ultrasonic Examination Checklist

□ Protocol Image 1: Dorsal radiocarpal joint, intercarpal joint, longitudinal ±
power Doppler.
□ Protocol Image 2: Dorsal second metacarpophalangeal joint, longitudinal ±
power Doppler.
□ Protocol Image 3: Dorsal second proximal interphalangeal joint, longitudinal ±
power Doppler.
□ Protocol Image 3a (optional): Dorsal distal second phalanx extensor tendon
insertion, longitudinal ± power Doppler.
□ Protocol Image 4: Dorsal third metacarpophalangeal joint, longitudinal ± power
Doppler.
□ Protocol Image 5: Dorsal third proximal interphalangeal joint, longitudinal ±
power Doppler.
□ Protocol Image 5a (optional): Dorsal distal third phalanx extensor tendon inser-
tion, longitudinal ± power Doppler.
□ Protocol Image 6: Dorsal fifth metacarpophalangeal joint, longitudinal ± power
Doppler.
□ Protocol Image 7: Distal ulna, longitudinal ± power Doppler.
□ Protocol Image 8: Ulnocarpal joint, longitudinal ± power Doppler.
□ Protocol Image 9: Volar wrist, transverse ± power Doppler.
□ Protocol Image 10: Volar second metacarpophalangeal joint, longitudinal ±
power Doppler.
□ Protocol Image 11: Volar second proximal interphalangeal joint, longitudinal ±
power Doppler.
□ Protocol Image 12 (optional): Volar third metacarpophalangeal joint, longitudi-
nal ± power Doppler.
□ Protocol Image 13 (optional): Volar third proximal interphalangeal joint, longitu-
dinal ± power Doppler.
□ Protocol Image 14 (optional): Flexor tendon enthesis, longitudinal + power
Doppler.
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Chapter 6
Anterior Elbow

1. Antecubital elbow pain
2. Lateral elbow pain
3. Paresthesia or weakness in the hand in the distribution of the radial nerve or the
median nerve
4. Weakness of elbow flexion or supination
1. Is there a joint effusion? If so, what is the cause?
2. Is there compression of the median nerve or the radial nerve?
3. Is there an injury to the distal biceps brachii tendon?
4. Is there bicipitoradial bursitis?
Anatomy
Bones and Joints (Fig. 6.1)
The terminology of the bones of the anterior elbow is confusing. The distal humeral
ends are the capitellum (radial side) and the trochlea (ulnar side). The radial head is
a “process,” and the ulnar head is also a “process.” The latter is also known as the
States Government.

Switzerland AG 2023
148 6 Anterior Elbow
Fig. 6.1 Bony anatomy of

the anterior elbow
coronoid process. The anterior recess has two fossae on the anterior distal humerus:
the coronoid (ulnar) and radial. So, the bony landmarks, as we go from proximal to
distal on the anterior elbow, are as follows:
A. Ulnar (medial) aspect:
Coronoid fossa (of the humerus) to the humeral trochlea to the ulnar head
(coronoid process).
B. Radial (lateral) aspect:
Radial fossa (of the humerus) to the humeral capitellum to the radial head.
The three elbow joints are as follows:
A. Humeroulnar joint
B. Humeroradial joint
C. Radioulnar joint
Anatomy 149
Anterior Joint Recess
The coronoid and smaller radial fossa are concavities at the distal humerus within
the anterior joint recess [1]. Each fossa contains a hyperechoic triangular fat pad
sandwiched between the deeper synovium and the more superficial joint capsule.
Fat pads will displace anteriorly by a joint effusion. An anechoic joint effusion is
easy to visualize at the anterior recess and is accentuated on a dynamic ultrasound
(US) exam with forearm supination/pronation. However, be aware that you may find
a small amount of physiologic fluid posterior (deep) to the anterior fat pad.
Synovitis may occur in the anterior joint recesses due to chronic osteoarthritis,
inflammatory arthropathy (rheumatoid arthritis [RA], gout, pseudogout, etc.), or
infection [1]. Thickened synovium and hyperemia may be noted with RA. If syno-
vitis is present, also consider synovial proliferative disorders such as pigmented
villonodular synovitis or synovial osteochondromatosis (the latter may be seen as
multiple hyperechoic foci within the synovial fluid). The examiner may also dis-
cover intra-articular bodies in the anterior recess with movement of the bodies acti-
vated by a gently rocking motion of the patient’s elbow [2]. The capitellum may
demonstrate a defect in the articular hyaline cartilage, the donor site for the intra-
articular body, or bodies [1].
Muscles, Nerves, and Tendons
So, at the anterior elbow crease, the soft tissue structures from lateral to medial are
the brachioradialis muscle, the radial nerve, the brachialis muscle, the biceps bra-
chii muscle, the median nerve, and the pronator teres (Fig. 6.2). A suggested mne-
monic is as follows:
Bring Real Beer By My Porch
The radial nerve traverses the space between the brachialis and the brachioradia-
lis. More distally, the radial nerve splits into superficial and deep branches; the latter
is called the posterior interosseous nerve (PIN). The PIN most commonly passes
between the superficial and deep portions of the supinator muscles [3]. The median
nerve similarly traverses between the two heads of the pronator teres (PT) muscle.
Muscle Insertions [4]:
1. Brachioradialis muscle: distal radius.
2. Supinator muscle: proximal radius.
3. Brachialis muscle: coronoid process of the ulna.
4. Biceps brachii: radial tuberosity (via the distal biceps tendon) and deep forearm
fascia (via the lacertus fibrosus).
Fig. 6.2 Simplified soft

tissues of the anterior
elbow
The distal biceps tendon (DBT) has a paratenon and not a true tendon sheath;
therefore, no true tenosynovitis occurs in this location. The cubital bursa,
interposed between the DBT and radial tuberosity, facilitates smooth gliding
during pronation and supination [3]. The lacertus fibrosis is a flat aponeurosis
that expands out from the biceps brachii tendon and inserts into the deep forearm
fascia. It helps maintain the DBT in the correct position [1, 3].
5. Pronator teres: middle lateral radius.
Arteries
The brachial artery (BA) divides into the ulnar and radial arteries near or proximal
to the elbow [4].
Clinical Comments
The complaint of antecubital pain prompts an assessment. The examiner can evalu-
ate the anterior joint recesses, muscles tendons, nerves, arteries, and the bicipital
bursa. Dynamic examination (pronation/supination and flexion/extension) may elu-
cidate pathology undetected by a static MR study.
Effusion, Synovitis, Loose Bodies, and Erosions
The humeroulnar and humeroradial joints are evaluated. The anterior recesses have
fat pads that are displaced anteriorly in the presence of synovial effusion or synovi-
tis. An effusion may be caused by trauma, joint inflammation, degenerative changes,
or infection. Ultrasound reveals a hypoechoic or anechoic effusion in the anterior
recess with an anterior (superficial) displacement of the fat pad [3]. If you detect an
effusion, evaluate it for loose bodies which may be associated with osteochondro-
matosis, osteochondral fractures, and osteochondritis dissecans, three entities with
a proclivity to occur in the elbow. Synovitis may demonstrate power Doppler activ-
ity in inflammatory conditions such as rheumatoid arthritis [3]. Cartilage or bone
erosion may be evident at the humeroradial joint or the humeroulnar joint. Crystal
disease (gout and calcium pyrophosphate deposition disease [CPPD]) prefers other
joints but may occur in the elbow. On US, examine for urate deposits on the carti-
lage surface (double contour sign of gout), gouty tophi, and CPPD crystals within
the cartilage. Sonography may reveal gout and CPPD crystals within the joint,
bursa, and tendons.
Fractures
Conventional radiographs may reveal a conspicuous fracture. However, both well-

defined and occult fractures may produce a radiographic “sail sign,” in which a
secondary effusion elevates the fat pad, mimicking the appearance of a spinnaker
sail [5]. If the fat pad is elevated on US or radiographs, a careful sonographic inspec-
tion may reveal cortical bone irregularities [3]. If a fracture is still suspected after
radiographic and sonographic evaluations, further imaging is warranted.
Distal Biceps Tendon Pathology
Distal biceps tendon tears typically occur in middle-aged men, associated with activi-
ties such as weightlifting [6]. Distal biceps tendon ruptures are much less common than
proximal biceps tendon tears [3]. A complete DBT tear often presents with sudden
anterior elbow pain and a popping sensation after lifting a heavy object [1]. There may
be a soft tissue mass or a palpable defect in the antecubital fossa accompanied by weak-
ness in flexion and supination. A round lump along the anterior upper arm is described
as a “Popeye sign” and is formed by the proximally retracted tendon and muscle [7].
Since treatment of a complete tear is surgical, better results require a prompt
diagnosis [6]. If the diagnosis is clinically obvious, no imaging is required. However,
the diagnosis of nonretracted tears may be challenging [1, 6]. Partial or nonretracted
tears may occur due to intact lacertus fibrosis. The US image may be obscured by
significant edema and hemorrhage [1]. Again, it is essential to distinguish between
complete and partial tears since complete tears require surgery.
Partial tears of the DBT are best seen in longitudinal (LAX) view on US and
appear as anechoic or hypoechoic discontinuities of tendon fibers without retrac-
tion; there may be surrounding hypoechoic fluid. If the lacertus fibrosis is ruptured,
the tendon may retract, resulting in nonvisualization of the distal tendon in the
expected location [1, 3]. The finding of a posterior acoustic shadow deep to the
retracted tendon may increase diagnostic accuracy [8].
Incomplete ruptures may also appear as intratendinous hypoechogenicity with a
thickened or thinned tendon [3]. The slanting course of the DBT and attendant
hypoechogenicity create a sonographic imaging challenge, particularly at its attach-
ment to the radial tuberosity. Multiple sonographic approaches have been offered
[3]. Due to these imaging obstacles, US is unreliable to visualize tendon tears,
although dynamic US may help differentiate complete from incomplete tears [1].
Evaluating the contralateral elbow may be of help.
Thus, a pitfall is missing a DBT tear or tendinosis. To mitigate the impediment of
anisotropy, evaluate the tendon in transverse (TAX) and LAX, perform heel-to-toe
maneuvers, and use full forearm supination. Further, evaluate the tendon in LAX
with a segmental approach and assess any potential abnormality with varying degrees
of elbow flexion and extension [1]. In one study comparing US to surgical findings
in evaluating complete versus partial DBT tears, US demonstrated 95% sensitivity,
71% specificity, and 91% accuracy [6]. As always, the diagnostic results of US stud-
ies rely on the experience of sonographers performing a particular US examination.
A disadvantage of magnetic resonance imaging (MRI) is the typical delay in
obtaining approval for the study since diagnostic delay affects surgical outcomes
with complete tears. The disadvantage of US, however, is the technical challenge of
DBT evaluation [6]. Some recommend that US be the first-line study to evaluate
DBT injuries if a trained and experienced sonographer is available. Nevertheless,
MRI is still considered the gold standard for the evaluation of this tendon, particu-
larly at the distal attachment [9].
Bicipitoradial Bursitis
The DBT attaches to the radial tuberosity, located on the posteromedial aspect of
the radius [10]. Repetitive supination–pronation creates wear and tear on the
DBT. Since the DBT lacks a tenosynovium, contact between the tendon and the
radius is mitigated by the bicipitoradial bursa (BRB) [10]. The BRB surrounds the
DBT during forearm supination and is compressed against the radial tuberosity dur-
ing forearm pronation. This bursa does not communicate with the joint space [10].
The BRB may distend due to tears of the DBT, repetitive microtrauma, infection,
and inflammatory arthropathies such as RA and gout [3, 10].
Bursitis of the BRB, known as cubital (bicipitoradial) bursitis, may present as an
antecubital mass or with symptoms of compression of the nearby radial nerve [11].
If neurologic symptoms are present, there may also be local pain. Cubital bursitis,
while the most common bursitis in this area, may be challenging to diagnose since
the cubital bursa is in a deep location [3]. Thus, cubital bursitis may be misdiag-
nosed as biceps tendinitis.
Ultrasound can detect anechoic bursal distension surrounding the distal DBT,
best seen in TAX view with respect to the long axis of the tendon during forced
forearm supination [10]. Ultrasound reveals a thickened bursal wall associated with
distention and an anechoic effusion [3]. Bicipitoradial bursitis mimics synovial gan-
glion cysts and other soft tissue masses [1]. Additionally, US may help guide aspira-
tion or a therapeutic bursal injection [10].
Median Nerve Pathology
Median nerve (MN) entrapment may occur at several locations in the anteromedial
elbow [1]. The PT muscle has a humeral head and an ulnar head, which combine to
form a muscle belly that inserts distally onto the middle third of the radius. The PT
mainly pronates the forearm but also flexes the elbow. In more than 80% of indi-
viduals, the MN runs between the two heads and is less commonly posterior to the
ulnar (deeper) head [1]. The MN on US has a speckled appearance in the short axis
due to the hypoechoic nerve fascicles and intervening hyperechoic epineurium.
Median nerve (MN) compression between the two heads of the PT muscle causes
pronator teres syndrome (PTS) [12]. This produces paresthesia in the distal extrem-
ity, mimicking carpal tunnel syndrome (CTS). It occurs with repetitive forearm pro-
nation, an occupational hazard for carpenters, hairdressers, baseball pitchers,
violinists, and mechanics [12]. Tinel’s sign may be positive in the forearm. However,
PTS does not produce nocturnal paresthesia as occurs with CTS, and EPS studies
are often normal with PTS [12].
Struthers’ ligament, present in 1% of individuals, is a fibrous or muscular band
originating from the apex of the distal humeral supracondylar process that inserts on
the medial epicondyle [12]. This creates a “tunnel” inside which the MN or BA may
become entrapped. Radiographs of the humerus will detect this supracondylar pro-
cess which is a clue to the possibility of Struthers’ ligament compressing the MN
and thus mimicking CTS [12]. Reduced radial artery pulsation may occur with BA
compression in supination and forearm extension.
Other causes of proximal compression of the MN include pseudoaneurysms of
the brachial or axillary arteries, dialysis fistula, post-puncture hematoma, anatomic
variations, and compression by orthopedic material [12]. The lacertus fibrosis,
located between the bicipital tendon and PT fascia, may also compress the MN. The
PT muscle itself may also be injured with throwing sports, forearm fractures or dis-
locations, and during surgery [12].
Radial Nerve Pathology
The radial nerve (RN) at the elbow divides into the superficial radial nerve (SRN)
and the deep branch, also known as the PIN [13]. This division may occur anywhere
from 5 cm above to 1 cm below the radiohumeral joint line. The PIN may be com-
pressed at multiple locations: at the medial edge of the extensor carpi radialis brevis,
by fibrous bands near the head of the radius, by branches from the recurrent radial
artery (Leash of Henry), under the Arcade of Frohse (a fibrous arch at the proximal
edge of the superficial head of the supinator), and at the distal edge of the superficial
supinator muscle [13]. Other causes of PIN compression include ganglion cysts,
tumors, radial head and neck fractures, or posttraumatic scars [1, 14]. Compression
of the PIN may cause the following:
1. Pure motor dysfunction distally, with weakness of finger extension, local pain,
radial nerve palsy, and difficulty in extending the wrist [3].
2. The so-called radial tunnel syndrome may mimic lateral epicondylitis by causing
lateral elbow pain. Sensory fibers carried by the PIN may be the source of pain.
A variety of opinions in the literature makes this syndrome somewhat controver-
sial [13].
Use US to follow the PIN distally with TAX images and compare with the contra-
lateral unaffected side. Longitudinal views are more challenging due to the winding
course of the PIN [13]. Compression of the PIN appears sonographically as
hypoechoic enlargement proximal to the point of compression [1, 13]. Doppler
ultrasound may reveal atypical and prominent pulsating vessels near the nerve in
the case of PIN compression at the Leash of Henry [13]. PIN compression is best
determined if there is enlargement and hypoechogenicity of the nerve near these
vessels.
There may be normal PIN flattening at the Arcade of Frohse (just before the
PIN enters the plane between the supinator heads), which may simulate entrap-
ment, particularly on TAX view [14]. This pitfall is avoided by measuring the
cross-sectional area (CSA) of the nerve 1 cm proximal to and 1 cm distal from the
arcade. Another pitfall is that PIN appearance usually changes with pronation and
supination [13].
The PIN is best followed between the superficial and deep heads of the supinator
muscle while slowly pronating the forearm [13]. Magnetic resonance imaging is a
complementary modality when diagnosing PIN compression. Bicipitoradial bursitis
may uncommonly compress the SRN and the PIN [15]. Distal biceps tendon repair
may injure these nerve branches as well [13].
Pitfalls 155
Pitfalls
1. Tendinosis and tears of the DBT are easy to miss due to imaging challenges. To
minimize this error, first evaluate the tendon in the transverse axis (TAX) and
then evaluate the tendon in a longitudinal (LAX) segmental approach using heel-
to-toe maneuvers employing maximal forearm supination. Also, learn the “crab”
technique described in the Method section to delineate the DBT insertion on the
radial tuberosity [1, 16].
2. Median nerve entrapment may occur at several locations in the anteromedial
elbow and may mimic CTS. Nocturnal paresthesia, positive Tinel’s and Phalen’s
signs at the volar wrist, as well as an enlarged MN proximal to the transverse
carpal ligament, favors CTS. The diagnosis of more proximal MN entrapment
requires careful US examination of the entire course of the MN in TAX view.
3. Do not mistake the normal flattening of the PIN as it enters the Arcade of Frohse
(AF) for true compression. Always measure the CSA of the nerve 1 cm proximal
to and 1 cm distal from the arcade [13].
4. Do not mistake the change in appearance of the PIN with pronation and supina-
tion for true compression of the PIN.
5. Do not mistake radial nerve compression for lateral epicondylitis since both
cause pain near the lateral epicondyle.
6. Due to its deep location, cubital bursitis may be challenging to diagnose and may
be mistaken for biceps tendinitis, synovial ganglion cysts, and other soft tis-
sue masses.
Method
Based on the clinical history and location of the discomfort, try to determine what
structure is the most likely cause of the problem. The patient is recumbent with an
extended forearm resting on the examination table and palm up (supinated).
Alternatively, the patient may be seated, with a supinated, extended arm on the lap.
Use the middle depth or elbow preset.
rotocol Image 1: Anterior Distal Humerus, Transverse ± Power

P
Doppler (Fig. 6.3)
Start with the probe in TAX on the ulnar (inner or medial) side of the elbow, at a
point approximately 5 cm proximal to the elbow crease. Turn on the PD to visualize
the BA and any of its branches on the anterior elbow’s medial aspect. The MN is just
medial to the BA.

Anterior distal humerus,
transverse ± power
Doppler
rotocol Image 2: Anterior Distal Humeral Cartilage Ulnar,

P
To assess the cartilage of the distal humerus on the ulnar side (the trochlea), per-
form a distal TAX slide (move closer to the elbow crease) to visualize the wavy
cartilage of the distal humerus. The transducer should be at or just proximal to the
elbow crease. Note that this is not the true joint space, but the cartilage covering
the distal humerus. From medial to lateral, locate the PT, BA, MN, and the bra-
chialis muscle. The coronoid fossa is seen in the TAX view. The biceps brachii
may be seen transitioning to the smaller biceps tendon at its myotendinous
junction.
Method 157

Anterior distal humeral
cartilage ulnar, transverse
rotocol Image 3: Anterior Humeroulnar Joint, Longitudinal

P
(Fig. 6.5)
Visualize the humeroulnar joint (HUJ) (trochlea-ulnar joint) in TAX by performing

a slight distal TAX slide while still in TAX. The joint space, located immediately
distal to the wavy line (distal humeral cartilage), is reached when the bone “drops
out.” The probe is now centered over the actual joint space. Then, rotate the trans-
ducer 90° to LAX orientation to visualize the HUJ in LAX. Recognize the curved
humeral trochlea and the sharp, pointed ulnar head (coronoid process). Imaging
may require slight TAX slides in the lateral or medial directions. If necessary, per-
form a proximal LAX slide to see the coronoid fossa of the distal humerus in
LAX. The fat pad lies over the fossa; the anterior elbow fat pads are contained
within the joint capsule but outside the synovium.

Anterior humeroulnar
joint, longitudinal
rotocol Image 4: Anterior Humeroradial Joint, Longitudinal

P
(Fig. 6.6)
With the transducer still in LAX orientation to the forearm, perform a TAX
slide in the radial direction until the shallow radial fossa is seen at the distal
humerus. The fat pad overlies the fossa. A slight distal LAX slide reveals the
humeral-radial (radiocapitellar) joint with the curved hyperechoic humeral cap-
itellum and the radial head, which has a characteristic hyperechoic “flat top”
appearance.
Method 159

Anterior humeroradial
joint, longitudinal
rotocol Image 5: Median Nerve, Transverse ± Longitudinal ±

P
Power Doppler (Fig. 6.7)
Rotate the probe 90° into TAX, and then perform a proximal TAX slide back to
Protocol Image 2. The elbow remains extended and supinated. Move the transducer
in an LAX slide medially along the crease of the elbow to center it on the MN,
which is just medial to the BA. The artery can be located with power Doppler. Then
perform a distal TAX slide to observe the BA or one of its branches slip under the
MN. This verifies the identity of the MN. At this level, the BA has split off into the
ulnar and radial arteries, and the MN is between the two heads (ulnar and humeral)
of the PT muscle. Compression of the MN between the two PT muscles may cause
paresthesia, pain, or weakness and is called the pronator teres syndrome. See
the Clinical Comments section.
If necessary, dynamic assessment for MN compression between the deeper ulnar
head and the more superficial humeral head can be performed as follows. The
patient's elbow is flexed, and the examiner actively resists forearm pronation. This

Median nerve, transverse ±
Doppler
is followed by persistent, continued resistance to flexion, while the examiner pas-

sively extends the forearm [17]. Comparison to the contralateral, presumably unaf-
fected side, may also be helpful. If desired, the MN can be examined in LAX by
centering the image on the MN, rotating the transducer 90°, and performing a heel-
to-toe maneuver.
rotocol Image 6: Anterior Distal Humeral Cartilage Radial,

P
Next, turn the probe back to TAX and return to Protocol Image 2, that is, TAX at the
ulnar aspect of the distal humerus, just proximal to the joint line. The “wavy line”
of the distal humeral cartilage is again visible. Perform an LAX slide in a radial
(lateral) direction across the anterior elbow to see the distal humeral cartilage over
the humeral capitellum. The radial fossa, shallower than the coronoid fossa, is also
found here. The prominent hyperechoic diagonal line is the fascial plane (the lateral
intermuscular septum) between the brachialis and the more lateral brachioradialis
muscles. Sandwiched in between the two muscles is the radial nerve, which is start-
ing to split into superficial and deep branches.
A distal TAX slide past the humeroradial joint shows the radial nerve further
dividing into the deeper PIN and the SRN. The PIN is also known as the deep
branch of the radial nerve. As you move the probe distally in a TAX slide, the fas-
cicle that will become the PIN will dive deep between the two heads of the supinator
Method 161

Anterior distal humeral
cartilage radial, transverse
± power Doppler
muscle. This maneuver reveals which bundles in the lateral intermuscular septum
become the PIN and the SRN.
Turn on the PD to look for pulsating blood vessels surrounding the PIN fascicle,
which resembles a dog leash and is called the Leash of Henry and may be associated
with PIN compression. See the Clinical Comments section. If necessary, turn the
probe 90° to try to capture an optional image of the PIN in LAX, although this may
be challenging.
rotocol Image 7: Posterior Interosseus Nerve at Arcade

P
of Frohse, Transverse ± Longitudinal (Fig. 6.9)
Now, continue to move the probe distally in a TAX slide, following the PIN as it
enters the AF between the deep and superficial heads of the supinator muscle. This
is where the PIN may become symptomatically compressed, producing the supina-
tor syndrome. However, the PIN may normally appear flattened here. Measure the
CSA in TAX under the AF as well as 1 cm proximal to and distal from the AF to see
if there is an actual enlargement of the PIN. Verified proximal enlargement might
indicate actual nerve compression. The CSA of the PIN is normally about 1 mm2. It
may be entrapped if it has swollen to 2–3 mm2 [13].

Posterior interosseus nerve
at Arcade of Frohse,
transverse ± longitudinal
The PIN is easily seen with a probe fixed on the supinator muscle while the
patient slowly pronates and supinates the forearm, although the shape of the PIN
may normally change with this movement. If necessary, turn the probe 90° to cap-
ture an optional image of the PIN in LAX. Image acquisition may be aided by
slowly pronating the forearm.
rotocol Image 8: Biceps Tendon, Longitudinal (Composite

P
Extended View) (Fig. 6.10)
Next, return to Image 1, that is, a TAX view 5 cm proximal to the elbow crease.
Locate and center the probe on the cross section of the ovoid biceps muscle, just
superficial to the larger brachialis muscle. Follow the biceps muscle distally by
performing a TAX slide. The muscle decreases in size as it transitions to its myoten-
dinous junction and then to the anisotropic circular DBT Center the probe over the
DBT and rotate it 90°. The DBT is seen plunging downward at about a 30° angle
toward the radial tuberosity, a bony protrusion on the posteromedial aspect of the
radius just distal to the radial head.
Angle the probe about 10–15° in the radial direction and perform a heel-to-toe
maneuver while performing a slow LAX slide. Image acquisition is challenging.
Due to anisotropy, the bulk of the DBT is visualized as an anechoic or hypoechoic
longitudinal structure. Make sure the forearm is in complete supination. The DBT
needs to be examined in segments to mitigate the anisotropic mimicry of a tendon
tear. By tilting, slightly rotating, and using heel-to-toe maneuvers, you can trans-
form the appearance of several hypoechoic tendon segments into the hyperechoic
fibrillar echotexture necessary to assess the tendon. Beam steering, if available, may
be of assistance.
Method 163
Fig. 6.10 Protocol Image 8: Biceps tendon, longitudinal [composite extended view]
Segmental analysis reveals a composite picture of this long tendon. The bicipito-
radial bursa, if distended, may be seen surrounding the DBT in this view. The inser-
tion of the DBT onto the radial tuberosity is difficult to visualize in this view,
however.
rotocol Image 9: Distal Biceps Tendon Insertion, Longitudinal

P
(Fig. 6.11)
Visualizing the DBT insertion onto the radial tuberosity is challenging. However, an
innovative technique has proven useful [16]. The patient assumes the “crab posi-
tion,” in which the upper arm is extended backward at the shoulder, the elbow
is flexed down at about 90°, and the palm is flat on the table with the fingers facing
forward. This position exposes the posterior aspect of the radial tuberosity.

9: Distal biceps tendon
insertion, longitudinal
Place the transducer in LAX over the lateral epicondyle and the radial head to
visualize the humeroradial joint and the common extensor tendon. The probe is
turned 90°, and a slow distal TAX slide focuses first on the radial head and then the
hyperechoic curved radius. Continue the slow TAX slide to visualize the hyper-
echoic, prominent radial tuberosity where the DBT insertion can be seen as a “bird’s
beak” without anisotropy. Note that this view is longitudinal with respect to the long
axis of the tendon at its insertion.
Complete Anterior Elbow Ultrasonic Examination Checklist
□ Protocol Image 1: Anterior distal humerus, transverse ± power Doppler.
□ Protocol Image 2: Anterior distal humeral cartilage ulnar, transverse.
□ Protocol Image 3: Anterior humeroulnar joint, longitudinal.
□ Protocol Image 4: Anterior humeroradial joint, longitudinal.
□ Protocol Image 5: Median nerve, transverse ± longitudinal ± power Doppler.
□ Protocol Image 6: Anterior distal humeral cartilage radial, transverse ± power
Doppler.
□ Protocol Image 7: Posterior interosseus nerve at Arcade of Frohse, transverse ±
longitudinal.
□ Protocol Image 8: Biceps tendon, longitudinal (Composite Extended View).
□ Protocol Image 9: Distal biceps tendon insertion, longitudinal.
Method 165
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14. Dong Q, Jamadar DA, Robertson BL, Jacobson JA, Caoili EM, Gest T, et al. Posterior inter-
osseous nerve of the elbow: normal appearances simulating entrapment. J Ultrasound Med.
2010;29(5):691–6.
15. Tsz-Lung C, Tun-Hing L. Bicipitoradial bursitis: a review of clinical presentation and treat-
ment. J Orthop Trauma Rehabil. 2014;18(1):7–11.
16. Draghi F, Bortolotto C, Ferrozzi G. Distal biceps brachii tendon insertion: a simple method of
ultrasound evaluation. J Ultrasound Med. 2021;40(4):811–3.
17. Hsu SH, Moen TC, Levine WN, Ahmad CS. Physical examination of the athlete’s elbow. Am
J Sports Med. 2012;40(3):699–708.
Chapter 7
Posterior Elbow

1. Posterior elbow pain
2. Posterior elbow swelling
1. Is there olecranon bursitis?
2. Is there a joint effusion or synovitis?
3. Are there any intra-articular bodies?
4. Is there evidence for cartilage or bone erosion?
5. Is there a distal triceps tendon tear?
Anatomy
The principal elbow joint is the humeroulnar joint (Fig. 7.1). The olecranon process
of the ulna, shaped like a bottle opener, glides over the humeral trochlea during
elbow flexion and extension. The humeral trochlea and capitellum are scroll-like,
rounded bony structures best appreciated anteriorly. Proximal to the posterior aspect
of the humeral trochlea, the concave olecranon fossa contains the posterior joint
recess, including the hyperechoic posterior fat pad [1]. Bending the elbow enables
sonographic visualization of the posterior recess. A second joint, the humeroradial
joint, is also visible on ultrasound (US) from the posterior direction.
Superficial to the bones is the triceps muscle, which consists of three heads (the
long, lateral, and medial). The medial head is the deepest (Fig. 7.2). The three heads
form the triceps tendon, which inserts into the olecranon process [1]. Superficial to
States Government.

Switzerland AG 2023
168 7 Posterior Elbow

the posterior elbow
Fig. 7.2 Muscles of the

posterior elbow
the olecranon process and the triceps tendon is the subcutaneous olecranon bursa,
evident only when distended with fluid. The bursa is best visualized on US in elbow
extension using abundant transmission gel and a light transducer touch [1].
Clinical Comments
Joint Effusion
The posterior recess is the preferred location to view excessive joint fluid (effusion),
intra-articular loose bodies, and signs of inflammatory/erosive arthropathy [2].
Usually, fluid is undetectable within the recess, and the synovial membrane is invis-
ible unless pathologically thickened [3]. The posterior joint recess is normally filled
with an isoechoic posterior fat pad [1, 4]. An elbow effusion produces echogenically
variable fluid deep within the recess that dislocates the fat pad in a superficial and
proximal direction. The effusion is displaceable with transducer compression [1]. A
posterior elbow effusion is easily aspirated using US guidance.
If synovitis or synovial thickening is present, US may also detect this [1, 4].
Synovial hypertrophy is implied by local hyperemia on power Doppler (PD). If
synovial hypertrophy (synovitis) is present, consider inflammatory arthropathy
(e.g., rheumatoid arthritis, spondyloarthropathy, or gout), infection, or chronic
osteoarthritis [1]. Other causes of synovial hypertrophy include pigmented villon-
odular synovitis and synovial chondromatosis, the latter associated with calcified
hyperechoic foci. Evaluate the hyaline cartilage over the trochlea and capitellum for
erosion. If an intra-articular body is recognized on US or radiograph, you may dis-
cover the cartilage donor site [1].
Humeroradial Joint
Bone/Cartilage Erosion
Bone erosion may occur with inflammatory arthropathy.
Capitellum Osteochondritis dissecans
Capitellum osteochondritis dissecans (COCD) is a disorder of articular cartilage

and subchondral bone of the capitellum associated with repetitive trauma, most
commonly in teenage athletes who continually throw [5]. Conservative versus sur-
gical treatment depends on the stability of the osteochondral fragment. Ultrasound
may help evaluate fragment instability in COCD [6].
Triceps Brachii
Ultrasound can demonstrate tears and tendinosis of the distal triceps tendon (DTT)
[4]. Degenerative, noninflammatory triceps tendon enthesopathy may be associated
with localized pain [3]. The DTT may exhibit enthesopathy with spondyloarthropa-
thy, with or without PD activity [7].
Frank DTT tears are uncommon, but US can differentiate complete from partial
triceps tendon tears [3, 8]. Distal triceps tendon rupture may present as pain and
swelling at the posterior elbow after falling on an outstretched hand [8]. There may
be a bone avulsion from the tendon insertion on the olecranon. The surgical approach
depends upon whether the tear is partial or complete [8]. Factors associated with a
weakened triceps tendon include local steroid injections, attrition from degenerative
arthritis, and olecranon bursitis.
The diagnosis of DTT tear is clinically challenging. The initial evaluation may
be complicated by swelling and pain that limit strength and range of motion assess-
ments. Magnetic resonance imaging has been helpful in preoperative planning, but
US is gaining traction, particularly in the emergency department setting [8]. If a
complete DTT tear occurs, US may demonstrate a retracted, wavy tendon [1].
Snapping triceps syndrome is described in Chap. 9.
Olecranon Bursa
The subcutaneous olecranon bursa, located over the posterior aspect of the olecra-
non, facilitates the gliding of the skin superficial to the joint and triceps tendon dur-
ing elbow flexion and extension [3]. The olecranon bursa becomes visible when
pathologically distended with effusion or when the bursal walls are significantly
thickened, as occurs with synovial hypertrophy [3, 4]. Power Doppler activity
within the bursa indicates local active inflammation [4]. Hyperechoic spots within
the bursa may accompany crystal deposition. Since the olecranon bursa has a shal-
low location, it is crucial to use copious transmission gel and light touch to avoid
displacing the intrabursal effusion.
Ulnar Nerve Compression
Although the ulnar nerve (UN) is technically part of the posterior elbow, UN evalu-
ation at the elbow has been described in Chap. 9 since UN neuropathy often pro-
duces medial elbow symptoms.
Pitfalls
1. Avoid mistaking the anisotropy of the DTT for an insertional tear. Use sufficient
transmission gel and a heel-to-toe maneuver to compensate.
2. When evaluating for olecranon bursitis, use ample transmission gel and a light
touch to avoid displacing bursal fluid and missing the diagnosis. Extending one
finger along the side of the transducer will prevent gel dispersion.
3. If posterior elbow discomfort is present after a fall on an outstretched hand
injury, consider olecranon bone avulsion and triceps tendon tear since these
diagnoses are clinically challenging.
4. In young athletes who repetitively throw, evaluate the posterior and anterior sur-
faces of the capitellum to look for COCD.
5. The posterior recess of the elbow is the ideal location to look for an effusion.
Positioning the elbow facing downward enables gravity to assist the evaluation.
Method 171
Method
The patient is recumbent with the hand placed over the umbilicus, elbow flexed at
90°, and pointed downward at least 45°. In this position, the posterior recess is
gravity-dependent, which enhances effusion detection. Patients in pain usually tol-
erate this position. The examiner sets the transducer frequency at the midrange pre-
set. Some examiners advocate an alternative position called the “crab” position, in
which the forearm is internally rotated with the palm resting on the table [1].
rotocol Image 1: Posterior Joint Recess, Longitudinal ± Power

P
Doppler (Fig. 7.3)
Place the transducer parallel to the long axis of the humerus at the center of the
distal posterior elbow. Visualize the hyperechoic valley, the deep olecranon fossa,
and the more superficial triceps muscle with its tendon insertion on the bony olec-
ranon process of the ulna. Visualize the hyperechoic, curved trochlea. The posterior
joint recess’s hypoechoic or hyperechoic fat pad is within the olecranon fossa. The
fat pad is just deep to the joint capsule.
Small transverse axis (TAX) slides medially and laterally reveal the full extent of
the posterior recess. The hyperechoic, hill-like trochlea is covered by hypoechoic to
anechoic cartilage, as is the less prominent capitellum, located radially. Evaluate for
joint effusion, synovial hypertrophy, bone or joint erosion, loose bodies, and bone
fracture. If a fracture is suspected, look for a discontinuity or step-off deformity. If
there is a pathology question, rotate the probe 90° to verify in TAX.

Posterior joint recess,
Doppler

Distal triceps tendon,
Doppler
rotocol Image 2: Distal Triceps Tendon, Longitudinal ± Power

P
Doppler (Fig. 7.4)
Perform a slight distal longitudinal axis (LAX) slide halfway around the elbow bend
to visualize the bird’s beak configuration of the DTT insertion on the bony olecra-
non. Using adequate gel, perform a heel-to-toe maneuver, and tilt the probe to
decrease anisotropy. Small medial and lateral TAX slides help evaluate the full
extent of the DTT. Examine for sonographic evidence of enthesopathy, tendinosis,
partial or complete tears, and bony avulsion. Slightly extend the elbow to avoid
extreme tension on the tendon, which may ablate PD activity. Power Doppler activ-
ity might indicate active enthesitis. Rotate the probe 90° for a TAX view to verify
any pathology.
Protocol Image 3: Posterior Joint Recess, Transverse (Fig. 7.5)
Center the transducer over the posterior joint recess, and rotate it 90° to evaluate the
valley-shaped recess in TAX. The hypoechoic to hyperechoic fat pad is recognized
beneath the joint capsule. Perform small proximal and distal TAX slides to take in
the full extent of the posterior recess.
Method 173

Posterior joint recess,
transverse

Distal trochlea and
capitellum, transverse
rotocol Image 4: Distal Trochlea and Capitellum, Transverse

P
(Fig. 7.6)
Perform a TAX slide distally to visualize the hyperechoic hill-like humeral trochlea
and capitellum. The trochlea is medial (ulnar), and the capitellum is lateral (radial).
Between these two hyperechoic “hills” are the distal portion of the olecranon fossa
and its fat pad. Hyaline cartilage covers this distal portion of the humerus.

Posterior humeroradial
joint, longitudinal ± power
Doppler
rotocol Image 5: Posterior Humeroradial Joint, Longitudinal ±

P
Rotate the probe 90° back to the LAX orientation to the extremity. The transducer
should be at the elbow bend, angled about 30° with respect to the forearm axis.
Perform a TAX slide in a radial direction to visualize the humeroradial joint with the
hyperechoic large curved humeral capitellum and the smaller flat-to-curved radial
head. Verify any pathology in the TAX view. Turn on the PD, but remember that
extreme elbow flexion may diminish Doppler activity.
Protocol Image 6: Olecranon Process, Longitudinal (Fig. 7.8)
The patient then fully extends the elbow. Return to the probe location for Protocol
Image 1. Perform a distal LAX slide to center the probe over the bony olecranon
fossa. Using a light touch and a liberal amount of transmission gel, evaluate for effu-
sion or synovitis in the olecranon bursa (Fig. 7.9). Excessive pressure by the trans-
ducer will inadvertently disperse small amounts of olecranon bursal fluid, so float
the transducer. An extended finger along the long axis of the transducer will help to
keep the gel from dispersing.
Synovial hypertrophy may occur within this bursa due to inflammatory processes.
Particle movement from transducer compression or a lack of PD activity favors effu-
sion rather than synovial hypertrophy. Effusion within the bursa may occur with
infection, inflammatory arthropathy, or trauma. Chronic inflammatory processes
may cause bony erosion, depicted as cortical irregularities. Utilizing a higher fre-
quency may improve the detection of more superficial pathology. Note that with the
elbow extended, the insertion of the triceps tendon is not well-visualized.
Method 175

Olecranon process,
longitudinal
Fig. 7.9 Olecranon

bursitis
Complete Posterior Elbow Ultrasonic Examination Checklist

□ Protocol Image 1: Posterior joint recess, longitudinal ± power Doppler.
□ Protocol Image 2: Distal triceps tendon, longitudinal ± power Doppler.
□ Protocol Image 3: Posterior joint recess, transverse.
□ Protocol Image 4: Distal trochlea and capitellum, transverse.
□ Protocol Image 5: Posterior humeroradial joint, longitudinal ± power Doppler.
□ Protocol Image 6: Olecranon process, longitudinal.
References
2. Fessell DP, Jacobson JA, Craig J, Habra G, Prasad A, Radliff A, et al. Using sonography to
reveal and aspirate joint effusions. AJR Am J Roentgenol. 2000;174(5):1353–62.
3. Draghi F, Danesino GM, de Gautard R, Bianchi S. Ultrasound of the elbow: examination tech-
4. Radunovic G, Vlad V, Micu MC, Nestorova R, Petranova T, Porta F, et al. Ultrasound assess-
ment of the elbow. Med Ultrason. 2012;14(2):141–6.
5. van Bergen CJ, van den Ende KI, Ten Brinke B, Eygendaal D. Osteochondritis dissecans of the
capitellum in adolescents. World J Orthop. 2016;7(2):102–8.
6. Yoshizuka M, Sunagawa T, Nakashima Y, Shinomiya R, Masuda T, Makitsubo M, et al.
Comparison of sonography and MRI in the evaluation of stability of capitellar osteochondritis
dissecans. J Clin Ultrasound. 2018;46(4):247–52.
7. Hong WJ, Lai KL. The clinical experience of musculoskeletal ultrasound for enthesitis in sero-
negative spondyloarthropathy. J Med Ultrasound. 2021;29(4):237–8.
8. Tagliafico A, Gandolfo N, Michaud J, Perez MM, Palmieri F, Martinoli C. Ultrasound demon-
stration of distal triceps tendon tears. Eur J Radiol. 2012;81(6):1207–10.
Chapter 8
Lateral Elbow
Reasons to Do the Exam

1. Pain or swelling in the lateral elbow
2. Lateral epicondylar pain
3. Suspicion of “tennis elbow” (common extensor tendon tear or tendinosis)
4. Suspicion of lateral collateral ligament tear
5. Suspicion of elbow arthritis
6. Suspicion of elbow synovitis
7. Suspicion of elbow cartilage or bone erosion
1. What is causing the elbow pain?
2. Is the extensor tendon involved, and is the problem acute or chronic?
3. Is there enthesopathy at the lateral epicondyle?
4. Is there pathology of the lateral collateral ligament?
5. Is the pathology in the joint?
6. Is the visualized pathology the actual cause of the pain?
7. What is the mechanism of the condition?
8. Is impingement of a branch of the radial nerve mimicking tennis elbow pain?
Anatomy
Bones (Fig. 8.1)
States Government.

Switzerland AG 2023
178 8 Lateral Elbow

the lateral elbow
Fig. 8.2 Muscles and tendons of the lateral elbow
Muscles and Tendons (Fig. 8.2)
The common extensor tendon (CET), a single large tendon derived from multiple
extensor muscles, inserts onto the lateral epicondyle (LE) in a “bird-beak” configu-
ration. The CET arises from these muscles [1], as follows:
1. Extensor carpi radialis brevis (ECRB)
The ECRB is the deepest and largest muscle of the CET.
2. Extensor carpi radials longus (ECRL)
Anatomy 179
3. Extensor digiti minimi (EDM)

4. Extensor digitorum communis (EDC)
The EDC is the most superficial muscle.
5. Extensor carpi ulnaris (ECU)
A mnemonic derived from the bolded letters above is as follows:
Racquet Rabbits Dislike Doctors Usually
Joints (Fig. 8.3)
Fig. 8.3 Joints of the

lateral elbow
180 8 Lateral Elbow
Fig. 8.4 Ligaments of the

lateral elbow
Ligaments (Fig. 8.4)
Ligaments lie deep to the CET. The lateral collateral ligament complex stabilizes
the elbow and is comprised of three ligaments:
1. The lateral (or radial) collateral ligament (LCL).
2. The annular ligament (AL).
3. The lateral ulnar collateral ligament (LUCL).
The LCL, located just deep to the CET, originates at the LE and attaches to the
AL [2]. Its course is slightly oblique to the CET. The LCL inserts fibers into another
ligament, not directly onto the bone. The AL stabilizes the radial head and neck by
stretching from the anterior to the posterolateral ulna [2]. The LUCL originates
from the LE, deep to and posterior to the LCL; the LUCL is an effective stabilizer
against varus stress [1, 2]. The LUCL extends to the supinator crest of the ulna,
attaching just distally to the AL attachment. Note that the LCL is deep to the CET
and runs almost, but not entirely, parallel to it. Similarly, the LUCL lies deep to the
LCL and runs virtually, but not entirely, parallel to the LCL.
Clinical Comments
Lateral Epicondylitis
Also known as “tennis elbow,” this common disorder is usually due to repeti-
tive overuse causing microtears and chronic secondary degeneration of the ten-
don near its insertion. Lateral epicondylitis is a misnomer since acute
inflammation is generally lacking. Thus, lateral epicondylitis is more accu-

rately described as CET tendinosis [1, 3]. However, microtears may sometimes
progress to partial or even full-thickness tears. Lateral epicondylitis most often
involves tendon fibers derived from the ECRB, but other CET layers may also
be involved [1, 2].
Lateral epicondylitis clinically presents as localized tenderness with weakened
strength of handgrip and elbow supination or extension [1]. Ultrasound (US) is
helpful to confirm the diagnosis, evaluate disease severity and response to treat-
ment, and guide injections. Ultrasound is also beneficial to exclude other causes of
elbow symptoms. Sonography may demonstrate tendinosis with hypoechoic swell-
ing at the tendon insertion. Anechoic tendon clefts or discontinuities suggest tendon
tears. Doppler activity more commonly indicates neovascularization of an injured
tendon than inflammation [1–6]. The clinical circumstance affects the interpretation
of Doppler activity, for example, repetitive injury history versus spondyloarthropa-
thy suspicion. Calcium deposits or enthesopathic changes at the bony attachment
imply chronic tendinosis [1].
Regarding the diagnosis of lateral epicondylitis, US is specific but not sensitive
[7]. A pitfall is mistaking anisotropy of the ECRB origin for hypoechogenicity and
inferring tendinopathy or partial tear [1]. Be aware that CET tears may result from
repeated intratendinous corticosteroid injections (CSIs) used to treat tennis elbow
[8]. Long-term results after CSIs are less favorable than conservative treatment [9].
An entrapped posterior interosseous branch of the radial nerve may mimic tennis
elbow [6].
Ligament Pathology
With an injury to the LCL, US may demonstrate loss of ligament fibers and, if acute,
perhaps a hematoma close to the humeral capitellum [2]. Consider and evaluate for
concomitant LUCL and LCL injuries before treatment of lateral epicondylitis since
conservative treatment failure occurs if an occult ligament tear is present [1, 2, 10,
11]. Distinguishing the CET from the LCL on the lateral epicondyle is challenging
with US. A cadaver study described that the LCL footprint comprises 54% of the
combined attachment of the CET and LCL [10]. Therefore, in most cases, the CET
and the LCL each occupy roughly half the bony expanse of the LE. Injury to the
LUCL may cause posterior rotatory joint instability with varus stress [10]. Perform
dynamic imaging with hand supination and pronation to evaluate LUCL injury and
abnormal radial head movement. However, magnetic resonance imaging is better
suited for LUCL evaluation than US.
182 8 Lateral Elbow
Joint Pathology
Ultrasound may detect joint effusion or synovitis at the humeroradial joint (HRJ).
Complex effusion suggests infection, bleeding, intra-articular bodies, or inflamma-
tion [1]. Abnormal power Doppler (PD) activity argues for synovitis rather than a
simple joint effusion; such synovitis may be due to inflammatory arthropathy, infec-
tion, or osteoarthritis. If synovitis is detected, consider pigmented villonodular
synovitis or synovial osteochondromatosis, the latter displaying hyperechoic foci
within the synovial fluid [1]. Additionally, US may guide joint aspiration.
Bone Pathology
1. Bone erosion may be noted at the humeroradial joint.

2. Occult fractures may be seen as step-off deformities at the epicondyle, the capi-
tellum, or the radial head and neck.
Nerves
(See Chap. 6 for further information.)
Pitfalls
1. Do not mistake normal anisotropy of the ECRB origin for hypoechogenicity of

tendinopathy or a partial tear [1].
2. Evaluate for occult ligament tears before conservative treatment of lateral epi-
condylitis since such treatment is likely to fail if there is a ligament tear [1].
3. Tennis elbow symptoms may be mimicked by entrapment of the posterior inter-
osseous branch of the radial nerve [6].
4. Interpret Doppler activity at the CET insertion in light of the clinical situation.
Doppler activity may indicate neovascularization of tendon injuries from repeti-
tive trauma. Alternatively, Doppler activity may suggest active enthesitis if spon-
dyloarthropathy is being considered.
Method
The patient is recumbent with the forearm in pronation. The elbow is bent to 90°
with the palm down and the hand resting on the abdomen or examination table.
Delineate any tender areas with a ballpoint pen. Palpate the LE and start with a
moderate depth preset.
Method 183
rotocol Image 1: Common Extensor Tendon Origin,

P
Place one end of the transducer over the bony, hyperechoic LE and the other over
the small, slightly rounded radial head. The LE may be a bit more posterior than you
think. The probe should roughly parallel the long axis of the forearm. Aim the distal
transducer end toward the distal radius at the wrist. Visualize the hyperechoic gentle
slope of the LE, the flat to slightly rounded distal humeral capitellum, and the small
rounded radial head. Also, note the triangular synovial fold in the humeroradial
joint and the CET, stretching distally from the most superficial portion of the
LE. The triangular synovial fold is also called the meniscal homologue or lateral
synovial fringe.
Visualize the fibrillar CET and its insertion on the LE by slightly rotating the
distal portion of the transducer in either direction. Individual CET tendon compo-
nents intermingle and cannot be separately delineated. While still in the longitudinal
axis (LAX) orientation, perform minor transverse axis (TAX) slides medially and
laterally to encompass the entire width of the CET. Look for CET tendinosis and
tears and LE cortical irregularities and enthesophytes.
Turn on the PD to look for active enthesitis at the CET insertion on the
LE. However, positive PD activity within the CET often indicates neovasculariza-
tion from chronic tendinosis rather than an inflammatory process. Again, the clini-
cal setting influences the interpretation of PD activity (e.g., repetitive trauma vs.
possible spondyloarthropathy).
The curved hyperechoic structure just superficial to the radial head is the AL. The
annular recess, located at the radial neck, may be distended with effusion or synovi-
tis [8]. The brachioradialis muscle is superficial to the CET. The LCL lies deep to
the CET. Since the CET and the LCL are not entirely parallel, only one of these two
longitudinal structures may be in focus at a time. It is challenging to demarcate the
CET from the LCL.

Common extensor tendon
origin, longitudinal ±
power Doppler
184 8 Lateral Elbow
Tips to help distinguish the CET from the LCL:

1. Look distally to see the hyperechoic CET transform into a hypoechoic muscle.
2. The LCL is the deeper structure and more distally coalesces into the AL.
3. Extension of the fingers and wrist will elicit movement or tightening of the CET,
helping to discern this structure from the underlying LCL.
4. Realize that the LCL and CET footprints each take up about 50% of the span
of the LE.
5. After viewing the CET, rotate the distal end of the transducer 5–10° in a postero-
lateral direction to help delineate the LCL as a separate structure from the CET
(see Protocol Image 2).
If you detect an abnormality, rotate the probe 90° to verify in a TAX view.
rotocol Image 2: Lateral Collateral Ligament, Longitudinal

P
(Fig. 8.6)
The LCL lies deep to the CET, but the two structures are not quite parallel. The LCL
may best be appreciated by rotating the transducer 5–10° in a posterolateral direc-
tion and tilting the transducer to visualize the hypoechoic to hyperechoic LCL
shaped like a deep bowl.

Lateral collateral ligament,
longitudinal
Method 185

Lateral ulnar collateral
ligament, longitudinal
rotocol Image 3: Lateral Ulnar Collateral Ligament,

P
To complete the sonographic evaluation of the lateral collateral ligamentous com-

plex, evaluate the third ligament, the LUCL. This ligament is also deep and not quite
parallel to the CET. To demonstrate the LUCL, move the probe in a TAX slide pos-
terolaterally until the LE becomes a straight hyperechoic line. Then rotate the distal
portion of the transducer posterolaterally to about a 45° angle to the long axis of the
humerus. The curved radial head will fade out and be replaced by the ulna’s hyper-
echoic supinator crest (SC). The hypoechoic longitudinal structure bridging the gap
between the inferior portion of the LE and the SC is the LUCL. Remember, the
LUCL is a primary elbow stabilizer.
rotocol Image 4: Humeroradial Joint, Longitudinal + Dynamic

P
(Fig. 8.8)
Return the transducer to the position in Protocol Image 1. Perform a distal LAX
slide to center the probe over the HRJ. Examine the triangular synovial fold within
the joint, the cartilage covering the superficial surface of the humeral capitellum,
and the radial head. The radial head has a slightly rounded shape. A curved hyper-
echoic structure, the AL is just superficial to the radial head cartilage. The AL
extends distally to the radial neck.
At the radial neck, just distal to the radial head, is the location of the annular
recess; the annular recess is detectable if distended by an effusion [8]. Look for
synovitis (with or without PD activity), cartilage erosion, and effusion in the annular
recess. To examine these structures more fully, perform tiny TAX slides slightly in
186 8 Lateral Elbow
Fig. 8.8 Protocol Image 4: Humeroradial joint, longitudinal + dynamic
lateral and medial directions. Discontinuity in the smooth cortex of the radial head
and neck suggests an occult fracture in the appropriate clinical setting. To perform
a varus dynamic stress test for LCL complex laxity, place a bolster under the elbow
and manually press the distal forearm toward the table.
rotocol Image 5: Radial Head, Transverse + Dynamic

P
(Fig. 8.9)
Center the probe over the radial head and rotate it 90° to see the round hyperechoic
bony cortex of the radial head in a transverse view. Perform tiny TAX slides proxi-
mally and distally. You can see the overlying anechoic cartilage and, superficially,
Method 187
Fig. 8.9 Protocol Image 5: Radial head, transverse + dynamic
the hyperechoic AL. Small bony cortical irregularities may be present. The ECRB
muscle has, at this point, become a tendon, but the EDC and ECRL are still muscles
in this location. The AL may be seen inserting posterolaterally on the supinator crest
of the ulna.
Manually pronate and then supinate the forearm to verify the margins and integ-
rity of the AL. Portions of the AL may exhibit anisotropy. This maneuver reveals a
fuller view of the radial head cortex and its cartilage cover when evaluating for
erosive disease. A distal TAX slide will also examine the radial neck and annular
recess in cross-section.
Complete Lateral Elbow Ultrasonic Examination Checklist
□ Protocol Image 1: Common extensor tendon origin, longitudinal ± power
Doppler.
□ Protocol Image 2: Lateral collateral ligament, longitudinal.
□ Protocol Image 3: Lateral ulnar collateral ligament, longitudinal.
□ Protocol Image 4: Humeroradial joint, longitudinal + dynamic.
□ Protocol Image 5: Radial head, transverse + dynamic.
188 8 Lateral Elbow
References
2. Radunovic G, Vlad V, Micu MC, Nestorova R, Petranova T, Porta F, et al. Ultrasound assess-
ment of the elbow. Med Ultrason. 2012;14(2):141–6.
3. Potter HG, Hannafin JA, Morwessel RM, DiCarlo EF, O’Brien SJ, Altchek DW. Lateral epi-
condylitis: correlation of MR imaging, surgical, and histopathologic findings. Radiology.
1995;196(1):43–6.
4. Levin D, Nazarian LN, Miller TT, O’Kane PL, Feld RI, Parker L, et al. Lateral epicondylitis of
the elbow: US findings. Radiology. 2005;237(1):230–4.
5. Connell D, Burke F, Coombes P, McNealy S, Freeman D, Pryde D, et al. Sonographic exami-
nation of lateral epicondylitis. AJR Am J Roentgenol. 2001;176(3):777–82.
6. Kotnis NA, Chiavaras MM, Harish S. Lateral epicondylitis and beyond: imaging of lateral
elbow pain with clinical-radiologic correlation. Skelet Radiol. 2012;41(4):369–86.
7. Miller TT, Shapiro MA, Schultz E, Kalish PE. Comparison of sonography and MRI for diag-
nosing epicondylitis. J Clin Ultrasound. 2002;30(4):193–202.
8. Draghi F, Danesino GM, de Gautard R, Bianchi S. Ultrasound of the elbow: examination tech-
9. Coombes BK, Bisset L, Brooks P, Khan A, Vicenzino B. Effect of corticosteroid injection,
physiotherapy, or both on clinical outcomes in patients with unilateral lateral epicondylalgia:
a randomized controlled trial. JAMA. 2013;309(5):461–9.
10. Jacobson JA, Chiavaras MM, Lawton JM, Downie B, Yablon CM, Lawton J. Radial collateral
ligament of the elbow: sonographic characterization with cadaveric dissection correlation and
magnetic resonance arthrography. J Ultrasound Med. 2014;33(6):1041–8.
11. Clarke AW, Ahmad M, Curtis M, Connell DA. Lateral elbow tendinopathy: correlation of ultra-
sound findings with pain and functional disability. Am J Sports Med. 2010;38(6):1209–14.
Chapter 9
Medial Elbow

1. Evaluation of elbow pain
2. Dynamic evaluation of the ulnar nerve (UN)
3. Dynamic evaluation of the medial head of the triceps muscle (MHTr)
4. Possible compression of the UN in, or proximal to, the cubital tunnel
5. Evaluation of soft tissue swelling
6. Evaluation of the common flexor tendon (CFT) for tears, tendinosis, and
tenosynovitis
7. Evaluation of the ulnar collateral ligament (UCL) (also known as the medial col-
lateral ligament or MCL)
8. Evaluation for inflammatory arthritis
1. What is causing the elbow pain?
2. Is the CFT involved, and is the problem acute or chronic?
3. Is there enthesopathy at the insertion at the medial epicondyle (ME)?
4. Is there pathology of the UCL?
5. Is the pathology within the joint itself?
6. Is the visualized pathology the actual cause of the pain?
7. What is the mechanism of the condition?
8. Is the UN or the MHTr creating the problem dynamically?
9. Is the UN compressed proximal to or within the true cubital tunnel (TCuT)?
10. What is the next step to help the problem?
States Government.

Switzerland AG 2023
190 9 Medial Elbow
Fig. 9.1 Muscles and

common flexor tendon
Basic Anatomy
The Medial Epicondyle and Common Flexor Tendon (Fig. 9.1)
The ME is a smooth bony ridge to which the CFT and the UCL attach, with the CFT
being more superficial. The CFT is the confluence of four or five tendons that insert
on the most superficial part of the ME. The tendons include the flexor carpi radialis,
palmaris longus (PL), flexor digitorum superficialis, pronator teres, and flexor carpi
ulnaris (FCU). The PL may not be present in up to 15% of normal individuals [1].
A mnemonic to remember the five tendons that form the CFT is as follows:
Five People Found Peace Forever
The CFT is mostly muscular and has a smaller tendon than the CET. The exam-
iner may evaluate this tendon for enthesitis on power Doppler (PD).
Ulnar Collateral Ligament (Fig. 9.2)
Deep to the CFT is the UCL. The UCL also inserts on the ME, but further (deeper)
down the slope. The mnemonic “CU down the slope” reminds us of the locations.
The UCL stretches from the ME to the ulna and may exhibit enthesitis at its attach-
ment to the ME. The UCL comprises three bands: the anterior oblique, posterior
oblique, and transverse. The anterior band is the most important of the three in terms
of elbow joint stabilization and is a common location of pathology [2]. This band of
the UCL is triangular-shaped, with the apex attaching distally to the ulnar coronoid
(sublime) tubercle. The anterior band is most often injured in athletes, particularly
baseball pitchers [2]. “Tommy John surgery” is a popular surgery in which an autolo-
gous graft replaces the torn anterior band of the UCL. On a sonographic longitudinal
(LAX) view, the anterior band is often hypoechoic due to anisotropy but will appear
hyperechoic with fibrillar echotexture if the angle of insonation is precisely 90°.
Basic Anatomy 191
Fig. 9.2 Ulnar collateral

ligament bands
Fig. 9.3 Posteromedial

elbow simplified
Posteromedial Elbow (Fig. 9.3)
We include posteromedial elbow anatomy in the medial elbow discussion since UN

compromise may cause medial elbow pain. The UN lies within the sulcus formed by
the ME and the olecranon. Here, the UN is covered with Osborne’s fascia. More dis-
tally, within the TCuT, the nerve runs deep to Osborne’s ligament, the latter uniting
the two heads of the flexor carpi ulnaris muscle. The terminology is confusing.
Osborne’s ligament and Osborne’s fascia go by different names in the literature,
including the arcuate ligament of Osborne, the cubital tunnel retinaculum, and
Osborne’s band, among others. Our convention is to call the connective tissue over the
sulcus “Osborne’s fascia” and that forming the roof of the TCuT “Osborne’s ligament.”
Sonographic Anatomy
We use US to evaluate the areas we label the three “S’s”: ski slope, Sisyphus, and
spectacles. The “ski slope” is the LAX view of the ulnar aspect of the bony ME,
where the CFT and the UCL attach. The “Sisyphus” area is the posterior and radial
aspect of the ME seen in sonographic transverse (TAX), where a dynamic exam is
192 9 Medial Elbow
performed to see if the UN or the MHTr moves up and perhaps over the apex of the
ME. Sisyphus, a Greek mythological figure, was doomed to eternally push a boul-
der up a hill, only to have the boulder roll back down each time. Our “boulder” is
the UN, which may move out of the ulnar sulcus (groove) and partially climb (sub-
luxation) or completely go over (dislocation) the peak of the ME.
The “spectacles” area of interest is where the UN travels distally to the ulnar
sulcus. This area is the TCuT, where the two ovoid heads of the FCU, tethered by
Osborne’s ligament, give the appearance of spectacles. The UN is the round “nose”
upon which these spectacles rest. Osborne’s ligament is a bit unusual in that most
ligaments typically bind bone to bone; however, this ligament attaches muscle to
muscle and is the roof of the TCuT [3]. By examining this area in TAX and LAX,
we can sonographically confirm or refute clinical suspicion of CuT syndrome
(CuTS), that is, compression of the UN in the TCuT.
Clinical Comments
The causes of medial elbow pain detectable on US include medial epicondylitis,

UCL injury, UN compression, snapping UN, and snapping MHTr [4].
The Medial Epicondyle
Medial epicondylitis is also called “golfer’s elbow.” Medial epicondylitis is a mis-

leading term since, in most cases, it is caused by tendinosis of the CFT rather than
actual inflammation. Doppler activity in this tendon may be from tendon injury or
active enthesitis, such as in spondyloarthropathy. The clinical setting is critical.
When evaluating the UCL, the goal is to delineate a partial or complete tear in
this oft-injured ligament [5]. Extend the elbow to look at the UCL fibers crossing
the humeroulnar joint [6]. However, the more distal portion of the UCL is best seen
with the elbow flexed so that the ligament is taut. Visualization of both UCL tears
and laxity is enhanced on US when the examiner does a dynamic valgus stress test
while observing if the humeroulnar joint enlarges when stressed [7].
Ulnar Nerve Entrapment
Ulnar nerve compromise at the elbow is included in the medial elbow despite the
nerve’s location on the posterior elbow, as pain from ulnar neuropathy is often expe-
rienced in the medial elbow. Ulnar neuritis may be caused by entrapment in differ-
ent locations, but it most commonly occurs under Osborne’s ligament in the TCuT
[4]. Again, such entrapment is termed CuTS [8]. In ulnar neuritis of any origin,
paresthesia may radiate to the fourth and fifth fingers.
Entrapment of the UN occurs at the entrance to the TCuT, which lies beneath
Osborne’s ligament and the humeral and ulnar heads of the FCU. The TCuT entrance
is our “spectacles” location and reminds us to look carefully at this site. If com-
pressed within the TCuT, the UN may enlarge proximally, with swelling apparent
near the ME. In this scenario, the UN will have a smaller caliber within the TCuT,
that is, under Osborne’s ligament.
It is important to note that nerves tend to enlarge proximally to compression when
squeezed within tight fibro-osseous canals such as the TCuT and the carpal tunnel
[9, 10]. One criterion for CuTS is a cross-sectional area (CSA) of the UN greater
than 9 mm2 [11]. An alternative criterion is a ratio greater than 2.8 when comparing
the CSA of the UN at the site of maximal swelling to a proximal site [12]. It is essen-
tial to recognize that some normal (physiologic) UN enlargement may occur with
asymptomatic UN subluxation/dislocation out of the ulnar sulcus [13]. However, in
the proper clinical setting, a de facto diagnosis of CuTS can best be made on US in
LAX view if the UN is enlarged proximal to the entrance of the TCuT [9].
It is noteworthy that at the elbow, the UN typically does not have the familiar
honeycombing that we expect to see in TAX. This appearance may be due to anisot-
ropy or mild edema due to daily microtrauma. The usual UN in the elbow has a
hypoechoic or anechoic center surrounded by a thicker, hyperechoic epineurium.
UN neuropathy at the elbow may occur in three circumstances:
1. Compromise within the TCuT [10].
2. Repetitive subluxation of the UN out of the sulcus may cause chronic pressure
damage and UN swelling [10, 13].
3. Compression by a space-occupying lesion, including ganglia, lipomas, anconeus
epitrochlearis (AE), osteophytes from the humeroulnar joint (HUJ), HUJ syno-
vitis, intra-articular bodies, hemorrhage, and MHTr dislocation [10].
The AE is an accessory muscle present in up to 23% of the population (Fig. 9.4)
[14]. It connects the ME to the olecranon process. It is proximal to the TCuT and
appears as a hypoechoic structure superficial to the UN in the ulnar sulcus, in the
expected location of Osborne’s fascia. The AE and MHTr are both adjacent to the
UN at elbow flexion, but the MHTr separates from the UN in elbow extension.
Fig. 9.4 Anconeus

epitrochlearis
194 9 Medial Elbow
Avoid confusing the AE with a ganglion. The AE compression of the UN may occur
in an extended elbow. Not only can an AE mimic CuTS by compressing the UN, but
the AE may also mimic a snapping MHTr by subluxing over the ME [9].
Other Ulnar Nerve Syndromes
Dynamic US of the posteromedial elbow is a priceless diagnostic modality when

focusing on two potentially mobile structures: the UN and the MHTr. In ulnar
nerve instability (UNI), the UN chronically subluxes and relocates with elbow
flexion and extension [15]. The UN fully dislocates in 20% of normal elbows and is
usually without symptoms [16]. However, UNI may increase UN vulnerability to
trauma, mainly when the UN lies superficially on the ME [17]. The most probable
cause of UNI is ligamentous laxity. Ulnar nerve instability may occur with or with-
out radiating paresthesia or a snapping UN or MHTr [17, 18]. It is separate from UN
compression, although UNI may cause friction neuritis, producing radiating pares-
thesia mimicking CuTS [17].
Snapping ulnar nerve occurs in elbow flexion (between 70° and 90°) when the
UN dislocates over the apex of the ME. This condition is typically painful and often
accompanied by a palpable and audible snap [19, 20]. Neurologic symptoms from
the snapping UN are rarely reported, with the most common symptom being local-
ized pain [19]. Another potential cause of elbow pain in a throwing athlete with UN
dislocation is pain upon extension of the elbow when the UN rapidly relocates over
the apex of the ME [21].
Snapping triceps may or may not be painful. Snapping triceps occurs with about
115° of elbow flexion when the distal MHTr displaces over the apex of the ME. There
may be audible/palpable snapping, and the MHTr may push the UN out of the
groove (subluxation) and perhaps even further to a point over the apex of the ME
(dislocation). Hypertrophy of the triceps may predispose to UN subluxation, dislo-
cation, and snapping triceps syndrome [4]. Snapping MHTr itself is associated with
UN dislocation [20]. If both snapping UN and MHTr are present, there may be two
separate palpable or audible sequential snaps [9].
Again, dislocation of the UN and MHTr may occur without pain or snapping.
Symptoms of pain, snapping, and dislocation of the UN or MHTr may only be
apparent with resistance provided by the examiner [22]. When examining the elbow
for snapping UN and MHTr, sequentially evaluate the elbow with passive, active,
and resisted flexion and extension.
Pitfalls
1. To correctly interpret Doppler activity at the CFT insertion, consider the clini-
cal situation. Doppler activity may occur after repetitive tendon injuries,
whereas acute enthesitis may be due to spondyloarthropathy.
Method 195
2. When examining the elbow for snapping UN and MHTr, scan the elbow with
passive, active, and resisted flexion and extension. Do not forget to do the
dynamic exam with resistance; this maneuver is critical for snapping
UN/MHTr.
3. Cutoff values and CSA ratios of the UN will help diagnose CuTS, but UN com-
pression in LAX view is a strong sign of CuTS in the right clinical setting.
4. Do not mistake the appearance of the UN as necessarily abnormal. The UN
typically has some edema, possibly due to TCuT compression with repeti-
tive elbow flexion. In addition, it does not always have a honeycomb
appearance.
5. UN swelling may also be due to repetitive dislocation trauma over the ME and
may not necessarily indicate UN compression in the TCuT.
6. Examine the UCL thoroughly to look for UCL tears. The UCL is hypoechoic in
elbow extension and becomes more hyperechoic as it tightens with elbow
flexion.
7. Valgus stress testing of the UCL with only gravity is sufficient.
8. Remember that a dislocating UN or MHTr may not cause pain.
9. Evaluate the contralateral elbow when evaluating a putative US abnormality.
10. Nerves tend to enlarge proximally to compression when squeezed within tight
fibro-osseous canals such as the TCuT and the carpal tunnel.
11. Avoid immediately assuming that ulnar neuropathy is due to CuTS, even if you
note a swollen UN. Look for more proximal causes of ulnar neuritis, such as
UN trauma or compression near the ME. Also, do not forget about more distal
causes of ulnar neuropathy, including compression within the ulnar (Guyon’s)
canal in the wrist with possible retrograde paresthesia.
12. The AE will appear as a hypoechoic structure superficial to the UN in the ulnar
sulcus, proximal to the TCuT. Avoid confusing the AE with a ganglion.
13. The AE may mimic either CuTS by compressing the UN or a snapping MHTr
by subluxing over the ME.
14. The elbow offers an extraordinary diagnostic window. Do not neglect to care-
fully examine the elbow for bone/cartilage erosion, step-off deformity of an
occult fracture, rheumatoid nodules, double contour sign of gout, and calcium
deposition in cartilage.
Method
The patient is recumbent with a pillow supporting the elbow, which is externally
rotated, abducted, and extended. Slight flexion of the elbow will likely occur with
this maneuver and is expected. Use a transducer with a frequency of at
least 12 MHz.
196 9 Medial Elbow
Fig. 9.5 Protocol Image 1: Medial epicondyle, longitudinal, extension ± power Doppler
rotocol Image 1: Medial Epicondyle, Longitudinal, Extension

P
± Power Doppler (Fig. 9.5)
Palpate the ME and place the probe in LAX over the joint along the anterior medial
elbow to visualize the HUJ. See the bony hyperechoic curved “ski slope” of the ME
leading down the curved valley, the coronoid recess, and then a smaller “hill,” the
trochlea of the humerus. The proximal ulna is distal to the trochlea and separated by
the joint space. Look at the CFT, its muscle, and the insertion on the ME. Elbow
extension enhances CFT visualization. Look for signs of enthesopathy, muscle
tears, and bony avulsions. Next, turn on the PD to look for active enthesitis. Deep to
the CFT and muscles is the UCL‘s anterior bundle, which we will refer to simply as
the “UCL.” To delineate the separation of the CFT from the UCL, look at the more
hypoechoic CFT muscle just superficial to the ligament. In elbow extension, the
UCL is hypoechoic. Look for gaps that may indicate partial or complete UCL tears.
Turn on the PD to look for Doppler activity suggestive of active enthesitis or an
acute ligament tear.
Method 197

Medial epicondyle,
longitudinal, flexion ±
power Doppler
rotocol Image 2: Medial Epicondyle, Longitudinal, Flexion ±

P
Flexing the elbow to 90° will create tension in the UCL. This results in a more
hyperechoic echotexture and improves UCL visualization. Rotate the probe to a
position nearly parallel to the forearm to better align the transducer with the liga-
ment. Look for alteration of the normal fibrillar echostructure, hypoechoic areas,
and ligament swelling. In males, the average ligament thickness ranges from 2.6 to
4 mm [23]. However, comparing the (unaffected) contralateral side might be more
revealing. Irregularity or protrusion of a portion of the medial epicondyle may point
to a prior UCL avulsion injury [24]. Again, look for interruptions in the integrity of
the ligament, which may indicate partial or complete ligament tears. Look at the
enthesis on the ME for evidence of enthesopathy. Turn on the PD to evaluate for
active enthesitis or an acute ligament tear.
rotocol Image 3: Medial Epicondyle, Valgus Maneuver,

P
Then, perform a valgus stress maneuver to test the structural integrity of the UCL,
mainly the anterior band. The elbow should be flexed to 30° or more during the
valgus maneuver. Place a roll of paper towels beneath the elbow. Stabilize the elbow
with the probe and let gravity perform the valgus maneuver [25]. Note that the UCL
is even better defined when it is taut during the valgus stress maneuver. During the
stress maneuver, measure the width of the HUJ space to see if it enlarges. Comparison
with the contralateral (unaffected) side is helpful. The expected change in the UCL
space with stress valgus is <1.3 mm. If the difference in UCL joint space with val-
gus stress on the affected side is at least 1 mm more than on the unaffected side,
suspect a UCL tear [26].
198 9 Medial Elbow
Fig. 9.7 Protocol Image 3: Humeroulnar joint, valgus maneuver, longitudinal
rotocol Image 4: Ulnar Nerve at the Medial Epicondyle,

P
Transverse + Measurement (Fig. 9.8)
Next, extend the elbow off the examination table while maximally supinating the
forearm. Rotate the probe 90° to a TAX position and then center the transducer over
the ME. Slide the probe posteriorly, still in TAX, to see the UN in TAX. The two
bony landmarks on opposite sides of the picture are the ME and the olecranon pro-
cess. The probe should bridge these two bones. The posterolateral portion of the ME
is hyperechoic and looks like a hill. The UN appears to have a central hypoechoic
area with a thick hyperechoic rim. The UN seems round, like Sisyphus’s boulder,
sitting at the bottom of the hill. Note that the UN, in this view, may not exhibit a
classic honeycomb appearance due to anisotropy. The UN lies close to and may
abut the ME.
In this location, there may or may not be a retinaculum called Osborne’s fascia,
which stretches between the ME and the olecranon superficial to the UN. Note
again that Osborne’s fascia is not the same as Osborne’s ligament; the fascia (if
present) becomes Osborne’s ligament more distally, the latter connecting the two
heads of the FCU. Verify the identity of the UN by moving the probe 1–2 cm dis-
tally to follow this circular structure. Once you have confirmed that the visualized
circular form is indeed the UN, reverse course and move the probe proximally back
to the ME. Be aware that the UN may split into two separate or connected rounded
sections for some individuals. The AE is an accessory muscle that may be present in
place of Osborne’s fascia and reside just superficially to the UN. It may have clinical
Method 199

Ulnar nerve at the medial
epicondyle, transverse +
measurement
significance since it may cause UN compression. Measure the CSA of the UN in

TAX. The typical CSA of the UN is 8–12 mm2; however, a CSA of the UN >9 mm2
may indicate pathology [11].

P
Transverse, Dynamic Exam, Passive Flexion (Fig. 9.9)
With a light touch of the probe, grasp the forearm and very slowly flex the elbow to
look for UN subluxation. Try to keep the ME in focus. We are watching for the UN
to ascend the ME with passive elbow bending. In flexion, the UN may normally
climb the ME (subluxation), like in the Sisyphus allegory. The UN may even go
over the peak of ME (dislocation). However, these UN movements may be asymp-
tomatic. Alternatively, the UN subluxation or dislocation may be associated with
pain or an audible snap. The examiner may see the snap or feel a “popping” sensa-
tion through the transducer.
200 9 Medial Elbow
Fig. 9.9 Protocol Image 5: Ulnar nerve at the medial epicondyle, transverse, dynamic exam, pas-
sive flexion
Recurrent subluxation or dislocation may predispose to UN injury. With repeti-

tive trauma from dislocating and relocating, the UN itself may occasionally swell to
the point that it can mimic the swelling associated with nerve compression. The
MHTr may also move over the ME in elbow flexion, producing a snapping sensation
known as the snapping triceps syndrome. The UN’s snapping over the ME’s peak
occurs at about 80° of elbow flexion, while MHTr snapping takes place at about
115° of elbow flexion. When both the UN and the MHTr dislocate over the ME, the
MHTr may appear to be propelling the UN.
Method 201

P
Transverse, Dynamic Exam, Active Flexion
The patient actively but slowly flexes the elbow while the examiner observes for UN
and MHTr subluxations.

P
Transverse, Dynamic Exam, Resisted Flexion
The patient flexes the elbow against resistance provided by the examiner or an
assistant while the examiner observes for UN and MHTr subluxations. Resistance
may best evoke subluxation.
rotocol Image 8: Ulnar Nerve in the True Cubital Tunnel,

P
With the transducer still in TAX, perform a distal TAX slide toward the TCuT,
focusing on the UN. You have reached the TCuT when the UN looks like a
round nose under a pair of oval eyeglass lenses. The “spectacle lenses” are the
two heads of the FCU; the “bridge” or “nosepiece” is Osborne’s ligament con-
necting the two heads of the FCU. The humeral head of the FCU is on the same
side as the ME. Again, this is the TCuT, the most common site of UN entrap-
ment. As you move more distally away from the TCuT, the two FCU heads
coalesce, and the UN is just beneath the single FCU. Just proximal to the TCuT,
the UN may be enlarged (pseudoneuroma) if there is chronic compression
within the TCuT. If you suspect compression, measure the CSA of the UN at its
largest circumference and compare it with the CSA more proximally. Comparison
with the unaffected side may often help. Normal UN CSA is 8–12 sq. mm. in
this location [11].
202 9 Medial Elbow
Fig. 9.10 Protocol Image 8: Ulnar nerve in the true cubital tunnel, transverse
Method 203

9: Ulnar nerve in true
cubital tunnel, longitudinal
rotocol Image 9: Ulnar Nerve in True Cubital Tunnel,

P
Visualize and center the UN under Osborne’s ligament within the TCuT, and slowly
rotate the probe 90° to visualize the UN in LAX. Note the caliber of the UN proxi-
mal to, within, and distal to the TCuT. If there is a discrepancy, measure the CSAs
in TAX in these three areas.
In the LAX view, and in the appropriate clinical setting, the finding of a com-
pressed UN within the TCuT with clear-cut proximal swelling often defines
CuTS, irrespective of the measurements. Again, be aware that the UN may swell
with repetitive trauma, such as traumatic dislocation and relocation over the ME,
mimicking swelling from chronic compression either within or proximal to
the TCuT.
rotocol Image 10: Ulnar Nerve in Forearm, Transverse

P
(Fig. 9.12)
Next, rotate the probe back to TAX and attempt to follow UN distally to the fore-
arm. You will need to straighten the elbow. Remember, as you move more distally,
the two FCU heads coalesce, and the UN is just deep into the single FCU. You can
follow the UN to the ulnar canal (Guyon’s) in the wrist.
204 9 Medial Elbow

10: Ulnar nerve in forearm,
transverse
rotocol Image 11 (Optional): Ulnar Nerve Proximal

P
to the Medial Epicondyle
Starting at the ME, examine the proximal UN in TAX as much as possible. If there
is a question of UN enlargement, measure the CSA and compare it with that in a
more distal location of potential compression, such as may occur with AE compres-
sion of the UN in the ulnar groove.
Complete Medial Elbow Ultrasonic Examination Checklist
□ Protocol Image 1: Medial epicondyle, longitudinal, extension ± power Doppler
□ Protocol Image 2: Medial epicondyle, longitudinal, flexion ± power Doppler
□ Protocol Image 3: Medial epicondyle, valgus maneuver, longitudinal
□ Protocol Image 4: Ulnar nerve at medial epicondyle, transverse + measurement
□ Protocol Image 5: Ulnar nerve at medial epicondyle, transverse, dynamic exam,
passive flexion
active flexion
resisted flexion
□ Protocol Image 8: Ulnar nerve in true cubital tunnel, transverse
□ Protocol Image 9: Ulnar nerve in true cubital tunnel, longitudinal
□ Protocol Image 10: Ulnar nerve in forearm, transverse
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elbow laxity by gravity stress radiography: comparison of valgus stress radiography with grav-
ity and a Telos stress device. J Shoulder Elb Surg. 2014;23(4):561–6.
26. Roedl JB, Gonzalez FM, Zoga AC, Morrison WB, Nevalainen MT, Ciccotti MG, et al. Potential
utility of a combined approach with US and MR arthrography to image medial elbow pain in
baseball players. Radiology. 2016;279(3):827–37.
Chapter 10
Shoulder

1. Shoulder pain [1]
1. What is causing the shoulder pain?
2. Is the pain directly from the shoulder, or is it referred from elsewhere?
3. Is the shoulder pain from a structural problem or an inflammatory condition such
as rheumatoid arthritis (RA) or spondylarthritis (SpA)?
4. Does the pathology on the image represent the actual cause of the pain?
5. Is the pain caused by movement?
6. Is a “frozen shoulder” (adhesive capsulitis [AC]) present, and if so, is it the
source of pain?
Basic Anatomy
The bony shoulder architecture is depicted in Fig. 10.1. There are four shoulder
joints: glenohumeral (GHJ), acromioclavicular (ACJ), scapulothoracic, and sterno-
clavicular (SCJ) [2].
Shoulder soft tissue anatomy is complicated; however, a few simple anatomic
concepts are worth remembering. Also, bear in mind that the long head of the biceps
tendon (LHBT) is not part of the rotator cuff and is just “passing through,” straight
up the middle. However, as you will see, impairment of other shoulder structures
may negatively influence the LHBT. The key to understanding the shoulder is the
rotator cuff tendons and their insertions (Fig. 10.2). The time-honored mnemonic
States Government.

Switzerland AG 2023
208 10 Shoulder
Fig. 10.1 Shoulder bony anatomy
Fig. 10.2 Rotator cuff tendons
acronym for the names of the rotator cuff tendons and muscles is SITS: supraspina-
tus (SST), infraspinatus (IST), teres minor (TMT), and subscapularis (SSCT) [2].
To remember the function of the rotator cuff muscles, think of the physical actions
of the muscles that produce specific tennis strokes:
Tennis players with a subpar forehand and a terribly inferior backhand must rely on a
supreme serve.
The four tendons insert on two tuberosities, namely the greater tuberosity (GT)
and the lesser tuberosity (LT). The subscapularis tendon inserts on the LT. The GT
has three facets: superior (SF), middle (MF), and inferior (IF) [3]. To remember the
GT tendon insertion locations, consider this story (Fig. 10.3):
Basic Anatomy 209
Fig. 10.3 Greater

tuberosity attachments
cartoon
There were three Sit brothers, Supra, Infra, and Terry, who lived in a great town (GT).
Firstborn Supra lived high and mighty in a superior house (SF). Infra, the middle child
(MF), lived nearby. Terry, the youngest, lived far away from his older siblings since he felt
inferior (IF) to them. Supra and Infra were close and spent time at each other’s houses (GT
insertional overlap). Supra, however, was rambunctious and tended to get “tore up,” some-
times extending his damage to nearby Infra. Terry stayed out of the way and was rarely
injured.
Fluid accumulation detectable by US occurs in three recesses (anterior, poste-

rior, and axillary), two bursae (subcoracoid and subacromial-subdeltoid [SASDB]),
and the LHBT sheath. The posterior recess is most accessible on US when the
shoulder is in external rotation (Fig. 10.4) [4].
The term rotator cable (RC) (Fig. 10.5) refers to a semicircular ovoid thickening
of the GHJ capsule stretching from the lateral aspect of the LT to the GT. This cable
runs just deep to the SST and IST and anchors them to the tubercles, functioning
like a suspension bridge cable [5]. The RC is superficial to the LHBT. On US, the
RC may be seen as a thickened hyperechoic curved structure underlining the SST
and may be confused with calcium deposition of the deeper aspect of the tendon [6].
The RC fibers are perpendicular to the tendon fibril orientation.
The rotator cuff interval (RCI) is the triangular space bordered by the SST, the
SCCT, and the coracoid process [7]. On US, we look at the base of this triangle,
delineated as the space between the insertion areas between the SST and the SSCT
insertions on the anterior-superior GT and superior LT, respectively (Fig. 10.6).
210 10 Shoulder
Fig. 10.4 Shoulder bursae

and tendon sheath
Fig. 10.5 Rotator cable
Fig. 10.6 (Intra-articular)

Rotator cuff interval
The proximal portion of the RCI is where the LHBT is ovoid (intra-articular). In
this location, the LHBT does not touch bone since it is supported by two ligaments
that form a sling, the biceps pulley system. These ligaments are the more superfi-
cial coracohumeral ligament (CHL) and the deeper superior glenohumeral ligament
(SGHL). More distal in the RCI, the LHBT becomes more circular and touches the
base of the biceps groove, tethered in place by the transverse humeral ligament
(THL). The RCI encompasses the path of the LHBT as it traverses this area and is
best seen in the transverse (TAX) view in a modified Crass position.
Clinical Comments
Shoulder pain is common. It is impractical to order a magnetic resonance imaging

(MRI) study for everyone with shoulder pain. Point-of-care ultrasound (US) excels
in delineating many causes of shoulder pain and is complementary to MRI [8].
However, shoulder US can be challenging, humbling, and loaded with potential
pitfalls [9]. We call it a shoulder exam, but US assesses soft tissue more than actual
shoulder joints. A shoulder US exam typically visualizes the posterior GHJ but not
the scapulothoracic joint. The ACJ is the shoulder joint best evaluated by US. The
SCJ joint can also be assessed by US, although it is not part of our standard
protocol.
Since clinical evaluation imperfectly pinpoints the source of shoulder pain, it is
essential to perform a complete shoulder US examination in almost every case [10].
If the exam is unremarkable, the pain may have been referred to the shoulder from
elsewhere. The radiograph is a valuable roadmap for the US exam. It will demon-
strate the shape of the acromion, the humeral head (HH) position with respect to the
glenoid fossa, the presence or absence of an os acromiale variant, GT cortical irreg-
ularity, osteophytes that may cause impingement, calcium deposition in the soft
tissue, and the status of the GHJ and ACJ [11].
Rotator Cuff Impingement

Anterosuperior Impingement
Anterosuperior impingement describes compression of the SASDB (and sometimes

even the SST itself) under the coracoacromial arch (CAA) (Fig. 10.4). The CAA
consists of the distal acromion, the coracoid process, and the coracoacromial liga-
ment (CAL). Shoulder abduction provokes compression. Impingement catalysts are
structural (downsloping distal acromion or osteophytes, os acromiale, large SST
calcium deposits, SASDB thickening) or functional (SST tendinosis or tears, SST
weakness from neurologic disease) [12]. However, functional impingement may
occur in healthy over-head throwing athletes due to humeral head instability while
throwing [13].
In severe impingement, the bony GT can abut the undersurface of the distal acro-
mion in abduction. Impingement may result from a complete SST tear since this
tendon keeps the HH tamped down. So, impingement of the SST under the CAA
may cause an SST tear, and a large SST tear itself may cause or exacerbate
212 10 Shoulder
impingement due to an ascending HH, creating a vicious cycle. Impingement syn-

drome can lead to chronic SASD bursitis/bursal thickening, SST tendinosis, and
ultimately tearing. Some suggest that impingement under the CAA initiates the bulk
of rotator cuff tears [14]. The sonographer tests for impingement using passive
shoulder abduction. Positive findings include bursal material or fluid accumulating
at the point of impingement (“rug-under-the-door sign”) or simply sluggish gliding
of the bursa [8, 15]. Also, be aware that SASDB impingement may occur under the
CAL and not just under the distal acromion [4].
Subcoracoid Impingement
Only rarely is the SSCT truly impinged under the coracoid. See the Dynamic Views
section below.
Posterosuperior Impingement Syndrome
Posterosuperior impingement syndrome, also called internal impingement, occurs

most often in over-head throwing athletes. The posterior rotator cuff is pinched at
the junction of the SST and IST between the GT and the posterosuperior glenoid
rim in maximal abduction and external shoulder rotation (the cocking phase for
throwing). It causes SST, undersurface tendinosis, and tears [16].
Rotator Cuff Tears
Rotator cuff tears most commonly occur in the SST, but isolated tears may also
occur in the IST and the SSCT, usually as an extension of an SST tear [17, 18]. The
most common partial-thickness SST tear is articular-sided on the anterior portion of
the SST near its insertion on the GT [19]. Such tears may account for 70% of all
partial-thickness rotator cuff tears. Critical zone (approximately 1 cm proximal to
the GT insertion) and bursal-sided tears are less common [19]. Thus, the “critical
zone” of the SST is not as vulnerable to tears as previously thought.
The rotator cuff tear you detect on US may not be the source of pain. Rotator cuff
tears are common, and their prevalence increases with age. In one study, full-
thickness tears were present in about 11% of males in their 50s and 37% in their 80s
[20]. The tears were asymptomatic in half of the males in their 50s and in 2/3 of the
males in their 80s. Comparing US to MRI and magnetic resonance imaging arthrog-
raphy (MRA) for the detection of rotator cuff tears, MRA was shown to be more
sensitive and specific than either US or MRI [21]. For all tears, the sensitivity of US,
MRI, and MRA, respectively, is about 85%, 85%, and 92%, respectively. Specificity
is about 82%, 90%, and 97% [21]. Therefore, US and MRI are comparable in both
sensitivity and specificity. US and MRI detect about 2/3 of partial-thickness tears,
whereas MRA detects 86% [21]. All three modalities were greater than 90% spe-
cific for partial-thickness tears. Thus, even if you do not see a tear on US, one can
still be present.
Description of Rotator Cuff Tears
To avoid confusion, remember that the tendons are three-dimensional, so tears vary
in width, depth, location, and extent. Adding to the bewilderment are descriptions of
tendon tears such as a rim-rent tear, which is also called a PASTA (partial articular
side tear). Tears can be defined as being either complete or incomplete. A complete
tear means that the tendon has torn to the point of having no interconnecting fibers
on either side of the tear. In an incomplete tendon tear, communicating remnants
persist. Furthermore, incomplete tears may be partial, intrasubstance, or even full-
thickness. However, incomplete full-thickness tears do not encompass both the ten-
don’s depth and width.
Verifying tears in two orthogonal planes is essential. The US report description
should include the location of the tear in the cross-sectional plane (e.g., anterior,
middle, or posterior) or longitudinal plane. Also, depict the tear shape, length, and
note if retraction (partial or complete) is present [8]. In our institution, we use
descriptive terms such as full- or partial-thickness and full- or partial-width to
describe tears. We further describe the extent of partial tears by percent. For instance,
“partial articular-side tear involving 50% of the tendon thickness” [9].
Specific Types of Tears (Fig. 10.7)

Partial-Thickness Tears
Partial-thickness or incomplete tears are tears that do not completely penetrate the
full thickness of the tendon. The partial-thickness tear should have a well-delineated
anechoic to hypoechoic discontinuity, to differentiate it from tendinosis, which is
verified in two orthogonal planes [9]. However, tendinosis may coexist with and be
confused with an intrasubstance tear. Cortical irregularity at the GT footprint may
be a clue to the presence of intrasubstance tears [9]. Measure the depth in mm or
a fraction of the tendon depth involved, the location in the tendon, and add a loca-
tion descriptor:
(a) Bursal: The tear communicates with SASDB but may be difficult to delineate
due to SASDB synovial fluid or synovitis filling the gap. Transducer pressure
may accentuate the migration of the SASDB into the tear defect in bursal-sided
tears [8].
214 10 Shoulder
Fig. 10.7 Types of rotator

cuff tears
(b) Articular: The tear communicates with GHJ and may cause a cartilage inter-
face sign (CIS) (see Chap. 1 for more information). A CIS is a detection clue for
articular-sided tears and occurs when fluid in the tear reaches the cartilage,
producing a thin hyperechoic interface on the surface of the cartilage [22].
(c) Intrasubstance: The tear occurs in the middle of the tendon and does not com-
municate with the bursa or the joint. Intrasubstance tears may involve the
insertional footprint (as long as they do not concomitantly involve the bursa or
articular side) [3]. Logically, intrasubstance tears noted on US or MRI are invis-
ible to arthroscopy.
Focal/Incomplete Full-Thickness Tears
This tear goes through the complete depth of the tendon, thereby communicating
with the GHJ and the SASDB; however, the tendon width is not entirely involved.
Like a partial-thickness tear, a full-thickness tear is delineated on US as an anechoic
or hypoechoic tendon defect. Partial tendon retraction may be seen; granulation tis-
sue and scarring may fill the space where the tendon once existed [8]. Effusion of
the SASDB or the GHJ is found in about 2/3 of acute rotator cuff tears and about 1/3
of chronic rotator cuff tears [23].
Complete Tear
A complete tear is a full-thickness (depth) tear that involves the tendon’s full width;
this is a 100% total tendon tear. There may be no residual tendon remnant, and the
stumps may not be appreciated. Debris or other structures may shift into the area. A
classic example is that after a massive SST tear, the deltoid muscle shifts into and
fills the tendon defect [24]. Alternatively, as may occur with incomplete full-
thickness tears, granulation tissue and scarring may fill the space where the SST
previously resided [8]. Look for at least some evidence of fibrillar echotexture, or
else you may not be looking at a tendon.
Clues That Point Toward a Full-Thickness Rotator Cuff Tear
1. Loss of volume of the tendon

With a SST tear, the normal convex contour of the tendon may become flat or
even slightly concave. The SASDB, the peribursal fat pad, or even the deltoid
muscle may outline the new, abnormal SST silhouette; the latter is called the
deltoid herniation sign [25]. Loss of volume is often more noticeable in bursal-
sided tears but also occurs with full-thickness tears. External probe pressure
may highlight this “flat-tire sign.” Small tears will not cause significant vol-
ume loss.
2. A total absence of the tendon [26]
3. Superior facet GT cortical irregularity (for supraspinatus tears only)
This bone abnormality is present in 86% of full-thickness tears and 50% of
articular-sided partial-thickness tears [26]. However, there are two caveats to
consider: (1) Ccortical irregularity may occur in 21% of patients without a tear,
and (2) Do not mistake a step-off deformity of a GT fracture for cortical irregu-
larity [26].
4. Effusion in the GHJ, SASDB, and LHBT sheath [26]
Recall that the GHJ and LHBT sheaths usually communicate with each other.
Also, recall that the SASDB may or may not communicate with the GHJ, but
will often do so in the presence of a rotator cuff tear [27]. However, effusion in
the LHBT sheath or the SASDB is not unambiguous evidence of a rotator cuff
tear [28].
5. The CIS
The CIS is a hyperechoic line covering articular cartilage, it is magnified by
fluid within a tear that reaches the articular side. Thus, the CIS is an acoustic
enhancement artifact due to the tendon tear extending to the articular surface,
whether a partial- or full-thickness tear [26].
216 10 Shoulder
Supraspinatus Tendon Tears
The etiology of SST tears is often multifactorial [29]. Degenerative cuff defects are
common, occurring in more than 65% of people, often with no symptoms [30]. This
degenerative (intrinsic) change, perhaps starting in middle life, coupled with extrin-
sic factors such as subacromial impingement, glenohumeral instability, and internal
impingement, creates a perfect storm for rotator cuff tears. Younger patients may
likewise develop rotator cuff tears, often from trauma [30]. Indeed, trauma may also
play a role in middle-aged athletes with preexisting degenerative rotator cuff
changes. In those individuals, clues to chronic degenerative change are tendinosis or
GT cortical irregularity [31].
1. Bursal-sided tears of the SST may be obscured by the encroachment of
SASDB material, synovial fluid, peribursal fat, or even the deltoid muscle
upon the damaged SST. You may only see a flattening or reversal of the normal
SST convexity accentuated by probe pressure (“flat tire sign”). If the tear pro-
gresses to a complete tear, the deltoid muscle may migrate into the former
position of the SST and mislead the sonographer into believing that the SST is
present.
2. Articular-sided tears are more common; look for fluid in the gap or a CIS.
3. Intrasubstance tears are longitudinal and do not break through to the bursal or
articular surface. Remember, an SST tear extending to the GT footprint but not
reaching either the articular or bursal sides is still called an intrasubstance tear.
Tilt the probe and evaluate in transverse (TAX) and longitudinal (LAX) views to
verify that the hypoechoic area you identify as a putative intrasubstance tear is
not simply anisotropy.
4. Full-thickness tears are full-depth. They are termed “complete tears” when the
full width is also involved. The larger the tear size, the greater the chance for
tendon stump retraction. Measure the distance between the two stumps. If you
see a complete SST tear, look carefully for an extension to the IST and check for
IST insertion integrity with dynamic maneuvers [18].
5. Rim-rent tears are distal partial-thickness articular-sided tears adjacent to the
GT. If a rim-rent tear has an additional bony avulsion from the GT, this is called
a PASTA (partial articular-sided supraspinatus tear with avulsion) lesion.
Subscapularis Tendon Tears
The SSCT stabilizes the anterior shoulder [8]. Isolated tears may be sports-related;
however, in many cases, an SSCT tear may be caused by an SST tear extending
anteriorly right across the RCI. The SSCT fibers blend into the CHL and the THL,
and, thus, SSCT tears may be associated with LHBT instability due to the loss of
integrity of the THL [8]. The LHBT will subluxate or even dislocate medially if this
occurs; this is most apparent during a dynamic US examination.
Infraspinatus Tendon Tears
Infraspinatus tendon tears are rarely isolated to the IST but often result from an SST
tear extending posteriorly [6]. If an SST tear extends posterolaterally by more than
2.5 cm, then there is a high likelihood that this tear has spread to the IST. Like SST
tears, these tears may be partial-thickness, intrasubstance, full-thickness, or com-
plete. One special mention is a partial-thickness articular-side tear of the IST, which
may occur with posterosuperior impingement syndrome. Impingement between the
posterior HH and glenoid during external rotation can cause a posterior labral tear
and significant posterior cortical irregularity of the posterior GT. However, this
“bare area” may normally have some irregularity since it is not covered by cartilage.
Teres Minor Tendon Tears
Teres minor tendon tears are rare, unrelated to IST tear extension, and may be due
to acute shoulder trauma. Measure the length of the tear or describe the percent of
the tendon involved. An acute tear may demonstrate neovascularization with power
Doppler (PD).
Other Findings
Tendinosis: Tendinosis is sonographically represented initially by tendon thicken-

ing and enlargement and later by focal or diffuse hypoechogenicity with loss of
the normal fibrillar echotexture [8]. Tendinosis may occur in the SST, the LHBT,
the IST, and the SSCT. Doppler activity may or may not be seen. Any abnormal-
ity should be defined as a tear only when a genuine defect is documented in both
TAX and LAX and an anisotropy effect is ruled out. Tendinosis is a precursor to
a tear but may be challenging to separate from an actual tear [8]. Tendinosis,
often referred to as tendinopathy, may be caused by age-related degeneration,
overactivity, trauma, or chronic impingement, such as may occur in the SST
under the CAA [14, 32, 33]. Statin medications may increase the incidence of
tendinopathy [34]. Likewise, quinolone antibiotics may facilitate supraspinatus
tendinopathy [35]. Sonopalpation may be diagnostically helpful in specific areas:
1. SST impingement at the distal acromion
2. Tenderness over the LHBT
3. Tenderness over an acute tendon tear
4. Tenderness over tenosynovitis, such as along the LHBT sheath
Bursitis: Bursitis, an inflamed and distended bursa, may be detected in the SASDB
and the subcoracoid bursa. Bursitis may be caused by repetitive pressure irrita-
tion, infection, crystal disease, or inflammatory conditions.
218 10 Shoulder
Glenohumeral joint effusion: Excess synovial fluid can reliably be demonstrated

in the posterior GHJ recess (in external rotation) and the LHBT sheath since the
latter communicates with the GHJ [36]. In the posterior GHJ recess, an
anechoic or hypoechoic effusion may be located deep to the IST but superficial
to the junction of the HH and the glenoid labrum [4].
Synovitis: Shoulder US may detect synovitis in the LHBT sheath, the GHJ poste-
rior recess, the SASDB, the ACJ, and the subcoracoid bursa. One study described
more significant bursal synovitis with PD activity in elderly onset RA compared
with polymyalgia rheumatica (PMR) [37].
Enthesitis: Entheses can be evaluated at all three GT facets (SST, IST, and TMT)
and the LT’s SSCT insertion.
Dynamic Views
A significant strength of US is dynamic evaluation; MRI cannot duplicate this.

Dynamic US uses:
1. Abduction detects SST impingement under the CAA.
2. External rotation detects small to moderate posterior GHJ recess effusions.
3. External rotation detects SSCT impingement under the coracoid due to coracoid
process anatomic variations, chunks of calcium within the SSCT, and ganglion
cysts [4, 38, 39].
4. External rotation discloses medial LHBT subluxation if there is a loss of integ-
rity of the biceps pulley system or the THL.
Adhesive Capsulitis
Adhesive capsulitis results in markedly decreased shoulder range of motion (ROM),

often with pain [4]. Although often idiopathic, causes include diabetes, certain med-
ications, and prolonged immobilization after surgery or trauma. It starts with syno-
vial proliferation, followed by collagen deposition, and ultimately articular volume
contraction, resulting in severe stiffening and decreased GHJ ROM. Also known as
“frozen shoulder,” it progresses in three stages: freezing, frozen, and thawing.
Doppler activity may occur before it becomes frozen. There are four sonographic
signs of AC on US. Using the first 3 (a–c) parameters, US has high sensitivity and
specificity (100% and 87%, respectively) for the diagnosis of AC of the shoulder
[40]. Power Doppler activity (d) is also diagnostically helpful [41].
(a) Decreased dynamic movement of the SSCT under the coracoid.
(b) Decreased SST dynamic movement under the acromion.
(c) Increased RCI size due to swelling of the ligaments surrounding the LHBT.
(d) ± PD activity in the RCI.
Rotator Cuff Muscle Atrophy
Atrophic muscles are hyperechoic (whiter), but be aware that diabetes may produce
bright-appearing muscles with increased echogenicity. Compare the muscle size
and echogenicity to normal contiguous and contralateral muscles. Additionally,
look for a loss of normal muscle echotexture and contour [3, 8]. Ultrasound com-
pares favorably to MRI for detecting rotator cuff atrophy, but is sonographer-
dependent [42, 43]. One important use of US is to evaluate the infraspinatus muscle
(ISM) for atrophy by comparing it to the teres minor muscle (TMM) in TAX, since
an atrophic IST predicts poor outcomes of rotator cuff repair [44–46]. In the TAX
view at the scapula ridge, the cross-sectional area of the normal ISM is approxi-
mately twice that of the TMM [3].
Postoperative Rotator Cuff Repair
Ultrasound is useful for assessing postoperative rotator cuff repair if the shoulder
has had sufficient time to heal. Most rotator cuff repairs are simply decompression
procedures, done arthroscopically to alleviate impingement on the SST [47]. The
surgeon resects any structure encroaching upon the SST. Tendon reattachment pro-
cedures can be done for complete rotator cuff tears. Even large tears may be ame-
nable to arthroscopic repair [48].
First, look at plain films as a roadmap to evaluate a post-op cuff repair. The reat-
tachment site appears as a trough, and you may see hyperechoic sutures [49]. If a
bursectomy was done, then the SASDB would not be identified. Distorted tendon
sonoanatomy complicates perioperative interpretation due to variable thickness and
echogenicity. Ultrasound image clarity improves with time, perhaps 6–9 months
post-op, as the tendon gradually resumes a more “normal” hyperechoic and fibrillar
echotexture and shape [49]. Recurrent rotator cuff tears may be noted, ranging from
focal to complete tears, sometimes with complete retraction. Free-floating metal
sutures may indicate a recurrent tear [49].
After tendon repair, US can diagnose recurrent tears with an accuracy of 89%
[50]. A recurrent tear may not correlate with pain or dysfunction; however, an intact
rotator cuff correlates with greater strength [51]. Thus, ultrasonic detection of a
recurrent tear does not necessarily warrant repeat surgery. Dynamic scans help
determine the repair integrity or the emergence of adhesive capsulitis.
Postoperative Arthroplasty
Total shoulder replacements (TSR) and hemiarthroplasties are done with an intact
rotator cuff. Both procedures preserve the rotator cuff and the tuberosities into
which the rotator cuff inserts. A “reverse shoulder” prosthesis is performed for
patients who lack an intact rotator cuff [52]. Look at plain films for the position of
the prosthesis, fracture, hardware aberrancy, and periprosthetic lucency >2 mm; the
220 10 Shoulder
latter suggesting prosthesis loosening [49]. On US, the prosthesis is echogenic,

smooth, and has posterior reverberation artifacts. Evaluate the overlying rotator cuff
tendons and their insertions to see if they remain intact. Since the prosthetic metal
humeral head artifact is deep to the rotator cuff, US assesses the integrity of the rota-
tor cuff and the position of surgical screws. Normal, intact rotator cuff tendons
appear hypoechoic and heterogeneous immediately after surgery. The diagnosis of
tendinosis or even a tear is challenging unless you see a clear-cut tendon defect with
anechoic fluid [49]. A dynamic US exam may demonstrate hardware instability.
Calcium in the Shoulder
Calcium deposits are common, consist primarily of hydroxyapatite, and occur

mainly in the SST, the LHBT, and the SADSB [8]. Calcium deposition is a dynamic
process of unknown cause, typically occurring in people aged 30–50 [53]. The
calcium deposits may be appreciated on plain films. On US, calcium is hyper-
echoic, perhaps with an acoustic shadowing artifact [8]. The three stages are: pre-
calcific, calcific (formative and resorptive phases), and postcalcific [54]. Pain, and
often Doppler activity, is most prominent in the resorptive phase [8]. Treatment is
not needed if asymptomatic, but if symptomatic, conservative treatment is
tried first.
Calcific Tendinosis Stages
1. Thin/linear stage
This is a degenerative stage. Do not aspirate, and do not confuse this
with a CIS.
2. Well-defined or globular stage
This may cause inflammation and may respond to aspiration. Determine if a
block of calcium is causing impingement. If so, needling the calcium (barbo-
tage) and saline lavage and aspiration may help [55].
3. Resorptive or “slurry” stage
The deposits are in liquid or semiliquid (“toothpaste”) form and can simply
be aspirated if necessary [56]. Positive Doppler and pain reproduction with sono-
palpation help determine if the calcium deposit is symptomatic.
Aside from hydroxyapatite, there are other causes of calcium deposition in the
shoulder. Calcium deposition may occur with calcific arthropathy, such as calcium
pyrophosphate deposition (CPPD) disease. Calcium in the SASDB may migrate
from calcium deposition in the SST, perhaps resulting in bursitis of the SASDB [17,
57, 58]. Loose bodies may occur when cartilage pieces detach and calcify in the
synovial fluid [59]. This process may occur in the joint recess, the LHBT sheath,
and the bursae. Loose bodies are benign, occasionally painful, and are best demon-
strated on dynamic US.
Other Shoulder Structures
Biceps Tendon
Although not technically part of the rotator cuff, LHBT pathology may be associ-
ated with disorders of the rotator cuff, the glenoid labrum, and LHBT impingement
[8]. The biceps’ brachii muscle, the classic symbol of strength, is interesting. The
LHBT originates from the spinoglenoid tubercle, but 50% of the time, there is a dual
attachment to the glenoid labrum [60]. Consequently, this tendon may be partially
attached to a cartilage structure. The proximal LHBT drapes over the HH, acting as
a secondary stabilizer of the HH. The tendon curves downward about 40° as it
enters the intertubercular sulcus or groove. Like many tendons that rub against
bone, friction is reduced by a surrounding protective sheath, the tenosynovium.
More distally, the LHBT transitions into the myotendinous junction. Beyond the
muscle, the distal biceps tendon inserts on the radial tuberosity and the bicipital
aponeurosis.
Many presume the biceps to be the ultimate elbow flexor, but it is subordinate to
the underlying brachialis muscle regarding elbow flexion. However, the biceps mus-
cle is the primary forearm supinator. The origin and course of the LHBT expose the
tendon to bystander damage from impairment of the GHJ, the glenoid labrum, the
SASDB, and particularly the SST. A completely torn SST encourages the HH to
migrate upward; the proximal biceps tendon will mitigate such movement to its own
detriment. Another example of collateral damage would be the effect of a glenoid
labrum tear in a person whose LHBT is partially anchored to the labrum. Thus, the
LHBT is, in a sense, the barometer of the shoulder. In the case of a complete LHBT
tear, hyperechoic tissue, including hematoma and synovitis, may mimic an intact
LHBT within the biceps groove on the TAX view. Again, look for the familiar fibril-
lar echostructure of the tendon to verify that the LHBT is in the groove. The LHBT
can be associated with several pathologic findings:
1. Tendinosis
The LHBT is a bit different from many tendons. With tendinosis, the tendon
swells, but fibrillar echotexture may persist, barring a frank tear. However, the
presence of some hypoechoic areas may indicate tendinosis [8]. In the tendon
groove, the LHBT with tendinosis appears enlarged. Like other disorders of the
LHBT, tendinosis is often a secondary event [61]. Occasionally, isolated LHBT
pathology may occur in younger athletes. Additionally, the LHBT may be sub-
ject to adverse effects from medications (e.g., statins, quinolone antibiotics, or
injected or systemic corticosteroids) [62].
2. Tears
Tears of the LHBT may be associated with a complete SST tear; in this case,
the BT becomes the HH’s main depressor, resulting in excess stress on the ten-
don. The LHBT may even split. An LHBT tear will cause distal tendon sheath
222 10 Shoulder
effusion and loss of fibrillary echotexture, which may occur at the intra-articular
or extra-articular level. If a proximal LHBT tear occurs, suspect a glenoid labrum
(SLAP) tear [63]. However, with such a proximal LHBT tear, the detached
LHBT may remain in the biceps groove. Consider a labral tear with appropriate
signs and symptoms, particularly in an overhead throwing athlete. Again, the
best test for a labral tear is an MRA of the shoulder [63].
Complete LHBT tears result in Popeye’s sign due to a balling up of the mus-
cle. Acutely, this is painful and may have a dramatic appearance, but the pain
subsides eventually, and elbow flexion strength is minimally affected. These
tears are often spontaneous and tend to occur in people older than 50 [64]. It may
be challenging to visualize partial tears of the LHBT on US. The strength of
sonography lies in confirming an intact LHBT or full-thickness tear, but it is less
accurate in diagnosing partial-thickness tears [65, 66].
Tracking the tendon from proximal and distal locations is imperative since
debris may mimic an intact LHBT. There may be visible, retracted tendon
stumps. If the rupture occurs at the myotendinous junction, then the LHBT may
still be in the groove proximally. Most LHBT tears are associated with SST or
SSCT tears. Treatment is usually conservative, but surgery may be needed for a
young, high-level athlete. It is not uncommon for anomalous biceps muscle
heads to be present and have separate tendons in the biceps groove [67]. Such a
variant may mimic a split LHBT [68].
3. Tenosynovial effusion
The LHBT communicates with the GHJ, so pathology in the GHJ may be
reflected by increased synovial fluid, perhaps with calcified intra-articular bodies
originating from the GHJ. In TAX views of an LHBT tenosynovial effusion,
synovial fluid almost wholly surrounds the tendon. If there is increased synovial
fluid in the LHBT sheath, look posteriorly at the GHJ in external rotation for
effusion and consider potential causes of increased GHJ synovial fluid, including
a rotator cuff tear.
4. Tenosynovitis
The tendon sheath may demonstrate anechoic fluid, synovial hypertrophy, or
PD activity [8]. Such findings should prompt a search for an underlying inflam-
matory condition such as RA. Power or color flow Doppler may produce spec-
tacular diagnostic images. The SASDB, if distended, may mimic an LHBT
sheath effusion or tenosynovitis in TAX view at the biceps groove but will not
completely surround the LHBT; the SASDB will be located superficially to
the LHBT.
5. Instability
The accuracy of US in detecting LHBT instability is high [66]. The LHBT is
held in place by the bicipital groove, the biceps pulley at the intra-articular level,
and, more distally, by the THL at the extra-articular level. The SSCT gives sup-
porting fibers to the THL, so if the SSCT tears, the THL may also be impaired.
A compromise of the tethering effect of either the biceps pulley or the THL may
result in LHBT subluxation or dislocation.
During the external rotation dynamic exam, the LHBT may medially sublux-
ate/dislocate superficial to or even into an SSCT tear. The LHBT may even dis-
locate under the coracoid, thus becoming invisible to the US beam. So, start
distally and follow the LHBT proximally to look for dislocation. In summary, if
dynamic US reveals LBHT subluxation, consider an injury to the SSCT, the
THL, or the biceps pulley [8, 69].
6. Entrapment
The LHBT may rarely become impinged between the HH and the glenoid
during forward arm elevation [4]. This may result in an “hourglass” configura-
tion of the LHBT [70]. There may be buckling of the LHBT as it is squeezed
between the HH and the glenoid [71].
7. Acromial impingement
If the SST completely tears, the HH may rise toward the acromion. By default,
the LHBT becomes a tether of last resort, ineffectually impeding the HH’s ascen-
sion. The LHBT itself may become impinged under the acromion, often damag-
ing the tendon [72].
Subacromial-Subdeltoid Bursa
This synovial-lined bursa, the largest in the body, separates the rotator cuff from the
CAA and the deltoid muscle [27]. It extends from the coracoid process to beyond
the GT and decreases tendon friction [8, 73]. It is surrounded by a hyperechoic peri-
bursal fat layer, the latter producing a “tram-track” appearance [8]. The SASDB is
hypoechoic, ordinarily 1–2 mm deep, and may typically contain a slight amount of
fluid [8]. It can thicken with underlying SST pathology or recurrent impingement
under the CAA [27]. A clue to a bursal-sided SST tear is the downward dipping of
the SASDB into the usually convex outer tendon layer. In the event of a complete
SST tear, a thickened SASDB may move into the vacant area to mimic an intact SST
[9]. With an effusion, the distended SASDB may be seen in TAX to overlie the
LHBT, resembling the beam and fulcrum of a teeter-totter or seesaw. Use probe
pressure to verify whether an effusion is present or not.
The bursa may become distended due to inflammation, even if it does not com-
municate with the GHJ [8]. It can harbor effusions, synovitis, and calcium deposits
[8]. Power Doppler activity may be present with synovitis or an infection. Causes of
noncommunicating SASDB distension include direct bursal trauma, repetitive
trauma, and inflammatory disease affecting the synovium [27]. The major causes of
SASDB distension are [8]:
1. Effusion
2. Synovitis (RA, spondyloarthropathy [SpA], PMR [74])
3. Crystal arthropathy (gout, CPPD, calcium hydroxyapatite)
4. Hemorrhage
5. Impingement
6. Infection (septic bursitis)
224 10 Shoulder
7. Rotator cuff tear

8. Amyloidosis
9. Synovial proliferative disorder (pigmented villonodular synovitis, synovial
osteochondromas)
The SASDB may be isoechoic with the deltoid muscle and thus challenging to
delineate [8]. However, since the distended SASDB extends beyond the SST, the
sonographer can detect the tip of a dependent SASDB effusion lateral to the inser-
tion of the SST on the GT [27]. Additionally, PD activity within the bursa may
indicate acute inflammation [8]. The SASDB does not usually communicate with
the GHJ but often does so with a rotator cuff tear; more than 90% of rotator cuff
tears are associated with SASDB distension [27].
Acromioclavicular Joint
The most commonly seen ACJ abnormality is osteoarthritis. The fibrous capsule
and coracoacromial and coracoclavicular ligaments (CAL and CCL, respectively)
stabilize the joint [75]. The os acromiale (an anomalous nonfused accessory bone in
about 8% of people) may be seen on the superior acromion [76]. An os acromiale
has a distinct US appearance, with the extra bony fragment being readily apparent
adjacent to the distal acromion [77]. An os acromiale can cause SST impingement
syndrome if the deltoid inserts on it, tugging it down and compressing the
SST. Alternatively, the os acromiale may develop a downward osteophyte that
impinges on the SST [78]. Cysts over the ACJ are painless or slightly tender masses
associated with ACJ degenerative joint disease and full-thickness rotator cuff tears
[79]. Other ACJ findings include:
1. Geyser sign: Fluid tracks into the ACJ from an underlying SST tear. This fluid
accumulates superficially to the ACJ and is known as a geyser sign. Probe pres-
sure shows debris moving back and forth across the ACJ [80].
2. Synovitis and bony erosion: This may occur with RA. The ACJ may also be
affected by other inflammatory polyarthropathies, including CPPD.
3. Effusion: In this case, the ACJ capsule can be distended with effusion, perhaps
with PD activity. Effusion causes include degenerative changes, infections, and
inflammatory conditions [8].
4. Instability: This may be painful and caused by trauma or osteoarthritis; it is
classified according to the ACJ space width and degree of ligament injury [81].
A dynamic exam of an injured ACJ will show a narrowing of the joint space in
cross-arm adduction [4]. A comparison with the contralateral, uninjured joint is
useful. A 2–3 mm discrepancy between sides is abnormal if this correlates with
the clinical situation [75]. Tossy type I–III instability grades can be determined
by US [82]. Significant tears of the acromioclavicular ligament may result in
misalignment of the acromion and clavicle, resulting in an elevated clavicle.
5. Widening of the ACJ: This may occur with effusion, hematoma, surgical resec-
tion, post-traumatic osteolysis, distal clavicle resorption from RA, systemic scle-
rosis, or hyperparathyroidism.
Sternoclavicular and Costochondral Joints
Trauma may result in SCJ instability or dislocation, which US can diagnose [83].
Synovitis is quite detectable by US [84]. Ultrasound may also reveal bony erosion,
osteoarthritis, and even bone destruction from SCJ infection [85, 86].
Glenoid Labrum
This fibrocartilage rim augments the bony glenoid “socket” into which the “ball” or
humeral head fits. Ultrasound best visualizes the more superficial posterior labrum,
but other quadrants can be viewed [87]. The acronym “SLAP” refers to a superior
labrum tear from anterior to posterior. This injury may occur after a fall on an out-
stretched hand or repetitive overhead throwing by a younger patient. Symptoms
range from a dull ache to a loss of throwing strength or a catching sensation.
Posteriorly, the labrum has a triangular shape. Tears are anechoic or hypoechoic
fissures, but this may be a difficult call to make on US. However, US excels in deter-
mining if the posterior labrum is normal [88]. The presence of a paralabral cyst
implies a torn labrum. The posterior labrum is best visualized with the shoulder in
external rotation since this maneuver augments posterior recess distension, thereby
enhancing labral tear detection. However, external rotation may also enlarge a
suprascapular vein, which may be mistaken for a paralabral cyst (see the Pitfalls
section below). Paralabral cysts may also be seen in the spinoglenoid notch. With
the improved resolution of newer US equipment, it is possible to create images of
all four quadrants of the glenoid labrum [87]. Nonetheless, MRA is the best imaging
modality to evaluate the glenoid labrum [89, 90].
Glenohumeral Joint
Visualization of the GHJ is best in the posterior view. Even so, US is not a premier
technique for GHJ evaluation [8]. Simple radiographs are superior for the assess-
ment of arthritic changes. However, US may demonstrate cartilage loss, osteo-
phytes, humeral head bony cortex irregularity, or joint recess synovitis [8].
Glenohumeral Joint Instability and Dislocation
Humeral head instability or dislocation out of the glenoid fossa causes pain, dys-
function, and accelerated osteoarthritis. Radiographs are the gold standard for the
evaluation of dislocation. However, in experienced hands, US can be confirmatory
and accurate for diagnosing dislocation as a stand-alone modality [91]. Ultrasound
is also a valid tool for evaluating GHJ instability [92, 93]. Ultrasound also helps to
look for related pathology, such as rotator cuff tears. The cause of GHJ dislocation
may be a single significant trauma, repetitive lower-grade injury (e.g., throwing ath-
lete), ligamentous laxity, or neuromuscular causes such as axillary nerve injury [94].
226 10 Shoulder
1. Anterior dislocation: About 95–97% of shoulder dislocations are anterior [95,

96]. Radiographs, including axillary views, are diagnostic [96]. Anterior disloca-
tion may produce a Hill-Sachs deformity, a depressed area at the posterolateral
aspect of the HH from recurrent impact against the edge of the anterior glenoid
rim. Ultrasound may diagnose this deformity reliably [97].
2. Posterior dislocation: This accounts for 1–4% of shoulder dislocations, may be
challenging to identify, and is easily missed [98, 99]. The posterior glenoid may
impact the anterior HH, causing a fracture, which is referred to as a “reverse
Hill-Sachs lesion” or “McLaughlin lesion” [100, 101]. Additional axillary radio-
graphs may be needed to diagnose a posterior dislocation. An undetected poste-
rior dislocation may lead to chronic pain and disability [102]. In contrast to
Hill-Sachs lesions, McLaughlin lesions are not readily evaluated by US; this
requires a CT or MRI [101].
3. Superior dislocation: The HH tends to migrate superiorly with a complete SST
tear since the latter structure depresses the HH. With a substantial SST tear, the
HH may ascend to abut the inferior acromial surface, accelerating the develop-
ment of osteoarthritis [103, 104]. The plain radiograph and MRI can delineate
superior migration of the HH [105].
4. Inferior dislocation: Dynamic US has been favorably compared with stress
radiography for assessing and quantifying inferior glenohumeral laxity [93].
5. Multidirectional instability: This is due to excessive laxity in more than one
direction and may be due to recurrent shoulder injuries. Such instability may be
asymptomatic in elite swimmers [106]. Multidirectional instability may have
neurologic causes, including cerebrovascular accidents [107].
Suprascapular Nerve
With a SLAP tear, a paralabral cyst may develop and compress the nerve in the
spinoglenoid notch (SGN), causing weakness of the infraspinatus muscle. If you see
a cyst in the SGN, be concerned about a SLAP tear, and consider an MRA of the
shoulder to look for a labrum tear [108]. However, varicose veins in the SGN may
imitate a paralabral cyst. Varicosities may also compress the nerve, but varicosities
collapse with internal shoulder rotation (cross-arm maneuver) and expand with
external rotation [4]. Be cautious about placing a needle into a cystic structure in
this area since this may be a vein. Even if you successfully decompress a paralabral
cyst, the cyst will often recur unless you address the underlying cause, which is the
labral tear [8]. Since the SGN is a relatively deep structure, a cyst in the SGN may
be hypoechoic and not as well-demarcated as a more superficial cyst.
Inflammatory Disease
Rheumatoid arthritis and other inflammatory arthropathies may cause effu-

sion or synovitis in the bursae, joint recesses, and the LHBT sheath, as well as bone
erosion of the humeral head [109]. For polymyalgia rheumatica, US detection of
Pitfalls 227
bursitis, effusion, and tenosynovitis is incorporated in the 2012 EULAR/ACR clas-

sification criteria to improve sensitivity and specificity [110, 111].
Pitfalls
1. Always request and directly review baseline shoulder radiographs before the
US. Review the history and do a focused physical exam. Have the patient indi-
cate the pain location and shoulder positions that exacerbate the pain [112].
2. Use a ballpoint pen to draw topical bony landmarks before the exam.
3. Rotator cuff tears are common. The unambiguous rotator cuff tear you detect
may not be the source of the patient’s pain.
4. Based on the limits of the technology, if a rotator cuff tear is not observed, it
may still be present. It is best described in reports as “no tears were visualized.”
Be aware that the former location of a completely torn SST may fill in with
hyperechoic material or the SASDB, fooling even experienced sonographers.
5. Angle the probe downward (heel-to-toe maneuver) to look at the footprint of
the SST in LAX to minimize anisotropy [112].
6. The heel-to-toe maneuver is also critical in evaluating the LHBT in LAX to
correct for anisotropy since the tendon angles downward more distally [113].
7. Tilting the probe back and forth is critical when evaluating the LHBT in TAX
within the bicipital groove to avoid the effect of anisotropy [112].
8. In LAX view, don’t mistake a horizontal hypoechoic band in the anterior SST
for an intrasubstance tear. This line separates the superficial from the deeper,
flatter fibers of the SST. On TAX, the superficial fibers may appear as a
hypoechoic ovoid defect due to anisotropy, so don’t mistake this for a tear or
tendinosis [17].
9. Do not forget to externally rotate the shoulder to enhance the detection of small
to moderate-sized GHJ effusions in the posterior recess [36].
10. The suprascapular vein may distend in external rotation, mimicking a paral-
abral cyst. It will collapse in internal rotation, whereas a cyst will not [4]. Color
flow Doppler will help to delineate this.
11. Completely evaluate the entire width and insertion of the SST and the
SSCT [112].
12. Do not diagnose tendinosis or tears at the junction of the SST and IST on the
GT since this is where the two tendons intermingle at different angles, resulting
in a hypoechoic insertional overlap due to anisotropy [112].
13. Do not misconstrue the normal echotexture of the cross-section of the SSCT as
having tears [112, 113].
14. Ultrasound can look at the glenoid labrum to a degree, but not nearly as accu-
rately as an MRA.
15. In the LAX view, the SASDB and the SST sometimes blend and may be chal-
lenging to differentiate. To discern the two, follow the SASDB distally since
it extends beyond the GT [113]. Remember, the SASB lacks fibrillar
echotexture.
228 10 Shoulder
16. A dislocated or completely torn LHBT is a challenge to detect. Look for the
fibrillar tendon and search for a dislocated LHBT and retracted tendon stumps.
If you are uncertain, describe that this structure is not visualized [10, 113]. If
you do not locate the LHBT in the groove, track the LHBT from distal to proxi-
mal, starting with the musculotendinous junction.
17. Verify tendon tears in both TAX and LAX views; double-check for anisotropy
mimicking a tear.
18. Don’t mistake a CIS for calcific tendinopathy or a double contour sign (see
Chap. 8).
19. Don’t mistake the SASDB or the deltoid muscle for an intact SST with com-
plete SST tears. In this situation, the deltoid muscle, or the SASDB, occupies
the absent tendon position. Verify that the putative SST inserts on the GT and
has fibrillar echotexture.
20. Tendinosis of the SST may be confused with a tear. Tendinosis is hypoechoic
with a swollen tendon. Tears may also be hypoechoic, but they are often
anechoic and have a thin tendon [3].
21. Look very carefully at the anterior SST footprint, a common location for tears.
22. It is difficult to determine if an intrasubstance tear at the SST footprint on the
GT extends to the tendon’s articular surface (and thus would be called a partial
thickness, articular side tear, or “rim-rent” tear). Look for a CIS or simply fluid
in the tear and apply probe pressure to see if the anechoic discontinuity reaches
the articular side.
23. Look for clues to amplify your suspicion of SST tears. For instance, GT cortical
irregularity increases the probability of a tear.
24. The SASDB, if distended, may mimic LHBT sheath effusion or tenosynovitis,
but the SASDB, in this case, will not surround the LHBT; it will lie superficial
to the LHBT.
Method
At our institution, we have adopted the four regions “ASAP” protocol (anterior,
superior, anterolateral, and posterior) used by others [8]. Use a 12 MHz linear probe
except for the GHJ, which may require an 8 MHz frequency to reach a 6 cm depth.
Obtain static, moving, and dynamic imaging. Many views are labeled “A, B, C,
etc.,” which are standard views, but may not apply to every patient and are left to the
examiner’s discretion.
Position The patient sits with the elbow flexed to 90° and the forearm and hand on
the lap. The palm is up. Palpate the shoulder and, with a ballpoint pen, mark off
specific landmarks: the proximal biceps tendon (long head) in the biceps groove, the
coracoid process (if palpable), the ACJ, and the most lateral portion of the acro-
mion. These markings are beneficial for landmark identification during an examina-
Method 229
tion. The examiner may be in front of or behind the patient, whichever is more
comfortable.
Crass vs. Modified Crass (Fig. 10.8)
These are shoulder positions designed to bring the proximal SST out from under the
acromion. The Crass position is more extreme; the patient’s hand is placed in the
contralateral back pocket or across the mid-back. This maneuver rotates the
humerus, bringing the GT more anteriorly. The modified Crass (Middleton) position
is less extreme; the patient’s hand is placed in the ipsilateral back pocket. Most
patients with shoulder pain will not tolerate the Crass position. but do well with the
modified Crass position. For that reason, we favor the modified Crass position. The
advantages and disadvantages of these two positions are summarized as follows:
Crass
• More accurate for SST tear size in both planes [114]
–– Does not fully evaluate the anterior third of the SST
–– Difficult for patients with shoulder pain to maintain
Modified Crass
• Overestimates SST tears in LAX but is accurate in TAX [114]
–– Better demonstrates the intra-articular LBHT and the RCI
–– Easier for the patient in pain to tolerate
Fig. 10.8 Crass vs.

modified crass
230 10 Shoulder
rotocol Image 1: Long Head Biceps Tendon, Transverse ±

P
Place the probe transverse to the upper arm, centered over the LHBT, which sits in
the bony biceps groove, between the LT and the GT. The LT is medial, more pointed,
and perhaps more superficial. Move the probe proximally until you see the tendon’s
ovoid, hyperechoic fibrillar cross-section. Observe for fiber hypertrophy, disruption,
or loss of echogenicity. Tilt the probe to eliminate anisotropy. The oval appearance
of the LHBT indicates its intraarticular location. Turn on PD if you suspect an acute
tendon tear or synovitis. Just deep to the LHBT is the SGHL. Superficial to and sur-
rounding the LBHT is the CHL. The CHL combines with the SGHL to form the
biceps pulley system, or sling.
Next, move the probe in TAX more distally, where the LHBT assumes a round or
semiround shape and the biceps groove is better delineated. The LHBT is now
extra-articular. Look at the tendon sheath surrounding the LHBT for effusion or
synovitis. A small amount of fluid is normal, but it should not surround the tendon
[17]. Just superficial to the LHBT is the THL, which is composed of fibers from the
SST and SSCT. If you do not see the tendon, it may be dislocated (over the LT
superficial to or within the SSCT) or completely torn. Toggle the probe to sharpen
the image. Look for LHBT swelling, which may indicate tendinosis. If you see
excess fluid surrounding the LHBT, this is strong, albeit inconclusive, evidence for
a rotator cuff tear or a GHJ effusion. Power Doppler may indicate tenosynovitis or
perhaps an acute tendon tear. You will often visualize a branch of the anterior cir-
cumflex humeral artery on PD, just lateral to the LHBT. Avoid this vessel when
injecting the LHBT sheath.

1: Long head biceps
tendon, transverse ± power
Doppler
Method 231
With the patient’s elbow tucked into the body, you can passively externally and
internally rotate the forearm to see if the LHBT subluxes or even completely dislo-
cates medially over the LT. In the case of an SSCT tear, the LHBT may move into
the SSCT [4]. Resume the prior arm position and then move the probe in TAX dis-
tally until the tendon blends into the biceps muscle. Note that the biceps groove
becomes shallower. Look for the tendon of the pectoralis major muscle, seen as a
horizontal hyperechoic structure just superficial to the LHBT, near the tendon-
muscle junction.
rotocol Image 2: Long Head Biceps Tendon, Longitudinal ±

P
Next, center the probe on the LHBT and turn it 90° to see the fibrillar LHBT in
LAX. Slowly move the probe in a proximal LAX slide, repositioning the probe
slightly medially and then laterally as you go to visualize the entire width of the
LHBT. Make sure that the distal portion of the probe is angled downward in a
“heel-to-toe” orientation that parallels the diving tendon. Look for loss of normal
echotexture (tendinosis vs. tears), fluid in the distal tendon sheath (a small amount
of fluid is normal), calcium deposits in the tendon sheath, and tenosynovitis. Power
Doppler may help define acute tenosynovitis. Evaluate for partial or complete
tears. If the tear is complete, there may be tendon retraction. The clinical finding of
“Popeye’s sign” occurs with a complete tendon tear; US may confirm a ball
of muscle.

2: Long head biceps
tendon, longitudinal ±
power Doppler
232 10 Shoulder
rotocol Image 3: Subscapularis Tendon,

P
Longitudinal + Dynamic View (Fig. 10.11)
For conceptual expediency, we break with convention and describe LAX and TAX
views with respect to the SSCT itself. However, according to strict nomenclature,
the views should be described with reference to the upper arm axis. Therefore, what
we describe as our TAX view of the SSCT is the traditional LAX view, and vice versa.
To visualize the superior portion of the broad SSCT:
1. The patient keeps the elbow tucked in and then externally rotates the forearm to
rest on a stable surface.
2. Move the probe back into a TAX position with respect to the upper arm, start at
the biceps tendon groove, and perform an LAX slide medially (over the LT) to
see the first bird’s beak view, the SSCT insertion on the LT.
3. Medially, visualize the curved hyperechoic coracoid process.
Inspect the SSCT fibers for tears and the humeral head for bony irregularities.
Look for subcoracoid bursal (SCB) fluid or thickening. The SCB is anterior to the
SSC muscle and inferior to the coracoid process. It does not normally communicate
with the GHJ, but may connect with the SASDB. If you do not see the curved, bony
hyperechoic coracoid process, move the probe medially until it appears, since this
verifies that you are looking at the superior portion of the SSCT.
Have the patient keep the elbow tucked into the body while you gently internally
rotate the forearm and thereby the shoulder. Look for impingement of the
SSCT, which normally glides smoothly under the coracoid process. Look for an
enlarged SCB, which may be just superficial to the SSCT. If the SSCT does not slide
under the coracoid and does not appear to impinge, this may indicate adhesive

3: Subscapularis tendon,
longitudinal +
dynamic view
Method 233

4: Subscapularis tendon,
transverse
capsulitis. Only rarely is the SSCT truly impinged under the coracoid. Perform a
slight distal TAX slide to see the inferior portion of the SSCT and examine those
fibers for tears and loss of echotexture. The coracoid process disappears. A slight
lateral LAX slide and toggling the probe will sharpen the insertion on the LT.
rotocol Image 4: Subscapularis Tendon, Transverse

P
(Fig. 10.12)
Next, rotate the probe 90° to look at the SSCT in TAX (officially, LAX with respect
to the humerus). This image reveals our first “wagon-wheel” view. Note that you see
tendon (hyperechoic) alternating with muscle (hypoechoic). These are not tears!
You often see three pure tendon sections of the SSCT in this view. Move the probe
in a medial TAX slide to examine the proximal portion of the tendon. Then, move
the transducer laterally to look at the more distal portion of the tendon and its inser-
tion on the LT.
rotocol Image 5: Acromioclavicular Joint, Longitudinal ±

P
The patient then loosely hangs the arm downward. Place the probe parallel to and
above the clavicle, over your ink marks delineating the ACJ in LAX. Look at the
joint space and alignment. Look at the acromioclavicular ligament if it is visible.
Ascertain if the joint capsule is abnormally tented or distended. Hyperechoic
234 10 Shoulder

5: Acromioclavicular joint,
Doppler
fibrocartilage may sometimes be seen within the joint space. Acromial or distal
clavicle osteophytes may be noted superiorly. You may see synovitis and bone ero-
sion here in cases of RA. Os acromiale may be seen on the superior acromion. It
appears to be “a double ACJ.” Use PD if there is joint capsule distension.
Perform a dynamic exam if there is a question of instability [8]. The patient places
the hand of the extremity onto the contralateral shoulder to achieve cross-arm adduc-
tion, which may cause localized pain. Ultrasound may show significant joint narrow-
ing. If there is a widening of the ACJ, compare it with the other, presumably
unaffected side. Excessive widening may indicate an acromioclavicular ligament tear.
rotocol Image 6: Supraspinatus Tendon, Distal Acromion,

P
Longitudinal + Dynamic View (Fig. 10.14)
With the probe in the same LAX position, perform a lateral LAX slide; the distal
acromion is medial, and the bird’s beak of the SST is lateral. The probe is at a 45°
angle to the shoulder. Focus on the bird’s beak and the bony cortex of the distal
acromion. Each structure may be a bit out of focus. Inspect the location of the
SASDB just superficial to the SST. Take the patient’s forearm, bend it 90°, and
gently grasp it near the elbow. The patient points the thumb downward [8]. Gradually,
slowly, abduct the humerus to 90° as the forearm hangs downward. Watch the SST
and SASDB glide under the acromion. You and the patient may need to practice this
a bit since most patients with shoulder pain will guard and not initially permit the
examiner to freely move the shoulder until it is clear that the passive movement is
Method 235

6: Supraspinatus tendon,
distal acromion,
longitudinal +
dynamic view
slow and gentle. If there is impingement, note whether bursal fluid, the SASDB, or
the tendon bunches up (“rug under the door sign”) [115]. With impingement, the
patient almost always feels pain under the probe. This positive sonopalpation sign is
helpful if this maneuver reproduces the patient’s pain since asymptomatic bunching
is clinically irrelevant. Note that the GT may directly contact the acromion [4, 112].
If the SST does not slide under the acromion and does not impinge, this may indi-
cate adhesive capsulitis [40].
rotocol Image 7: Supraspinatus Tendon, Coracoacromial

P
Ligament, Longitudinal + Dynamic View (Fig. 10.15)
There may also be SST impingement under the CAL [4]. While focusing on the
SST, perform a TAX slide inferiorly until the bony distal acromion disappears. The
distal end of the transducer will need to be directed slightly downward to visualize
the fibrillar SST. Passively abduct the arm as done for Protocol Image 6 and look
for impingement under the CAL. You may see fluid within the SASDB fluid bunch-
ing up, accompanied by pain reproduction. The SASDB impingement under the
CAL may occur with or without concomitant impingement under the distal
acromion.
236 10 Shoulder

7: Supraspinatus tendon,
coracoacromial ligament,
longitudinal +
dynamic view

8: Rotator interval,
modified Crass position
rotocol Image 8: Rotator Interval, Modified Crass Position

P
(Fig. 10.16)
To visualize the RCI, the patient places the hand into the ipsilateral back pocket
(modified Crass position) to bring the SST out from under the bony acromion. The
elbow should be tucked into the body (adducted) and pointing backward. Place the
Method 237
probe in TAX to the humerus anteriorly over the ink marks of the LHBT and aim the
medial end of the transducer toward the ipsilateral nipple [3]. Visualize the oval
cross-section of the LHBT (intra-articular portion) again, along with the SSCT
medially and the SST laterally. This view best defines the intra-articular portion of
the RCI. A slight distal TAX slide reveals the LBHT with a more rounded appear-
ance; this is the extra-articular portion of the RCI.
rotocol Image 9a: Supraspinatus Tendon, Distal Anterior,

P
With the patient still in the modified Crass position, center the probe over the LHBT
and rotate the proximal end of the probe toward the distal end of the clavicle while
keeping the center of the probe and your focus on the LHBT. Watch the LHBT
elongate and visualize as much of the LHBT in LAX as possible. Next, move the
probe in a lateral TAX slide to see the large bird’s-beak of the SST insertion
on the GT.
The anterior SST is a common area for tendon tears [112]. Carefully examine the
distal anterior portion of the SST at its insertion on the SF of the GT. The hyper-
echoic bony SF is concave, with the distal portion of the concavity being somewhat

9a: Supraspinatus tendon,
distal anterior, longitudinal
± power Doppler
238 10 Shoulder
elongated and a bit flattened. Look at the GT for irregularities in the bone since this
may heighten suspicion of an SST tear. When looking at the SST in LAX, the goal
is to sharpen and “fill in the blanks” of the fibrillar SST by alternatively performing
heel-to-toe and tilting probe maneuvers.
At the insertion of the anterior portion of the SST on the SF, there is a very thin
hypoechoic line due to the SST insertional fibers’ downward curve; this causes
anisotropy. If you see a large anechoic area, then heel-to-toe the probe downward to
verify an SST footprint tear. A footprint tear is an intrasubstance tear unless it
extends to the bursal or articular sides. Note the loss of fibrillar echotexture from
tendinosis or tears. Fluid may fill a tear, making it more conspicuous. Look for a
CIS if there appears to be an articular-sided tear [112]. Measure the length and loca-
tion of any tear and observe for any calcium deposition. Look at the distal portion
of the SASDB, which may contain effusion or be thickened, perhaps indicating
synovitis. Look for any flattening or concavity of the substance of the normally
convex SST, which may indicate SST volume loss from a tear. Sometimes the bursa,
peribursal fat, or overlying deltoid muscle dips down into a torn area. The more
medial hyperechoic bone is the HH, covered by anechoic hyaline cartilage. Turn on
the PD to look for bursal synovitis or acute SST tears.
Avoid mistaking a horizontal hypoechoic band in the anterior SST for an intrasu-
bstance tear. This line separates the superficial from the deeper, flatter fibers of the
SST [17].
rotocol Image 9b: Supraspinatus Tendon, Distal Posterior,

P
Next, remain in LAX and perform a slow posterior TAX slide to look at the middle
facet and the posterior SST. The bird’s beak persists, but is smaller and sharper at
the end. The middle facet will be flatter, and there may be some hypoechoic areas of
the SST near the insertion on the GT. These areas, often mistaken for small tears or
tendinosis, are normal interdigitation of the insertional fibers of the IST coming
from a different direction, causing anisotropy. These thin hypoechoic lines may
resemble zebra stripes [112]. Perform probe maneuvers (heel-to-toe and tilting) to
“fill in the blanks” to avoid misinterpreting anisotropy for tendinosis or a tendon
tear. Be aware that the SST is about 2.5 cm wide, and you need to scan its entire
girth [112]. Again, the first 1.5 cm of the SST lateral to the biceps groove is “pure
SST,” but beyond that, the IST fibers may intermingle, causing anisotropy, simulat-
ing tendinosis, or tears [116].
Method 239

9b: Supraspinatus tendon,
distal posterior,
Doppler

9c: Supraspinatus tendon,
proximal posterior,
Doppler
rotocol Image 9c: Supraspinatus Tendon, Proximal Posterior,

P
Next, move the probe proximally in an LAX slide until the SST fibers disappear
beneath the bony distal acromion. Use the same probe maneuvers to “fill in the
blanks” as before, and turn on the PD if necessary.
240 10 Shoulder

9d: Supraspinatus tendon,
proximal anterior,
Doppler
rotocol Image 9d: Supraspinatus Tendon, Proximal Anterior,

P
With the most proximal portion of the probe abutting the bony acromion, perform a
TAX slide anteriorly (medially), and you will quickly lose sight of the bony acro-
mion. You are now looking at the proximal anterior portion of the SST, which runs
deep to the CAL. Carefully scan this portion of the SST.
rotocol Image 10a: Supraspinatus Tendon, Anterior,

P
Next, rotate the probe into TAX and place it in a position to once again visualize the
RCI (Protocol Image 8). The patient remains in the modified Crass position. Move
the transducer with a slight lateral LAX slide to center it on the SF of the GT to
visualize the anterior portion of the SST; this is the second “wagon-wheel” view.
Scan the tendon proximally in TAX for evidence of tears, splitting, or tendinosis.
The average SST is about 6 mm in thickness. You may see the RC, which is a hyper-
echoic curved line running along the deepest portion of the SST. It may be mistaken
for a calcium deposit. Also, remember that the superficial SST fibers are oriented
differently from the deeper, flatter fibers and may normally appear as a hypoechoic
ovoid defect due to anisotropy; don’t mistake this area for a tear or tendinosis [17].
Check the SASDB for fluid, thickening, and peribursal fat indentation/flattening/
bulging. Flattening or concavity of the usually convex SST itself may indicate
Method 241

10a: Supraspinatus tendon,
anterior, transverse,
modified Crass position
volume loss, a good indicator of a possible SST tear. The SASDB does not usually
communicate with the GHJ, but may do so after a full-thickness SST tear. Scan the
HH and the covering hyaline cartilage for irregularities; note if there are any cal-
cium deposits within the cartilage. The SST should be scanned proximally and then
distally to the insertion on the GT. You have reached the insertion on the GT when
tendon fibers drop off, replaced with bony cortex.
rotocol Image 10b: Supraspinatus Tendon, Posterior,

P
Refocus on the SF and perform a slight posterior LAX slide to visualize the flatter
MF. Then start a slow TAX slide proximally to scan the entire posterior portion of
the SST. The posterior SST fibers will disappear once you have reached the hyper-
echoic acromion. Remember that the posterior part of the SST inserts on the MF and
is interspersed with fibers from the IST. The IST fibers are oriented differently from
the SST, causing anisotropy that mimics a tear or tendinosis. As a general rule, start-
ing at the intra-articular LHBT and moving in a posterolateral direction, the first
1.5 cm of the SST in TAX is considered “pure SST” without interdigitating IST
fibers [116]. Again, if you recognize the flatter MF, you are looking at the SST, the
IST, or an overlap area of both.
242 10 Shoulder

10b: Supraspinatus tendon,
posterior, transverse

11a: Infraspinatus tendon
and muscle, proximal,
longitudinal
rotocol Image 11a: Infraspinatus Tendon and Muscle,

P
Proximal, Longitudinal (Fig. 10.23)
The patient places the hand on the thigh in a neutral position with an upward palm
as positioned for Protocol Image 1. Place the probe on the posterior shoulder
about a 2-3 cm caudal to the posterior acromion. The medial aspect of the
Method 243
transducer is rotated downward, resulting in a 35-45° angle. You will need more
depth to look at the posterior shoulder. Try to visualize the curved HH with a lin-
ear probe at its lowest frequency, but switch to a curvilinear transducer if neces-
sary. For a moment, focus on the curved hyperechoic surfaces of the HH and the
glenoid. Then concentrate more superficially on the IST in a longitudinal view.
Inspect the IST fibrillar echotexture for tears, tendinosis, and calcium deposits.
Perform a medial LAX slide to visualize the proximal portion of the IST, the myo-
tendinous junction, and the ISM.
rotocol Image 11b: Infraspinatus Tendon, Distal, Longitudinal

P
(Fig. 10.24)
With the transducer still at a 35–45° angle, perform a superolateral LAX slide to
look at the IST insertion on the middle facet (posterior aspect) of the GT. Ask the
patient to keep the elbow tucked in and externally rotate the forearm about 30° to
visualize a bird’s beak insertion. Again, look carefully for tendon tears, tendinosis,
and calcium deposits. Slow internal and external rotation of the shoulder reveals
insertional integrity.

11b: Infraspinatus tendon,
distal, longitudinal
244 10 Shoulder

12: Teres minor tendon,
longitudinal
rotocol Image 12: Teres Minor Tendon, Longitudinal

P
(Fig. 10.25)
If your examination requires an evaluation of the TMT, go back to the transducer

position for Protocol Image 11a and then perform a TAX slide in a caudal direc-
tion, maintaining the same oblique angle. The patient’s hand should be resting on
the thigh (neutral shoulder rotation). The TMT, a bit more superficial than the IST,
inserts into the IF of the GT. The bird’s beak insertion is small. Passive internal and
external shoulder rotation will check for the insertional integrity of the TMT.
rotocol Image 13: Posterior Glenohumeral Joint, Longitudinal,

P
Internal + External Rotation ± Power Doppler (Fig. 10.26)
The patient places the hand on the contralateral shoulder to produce internal rota-
tion. Reestablish Image 11a, the IST in LAX. Rotate the transducer to a horizontal
position. Perform small cephalad and caudal TAX slides until you visualize the
hyperechoic curved cortex of the HH and the smaller hyperechoic bony cortex of
the glenoid. Between these two bones lies the triangular, hyperechoic posterior gle-
noid labrum. Clarify the labrum borders by toggling the probe. The superficial edge
of the labrum is the joint capsule, which extends laterally over the humeral cartilage.
Observe for tears, maceration (disruption), or paralabral cysts. Use the highest fre-
quency that will still enable you to visualize the labrum. The time-gain control may
Method 245
a b
Fig. 10.26 (a, b) Protocol Image 13: Posterior glenohumeral joint, longitudinal, internal + exter-
nal rotation ± power Doppler
be useful to elucidate posterior labrum echotexture. Report if you do not see the
labrum; it may not be well visualized with a larger body habitus. If there is a tear,
use the PD to determine if it is acute.
Next, perform a dynamic scan to evaluate for an effusion in the posterior recess
of the GHJ. With the elbow tucked into the chest, the patient slowly externally
rotates the forearm to see if an effusion distends the posterior recess joint capsule.
Anechoic fluid will be seen superficially and anteriorly to the labrum in external
rotation, but a large effusion will distend the posterior recess even in a neutral posi-
tion. An effusion height (measured from the HH to the IST) >3 mm is abnormal
[117]. External rotation may enhance posterior glenoid labrum visualization as well.
rotocol Image 14: Spinoglenoid Notch, Longitudinal + Power

P
Doppler (Fig. 10.27)
Perform a medial LAX slide to assess the hyperechoic SGN. The SGN connects
the supraspinatus and infraspinatus fossae [8]. The “U-shaped” notch is deep to the
IST myotendinous junction. Slightly rotate the transducer to delineate the SGN
sharply. The suprascapular artery and nerve are occasionally seen in this notch [4].
Power Doppler may assist in locating the artery; however, the nerve is challenging
to see. A paralabral cyst in the notch implies a glenoid labrum tear. The cyst can
entrap the suprascapular nerve [4]. An enlarged suprascapular vein may simulate a
paralabral cyst in external rotation, so turn on the CF to delineate this. Do a dynamic
maneuver; if this is varicosity, it should collapse when the shoulder is internally
rotated [4].
246 10 Shoulder

14: Spinoglenoid notch,
longitudinal + power
Doppler
rotocol Image 15 (Optional): Infraspinatus and Teres Minor

P
Muscles, TAX (Fig. 10.28)
The patient’s hand should be resting on the thigh (neutral shoulder rotation). Rotate
the transducer so that it is parallel to the spine. Perform a medial TAX slide to see
the bony cortex of the scapula edge. Then perform a slow caudal LAX slide to look
for a bony protuberance (the posterior scapula ridge). At this protuberance, the ISM
and TMM are adjacent and easily delineated, separated by a diagonal fascial plane
[3]. When assessing for atrophy of the ISM, compare its thickness at the posterior
scapula ridge to that of the TMM. The normal ISM should be about twice the size
of the TMM [3]. A hyperechogenic ISM (compared with the echogenicity of the
TMM) may also indicate atrophy.
Method 247

15: Infraspinatus and teres
minor muscles, TAX
Complete Shoulder Ultrasonic Examination Checklist

□ Protocol Image 1: Long head biceps tendon, transverse ± power Doppler.
□ Protocol Image 2: Long head biceps tendon, longitudinal ± power Doppler.
□ Protocol Image 3: Subscapularis tendon, longitudinal + dynamic view.
□ Protocol Image 4: Subscapularis tendon, transverse.
□ Protocol Image 5: Acromioclavicular joint, longitudinal ± power Doppler.
□ Protocol Image 6: Supraspinatus tendon, distal acromion, longitudinal +
dynamic view.
□ Protocol Image 7: Supraspinatus tendon, coracoacromial ligament, longitudinal
+ dynamic view.
□ Protocol Image 8: Rotator interval, modified Crass position.
□ Protocol Image 9a: Supraspinatus tendon, distal anterior, longitudinal ± power
Doppler.
□ Protocol Image 9b: Supraspinatus tendon, distal posterior, longitudinal ± power
Doppler.
□ Protocol Image 9c: Supraspinatus tendon, proximal posterior, longitudinal ±
power Doppler.
□ Protocol Image 9d: Supraspinatus tendon, proximal anterior, longitudinal ±
power Doppler.
□ Protocol Image 10a: Supraspinatus tendon, anterior, transverse.
□ Protocol Image 10b: Supraspinatus tendon, posterior, transverse.
□ Protocol Image 11a: Infraspinatus tendon and muscle, proximal, longitudinal.
□ Protocol Image 11b: Infraspinatus tendon, distal, longitudinal.
□ Protocol Image 12: Teres minor tendon, longitudinal.
□ Protocol Image 13: Posterior glenohumeral joint, longitudinal, internal + exter-
nal rotation ± power Doppler.
□ Protocol Image 14: Spinoglenoid notch, longitudinal + power Doppler.
248 10 Shoulder
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Chapter 11
Anterior Ankle

1. Anterior ankle pain
2. Dorsal foot pain
3. Foot or toe extension dysfunction
4. Evaluate for underlying systemic diseases such as rheumatoid arthritis (RA),
spondyloarthropathy (SpA), or crystalline disease
1. What is causing foot dorsum or anterior ankle pain?
2. What is the cause of foot dorsum pain/swelling?
Basic Anatomy (Fig. 11.1)
Bones, Joints, Recesses of the Hindfoot and Midfoot
1. Tibiotalar joint
2. Chopart joint (transverse tarsal joint) is the talonavicular joint combined with
the calcaneocuboid joint.
3. Naviculocuneiform joint
4. More distally, the three cuneiforms and the cuboid bone articulate with the meta-
tarsal bones to form the Lisfranc joint (tarsometatarsal joints).
States Government.

Switzerland AG 2023
256 11 Anterior Ankle
Fig. 11.1 Basic bony

anatomy
Soft Tissue Structures (Fig. 11.2a) [1]
1. Tibialis anterior tendon (TAT)

(a) Origin: proximal tibia and interosseous membrane
(b) Insertion: base of the first MT and medial cuneiform
2. Extensor hallucis longus (EHL) tendon
(a) Origin: fibula and interosseous membrane
(b) Insertion: distal phalanx of the first toe
3. Extensor digitorum longus (EDL) tendon
(a) Origin: tibia, fibula, interosseous membrane
(b) Insertion: phalanges of the second-fifth toes
4. Peroneus tertius
The peroneus tertius is an accessory tendon that, if present, may lie within the
same tendon sheath as the EDL [2].
(a) Origin: fibula and interosseous membrane
(b) Insertion: base of the fifth MT or the cuboid
5. Anterior tibial artery (ATA), which becomes the dorsalis pedis artery (DPA)
at the anterior ankle joint
6. Deep peroneal nerve (DPN)
7. Superior extensor retinaculum (SER)
8. Inferior extensor retinaculum (IER)
9. Anterior recess superficial to the tibiotalar joint
Basic Anatomy 257
a b
Fig. 11.2 (a) Soft tissue structures (b) Soft tissue structure mnemonic
Soft Tissue Information
A mnemonic for many of the soft tissue structures of the anterior ankle, from medial
to lateral (Fig. 11.2b):
“Tom Has Nine Awesome Dogs” (TAT, EHL, nerve, artery, EDL)
Additional Tips
1. The anterior tendons are held in place by the SER and IER.
2. The ATA goes beneath the SER to become the DPA between the EHL and EDL
tendons.
3. The DPN medially follows the ATA/DPA, then may cross to the lateral aspect of
the artery [3].
Clinical Comments
Ligaments
The anterior ligaments that are sonographically accessible are the anterior talofibu-
lar ligament (ATaFL) and the anterior inferior tibiofibular ligament (AITiFL).
Tendons
The extensor tendons are rarely affected by tendinosis and tenosynovitis; complete
tears are even less common [4]. These disorders arise from trauma, overuse, infec-
tions, or inflammatory conditions. Since the extensor tendons follow linear courses,
uninjured tendons exhibit pristine fibrillar echotexture; however, of all the extensor
tendons, the TAT is most often damaged [5].
Tendinosis
With tendinosis, the tendon swells with heterogeneous hypoechoic distortions

within the ordinarily well-defined linear fibrillar echotexture, but it is impossible to
delineate low-grade tears [6, 7]. Power Doppler (PD) activity may be appreciated,
indicating local hypervascularity [6]. Comparison with the unaffected contralateral
tendon is quite helpful. The TAT may develop tendinosis distally near its two inser-
tions, which may present as medial midfoot burning [8]. Osteophytes might exert an
abrasive effect on the undersurface of the distal TAT, causing hypoechoic swelling,
sometimes with PD activity and pain during sonopalpation.
Tenosynovitis
Tenosynovitis is represented on ultrasound (US) as thickening of the tendon sheath

with increased anechoic or hypoechoic synovial fluid within the sheath, perhaps
with PD activity [3, 6]. Tenosynovitis may be due to repetitive trauma, infection, or
inflammatory polyarthropathy such as RA or SpA. Tenosynovitis of the EDL occurs
most frequently; next is the TAT [9]. The myotendinous junction of the EHL may be
mistaken for tenosynovitis. The extensor tendons present with serous tenosynovitis,
in contrast to the medial and lateral ankle tendons, which frequently show prolifera-
tive tenosynovitis. If you can visualize the TAT sheath, then tenosynovial pathology
is likely [8].
Tears
Anterior tendon tears are uncommon and may be caused by impingement from
osteophytes or orthopedic hardware, local steroid injection, penetrating trauma, or
possibly a fracture [5, 6, 8, 10]. Dynamic US reveals the underlying impinging
source if the tendon has not been torn completely. The TAT is the most frequently
torn of the extensor tendons, with tears occurring beneath the extensor retinaculum
[6]. Partial tears include longitudinal splitting, best delineated when filled with
anechoic fluid; however, if debris fills the fissure, it may be impossible to differenti-
ate them from tendinosis. Complete tears may show retraction, gap separation on
dynamic US, or present as a dorsal foot mass [6].
Muscles
Herniation
Muscle herniation most often occurs in the lower leg, primarily affecting the tibialis
anterior muscle [8]. Causes include athletic activities, occupational stresses, direct
trauma, and chronic compartment syndrome. The muscle protrudes through a defect
in the fascia and the subcutaneous fat, presenting as a soft tissue mass that may be
mistaken for a tumor. Dynamic US, in which the patient contracts the muscle, will
delineate defect margins and, thus, the true nature of the mass.
Atrophy
Tibialis anterior muscle atrophy may occur with direct trauma, common peroneal
neuropathy, knee dislocation, fibula fracture, tumors, or a tight cast. Ultrasound
objectively evaluates foreleg muscle atrophy by assessing thickness compared to the
contralateral side [8]. Atrophic muscle tissue converts to fat and fibrosis, increasing
reflectivity and rendering the echotexture hyperechoic.
Calcification
Foreleg calcification presenting as a soft tissue mass occurs with calcific myonecro-
sis, hematoma, synovial sarcoma, or osteosarcoma [8]. Calcific myonecrosis from
blunt trauma may appear as a hypoechoic mass with internal irregular linear echoes
and posterior acoustic shadowing. Other causes of soft tissue calcification in the
foreleg are myositis ossificans, posttraumatic pseudoaneurysms, dermatomyositis
or polymyositis, tumoral calcinosis, and diabetic myonecrosis [8].
Anterior Retinacula
The SER and the IER, composed of deep fascia, stabilize the extensor tendons dur-
ing muscle contraction to prevent bowstringing [11]. The anterior retinacula (AR)
may be injured playing sports, acutely, or by repetitive microtrauma. The AR is best
seen sonographically with the probe transverse (TAX) to the foot so that the linear,
thin hyperechoic fibrillar bands are displayed superficial to the tendons. The aver-
age normal AR thickness is approximately 1 mm [12]. Injured retinacula appear
thickened and hypoechoic; hyperemia, delineated by PD, may be present in acute
and subacute stages. Chronic injuries lead to retinacular loosening and secondary
tendon instability. Retinacula integrity can be assessed with dynamic US by pas-
sively or actively dorsiflexing the foot or digits [11]. The AR may also play a role in
stabilizing the subtalar joint since AR injuries are implicated in subtalar instability.
Anterior Tibiotalar Joint
Effusion
Joint effusion may result from infection, fractures, inflammatory polyarthritis, gout,
hemophilia, sickle cell disease, and amyloid arthropathy [13]. Anechoic or
hypoechoic fluid beneath the fat pad is best seen on a sagittal view with the ankle in
maximal plantar flexion [4, 6, 13]. The effusion displaces or floats the fat pad ante-
riorly (superficial on the US image). Be aware that up to 3 mm of synovial fluid may
be expected within the anterior recess, so do not mistake physiologic synovial fluid
for effusion [4, 14]. Likewise, do not mistake anechoic cartilage for effusion.
To differentiate effusion from cartilage, note that compared to talar dome carti-
lage, fluid appears anechoic, and transducer pressure displaces fluid but not carti-
lage [4]. For effusion detection, US is more sensitive than lateral radiography, but
less sensitive than magnetic resonance imaging. Clues about the cause of effusion
may be in plain sight: osteophytes indicating osteoarthritis, intra-articular tophi, a
double contour sign (DCS) of gout over the talar dome cartilage, or perhaps carti-
lage erosion from inflammatory polyarthritis.
Echogenic fluid can mimic synovial proliferation or active synovitis [15].
Synovitis may or may not have PD activity; however, effusion lacks PD. Hence, PD
activity argues for synovitis. It is best to evaluate for effusion and PD activity at both
the lateral and medial aspects of the tibiotalar joint; these areas are more superficial
than the deeper central portion of the joint [9].
Dynamic imaging with dorsiflexion and plantar flexion may reveal movement of
an effusion; synovitis will not reveal such action [15]. Plantar flexion facilitates
synovial fluid flow from the posterior recess into the anterior tibiotalar joint and
recess [3, 7, 13, 16]. Directly compressing an effusion with the probe may differen-
tiate simple from complex effusions since there may be debris swirling with the
latter [14]. Consider fluid aspiration under direct US guidance; however, synovial
fluid aspiration is mandatory if an infection is of concern.
Synovitis
Synovitis of the tibiotalar joint is located deep to the fat pad in a similar location to
an effusion; however, US reveals synovitis to be slightly hypoechoic compared to
anechoic effusion. Synovitis appears as soft tissue thickening and has minimal to no
compressibility to probe pressure [16]. Tibiotalar joint synovitis in RA appears as a
hypoechoic area superficial to the talar dome [9]. Synovitis causes include infec-
tion, inflammatory joint disease, osteoarthritis, and noninflammatory synovial pro-
liferation [7]. The latter can be seen with pigmented villonodular synovitis (PVNS)
and synovial osteochondromatosis. PD may indicate acute inflammation.
Erosion
Erosion of the cartilage and bone of the tibiotalar joint occurs less commonly than
one might expect.
Arthritis
Here, we refer to causes of tibiotalar arthritis, not periarticular mimics of ankle

arthritis.
1. Osteoarthritis
Osteoarthritis occurs much less commonly in the ankle than in the knee and
hip [17]. When it does happen, it is not usually primary but secondary to pre-
ceding physical trauma or the end-stage result of RA, hemochromatosis, recur-
rent bleeding, avascular necrosis, or postinfectious arthritis. The low prevalence
of primary osteoarthritis of the ankle is surprising considering its weight-bear-
ing burden. A putative biomechanical protective factor may be the difference in
cartilage density and stiffness over the talar dome compared with other
joints [18].
2. Spondyloarthropathy
This includes axial and peripheral SpA, psoriatic arthritis, and SpA associ-
ated with inflammatory bowel disease [17].
3. Rheumatoid arthritis
Please see the section below on RA.
4. Other systemic rheumatic diseases
While both lupus and systemic sclerosis may cause ankle arthralgia, occa-
sionally, true ankle synovitis is noted with systemic sclerosis [17].
5. Infectious arthritis
(a) Bacterial
The ankle is the third most infected joint after the knee and hip [19].
Gonococcal disease is also included in this category [17].
(b) Viral
This includes hepatitis B and C, chikungunya, and human immunodefi-
ciency virus infections [17].
(c) Mycobacterial [17]
6. Crystal disease
Gout frequently involves the ankle [17]. Calcium pyrophosphate deposition
disease (CPPD), although more common in the wrist and knee, may sometimes
involve the ankle.
7. Sarcoidosis
Older literature describes frequent ankle involvement in sarcoidosis; how-
ever, closer inspection reveals that sarcoidosis more commonly surrounds soft
tissue with panniculitis and tenosynovitis instead of directly involving the
ankle [17].
8. Intra-articular bodies
These bodies, comprised of cartilage or bone, are caused by damage to the
articular surface. They may be asymptomatic or painful. Causes include osteo-
chondral fractures, osteochondritis dissecans (see below), PVNS (see below),
osteoarthritis (see above), and synovial osteochondromatosis [20]. Loose bodies
are located within the joint capsule or the tendon sheath [4]. Dynamic US con-
firms loose body movement.
Rheumatoid arthritis usually starts in the hands, but 20% of patients first develop
symptoms in the foot or ankle [21]. Nearly 90% of RA patients develop foot or
ankle involvement during the disease course [22]. Sonographic evaluation of teno-
synovitis, erosion, and PD activity informs diagnosis, prognosis, and treatment
selection [23]. When evaluating RA in the ankle, the regions of interest are the tib-
iotalar and talonavicular joints, the tendons, and the tenosynovial sheaths. Fluid
distending the recesses by more than 3 mm in the tibiotalar joint or 2.6 mm in the
talonavicular joint is regarded as an effusion [24]. An inflammatory effusion may
also present in the subtalar joint, best viewed laterally at the sinus tarsi (see Chap.
13 for more information). Definitions of tendinosis, erosions, synovitis, and tenosy-
novitis, as well as scoring of PD vascularity, synovitis, tenosynovitis, and erosions,
have been described in Chaps. 1 and 5.
In one study of 63 patients with active disease, evaluation of the tibiotalar and
talonavicular joints, ankle tendons, and tenosynovial sheaths revealed RA ankle
involvement in 44% [22]. The right (dominant) ankle had more findings than the left
ankle, indicating the need to evaluate both ankles. Tenosynovitis was the earliest
sign of RA and correlated with disease activity scores. However, bone erosion was
associated with disease duration and the presence of rheumatoid factor. A second
study compared 100 symptomatic ankles in 74 patients with early RA (<6 months
duration) and established RA (>6 months duration) [25]. Nearly 70% of the early
RA patients had tenosynovitis, which most often occurred in the medial flexor ten-
dons. Thus, the shorter the disease duration (and perhaps less exposure to treat-
ment), the greater the chance of detecting ankle tenosynovitis.
If RA is suspected in a patient with ankle pain, US examination of ankle joints
and tendon sheaths may aid in diagnosis. When a patient presents with a clinically
inflamed ankle, evaluate the contralateral ankle to look for subclinical signs of syno-
vitis or tenosynovitis.
Masses and Cysts
Ultrasound will locate a mass in relation to other structures and will define the inter-
nal echogenic character (e.g., cystic, solid), compressibility, vascularity, and the
presence of nearby nerves and vessels [6]. Serial US examinations can follow
masses over time to verify stability or changes in size. However, other modalities,
or ultimately, a biopsy may be necessary to determine the precise diagnosis.
Ultrasound can help safely guide the biopsy [6]. Neoplasms are rare on the foot
dorsum. Several other entities may present as a foot mass.
Ganglion Cyst
The familiar, benign ganglion cyst may be uni- or multiloculated and has a narrow
stalk connecting it to a nearby joint or tendon sheath [6]. Ganglia appear anechoic
or hypoechoic on US, but may be so tense as to mimic a solid mass or bone on pal-
pation [26].
Nerve Sheath Tumors
These may occur on the DPN in the anterior compartment or the superficial pero-
neal nerve at the distal fibula [16]. Schwannomas and neurofibromas are the most
common types of peripheral nerve sheath tumors. Usually benign, they rarely
undergo malignant transformation. Most are homogeneous and hypoechoic on
US. Other sonographic features include posterior acoustic enhancement, target
appearance (hyperechoic center with hypoechoic periphery), and PD activity.
These tumors may mimic ganglion cysts; however, if PD activity is present, a
ganglion cyst is ruled out [6, 16]. Benign and malignant peripheral nerve sheath
tumors have variable sonographic features; thus, sonography cannot reliably
differentiate the tumor type or presence of malignancy [27]. Sonographic imaging

of the nerve entering the mass (peripheral nerve continuity) supports the diagnosis
of a peripheral nerve sheath tumor [6, 27].
Gouty Tophus
A tophus may appear as a localized mass on an extensor tendon [6]. Tophaceous

material within the tendon may cause it to lose its typical fibrillar pattern; there may
also be associated tenosynovitis and surrounding soft tissue swelling. There may or
may not be a classic sonographic picture of a tophus. Clinical history and physical
examination, as well as the presence of a DCS in the ankle or other joints, support
the diagnosis. Fluid aspiration and sometimes direct aspiration of the mass with
polarized microscopic analysis may be diagnostic.
Retained Foreign Body
A foreign body may incite a reactive inflammatory mass depicted on US as a hyper-

echoic foreign body surrounded by a hypoechoic rim [6]. The foreign body itself
may produce reverberation artifacts if it is smooth and flat [28]. Acoustic shadowing
may be seen if the body is irregular with a small, curved radius.
Complete Tendon Tear
A complete tendon tear with retraction may produce a mass on the foot dorsum [6].
Extensor Muscle Herniation
See Muscle Disorders, Herniation, above.
Calcium-Containing Masses
See Muscle Disorders, Calcifications, above.
Pigmented Villonodular Synovitis
Also known as a tenosynovial giant cell tumor or a giant cell tumor of the tendon
sheath, PVNS is a rare, localized, potentially aggressive lesion involving the
synovial lining of joints, tendon sheaths, or bursae [29]. PVNS occurs more often
in the knee, hand flexor tendons, and hip than in the foot or ankle. Due to the high
recurrence rate (up to 50%), some authors refer to this condition as a semi-malig-
nant tumor [30]. In the foot, PVNS may occur in the ankle joint, the tenosy-
novium, or other areas [31]. The lesion may present as monoarticular arthritis or
as a palpable, painful or painless mass. Magnetic resonance imaging (MRI) is the
most useful noninvasive means of diagnosis; however, it is sensitive but nonspe-
cific. A biopsy is often necessary. Radiography may reveal localized bony erosion
[32]. Ultrasound shows the relationship of the nodule to the adjacent tendon dur-
ing dynamic evaluation. The mass is usually homogeneous, lobulated, and
hypoechoic, with internal vascularity on PD. Maintain a high index of suspicion
of any painless or painful mass in the foot and ankle, despite the rarity of this
condition [31].
Aneurysm/Pseudoaneurysm
Vascular injury may follow direct trauma, ankle arthroscopy, or extreme plantar
flexion or inversion [33]. Such damage may present as swelling, hemarthrosis, vas-
cular insufficiency, a pulsatile mass, or a compartment syndrome and may result in
severe pain, ulceration, or ischemia. Doppler US accurately detects injury to the
anterior tibial artery; however, a transfemoral arteriogram is the gold standard for
diagnosis [6, 33, 34].
Abscess
The sonographic appearance of an abscess may be hyper- or hypoechoic, often with

an echogenic rim and perhaps hyperemia [6]. The abscess lacks internal Doppler
flow. Transducer pressure may produce swirls of complex fluid.
Lipoma
These are well-defined, mildly hyperechoic, ovoid masses parallel to the skin sur-
face that lack internal blood flow on Doppler evaluation [5]. The appearance may
overlap with other masses, and MRI is typically diagnostic.
Subcutaneous Tissue
Edema
On US, hypoechoic fluid separates soft tissue and creates a marbled appear-
ance [6].
Subcutaneous Gas
Due to infection or invasive intervention, subcutaneous gas produces reflective foci

with shadowing [6].
Anterior Ankle Impingement Syndrome
A common clinical syndrome due to synovial tissue crowding the anterolateral

recess and tibiotalar joint space, anterior ankle impingement syndrome (AAIS), is
associated with bone and soft tissue abnormalities [35, 36]. This condition is often
due to repetitive microtrauma injuries with dorsiflexion, occurring in soccer players,
gymnasts, runners, and ballet dancers [35]. There is often previous joint instability
[37]. Direct ankle trauma may also be the trigger. Cartilage or osteochondral lesions
may result in the abnormal growth of scar tissue and synovial abnormalities [38].
Anterior ankle impingement syndrome may culminate in chronic anterior ankle
pain, soft tissue swelling, pain with motion (especially dorsiflexion), or decreased
range of motion [35, 36]. Dorsiflexion may increase pain since it reduces articular
joint space volume [39]. Premature ankle osteoarthritis and spur formation are also
associated with AAIS, although cause and effect are not always clear.
Imaging delineates associated ligament injuries, articular cartilage damage to the
talar dome, intra-articular foreign bodies, and peroneal tendon disorders [36].
Radiographs may show spurs at the distal tibia or talus; however, the presence of
bony spurs is insufficient for the diagnosis. MRI shows synovial hypertrophy and
talofibular ligament damage, while MR or CT arthrography further increases diag-
nostic accuracy. Ultrasound is less accurate than the above contrast studies, but may
be helpful [36]. Ultrasound may detect a preexisting anterior talofibular ligament
injury. Sonopalpation causing pain over a synovial mass may be diagnostically use-
ful. PD activity within a synovial mass implies an underlying pathological origin
[40]. Initial conservative treatment includes rest, physical therapy, and shoe modifi-
cation [35]. Injection guided by US may be beneficial [36]. Surgical procedures are
often necessary, including arthroscopic procedures [41].
Osteochondritis Dissecans
Persistent pain after an ankle sprain should prompt consideration for AAIS, instabil-
ity, and osteochondral lesions [42]. Osteochondritis dissecans (OCD) of the dome
of the talus may cause chronic posttraumatic ankle pain [43]. Delay in diagnosis and
treatment of OCD may cause loose body arthritis and long-term morbidity [44].
OCD results from sudden impacts causing bone contusions or prolonged repetitive
Method 267
microtrauma such as excessive weight-bearing [43]. Such bony trauma causes a

secondary microscopic fracture, bone marrow edema, and eventual detachment of
the osteochondral fragment with intra-articular loose body formation. The patient
complains of vague pain exacerbated by weight-bearing, swelling, stiffness, and the
sensation of ankle instability and giving way. The diagnostic gold standard is the
MRI [45, 46]. If traumatic ankle pain becomes chronic, the US finding of a large
ankle effusion should heighten suspicion of OCD [43].
Pitfalls
1. Evaluate the anterior joint recess over the tibiotalar joint with the foot in plantar
flexion since this maximizes detection of joint effusion.
2. In a patient with persistent pain after an ankle sprain, consider impingement
syndrome, instability, and osteochondral lesions [42].
3. Don’t overlook OCD in a patient with a history of an ankle sprain or other ankle
trauma who has persistent ankle pain, but presents with only a tibiotalar effu-
sion on US.
4. Do not mistake cartilage for effusion of the tibiotalar joint.
5. When evaluating a tibiotalar joint effusion, do not neglect to perform PD, com-
press the effusion with the probe, and compare it with the contralateral, nor-
mal side.
6. There may be a cartilage interface sign (CIS) over the talus with a tibiotalar effu-
sion [47]. CIS may imitate a DCS. In contrast to a DCS, the CIS is very thin and
will disappear with a slight change in the angle of insonation.
7. Clues about the cause of effusion may be in plain sight: osteophytes indicating
osteoarthritis, intra-articular tophi, a DCS over the talar dome cartilage, or per-
haps cartilage erosion from inflammatory arthritis.
8. If RA is suspected in a patient with ankle pain, do not neglect to perform an US
examination of the ankle joints and tendon sheaths to evaluate for synovitis or
tenosynovitis to support the diagnosis.
9. If RA is suspected of causing ankle monoarthritis, the lack of inflammatory find-
ings in the contralateral ankle should raise doubts about the diagnosis.
Method
Although located anteriorly, the anterior talofibular ligament and the anterior infe-
rior tibiofibular ligament are included on the lateral foot US examination.
The patient is supine with the knee flexed at 90°, the foot flat on the exam table,
and slightly rotated inward. Choose a linear probe with an ankle or mid-depth preset.
rotocol Image 1: Tibialis Anterior Tendon + Extensor Hallucis

P
Longus, Transverse ± Power Doppler (Fig. 11.3)
Place the probe in TAX at the medial aspect of the distal anterior tibia. Move the
probe distally in a TAX slide. The hyperechoic tibial surface will drop off to
reveal another hyperechoic bone that looks like a mountain with a gentle slope
and a steep cliff on the medial aspect. This is the medial process of the proximal
Fig. 11.3 Protocol Image 1: Tibialis anterior tendon + extensor hallucis longus, transverse ±
power Doppler
Method 269
talus, the talar dome. The appearance on US has been likened to the corner of the
roof of a pagoda.
Look at the soft tissue structures superficial to the bone. To verify the identity of
the structures, turn on the PD to see the more central DPA. Superficial and slightly
medial to the DPA is the EHL; medial to the EHL is the TAT. This is the “home
base” position, and if the probe is sufficiently long, you should be able to simultane-
ously see the TAT, the EHL, the neurovascular bundle, and at least part of the
EDL. The SER is superficial to all three tendons, is hyperechoic, and exhibits
anisotropy. If present, the accessory peroneus tertius tendon is lateral to the EDL
and often lies within the same synovial sheath [2]. Tilting the probe will diminish
tendon anisotropy.
Center the probe on the large TAT. Manually dorsiflex and invert the foot to
verify tendon movement and that this tendon is, in fact, the TAT [16]. Look for
tendon sheath fluid or tenosynovitis surrounding the TAT. Examine the hypoechoic
or anechoic cartilage covering the surface of the talar dome for damage. Verify
the identity of the EHL by passively flexing and extending the large toe. The
musculotendinous junction of the EHL is somewhat distal; thus, the EHL muscle
may sometimes be confused with tenosynovitis. The DPA is deep and slightly
lateral to the EHL. Contiguous to the DPA, the small DPN may at first be medial
to and then cross over to the lateral aspect of the artery. Use PD to confirm the
DPA location since the DPN may be difficult to discern. The DPN displays a
honeycomb appearance; tilting the probe delineates the nerve by exploiting its
anisotropy. If necessary, the DPN and the DPA can each be followed distally in
TAX view.
Hints:
1. The TAT is double the size of the other extensor tendons. Normal ankle tendon
synovial sheaths cannot be delineated.
2. The DPN is adjacent to, or “hugs,” the medial aspect of the DPA. At this level, it
is often medial to the DPA, but sometimes it is on the lateral aspect of the DPA.
rotocol Image 2: Extensor Digitorum Longus, Transverse ±

P
Next, move the probe laterally to center it over the EDL. This tendon or tendon
group is lateral to the EHL. Verify the tendon identity by observing tendon move-
ment while manually dorsiflexing the second through fifth toes [16]. Note several
tendons on their course to the digits and examine them for tenosynovitis.

2: Extensor digitorum
longus, transverse ± power
Doppler

3: Tibiotalar joint, dorsalis
pedis artery, longitudinal ±
power Doppler
rotocol Image 3: Tibiotalar Joint, Dorsalis Pedis Artery,

P
Once again, go back to “home base” and center the probe on the DPA. Rotate the
probe 90° to see the DPA in a longitudinal (LAX) view. This is the first look at the
tibiotalar joint. Note the two curved hyperechoic bones, the hypoechoic or anechoic
cartilage covering the more distal talus, and the mildly hyperechoic triangular or
hammock-shaped fat pad within the joint space. Superficial to the fat pad is the
Method 271
hyperechoic joint capsule, which is sometimes challenging to discern. The joint

recess is deep to the fat pad and may typically contain a small amount of anechoic
synovial fluid. An abnormal effusion is noted when the fat pad is elevated or “floats”
on the excess liquid. This image may demonstrate joint effusion, synovitis, DCS, or
cartilage erosion. This joint may typically contain up to 3 mm of synovial fluid [4,
14]. Next, perform a TAX slide medially and laterally to examine the entire width
of the tibiotalar joint in LAX. The cartilage covering the talar dome is usually thin-
ner laterally [48].
Hints:
1. Maximal plantar flexion will expose more of the talar dome cartilage and accen-
tuate an abnormal effusion.
2. There may be osteophytes on the distal tibia or the talus, which may be associ-
ated with AAIS.
3. The shallower lateral and medial aspects of the tibiotalar joint may best demon-
strate effusion.
rotocol Image 4: Talonavicular Joint, Longitudinal ± Power

P
Doppler (Fig. 11.6)
Move the probe more distally, still in LAX, and center on the talonavicular joint. If
necessary, examine the full breadth of this joint by performing a slow medial and
then lateral TAX slide, similar to what was done for the tibiotalar joint. Turn on PD
to look for active synovitis.

4: Talonavicular Joint,
Doppler

5: Tibialis anterior tendon
over tibitotalar joint,
Doppler
rotocol Image 5: Tibialis Anterior Tendon over Tibiotalar

P
Return to the “home base” view in TAX and center the probe on the TAT. Turn the
probe 90° into LAX. Move the transducer distally, moving it slightly laterally and
medially as you go to see the complete TAT in LAX. As you look at the talus from
proximal to distal, you will sequentially visualize the tibiotalar joint, the talar dome,
the talar neck, the talar head, and finally, the talonavicular joint.
rotocol Image 6: Extensor Hallucis Longus over Tibiotalar

P
Perform a TAX slide laterally to center the probe over the EHL. Move the probe
proximally and then distally, as well as laterally and medially, to visualize the
full EHL. Look for the fibrillar echotexture of the EHL, but be aware that the
Method 273

6: Extensor hallucis longus
over the tibiotalar joint,
Doppler
EHL muscle may be present at the tibiotalar joint; the muscle may mimic
tenosynovitis.
rotocol Image 7 (Optional): Tibialis Anterior Tendon at

P
Naviculocuneiform Joint, Longitudinal ± Power Doppler
Return to the view in Protocol Image 5 for the LAX view of the TAT. Continue to
move the probe in LAX distally, following the TAT. The next joint distal to the talo-
navicular joint is the naviculocuneiform joint. Technically, you are looking at the
navicular-medial cuneiform joint.
rotocol Image 8 (Optional): Tibialis Anterior Tendon at Medial

P
Cuneiform Insertion, Longitudinal ± Power Doppler
Continue to move the probe distally, following the TAT, to see its insertion on the
distal medial cuneiform. Turn on PD at the insertion if there is a question of active
enthesitis.
rotocol Image 9 (Optional): Tibialis Anterior Tendon at Medial

P
Cuneiform Insertion, Transverse ± Power Doppler
Turn the probe 90° into the TAX position. Perform small proximal and distal TAX
slides to examine the tendon and to see the part of the TAT that inserts on the medial
cuneiform. This image may require tilting the probe to minimize anisotropy.
Confirm any PD findings in transverse view.
rotocol Image 10 (Optional): Extensor Hallucis Longus at

P
Insertion on First Phalanx, Longitudinal ± Power Doppler
Return to the view in Protocol Image 6 for the LAX view of the EHL. Move the
probe distally in LAX to visualize the insertion on the first digit phalanx. Power
Doppler may help delineate active enthesitis.
rotocol Image 11 (Optional): Extensor Hallucis Longus at

P
Insertion on First Phalanx, Transverse ± Power Doppler
Turn the probe 90° into TAX to examine the tendon insertion on the dorsum of the
first toe’s distal phalanx. Again, confirm any PD findings.
rotocol Image 12 (Optional): Extensor Digitorum Longus at

P
Tibiotalar Joint, Longitudinal ± Power Doppler
Return to the “home base” view of Protocol Image 1 in TAX and center the probe
on the EDL. Note how this flat tendon divides into four slips, each inserted sepa-
rately on the bases of digits 2–5. Lift each toe manually to ensure that you look at
the correct tendon. Rotate the probe 90° to see the EDL in LAX. Since this is often
the area of the myotendinous junction of the EDL, you may see muscle, tendon, or
a combination.
rotocol Image 13 (Optional): Extensor Digitorum Longus at

P
Insertion on Digits 2–5, Longitudinal ± Power Doppler
Next, move the probe distally to view the EDL insertions on digits 2–5.
References 275
rotocol Image 14 (Optional): Extensor Digitorum Longus

P
Insertion on the Base of Digits 2–5, Transverse ± Power Doppler
Rotate the probe 90° into TAX to examine the tendon insertion on the dorsum of
each digit 2–5.
Complete Anterior Ankle Ultrasonic Examination Checklist
□ Protocol Image 1: Tibialis anterior tendon + extensor hallucis longus, transverse
± power Doppler.
□ Protocol Image 2: Extensor digitorum longus, transverse ± power Doppler.
□ Protocol Image 3: Tibiotalar joint, dorsalis pedis artery, longitudinal ± power
Doppler.
□ Protocol Image 4: Talonavicular joint, longitudinal ± power Doppler.
□ Protocol Image 5: Tibialis anterior tendon over tibiotalar joint, longitudinal ±
power Doppler.
□ Protocol Image 6: Extensor hallucis longus over tibiotalar joint, longitudinal ±
power Doppler.
□ Protocol Image 7 (optional): Tibialis anterior tendon at naviculocuneiform joint,
longitudinal ± power Doppler.
□ Protocol Image 8 (optional): Tibialis anterior tendon at medial cuneiform inser-
tion, longitudinal ± power Doppler.
□ Protocol Image 9 (optional): Tibialis anterior tendon at medial cuneiform inser-
tion, transverse ± power Doppler.
□ Protocol Image 10 (optional): Extensor hallucis longus at insertion on first pha-
lanx, longitudinal ± power Doppler.
□ Protocol Image 11 (optional): Extensor hallucis longus at insertion on first pha-
lanx, transverse ± power Doppler.
□ Protocol Image 12 (optional): Extensor digitorum longus at tibiotalar joint, lon-
gitudinal ± power Doppler.
□ Protocol Image 13 (optional): Extensor digitorum longus at insertion on digits
2–5, longitudinal ± power Doppler.
□ Protocol Image 14 (optional): Extensor digitorum longus insertion on the base of
digits 2–5, transverse ± power Doppler.
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Chapter 12
Posterior Ankle and Heel

1. Posterior or inferior heel pain
1. What is causing posterior ankle pain?
(a) Is there evidence for an Achilles tendon tear or tendinopathy?
(b) Is there evidence for a systemic disease such as crystalline arthritis (gout,
pseudogout), spondyloarthropathy (SpA), rheumatoid arthritis (RA), etc.?
(c) Is there evidence for bursitis?
(d) Is there evidence for Haglund’s syndrome?
(e) Is there evidence for Achilles paratenonitis, masses, or calcium deposits?
2. What is causing posterior calf pain?
(a) Is there evidence of a muscle or tendon tear?
3. What is causing inferior heel pain?
(a) Is there an inferior calcaneal spur?
(b) Is there evidence for SpA?
(c) Is there evidence for plantar fascial tears, plantar fasciitis, or fibromatosis?
(d) Is there compression of Baxter’s nerve (first branch of the lateral plantar
nerve) [1]?
(e) Is there a mass?
(f) Is the ultrasound (US) exam normal?
States Government.

Switzerland AG 2023
280 12 Posterior Ankle and Heel
Bony Anatomy
The ankle structure evokes an ancient Egyptian pyramid; the base is the heel, or
calcaneus, which contacts the ground. “Calx” is Latin for chalk or limestone. The
ancient Egyptians constructed pyramids with limestone, a material that could sup-
port a great deal of weight. Stubborn people who are recalcitrant are always digging
in their heels. Perched on the calcaneus is the talus, a curved bone similar to an
eagle’s talon. On the back of a United States dollar bill are a pyramid and an eagle,
a convenient mnemonic device.
Posterior Heel Anatomy (Fig. 12.1)
The Achilles tendon (AT), the chief ankle plantar flexor, is formed proximally by the
soleus and medial and lateral gastrocnemius muscles and inserts on the posterior cal-
caneus. The mean AT thickness is 4.3 mm when measured 2 cm proximal to the cal-
caneus [2]. Deep (anterior) to the AT and abutting the proximal posterior calcaneus is
the retrocalcaneal (subtendinous) bursa. It may normally contain fluid measuring up
to 3.4 mm in thickness [2, 3]. The normal retrocalcaneal bursa is comma-shaped [4].
More proximal, Kager’s fat pad (KFP), rests on the calcaneus. Superficial (posterior)
to the AT is the subcutaneous calcaneal bursa (also called the retro-Achilles, pre-
Achilles, precalcaneal, superficial, or Achilles bursa), usually undetectable unless
pathologically distended [3]. The thin plantaris tendon (PT) along the medial aspect
of the AT may be absent in up to 20% of people [3, 5]. The PT may mimic intact AT
fibers in the event of a complete AT rupture [3]. There may be a normal variant acces-
sory soleus muscle in approximately 3% of people, which runs parallel and adjacent
to the anteromedial aspect of the AT near Kager’s fat pad [6]. The tendon inserts into
the AT, or the calcaneus, and appears as a mass displaying muscle echotexture. It may
be asymptomatic, but may also cause pain and swelling after exercise.
Proximal/Posterior Calf Anatomy (Fig. 12.2)
The AT is formed by the gastrocnemius muscles (medial and lateral heads) (MHG
and LHG, respectively) and the deeper soleus muscle [7]. The hyperechoic muscle
fascia separates these unipennate muscles. The long, thin, ovoid PT, variably absent
Bony Anatomy 281
Fig. 12.1 Posterior heel bone and soft tissue anatomy
in normal people, originates from the distal lateral femur [8]. The PT moves distally
from lateral to medial, sandwiched between the MHG muscle and the deeper soleus
muscle. The PT has various insertion points, including the calcaneus or the AT [8].
Again, the PT can be mistaken for intact AT fibers or perhaps even a nerve. The
biomechanical properties of the PT are unclear, but it may be used as a graft in
orthopedic surgery [9].
Fig. 12.2 Proximal calf

anatomy
Inferior Heel Anatomy (Fig. 12.3)
The calcaneus is the primary bony landmark of the inferior hindfoot. The normally
fibrillar plantar fascia (PF) is a ligamentous structure connecting the inferior calca-
neus to the toes and maintaining the foot’s arch. It has three bundles (central, lateral,
and medial), with the maximal normal thickness of the central bundle being
4.0 mm [10].
Fig. 12.3 Inferior heel anatomy
Clinical Comments
Posterior and inferior heel pain complaints are common. History, a physical exam,
and radiographs are the first lines of evaluation. Radiographs may help delineate
fractures, Haglund’s deformity (superior calcaneal prominence), posterior or infe-
rior bony spurs (enthesophytes where ligaments or tendons attach to bone), foreign
bodies, or osteomyelitis. Ultrasound should be the next step if further workup
is needed.
Posterior Heel Potential Ultrasound Findings
1. Haglund’s syndrome consists of calcaneal cortical irregularity with adjacent

subcutaneous and retrocalcaneal bursitis, an abnormally prominent posterosu-
perior calcaneal corner, and associated AT thickening or swelling (tendinosis)
[3, 11]. The calcaneal prominence is often called a “pump bump” (Fig. 12.4).
Radiographs reveal a prominent posterosuperior calcaneus. The US may dem-
onstrate swelling of the distal AT, perhaps with power Doppler (PD) activity
[11, 12]. One or both posterior heel bursae may reveal an anechoic fluid collec-
tion. Ill-fitting shoes produce bony enlargement of the posterior calcaneus and
subsequent soft tissue inflammation, resulting in Haglund’s syndrome [12].
2. Bony spurs (enthesophytes) at the insertion of the AT on the posterior calca-
neus may be associated with osteoarthritis, RA, or SpA [13–15].
3. Crystal disease. Calcium deposits from calcium pyrophosphate deposition dis-
ease (CPPD) may appear within the AT, as can monosodium urate (MSU)
deposits, the latter suggesting gout. Gouty tophi may develop within or outside
the AT or within the two posterior bursae [16–18].
Fig. 12.4 Elements of Haglund’s syndrome
4. Rheumatoid arthritis may produce paratenonitis and retrocalcaneal bursi-

tis [19].
5. Enthesopathy with or without PD activity may be seen at the AT insertion on
the posterior calcaneus or the PF insertion on the inferior calcaneus.
6. Achilles tendon tear (complete or partial). Tears of the AT, often caused by
forceful dorsiflexion, most frequently occur 2–6 cm from the calcaneal inser-
tion, also known as the “critical zone” [20]. For a complete AT rupture, the
decision to treat it surgically or conservatively may be determined by how
closely the two stump ends approximate each other in plantar flexion [21].
Partial tears appear as anechoic or hypoechoic areas or perhaps as clefts with a
fibrillar interruption [3]. An AT thickness greater than 10 mm suggests a partial
tear [3]. Other sonographic signs of an AT tear include distortion of the normal
fibrillar echotexture, PD activity at the edge of a tear, hematoma, and possibly
a gap in the tendon [22]. A healed AT tear may show residual fibrillar echotex-
ture alteration, anterior local bulging, or a hypoechoic area at the site of the tear.
Partial tears may be associated with Haglund’s syndrome.
7. Tendinosis of the Achilles tendon may appear as focal or diffuse hypoechoic
swelling with or without fibrillar disruption; there may also be loss of the ante-
rior concavity of the AT in the transverse plane [23]. Tendinosis most often
occurs in the proximal two-thirds of the AT and is best measured in the trans-
verse axis (TAX) view [24, 25]. Tendinosis may be associated with pain; how-
ever, it is challenging to differentiate tendinosis from a partial thickness AT
tear [12].
8. Power Doppler activity in the AT is abnormal, represents neovascularization,

and may occur with inflammation, tendinosis, paratenonitis, an acute AT tear, or
infection [26]. Keep the foot in a neutral position to avoid extreme tension on
the AT, which may falsely obliterate PD activity [27].
9. Paratenonitis. The AT has no proper tenosynovial sheath, so swelling border-
ing the outside of the AT may be due to paratenonitis. Paratenonitis may appear
as isoechoic/hypoechoic soft tissue thickening or hypoechoic fluid, perhaps
with PD activity [3, 26]. Paratenonitis is best appreciated at the posterior aspect
of the AT [19]. Paratendinopathy is often due to overuse and may occur with AT
degeneration [28].
10. Retrocalcaneal bursitis can be caused by mechanical compression (shoes),
direct or repetitive trauma, gout, RA, SpA, or Haglund’s deformity [29].
Haglund’s deformity impinges on the bursa during ankle dorsiflexion [30].
Another cause of retrocalcaneal bursitis is a misalignment of the subtalar joint
axis [31].
11. Subcutaneous calcaneal bursitis may be seen on US superficial to the AT and
can be due to direct pressure from the back of a shoe [29].
12. Xanthomas are painless soft tissue masses due to fat accumulation. Usually
occurring in the distal AT, xanthomas may be present bilaterally. Ultrasound
reveals a thickened and speckled (reticular) pattern within the AT due to
hypoechoic xanthoma foci [12, 32].
13. Integrity of Achilles tendon repair. After repair, the AT may have heteroge-
neous echogenicity; however, if the fibers are continuous and there is no retrac-
tion on passive maneuvers, the repair is likely intact [33].
14. Calcium deposits within the Achilles tendon may be due to prior trauma
(dystrophic), CPPD, or hydroxyapatite deposition disease.
Proximal Calf Potential Ultrasound Findings
1. “Tennis leg” or MHG muscle tear occurs near the aponeurosis, resulting in dis-
rupted fibers and possible tendon retraction [3].
2. Plantaris tendon tears can occur in conjunction with the MHG muscle tear
or more distally associated with an AT tear. In addition, isolated PT tears
rarely occur but can mimic a partial AT tear, thrombophlebitis, or a ruptured
popliteal cyst [34]. Isolated PT tears are usually benign and do not require
surgery.
3. Other calf injuries, such as those to the soleus, LHG contusion or tear, deep
venous thrombosis, or ruptured Baker’s cyst, may be delineated by US [35, 36].
Inferior Heel Potential Ultrasound Findings
1. Enthesopathy (with or without PD activity) may be seen at the PF insertion on

the inferior calcaneus [37].
2. Hypoechoic thickening (>4 mm) of the proximal PF near the calcaneus may
be due to enthesitis, plantar fasciitis, PF tears, degeneration, or edema. Tears of
the PF may demonstrate partial or complete fiber disruption. However, edema
may obscure these tears on US [38]. Look for PF tears in track and field athletes
and patients previously treated with local corticosteroid injections [39, 40].
Confirm tears with a dynamic US exam to demonstrate the widening of any
gap [1].
3. Plantar fasciitis is suggested by painful enlargement and hypoechogenicity of
the PF near the calcaneal insertion, often with calcaneal cortical irregularities
[38] (Fig. 12.5). Plantar fasciitis is frequently a result of repetitive stress in the
presence of biomechanical risk factors (foot deformities, excess body mass,
improper footwear, etc.). There is a loss of fibrillar echotexture and possibly
increased perifascial soft tissue, calcifications, and hyperemia [38]. The origin is
often degenerative; hence, a better term is plantar fasciopathy. However, SpA
and RA may be associated conditions [41]. The presence of inferior calcaneal
spurs (enthesophytes) may be present, but is not specific for plantar fasciitis
since they occur in asymptomatic people. In one study, the mean PF thickness
was 5.9 mm in patients with plantar fasciitis and 3.3 mm in asymptomatic
controls [42]. Thus, PF thickening greater than 3–4.5 mm is considered abnor-
mal, although comparison with the contralateral asymptomatic side should be
taken into consideration [19]. Thickening of the proximal plantar fascia at the
calcaneal origin is best seen in the LAX view [43].
Fig. 12.5 Plantar fasciitis

4. Plantar fibromatosis (Ledderhose’s disease) is a benign condition that may or

may not cause ambulatory pain in the central, medial, or more distal aspect of the
PF [38, 44] (Fig. 12.6). The proliferation of fibroblasts in the PF may appear as
fusiform nodules of varied echogenicity, often isoechoic or hypoechoic. The
subcutaneous nodules are usually solitary, less than 3 cm in diameter, and well-
demarcated, perhaps with calcium or fluid collection [38]. Ledderhose’s disease
may be associated with Dupuytren’s contracture [45]. The nodules may be
superficial and clinically visible distal to the calcaneus. The nodules are often
bilateral and may demonstrate increased through-transmission and vascular-
ity on PD.
5. Inferior calcaneal spurs (enthesophytes) at the insertion of the PF may be a
primary pain source. Again, inferior calcaneal spurs are not specific to plantar
fasciitis, but may be associated with chronic heel pain in the presence of fat pad
abnormalities [38, 46].
Fig. 12.6 Ledderhose’s

disease
6. Other lesions: Xanthomas, usually asymptomatic nodules with a speckled pat-

tern on US, may occasionally be seen near and within the PF [38, 47]. Likewise,
foreign bodies, inclusion cysts, and adventitial bursae may be sonographically
visualized at the inferior heel.
Lack of Ultrasound Findings with Heel Pain
Medial plantar fascial pain with an unremarkable US examination suggests flexor

digitorum brevis tendinosis (the muscle deep to the plantar fascia) [48]. Another
mimic of plantar fasciitis pain is entrapment of Baxter’s nerve deep to the PF or
between a calcaneal spur and a muscle [49] (see Chap. 14 for more information).
Other conditions such as occult calcaneal stress fracture, vascular disease, heel fat
pad atrophy, or necrosis may mimic plantar fasciitis [50–52].
Pitfalls
1. When examining posterior calcaneal radiographs, look for spurs (entheso-

phytes), since these bony protrusions may form a valley mimicking erosion on
US. Also, remember to look for Haglund’s deformity.
2. Scan the entire surface and verify posterior calcaneal and AT pathology in two
orthogonal views [53].
3. Use a heel-to-toe maneuver at the AT calcaneal insertion to minimize anisotropy,
which can mimic an insertional tear.
4. After a complete AT tear, the medially located PT may migrate posteriorly into
the space previously occupied by the AT. This wandering tendon may mimic
intact AT fibers and mislead the examiner into thinking there is only a partial AT
tear [3].
5. The normal retrocalcaneal bursa may be challenging to visualize, but it is more
detectable when distended by a pathologic process [54]. If this bursa is >2–3 mm,
it may be abnormal.
6. Extreme tension of the AT (foot dorsiflexion) may falsely eliminate PD activity.
7. Ultrasound guidance enhances injection accuracy into the PF. However, for a
procedure such as fenestration of the PF, a tibial nerve block at the medial ankle
will improve patient comfort.
8. The AT and PF may be thickened with diabetes mellitus; PF thickness is particu-
larly affected by body mass [55].
9. When investigating enthesopathy, remember that magnetic resonance imaging
is a valuable adjunct to US since it can detect insertional bone marrow
edema [56].
Method 289
Method
The patient is preferentially prone, with the foot hanging off the table and slightly
dorsiflexed. Choose a linear probe with an ankle or mid-depth preset. The virtual
convex setting will extend the viewing field for the Achilles tendon, the plantar fas-
cia, and the posterior ankle joints if needed.
rotocol Image 1: Achilles Tendon, Longitudinal ± Power

P
Doppler (Fig. 12.7)
Place the probe along the longitudinal axis (LAX) with the distal end over the supe-
rior posterior calcaneus. This position is the “home base.” Move the probe laterally
and medially to encompass the entire width of the AT. Look for the AT insertion on
the posterior calcaneus. The insertion point is approximately 1 cm long and is
hypoechoic or anechoic due to the anisotropy of AT fibers. Use the heel-to-toe
maneuver and slightly increase foot dorsiflexion to diminish anisotropy.
Look for AT tears, swelling, hypoechogenicity, calcifications, MSU aggregates,
or tophi adjacent to or within the AT. Outside the AT, look for bony posterior calca-
neal spurs, bursitis, signs of Haglund’s syndrome, KFP location, calcaneal spurs,

1: Achilles tendon,
Doppler
and paratenonitis. Move the probe proximally to evaluate the entire length of the
AT. The AT will merge into the gastrocnemius-soleus complex at the myotendinous
junction. Recognize the gastrocnemius muscles (medial and lateral heads) and the
deeper soleus muscle. These unipennate muscles are separated by hyperechoic mus-
cle fascia. The MHG is more prominent and is subject to tears in middle-aged ath-
letes (tennis leg). Such tears most often occur at the distal medial head.
rotocol Image 2: Achilles Tendon, Dynamic Scan,

P
Return to the “home base” position of Protocol Image 1. Keep the probe in place
and slowly, passively plantar and dorsiflex the foot to look for AT tears and the rela-
tionship of movement to the enthesis, the KFP, and the two bursae. If there is a sug-
gestion of more proximal pathology, perform this dynamic scan at that location.

2: Achilles tendon,
dynamic scan, longitudinal
Method 291
rotocol Image 3: Achilles Tendon at the Enthesis,

P
Longitudinal + Power Doppler (Fig. 12.9)
Turn on PD and scan the AT calcaneal insertion with TAX slides medially and later-
ally to look for enthesitis. Again, avoid extreme foot dorsiflexion since this may
falsely abate the PD signal.
rotocol Image 4: Achilles Tendon, Transverse ± Power Doppler

P
(Fig. 12.10)
Return to the calcaneus and rotate the probe 90° to TAX. Look for spurs, but be
aware that some degree of posterior calcaneal irregularity is common and is not
truly a spur. Consider PD if indicated. Locate the hyperechoic ovoid AT in cross-
section, tilting the probe back and forth to enhance the hyperechogenicity. A trick to
verify that the visualized ovoid structure is truly the AT is to visualize the AT in
LAX, move the AT to the center, and then rotate the probe 90°.
Next, move the probe proximally to reach the mid tendon. The normal anterior
(ventral) AT should be flat or slightly concave but not convex. Achilles tendinopathy
may be supported by focal thickening, disruption of fibrils, and loss of anterior con-
cavity. If needed, compare this image with the contralateral AT at the same distance
from the calcaneal insertion. A discrepancy in the volume of the AT between two
sides may indicate tendinosis of the enlarged side. Now continue to perform a proxi-
mal TAX slide while following the AT to inspect the myotendinous junction.
Appreciate the emergence of the AT from the deeper lateral and medial

3: Achilles tendon at the
enthesis,
Doppler

4: Achilles tendon,
transverse ± power
Doppler
gastrocnemius muscles and the even deeper soleus muscle. Medial to the AT, the
thin, ovoid plantaris tendon may be seen deep to the gastrocnemius but superficial
to the soleus.
rotocol Image 5: Posterior Tibiotalar Recess,

P
Now, go back to the “home base” position of Protocol Image 1 in LAX, but increase
the depth to look at the deeper posterior tibiotalar and subtalar joints. The lower
frequency enhances bone visualization, and the virtual convex setting extends the
field of view. Passively dorsiflex the foot to open the joint space; this facilitates
detection of an effusion. An effusion may distend the posterior tibiotalar joint recess,
which normally contains a small amount of synovial fluid. The transducer is placed
just lateral to the midline of the posterior heel and tilted to aim the US beam toward
the midline to visualize posterior recess distension [57]. The bulk of the deep mus-
cle just superficial to the joint is the flexor hallucis longus (FHL), not the soleus.
Remember, as you move proximally in the calf, the soleus becomes dominant, and
the FHL muscle mass decreases.
rotocol Image 6: Plantar Fascia Origin, Longitudinal

P
(Fig. 12.12)
Place the probe in LAX at the center of the inferior calcaneus. The probe fre-
quency may need to be further reduced to visualize the calcaneus. Perform
TAX slides medially and laterally to examine the full extent of the fibrillar PF;
rocking the probe will help overcome the significant anisotropy of the PF. The
Method 293
Fig. 12.11 Protocol Image 5: Posterior tibiotalar recess, longitudinal ± power Doppler

6: Plantar fascia origin,
longitudinal
central cord of the PF is just superficial to the flexor digitorum brevis muscle
(FDB). Manually dorsiflexing the ankle may clarify the PF image. Use a heel-
to-toe maneuver (with plenty of gel) to diminish anisotropy, which might
mimic an insertional tear of either the PF or the FDB on the calcaneus. The PF
will lose fibrillar definition near the calcaneal origin, but this is normal if
there is no attendant PF thickening [58].

thickness measurement,
longitudinal
rotocol Image 7: Plantar Fascia Origin, Thickness

P
Measurement, Longitudinal (Fig. 12.13)
Measure the thickness of the plantar fascia. The average PF thickness is 3–4 mm [4,
58]. A comparison with the contralateral foot might be helpful. With plantar fasci-
itis, there may be increased thickness, hypoechoic changes with loss of fibrillar
echotexture, or poorly defined superficial and deep borders of the PF. In one study,
the mean PF thickness was 5.9 mm in patients with plantar fasciitis and 3.3 mm in
asymptomatic controls [42].
rotocol Image 8: Plantar Fascia, Longitudinal + Power

P
Turn on PD to look for active enthesopathy at the origin, which may be from SpA,
but may also occur with the more acute phase of plantar fasciitis [59]. The ankle
should not be maximally dorsiflexed since this may ablate PD activity.
References 295

Doppler
Complete Posterior Ankle Ultrasound Checklist

⎕ Protocol Image 1: Achilles tendon, longitudinal ± power Doppler
⎕ Protocol Image 2: Achilles tendon, dynamic scan, longitudinal
⎕ Protocol Image 3: Achilles tendon at the enthesis, longitudinal + power Doppler
⎕ Protocol Image 4: Achilles tendon, transverse ± power Doppler
⎕ Protocol Image 5: Posterior tibiotalar recess, longitudinal ± power Doppler
⎕ Protocol Image 6: Plantar fascia origin, longitudinal
⎕ Protocol Image 7: Plantar fascia origin, thickness measurement, longitudinal
⎕ Protocol Image 8: Plantar fascia origin, longitudinal + power Doppler
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Ultrasound Med Biol. 2004;30(4):435–40.
Chapter 13
Lateral Ankle

1. Lateral ankle pain or swelling
2. Ankle instability, particularly after sports trauma
3. Loss of ankle eversion and plantar flexion
1. What is the cause of lateral ankle pain?
2. Is an underlying inflammatory condition such as spondyloarthropathy (SpA),
rheumatoid arthritis (RA), or crystal disease causing the pain?
3. Is there a structural, functional, traumatic, or repetitive injury problem causing
lateral ankle pain, such as a ligament or tendon tear, retinaculum tear, or painful
os peroneum syndrome (POPS)?
Basic Anatomy
Bones (Fig. 13.1)
We primarily deal with the fibula, talus, and calcaneus of the lateral ankle.
States Government.

Switzerland AG 2023
300 13 Lateral Ankle

anatomy
Ligaments (Fig. 13.2)
Ligament names are daunting unless we remember two simple rules:

1. Ligament names start with the more prominent bone.
2. Ligaments that bind adjacent bones are logically deeper than superficial liga-
ments that bind nonadjacent bones.
The ligaments of the lateral ankle are divided into high ankle and low ankle liga-
ments [1].
High Ankle Ligaments
1. The anterior and posterior inferior tibiofibular ligaments (AITiFL and

PITiFL) extend from the tibia to the fibula.
2. The accessory anterior inferior tibiofibular ligament (Bassett’s Ligament)
extends from the tibia to the fibula.
3. The interosseous membrane (IOM) (interosseous or middle tibiofibular liga-
ment) stabilizes the tibia and tibia in relation to each other.
Low Ankle Ligaments
1. The anterior and posterior talofibular ligaments (ATaFL and PTaFL) extend
from the fibula to the talus.
2. The calcaneofibular ligament (CFL) extends from the fibula to the calcaneus
and is deep to the peroneal tendons.
Basic Anatomy 301
Fig. 13.2 Ligaments of the lateral foot
Muscles and Tendons (Fig. 13.3)
1. The Peroneus brevis tendon (PBT) inserts on the fifth metatarsal (MT) base
and enables ankle eversion and plantar flexion [2].
2. The Peroneus longus tendon (PLT) inserts on the first MT and medial cunei-
form and facilitates ankle eversion and plantar flexion.
3. An accessory tendon variant, the peroneus quartus tendon (PQT), has a vari-
able insertion, most often onto the lateral calcaneus. The PQT assists ankle ever-
sion, depending on the insertion.
Peroneus means “related to the fibula” [3]. The fibula is shaped like a colossal
hair brooch with a long stem and an oval head. The PBT and PLT tendons usually
arise from their foreleg muscles before curving around the posterior distal fibula;
however, the PLT myotendinous junction is more cephalad than the PBT.
We begin our sonographic focus primarily on the PBT and PLT at a point poste-
rior to the distal fibula. The PBT is more anterior in this location and typically
contacts the posterior fibula or retromalleolar groove. The PBT and the PLT curve
around the groove and extend distally on each side of the peroneal tubercle (PT) on
Fig. 13.3 Muscles/tendons of the lateral foot
their way to their respective insertions. The PBT is shorter (“briefer”), and the “B”
in brevis reminds us that the tendon is a “bone hugger.” In our protocol, we see it
first hugging the distal posterior fibula and, a bit more distally, sitting on top of the
PT on its way to its insertion. The PLT is longer than the PBT and goes lower (“L”)
and under the PBT on the way to its insertion.
Retinacula (Fig. 13.3)
The peroneal tendons are tethered by the superior and inferior peroneal retinacula [4].
1. The superior peroneal retinaculum (SPR) originates at the lateral malleolus
and inserts on the lateral calcaneus.
2. The inferior peroneal retinaculum (IPR) originates from the inferior extensor
retinaculum of the foot dorsum and inserts on the lateral calcaneus.
Clinical Comments
Lateral ankle injuries commonly occur during sports [5]. These injuries include
damage to ligaments, peroneal tendons, and bones. Weight-bearing radiographs
should be performed initially to evaluate for alignment and bone fracture. Ligaments
and tendons of the lateral ankle may be assessed by magnetic resonance imaging
(MRI) and ultrasound (US). MRI is the gold standard for evaluating intra-articular
and osteochondral abnormalities [5]. However, US dynamically evaluates tendon
motion, subluxation, and ligament integrity under stress.
Ligament Injury
About a fifth of sports-related injuries involve the lateral ankle; resultant sprains are
the primary cause of posttraumatic ankle osteoarthritis [6–8]. Ankle sprains from
inversion injuries cause ligament laxity and mechanical joint instability, which pre-
disposes to osteoarthritis, osteophytes, secondary synovitis, and perhaps even ante-
rior ankle impingement [6, 9, 10]. Chronic anterior ankle impingement occurs when
bone spurs and soft tissue thickening impair normal ankle mechanical function,
culminating in constant pain and reduced range of motion [7, 10].
The clinical context of the injury focuses the US exam on the specific ligament
tear(s) that may have occurred. Locate the target ligament(s) to observe the overall
appearance and for evidence of swelling, laxity, hypoechogenic areas, and partial or
complete disruption. Apply stress to assess mechanical strength.
Ultrasound appearance of ligament sprain grades [5]:
Grade 1 sprain is a stretch injury without a tear: US is normal.
Grade 2 sprain is a partial tear; US reveals hypoechoic thickening with a lax or
irregularly contoured ligament [11].
Grade 3 sprain is a complete tear. US demonstrates a lack of continuity (hypoechoic
gap), an absent ligament, and an abnormal stress (dynamic) test [11].
Ultrasound appearance of ligament sprains [5, 8]:
1. Acute partial thickness tears: heterogeneous echotexture and thickening of the
ligament, perhaps with power Doppler (PD) activity.
2. Chronic partial thickness tears: variable appearance with thickening or thin-
ning, ligamentous elongation, or wavy contour.
3. Chronic complete tears will show the absence of the ligament.
Interestingly, the Latin derivation of fibula is “clasp, bolt, pin, peg, or brooch.”
All are fasteners. Without the distal fibula as an anchor for the lateral ankle
ligaments, it is easy to see how quickly lateral ankle stability would unravel.
Remember this role of the distal fibula if a lateral ligament tear is suspected.
Ligament Injury by Location
Low Ankle Ligament Injury
Low ankle ligament sprains typically arise with excessively forceful inversion, such
as landing on the outside of the foot, as may occur when landing after jumping for
a rebound in basketball. Low ankle ligament sprains are much more common than
high ankle ligament sprains.
The following three ligaments listed comprise the Lateral Collateral Ligament
(LCL) complex of the ankle [1]:
1. The ATaFL restricts excess ankle inversion and anterior displacement [5]. It is
the weakest of the three ligaments and is almost always affected in an ankle
sprain [5, 12, 13]. Test for an ATaFL tear with passive plantar flexion and internal
rotation, known as the anterior drawer test [1]. The accuracy of US versus MRI
detection of ATaFL injury is 91% versus 97%; however, sonography may yield
false positives [14]. Be aware that the ATaFL is usually comprised of two bands,
so do not misinterpret this normal anatomy for a longitudinal tear [14].
2. The CFL primarily limits excessive inversion and is second only to the ATaFL in
injury frequency [5, 13]. Although isolated CFL sprains rarely occur, the CFL is
usually torn sequentially after the ATaFL during an inversion-induced injury
[13]. Since the CFL forms a sling for the peroneal tendons, CFL tears often
cause a secondary, telltale peroneal tendon effusion due to proximity [11].
3. The PTaFL works with the ATaFL and the CFL to stabilize the ankle [15]. While
sonographically accessible, the PTaFL is not routinely viewed since it is infre-
quently injured compared with its companion lateral ligaments.
High Ankle Ligament Injury
The ligamentous syndesmosis binding the distal tibia and fibula is located proximal
to the lateral malleolus. This high ankle stabilizer is formed by the following liga-
ments [16, 17]:
1. The AITiFL is the least resistant to shearing forces produced by external rotation
of the fibula [13]. An accessory AITiFL, also known as Bassett’s ligament, is
present in 94% of people and is located inferiorly to the AITiFL [17].
2. The PITiFL is the least often injured high ankle ligament and is best
assessed by MRI.
3. The intraosseous tibiofibular ligament controversially contributes to ankle stabil-
ity [17, 18].
High ankle ligament tears occur when an injury causes the foot and ankle to
externally rotate together, exceeding the mechanical ability of the syndesmosis to
withstand shearing forces acting to separate the fibula from the tibia [19]. Such
force occurs with sudden twisting, cutting, or turning movements, such as when
playing football, soccer, or basketball. High ankle ligament injuries occur in less
than 11% of ankle sprains [20].
The index of suspicion for a high ankle injury should be increased since it may
be challenging to diagnose and delayed treatment results in poor outcomes [11].
Based on the injury history, the presence of an AITiFL injury on US, radiographic
widening between the tibia and fibula, or a lateral malleolar fracture, it is reasonable
to order an MRI to confirm these findings and to examine the PITiFL and the ITL
[5, 20]. Be aware that US diagnostic sensitivity to diagnose a high-grade injury of
the AITiFL is only 66%. Hence, a negative US study warrants an MRI evaluation to
avoid missing this critical diagnosis [21].
Tendon Injury
The MRI is the gold standard for imaging peroneal tendon pathology, including
fixed subluxation or dislocation [5, 8, 22]. Ultrasound is 90% accurate for diagnos-
ing peroneal tendon injuries [23]. An advantage of US over MR is that it delineates
peroneal tendon subluxation/dislocation arising with movement [5].
The PBT and PLT are subject to acute tears and overuse injuries [5, 13]. Tendon
damage (tendinosis), a common occurrence near the lateral malleolus, may be
delineated by hypoechoic enlargement of the tendon with or without fiber disrup-
tion [5]. Tears appear as hypoechoic/anechoic fissures that may reach the tendon
surface or travel longitudinally through the tendon, perhaps splitting the tendon.
Longitudinal tears extend along the long axis and may split the tendon into two half
tendons, typically occurring when retromalleolar peroneal tendon instability causes
recurrent impingement between the tendon and the bone.
A common peroneal tendon sheath is present in the retromalleolar area and may
exhibit tenosynovitis [24]. Tenosynovitis may occur with a tendon tear, repetitive
injury, excessive tendon movement, inflammatory conditions, an enlarged PT, or
other contiguous structural problems [25]. Tenosynovitis of the peroneal tendons is
noted on US by anechoic or hypoechoic fluid in the tendon sheath with or without
PD activity [5]. However, a small amount of tenosynovial fluid in this area is nor-
mal [26].
Peroneus Brevis Tendon
A frank longitudinal split tear affects the PBT more than the PLT [5]. In such a tear,
the PLT may become interposed into the split PBT, and, in a transverse (TAX) view,
the two tendons appear as three tendons and resemble a “hotdog in a bun,” the bun
Fig. 13.4 Longitudinal

split tear of the peroneus
brevis tendon
being the split PBT (Fig. 13.4) [5, 27]. The PBT may also be affected by inflamma-
tory arthropathies such as RA or SpA, producing GS or Doppler evidence of enthesi-
tis at the insertion of the PBT on the fifth metatarsal [28].
Peroneus Longus Tendon
Isolated PLT tears are not typical and, if present, are usually observed near the
cuboid bone [13]. Partial tears may sonographically present as thinning or thicken-
ing of the tendon with hypoechoic loss of normal fibular echotexture. Full-thickness
tears are often associated with tenosynovitis and may be either longitudinal or com-
plete tendon tears with retraction. An os peroneum (OP) is a normal accessory ossi-
cle within the distal PLT near the cuboid bone; a comparable accessory bone on the
medial foot is the os naviculare. An OP fracture may be associated with a distal PLT
tear, instigating a search for PLT tendon stumps [24]. Likewise, a radiographic clue
to a full-thickness PLT tear may be a more proximal than expected location of
an OP [5].
Retinacula Injury
The SPR may be injured in athletes, thus predisposing them to tendon subluxation
or dislocation [5, 22, 29]. This dorsiflexion and eversion injury typically occurs dur-
ing skiing [30]. An acute SPR injury may be mistaken for an ankle sprain due to
swelling, bruising, and pain at the lateral malleolus [13]. The SPR may detach with
or without a bony fragment avulsion in such cases. Alternatively, the SPR may be
rendered lax, allowing abnormal tendon movement, which may become symptom-
atic [13]. A radiographic clue to an SPR injury is an avulsion fracture anchor site on
the lateral distal fibular cortex. Dynamic US maneuvers (ankle dorsiflexion, ever-
sion, or circumduction) may show the migration of one or both peroneal tendons out
of the normal position, indicating a loss of integrity of the SPR (Fig. 13.5) [5].
Pathologic peroneal tendon subluxation diagnosis is crucial since surgery may be
required for successful treatment [5].
Fig. 13.5 Subluxation by dynamic exam

A subtype of peroneal tendon subluxation is intrasheath subluxation, in which

the PLT and the PBT reverse regular positions within the sheath, but remain within
the retromalleolar groove with an intact retinaculum [31]. Reproduction of symp-
toms with sonopalpation in a symptomatic patient with “popping” or “snapping”
during ankle circumduction suggests that the intrasheath subluxation may be patho-
logic [5]. However, peroneal tendon instability is common in asymptomatic
patients [31].
Painful Os Peroneum Syndrome
The OP is an accessory sesamoid bone embedded within the PLT near the cuboid
bone [32]. Prevalence is 5–30% of normal feet [33]. Strong PLT contraction, as
occurs with sudden foot inversion, may damage the OP or the PLT, resulting in pain
[32, 34, 35]. An OP may be seen on an oblique radiograph; on US, it appears as a
hyperechoic curved structure with posterior acoustic shadowing [34, 36]. Painful
OP syndrome (POPS) may display on US as PLT tendinosis, tears, and a fractured
or retracted OP with pain to sonopalpation [37].
Sinus Tarsi Syndrome
The sinus tarsi is an anterolateral funnel-shaped tunnel formed by the talar and
calcaneal bones and is a conduit into the posterior subtalar joint (PSTJ) (see
Fig. 13.1). The sinus tarsi contains ligaments and neurovascular structures essen-
tial for ankle stability. The sinus tarsi syndrome (STS) is a poorly understood
condition associated with ankle ligament damage, instability, or inflammatory
arthritis. It results in pain or tenderness at the lateral hindfoot, and worsens with
ambulation, particularly on uneven ground. The MRI is the diagnostic tool of
choice to evaluate this affliction [38]. The PSTJ can be injected with a US-guided
needle via the sinus tarsi [39]. The PSTJ recess is best evaluated from a posterior
approach; this will detect an effusion and/or the efficacy of injection through the
sinus tarsi (see Chap. 12).
Crystalline Disease
Gout and pseudogout may present focally in the lateral ankle.

(See Chap. 24 for more information.) [5].
Pitfalls 309
Variants
Variants are not uncommon and may lead to painful pathology.
Low-Lying Peroneus Brevis Muscle
A low-lying peroneus brevis muscle belly may cause overcrowding of the soft tissue
in the retromalleolar groove, damaging the SPR; this may result in peroneal tendon
subluxation [32, 40].
Peroneus Quartus Muscle and Tendon
The peroneus quartus muscle (PQM) is an accessory muscle present in 22% of the
population [34]. The origin and insertion of the PQT vary greatly, but the most com-
mon insertion is at the lateral calcaneus [32]. The PQM may crowd the peroneal
tendons in the retromalleolar area, causing tenosynovitis, swelling, pain, and even
tendon tears [24, 36]. The PQM is best visualized on MRI [32]. The PQ is an imita-
tor in the retromalleolar area; it may appear as a third tendon, mimic a low-lying PB
muscle, or even simulate a longitudinal tear of the PBT [41].
Congenitally Shallow Retromalleolar Groove
This condition may facilitate peroneal tendon dislocation or subluxation [35, 42].
Peroneal Tubercle Prominence
Peroneal tubercle hypertrophy may irritate the PLT, causing tenosynovitis and a tear
[32]. An adventitial bursa may also develop over the tubercle, which can become
inflamed and symptomatic.
Pitfalls
1. The normal OP may be bipartite, so look for sonopalpation symptoms or retrac-

tion of the fractured bone segments. Fragment separation of >6 mm suggests an
OP fracture and a full-thickness PLT tear [43].
2. If the AITiFL is torn, consider evaluating the IOM by US or MRI.
3. If there is suspicion of a high ankle tear based upon the mechanism of the injury,
consider an MRI to evaluate further, even if the symptoms improve rapidly. These
tears are difficult to detect on US and may have chronic residuals if not treated
promptly.
4. If a lateral ligament tear is suspected after an inversion injury, focus on the ATaFL
since that is the most injured, and then carefully inspect the CFL and PTaFL.
5. Ultrasound is not as sensitive for ATaFL tear detection as an MRI. Do not neglect
to obtain an MRI if there is lingering suspicion of a lateral ligamentous
sprain [44].
6. Do not forget to compare sonographically detected pathology to the contralateral
side as a reference [45].
7. Since the ATaFL usually comprises two bands, do not misinterpret this normal
anatomy for a longitudinal tear.
8. For a complete evaluation of the CFL, remember to dorsiflex the foot to enhance
visualization.
9. When viewing the PBT and PLT in TAX along the lateral aspect of the ankle,
remember that the two tendons are not parallel; thus, one may appear to be
hypoechoic and imitate a ganglion cyst or other hypoechoic mass. Remember to
tilt the probe to enhance the echogenicity of each circular structure to verify that
you are looking at the tendon.
Method
The patient is supine with the knee flexed at 90° and the foot flat on the exam table.
The foot is slightly inverted to reveal the lateral side of the ankle. An alternate posi-
tion would be to have the supine patient extend the knee, placing the heel on a soft
pad with an upright forefoot. Again, the foot is slightly inverted. A second alterna-
tive is to place the patient in a lateral decubitus position with the lateral ankle facing
upward and a small pillow under the medial ankle. Use a stand-off pad if the con-
tours of the ankle make contact difficult. Set the preset to superficial. Remember,
the first seven protocol images focus on ligaments, and the remainder of the exam is
concerned with tendons.
rotocol Image 1: Anterior Talofibular Ligament,

P
Longitudinal + Anterior Drawer Test (Fig. 13.6)
Place the proximal portion of the probe on the lateral malleolus and aim the distal
portion of the probe toward the large toe until you see the hyperechoic, linear
ATaFL. You may need to sweep the distal end of the probe a bit more medially to
better visualize this ligament. The initial view may show ligamentous anisotropy,
which should aid in identification. Use the heel-to-toe maneuver to diminish
Method 311
Fig. 13.6 Protocol Image 1: Anterior talofibular ligament, longitudinal + anterior drawer test
anisotropy. If the patient has increased body mass, you may need to increase the
depth. Again, the ATaFL usually comprises two bands, so do not misinterpret this
normal anatomy for a longitudinal tear.
To check for ligament integrity, perform the anterior drawer test. Hold the probe
in place to watch the ATaFL. With your other hand, gently force the foot into simul-
taneous plantar flexion and internal rotation to see if the widening of the ATaFL
occurs. If so, this indicates a full-thickness ATaFL tear. This maneuver improves
ligament fibril visualization and thus helps to delineate partial-thickness tears
as well.
rotocol Image 2: Anterior Inferior Tibiofibular Ligament,

P
Longitudinal ± Dynamic View (Fig. 13.7)
Maintain the posterior edge of the probe on the lateral malleolus tip and cranially
rotate the distal edge to see the distal aspect of the hyperechoic tibia. The ankle
should be slightly inverted. Between these two bones, the hyperechoic fibrillar
AITiFL is visualized. The angle of the probe should be about 45°. The AITiFL is
short and thick. Elucidating the fibrillar echotexture may require slight probe rota-
tion and tilting.
Fig. 13.7 Protocol Image 2: Anterior inferior tibiofibular ligament, longitudinal ± dynamic view
An optional dynamic view can be performed if there is clinical suspicion of an

AITiFL tear. Passively dorsiflex the foot and maximally rotate the foot internally
and then externally, observing for a widening of the distance between the tibia and
fibula, which would indicate a complete tear [46]. This maneuver may likewise
illuminate partial tears since it will tighten the ligament to better demonstrate dis-
continuity in the fibrillar echotexture.
rotocol Image 2a (Optional): Accessory Anterior Inferior

P
Tibiofibular Ligament, Longitudinal
This accessory ligament is present in 94% of normal ankles and offers another view
of a potentially injured ligament. Perform a distal TAX slide to visualize this liga-
ment. Tilt and rock the transducer to maximally enhance the echogenicity of the
ligament. Look for full and partial tears with the same dynamic maneuver as in
Protocol Image 2.
Protocol Image 2b (Optional): Distal Interosseous Membrane
Evaluate the distal IOM if there is clinical suspicion of a high ankle sprain, mainly
if there is evidence of injury to the AITiFL or the accessory AITiFL. Place the trans-
ducer in TAX between the distal tibia and fibula proximal to the AITiFL anteriorly.
The IOM is thin and hyperechoic; nonvisualization may indicate injury.
Method 313
Fig. 13.8 Protocol Image 3: Calcaneofibular ligament, longitudinal + dynamic
rotocol Image 3: Calcaneofibular Ligament,

P
Longitudinal + Dynamic (Fig. 13.8)
Keep the proximal edge of the probe on the inferior lateral malleolus, and aim the
distal edge about 20° toward the heel tip. Look for the round peroneal tendons in
TAX. The ligament is deep to the peroneal tendons and is curved, so its visibility
will be impaired until dynamic maneuvers are performed.
For the dynamic view, the patient actively dorsiflexes the foot, or you passively
invert the ankle. The now taut CFL is better delineated: it is now linear, fibrillar, and
hyperechoic. If the ligament is intact, the peroneal tendons will be displaced super-
ficially (in a lateral direction). No peroneal tendon displacement implies a complete
ligament tear is present. Even with a dynamic view, there may still be anisotropy of
at least one of the peroneal tendons, imitating a complex ganglion cyst.
Protocol Image 4: Sinus Tarsi (Fig. 13.9)
The foot is in slight plantar flexion and inversion, but relaxed. Rotate the transducer
into a vertical position and perform a distal TAX slide so that the transducer slides
off the lateral malleolus. Once the curved calcaneus is located, perform a small
LAX cephalad slide so that the transducer is just distal (anterior) to the lateral mal-
leolus. Between the cephalad talus and the caudal calcaneus lies the sinus tarsi.
Do not mistake anisotropy of the peroneal tendons and/or normal tenosynovial
effusion for effusion or a cyst. The sinus tarsi is the gateway to injecting the
PSTJ. The injection of the PSTJ via the sinus tarsi is described elsewhere. [39].
Fig. 13.9 Protocol Image 4: Sinus tarsi
rotocol Image 5: Peroneal Tendons at Supramalleolar Region,

P
Next, place one end of the probe against the posterior aspect of the lateral malleolus
and aim the other end of the probe slightly downward toward the posterior portion of
the talus; the probe should be transverse to the fibula. If both the PBT and PBM are
“normal” (not torn, not displaced, or there is no low-lying PBM), the hyperechoic
PBT is seen hugging the lateral malleolus contiguous to the larger, rounder PLT,
which is more superficial. The even larger hypoechoic PBM is deep to the PBT. The
SPR, attached to the lateral malleolus, is superficial to both the PBT and the PLT.
rotocol Image 6: Peroneal Tendons at Lateral Malleolus,

P
Transverse ± Power Doppler + Dynamic (Fig. 13.11)
Angle the posterior portion of the probe down another 10–20° and perform a TAX
slide distally. Note the hyperechoic bony cortex of the lateral malleolus. If there is a
low-lying PBM, the PBT may not be fully present at this level. The hyperechoic
Method 315
Fig. 13.10 Protocol Image 5: Peroneal tendons at supramalleolar region, transverse ± power Doppler

6: Peroneal tendons at
lateral malleolus,
transverse ± power
Doppler + dynamic
horizontal structure deep to the tendons is the PTaFL, which is sometimes challeng-
ing to visualize [47].
Next, dorsiflex and evert the ankle to test the integrity of the SPR. If the peroneal
tendons transiently migrate (subluxate) out of their usual “stacked” position (with
the PBT normally touching the bone), the SPR may not be intact. In such a case, the
SPR may not be directly torn but may have avulsed from its periosteal insertion.
Alternatively, ask the patient to circumduct the foot by drawing a large imaginary
circle with the big toe. An alternative recommended patient position for dynamic
US evaluation is to have the patient lie prone to allow for muscle relaxation [48].
Use copious gel and a light touch when performing dynamic maneuvers to avoid
constraining abnormal tendon movement.
rotocol Image 6a: Peroneus Quartus at Lateral Malleolus,

P
Depending on the anatomy of the patient, you may not be able to obtain this image.
This accessory muscle and tendon may variably arise (from the PBM, the fibula, or
from distal fibers of the PLT) and usually course posteriorly to the peroneal tendons.
It variably inserts on the calcaneal tubercle, the fifth MT bone, and the cuboid. It
may be predominantly muscular or tendinous in the retromalleolar area. It is a com-
mon variant and may be a source of pain (if it crowds the retromalleolar peroneal
tendons) or confusion (mimics a longitudinal split PBT).

6a: Peroneus quartus at
lateral malleolus,
transverse
Method 317
rotocol Image 7: Peroneal Tendons at Peroneal Tubercle,

P
Move the probe (TAX slide) more distally, with the inferior edge now posteriorly
angled at about 80–90° to the horizontal. The probe is almost vertical. Slowly move
the probe distally off the lateral malleolus. Note that up to 3 mm of fluid within the
common peroneal tendon sheath is normal in this area [30, 49].
Continue to perform a TAX slide until you visualize a hyperechoic hill-like pro-
tuberance, the PT. The PBT and the PLT are on either side of the tubercle, with the
PBT being cephalad and resting on the tubercle. The two tendons are not parallel,
so one will exhibit anisotropy while the other does not, as seen when the probe is
tilted in either direction. This image is reminiscent of a pair of aviator glasses, with
the PT being the bridge and the peroneal tendons being the lenses. Do not mistake
either one of these two tendons for a ganglion cyst.
Fig. 13.13 Protocol Image 7: Peroneal tendons at peroneal tubercle, transverse ± power Doppler

8: Peroneus brevis tendon
at insertion,
Doppler
rotocol Image 8: Peroneus Brevis Tendon Insertion,

P
Center the probe on the PBT and rotate 90° to see the fibrillar, hyperechoic PBT in
LAX view. Follow the tendon distally to its insertion at the base of the fifth metatar-
sal; this insertion may be indistinct due to anisotropy, thus mimicking enthesitis
[50]. However, Doppler activity at the insertion may indicate genuine enthesitis [28,
50]. As always, minimize anisotropy by keeping the transducer (and US beam) per-
pendicular to the insertion when evaluating for enthesopathy [28].
rotocol Image 9 (Optional): Peroneus Longus Tendon Distal

P
to Peroneal Tubercle, Longitudinal ± Power Doppler
Go back to the view in Protocol Image 7 and center the probe in TAX on the PLT,
which is located closer to the plantar surface than the PBT. Rotate the probe 90° to
see the hyperechoic, fibrillar PLT in LAX. Perform a distal LAX slide, maintaining
the tendon in the center and tilting the probe back and forth, sustaining the hyper-
echoic appearance of the tendon. The tendon will plunge toward the sole of the foot
on its way to the insertion on the first metatarsal and the medial cuneiform. To
maintain tendon visualization, counter anisotropy by angling the distal transducer
end slightly downward toward the foot bottom and incorporating a heel-to-toe
maneuver. You may see a hyperechoic OP bone embedded in the PLT. If so, observe
its appearance and if it is tender to sonopalpation, particularly if this is an area of
complaint.
Complete Lateral Ankle Ultrasound Checklist
⎕ Protocol Image 1: Anterior talofibular ligament, longitudinal + anterior
drawer test
⎕ Protocol Image 2: Anterior inferior tibiofibular ligament, longitudinal ± dynamic view
References 319
⎕ P rotocol Image 2a (optional): Accessory anterior inferior tibiofibular lig-

ament, longitudinal
⎕ Protocol Image 2b (optional): Distal interosseous membrane
⎕ Protocol Image 3: Calcaneofibular ligament, longitudinal + dynamic
⎕ Protocol Image 4: Sinus tarsi
⎕ Protocol Image 5: Peroneal tendons at supramalleolar region, transverse ±
power Doppler
⎕ Protocol Image 6: Peroneal tendons at lateral malleolus, transverse ± power
Doppler + dynamic
⎕ Protocol Image 6a: Peroneus quartus at lateral malleolus, trans-
verse ± power Doppler
⎕ Protocol Image 7: Peroneal tendons at peroneal tubercle, trans-
⎕ Protocol Image 8: Peroneus brevis tendon insertion, longitudinal ± power Doppler
⎕ Protocol Image 9 (optional): Peroneus longus tendon distal to peroneal tubercle,
longitudinal ± power Doppler
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Chapter 14
Medial Ankle

1. Medial ankle pain
2. Medial ankle swelling
3. Evaluation for inflammatory polyarthropathy
4. Paresthesia or pain in the medial ankle or bottom of the foot
1. What is the cause of medial ankle pain?
2. Is there an underlying inflammatory condition such as spondyloarthropathy
(SpA), rheumatoid arthritis (RA), or crystal disease?
3. Is a structural, functional, traumatic, or repetitive injury causing medial ankle
pain, for example, a ligament, tendon, or retinaculum tear?
5. What is causing localized soft tissue swelling?
6. Does this patient have tarsal tunnel syndrome?
Basic Bone Anatomy (Fig. 14.1)
The bony anatomy is from superior to inferior to distal: Tibia, Talus, Calcaneus,
Navicular, Cuneiform, and Metatarsal. The mnemonic “Tim’s Talking Cat Nate
Cuts Metal” may be helpful to remember the bones in this location.
States Government.

Switzerland AG 2023
324 14 Medial Ankle

anatomy
Fig. 14.2 Medial ankle

ligaments
Ligament Anatomy (Fig. 14.2)

Deltoid Ligament
The deltoid ligament complex, shaped like a delta or triangle, stabilizes the medial
ankle [1, 2]. These ligaments all start with “tibio.” Again, think of the bones
involved, proximal to distal: the tibia, the talus, the calcaneus, and the navicular.
The deeper tibiotalar ligaments bind adjacent bones and have two parts, the
anterior and posterior. The more superficial ligaments that bind nonadjacent
bones are the tibionavicular, tibiospring, and tibiocalcaneal ligaments. One
exception is the posterior superficial tibiotalar ligament, which binds adjacent
bones but is superficial.
1. Deep Deltoid Ligaments [2]
(a) The anterior tibiotalar ligament (ATTL) may be absent as a normal
variant [1].
(b) The posterior tibiotalar ligament (PTTL) is the thickest medial ankle
ligament.
Basic Bone Anatomy 325
2. Superficial Deltoid Ligaments

(a) The tibionavicular ligament (TNL) is present in 55% of the general popu-
lation [1].
(b) The tibiospring ligament (TSL) inserts into the spring ligament, which is
unusual since most other ligaments tend to bind bone to bone [1, 3].
(c) The tibiocalcaneal ligament (TCL) is present in 88% of the general popu-
lation [1].
(d) The posterior superficial tibiotalar ligament (PSTL), not labeled in
Fig. 14.2, is the superficial layer of the PTTL.
Spring Ligament
Several ligaments constitute the spring ligament complex; however, the superome-
dial calcaneonavicular ligament is the main component, and we refer to it generally
as the “spring ligament” [4]. The spring ligament stabilizes the foot’s longitudinal
arch and supports the talar head [2]. The spring ligament, although not officially
part of the deltoid ligament complex, forms the distal horizontal base of the delta or
triangle.
Tendon Anatomy (Fig. 14.3)
The ankle flexor tendons are the tibialis posterior (TPT), the flexor digitorum
longus (FDLT), and the flexor hallucis longus (FHLT) [5]. All originate from
muscles in the calf and enter the tarsal tunnel (TT) posterior to the medial malleo-
lus (MM). However, the FHLT may be more muscle than tendon within the TT. The
three tendons continue posteriorly to the retromalleolar groove, which functions as
a pulley. Each tendon makes a 90° curve and is encouraged to “stay in its lane” by
the protruding medial calcaneal bony landmark, the sustentaculum tali (ST). Despite
the name ending in “tali,” the ST is part of the calcaneus. Above (cephalad to) the
ST runs the TPT. The FDLT crosses the medial aspect of the ST. The FHLT courses
beneath (caudal to) the ST in a groove. In cross-section, the three tendons and the
ST are reminiscent of a hill with three suns. The ST is similar to the lateral calca-
neus’s peroneal tubercle (PT) in that the ST separates the tendons and serves as a
sonographic landmark [5].
Tendon Comments [5]
1. Tibialis Posterior Tendon

(a) The largest and most anterior of the three tendons
(b) Held in place by the posterior MM sulcus and the flexor retinaculum
326 14 Medial Ankle
Fig. 14.3 Medial ankle

tendons
(c) Inserts on the navicular, medial cuneiform bones, and metatarsals 2–4
(d) Facilitates ankle and foot plantar flexion and inversion
(e) An essential part of the medial longitudinal arch
(f) May contain a sesamoid bone that goes by three different names (os tibiale
externum, os naviculare, or os navicularum), located proximal to the ten-
don’s insertion onto the navicular, present in 23% [6]
2. Flexor Digitorum Longus Tendon
(a) Slimmer and posterior to the TPT
(b) Inserts on the plantar aspects of the distal phalanges of digits 2–5 to facili-
tate flexion of these digits
3. Flexor Hallucis Longus Tendon
(a) Inserts on the first toe base at the distal phalanx to enable first toe and
ankle flexion
(b) Difficult to identify on ultrasound (US) in the TT (where it is more muscle
than tendon)
(c) May communicate with the tibiotalar joint via the tendon sheath [7]
Be aware of the potential presence of an accessory FHLT or FDLT [5].
Basic Bone Anatomy 327
Tarsal Tunnel Anatomy (Fig. 14.4)
The TT is posterior to the MM. From anterior to posterior, the structures within the
TT are memorialized by the mnemonic “Tom, Dick, and A Very Nervous Harry,”
which stands for TPT, FDLT, Posterior tibial Artery, Posterior tibial Vein, Tibial
Nerve, and FHLT. We designate the tibial nerve (TN) in the medial ankle as just
plain “tibial nerve,” although others call it the posterior tibial nerve or tibialis pos-
terior nerve. The tibial nerve terminal branches are as follows (Fig. 14.5) [8]:
1. Medial calcaneal nerve (MCN), which branches off the TN before entering the TT
2. Lateral plantar nerve (LPN)
3. Medial plantar nerve (MPN)
4. Inferior calcaneal nerve (ICN), or Baxter’s nerve, which branches off the
LPN or the TN just before the LPN forms and has mixed motor and sensory
components [9]
Fig. 14.4 Tibial nerve/

tarsal tunnel anatomy
328 14 Medial Ankle
Fig. 14.5 Tibial nerve

branches
Flexor Retinaculum
The flexor retinaculum (FR) covers the TT and stretches from the MM to the
calcaneus.
Clinical Comments
Ligaments
Deltoid Ligament
Sonographic detection of deltoid ligament tears may be difficult due to individual

variability and the two-layer ligament arrangement [2, 10]. An absent ligament may
indicate a complete tear or normal variability. When assessing the ligaments, move
from superficial to mid-depth to identify bony landmarks. Then, go back to the shal-
low depth to focus on the region of interest. Compare the affected foot ligaments
with those on the contralateral, unaffected side. The deltoid ligament is less often
injured than the lateral ankle ligaments due to the lower frequency of landing on an
everted ankle in sports [3].
The robust, deeper ligaments are crucial for ankle stability but are more often injured
than the superficial ligaments [2, 11]. Complete tears are less common than partial
tears. When a deltoid ligament injury occurs, the damage may be severe, perhaps asso-
ciated with a lateral malleolar fracture and lateral talar displacement [12]. Deltoid liga-
ment insufficiency due to injury may culminate in ankle joint osteoarthritis [13].
Ligament injuries may produce hypoechoic swelling, fibril disruption, and avul-
sion fracture fragments [3]. Full-thickness tears demonstrate ligament interruption,
soft-tissue edema, and hematoma, making visualization of specific ligaments diffi-
cult [2]. The (deeper) tibiotalar ligaments may falsely appear to have tears due to
anisotropy. Sonographic sensitivity for partial tears is only 50%; therefore, mag-
netic resonance imaging remains the gold standard when evaluating ankle instabil-
ity [2, 14].
Spring Ligament Complex
Injuries to the spring ligament (as well as to the TPT) promote pes planus (flatfoot
deformity) [15]. A spring ligament injury on US is seen as a thickening, thinning, or
frank discontinuity. The plantar components of the spring ligament complex are not
consistently visible on US [2]. For that reason, what we term the “spring ligament”
is technically the superomedial calcaneal ligament component, the more sonograph-
ically accessible component, and the one more likely to be injured [3].
Tendons/Tenosynovium
The tendons of the medial ankle may exhibit a range of pathologies, including ten-
dinosis, partial or complete tears, tenosynovitis, and enthesopathy [16]. In addition,
tendon subluxation, often associated with flexor retinaculum injury or dysfunction,
may be demonstrated with dynamic maneuvers. Tendinosis, a degenerative change
with hypoechoic enlargement, occurs in the tendon segments that abut bony struc-
tures, such as the posterior MM. Partial-thickness tears are seen as intrasubstance
hypoechoic or anechoic areas, often in the setting of underlying tendinosis.
Sometimes it isn’t easy to separate the two, although a tear is more likely to be pres-
ent if it is well-defined and anechoic. Complete tendon tears may also occur.
Each tendon is encased in a tenosynovial sheath. Infection, mechanical, or
inflammatory conditions may instigate tenosynovitis, producing anechoic fluid and
perhaps power Doppler (PD) activity. There may be associated tendon swelling,
indicating tendinopathy. Comparison with the contralateral tendon may be helpful.
The tibiotalar joint may normally communicate with medial tendon sheaths, espe-
cially the FHLT [17]. Thus, isolated tendon sheath distention without a tibiotalar
effusion argues for the presence of tenosynovitis.
Tibialis Posterior Tendon
Evaluate for tendinosis of the TPT and the nearby FDLT by comparing their relative
sizes. The TPT diameter is typically twice that of the FDLT, ranging from 4 to 6 mm
[18, 19]. The TPT is the most frequently damaged of the ankle flexor tendons, with
injury occurring at the MM and the distal insertions (entheses) [20]. Tendinosis and
partial tears are more common than complete ruptures. Pathology starts as tenosy-
novitis with progression to a tear; however, early treatment may prevent severe dis-
ability [21].
330 14 Medial Ankle
Tears of the TPT most often occur just distal to the MM or at the navicular inser-
tion. Complete TPT rupture often results in a flatfoot deformity [20, 22]. Rupture
may be associated with RA and SpA. The normal variant accessory sesamoid bone,
the os naviculare, may be embedded in the TPT proximal to its navicular bone inser-
tion and may be associated with TPT pathology due to altered mechanical stresses
[23]. The os naviculare can be mistaken for a bony avulsion or calcium deposition
within the TPT.
TPT subluxation may be due to damage to the FR and is detected using dynamic
maneuvers, namely ankle flexion and inversion [24]. Patients with RA and SpA may
demonstrate TPT enthesopathy at the TPT insertion on the navicular, which is best
appreciated when the transducer is tilted 30°–45° cephalad [25]. Tenosynovitis may
occur near the malleolus, but not distally near the navicular insertion since this seg-
ment of the tendon lacks a tenosynovial sheath [26].
Flexor Digitorum Longus Tendon
Pathology of the FDLT is rare, but tendinosis may occur in ballet dancers [20, 22,
27, 28].
Flexor Hallucis Longus Tendon
Injury to the FHLT occurs in sports such as ballet, soccer, or basketball, resulting in
tenosynovitis, stenosing tenosynovitis, and tendinosis [22, 29]. Nearby bony spurs
and os trigonum (see below) may predispose to FHLT tendon pathology [22].
Visualization of the FHLT is impeded by its depth, but is improved by dynamic
great toe flexion.
Specific Conditions
OS Trigonum Syndrome
The os trigonum variant, present in 7% of ordinary people, results from a lack of

bone fusion at the posterior talus [30, 31]. The os trigonum may compress posterior
ankle soft tissues, including the FHLT, causing tenosynovitis, chronic posterior
ankle pain, and swelling [32–34]. However, similar symptoms may be caused by
Achilles tendinosis or tear, Haglund’s syndrome, retrocalcaneal bursitis, and osteo-
chondral lesions [35]. Ultrasound has a role diagnostically and for injection guid-
ance, but other imaging modalities are preferred [32, 36]. Dynamic evaluation for
FHLT with plantar flexion may reveal bony impingement.
Intersection Syndrome
The FHLT and the FDLT cross the midfoot in the region known as the Master Knot
of Henry [37]. This crossover may develop into an intersection syndrome with ten-
dinosis, tenosynovitis, or tendon tears [38]. There may be fluid distention in both
tendon sheaths and entrapment of the adjacent medial plantar nerve.
Rheumatoid Arthritis and Spondyloarthritis
Rheumatoid arthritis may present with TPT and FHLT tenosynovitis [16]. Rupture
of the TPT distal to the MM or at the navicular insertion may be associated with RA
and SpA [25]. Distal longitudinal TPT imaging may show enthesopathy features in
both RA and SpA. Tilting the transducer in a 30°–45° cephalad direction improves
tendon evaluation.
Flexor Retinaculum Dysfunction
The FR is a thickened fascia that restrains flexor tendon movement [39]. The FR is
the TT roof, originating at the MM and extending to the medial calcaneus. On US,
the FR appears as thin (1 mm) hyperechoic fibrillar bands overlying the tendons,
best seen in the transverse (TAX) view [39]. When damaged, the FR has a thick-
ened, hypoechoic appearance and may demonstrate PD activity. Damage to the FR
may contribute to TPT dysfunction and, thus, to acquired pes planus.
Tarsal Tunnel Syndrome
Tarsal tunnel syndrome (TTS) occurs when the TN or one of its branches is compro-
mised within the TT, resulting in numbness, tingling, burning, dysesthesia, cramp-
ing, or pain in the distribution of the TN or branches [40]. Symptoms may occur at
rest or with different foot movements [41]. Compressive causes of TTS include
myriad bone and soft tissue abnormalities. Foot deformities such as a varus or val-
gus ankle, pes planus, and tarsal coalition predispose to nerve branch compression
[40]. Two other causes of TN, or branch compromise, are surgical injury and hard-
ware compression.
The diagnosis of TTS is complicated by the large variety of etiologies and vari-
ance of nerve branches that may be affected [40]. Reproduction of symptoms may
occur with transducer pressure or tapping over the involved nerve (Tinel’s sign).
Electrophysiologic studies are essential, but negative studies do not exclude
TTS. Only imaging will establish the compression site, cause, and proper treatment.
332 14 Medial Ankle
Radiographs may reveal structures with compressive potential. Magnetic resonance

imaging is the gold standard; however, high-resolution US is gaining support to
delineate nerve compression and to rule out commonplace TTS mimics such as
plantar fasciitis [40, 42–44]. Ultrasound evaluation while the patient stands may
augment plantar venous distension and exacerbate compression caused by bony
conditions, including compression of a TN branch by the talus with pes planus and
valgus foot [40]. An alternative technique to augment venous pressure is to use a
blood pressure cuff as a tourniquet in the lower extremity; this may reproduce
symptoms [41]. In contrast to carpal tunnel syndrome, there are no well-defined US
criteria for TTS. It is best to compare the cross-sectional area of the TN to that of the
asymptomatic contralateral side.
Baxter’s nerve impingement may cause pain at the medial calcaneus or the plantar
fascia, mimicking TTS or plantar fasciitis [45]. Another mimic of TTS is TN neuropa-
thy, which occurs with diabetes and other conditions. Treatment for TTS includes open
decompression, US-guided hydrodissection, or minimally invasive TT release [46, 47].
Pitfalls
1. A positive US Tinel’s sign occurs when transducer pressure over the TN or an

affected branch reproduces symptoms. However, avoid overzealous compression
of the nerve and branches during the examination since this may produce pares-
thesia even in ordinary people.
2. Always perform a dynamic examination to look for tendon subluxation, particu-
larly for the TPT [24].
3. The TPT insertion on the navicular and the middle cuneiform may falsely appear
to have tendinosis or a tendon tear due to anisotropy. Avoid mistaking this for
pathology by performing sonopalpation to look for symptoms in this area [24, 48].
4. Do not mistake an accessory navicular bone (os naviculare) for a bony avulsion
or tendon calcification. Sonopalpation will elicit symptoms if this finding is
pathologic [24].
5. With a complete TPT rupture, avoid confusing an intact FDLT for the TPT [24].
6. Do not neglect to tilt the transducer to a 30°–45° cephalad orientation when
evaluating the TPT in longitudinal (LAX) at the insertion on the navicular
[25, 49].
7. When evaluating for compressive causes of TTS, consider performing US in
the standing position to distend plantar veins or exacerbate bony compres-
sion [40].
Method 333
Method
The patient is supine, the knee is flexed at 90°, and the foot is slightly externally
rotated. Alternatively, the patient rolls onto the side to be examined with the foot off
the table and supported by a towel under the lateral aspect of the distal foreleg.
Protocol Images 1 through 6 evaluate the medial ankle ligaments. The deeper ante-
rior and posterior tibiotalar ligaments are first assessed. Note that the posterior tib-
iotalar ligament has both deep and superficial layers.
The tendons are next studied in Protocol Images 7 through 11. Protocol Images
7 and 13 evaluate the TN and its branches. Use PD to locate the posterior tibial
artery and Color Flow (CF) to find the posterior tibial veins. Avoid excessive probe
pressure, which might inadvertently compress the tibial veins, rendering them sono-
graphically invisible.
rotocol Image 1: Anterior Tibiotalar Ligament, Longitudinal

P
(Fig. 14.6)
To visualize the (deep) ATTL, place one end of the probe on the MM and aim
the distal end toward the base of the first metatarsal. Angle the probe downward
about 30°. Look for the MM, the talus, and the joint space between the two.
Toggle the probe until you see a hyperechoic band bridging the chasm between
the two bones.

1: Anterior tibiotalar
334 14 Medial Ankle

2: Posterior tibiotalar
rotocol Image 2: Posterior Tibiotalar Ligament, Longitudinal

P
(Fig. 14.7)
With the foot everted and dorsiflexed, lift the probe and place the proximal end on
the inferior-posterior portion of the MM. Aim the distal probe end toward the tip of
the heel to visualize the PTTL. Use the distal probe to look for the hyperechoic
talus. This ligament’s superficial and deep components bridge the valley between
the MM and the talus.
rotocol Image 3: Tibiocalcaneal Ligament, Longitudinal

P
(Fig. 14.8)
With the foot still everted and dorsiflexed, keep the proximal end of the probe on the
inferior aspect of the MM and then rotate the distal end to a near-vertical position to
display the TCL. You may need to rotate the distal end of the probe an additional
10° toward the tip of the heel to optimize the image.
Hint You should see the large TPT in TAX, just superficial to the ligament. Note
the ligament’s insertion on the ST of the calcaneus; the ST is about the same depth
as the MM. The posterior prominence of the talus is still deeper than the ST. Do not
mistake the posterior prominence of the talus for the ST.
Method 335

3: Tibiocalcaneal ligament,
longitudinal

4: Tibiospring ligament,
longitudinal
Protocol Image 4: Tibiospring Ligament, Longitudinal (Fig. 14.9)
Next, rotate the distal portion of the probe about 20° toward the toes. Perform a
slight TAX slide anteriorly, moving the probe along the inferior MM. The TCL with
its calcaneal insertion will disappear, leaving a view of the TSL that is proximally
attached to the MM but without a distal bony attachment. Look for a subtle distal
insertion of the TSL on the spring ligament, which, in TAX, appears as an oval
hypoechoic structure. Once again, the TSL is unique in that it inserts into another
ligament.
336 14 Medial Ankle

5: Tibionavicular ligament,
longitudinal
rotocol Image 5: Tibionavicular Ligament, Longitudinal

P
(Fig. 14.10)
Next, perform a LAX slide distally and just off the MM to see the tibiotalar joint
and, more distally, the talonavicular joint. The superficial TNL connects the
tibia to the navicular and is a curved ligament when the ankle is in a neutral
position.
rotocol Image 6: Spring Ligament Complex, Longitudinal

P
(Fig. 14.11)
The spring ligament complex consists of the calcaneonavicular ligaments, a group

of ligaments that parallel the bottom of the foot. The ligament complex has dorsal
and plantar components. We primarily focus on the most dorsal component, the
superomedial calcaneonavicular ligament, and refer to this component as the “spring
ligament.”
Rotate the foot externally and place it in dorsiflexion. Next, palpate the ST just
inferior to the MM. An alternative method to find the ST is to place the probe in a
vertical position with one end on the MM. The more distal bony protuberance at
about the same depth as the MM is the ST. Next, put one end of the probe on the ST
and rotate the distal end anteriorly until it parallels the plantar surface of the foot.
Move the probe in an LAX slide distally until the bony, curved navicular bone is
seen. The ST and the navicular are at about the same depth and bracket the spring
ligament, seen in LAX, connecting the ST and the navicular. The distal end of the
probe may need to be angled up or down to visualize the spring ligament. This
image may be challenging to obtain.
Method 337

6: Spring ligament
complex, longitudinal
Fig. 14.12 Protocol Image 7: Tarsal tunnel tendons at medial malleolus, transverse ± Doppler
rotocol Image 7: Tarsal Tunnel Tendons at Medial Malleolus,

P
Transverse ± Doppler (Fig. 14.12)
Next, examine the tendons within the TT. The patient’s leg is in a frog-leg position
with a pillow under the lateral malleolus. Alternatively, the patient may lie on their
side. The flexor retinaculum runs from the MM to the calcaneus. It is the roof of the
TT and, therefore, the most superficial part. Start in TAX with the probe posterior to
the edge of the MM. Recognize from anterior to posterior: TPT, FDLT (half the size
of the TPT), posterior tibial artery and veins, TN, and FHLT. The FHLT may be
338 14 Medial Ankle
muscle rather than tendon in this location; if so, it is hypoechoic and poorly visual-
ized compared with the other two tendons. The FHLT may also be deeper than the
other two tendons. Again, the mnemonic “Tom, Dick, and A Very Nervous Harry”
reminds us of the names. In this area, the tendon sheaths may collect synovial fluid.
Perform the following passive dynamic maneuvers to verify the identity of
each tendon:
1. TPT: inversion and plantar flexion
2. FDLT: flexion and extension of digits 2 through 5
3. FHLT: flexion and extension of the great toe
Anterior subluxation of the TPT may be demonstrated with resisted dorsiflexion
and inversion in the presence of a damaged flexor retinaculum [39]. Tibialis poste-
rior dysfunction is a cause of acquired pes planus. Use PD or CF to detect the pos-
terior tibial artery, usually located just deep to one of the posterior tibial veins.
Excess probe pressure may collapse the veins, which is a way to identify the artery
without Doppler. You may see “Mickey Mouse,” with the ears being two veins and
the artery representing Mickey’s head. The TN is often just posterior to the vascu-
lar bundle.
rotocol Image 8: Tibialis Posterior Tendon at Sustentaculum

P
Tali, Transverse (Fig. 14.13)
Center a small footprint transducer (still in TAX) on the ovoid TPT as it rests upon
the curved bony posterior MM; the TPT is 4–6 mm in diameter [19]. While focusing
on the TPT in TAX, follow it down as it curves around the retrocalcaneal groove to
the ST. There may be a small amount of normal tenosynovial fluid in the tendon
sheath of the TPT just distal to the MM. Rotate the probe around the MM to main-
tain TAX orientation to the TPT. Look for the ST, the bony protrusion of the medial
calcaneus. The TPT runs superior (cephalad) to the ST; the FDLT is medial and
superficial to the ST; and the FHLT is inferior (caudal) to the ST in a groove. These
locations relative to the ST help verify the identity of each tendon when examined
in TAX after exiting the TT. Again, this appears to be a “hill with three suns.”
rotocol Image 9: Tibialis Posterior Tendon Navicular

P
Insertion, Longitudinal (Fig. 14.14)
Center the TPT in the image and rotate the probe 90° to view the TPT in LAX. With
a LAX slide, follow the TPT to its first insertion point, the navicular. Tilting the
transducer upward (cephalad) at a 30°–45° angle improves the visualization of the
TPT insertion [25]. Anisotropy near the navicular insertion may mimic a tendon
tear. Near the navicular, you may find a curvilinear os naviculare within the TPT. Do
not mistake this normal, variant accessory bone for an avulsion or tendon
Method 339
Fig. 14.13 Protocol Image 8: Tibialis posterior tendon at sustentaculum tali, transverse
calcification. Sonopalpation will elicit symptoms if this finding is pathologic. The

rest of the TPT continues to insert on the plantar surface of the three cuneiforms and
the second to fourth metatarsal bases.
rotocol Image 10: Flexor Digitorum Longus Tendon at

P
Sustentaculum Tali, Longitudinal (Fig. 14.15)
Return to Protocol Image 7 (TT in TAX) and locate the FDLT, which is posterior
to and half the size of the TPT. Manually dorsiflex toes 2 through 5 to verify that
you are looking at the FDLT. Next, rotate the probe 90° into LAX and, in a LAX
slide, follow the FDLT around the curve of the posterior MM. Remember to
340 14 Medial Ankle
Fig. 14.14 Protocol Image 9: Tibialis posterior tendon navicular insertion, longitudinal

10: Flexor digitorum
longus tendon at
sustentaculum tali,
longitudinal
look for tendinopathy near the retromalleolar groove. After clearing the rear
MM, position the probe in a near-horizontal plane to see two hyperechoic
rounded protrusions: the proximal one is the talus, and the more distal one is the
protruding ST. The FDLT, in LAX orientation, lies superficial to these bony
protrusions.
Method 341

11: Knot of Henry,
longitudinal
Protocol Image 11: Knot of Henry, Longitudinal (Fig. 14.16)
Continue the LAX slide and follow the FDLT in LAX distally to the plantar surface
of the midfoot, where it crosses the FHLT to form the Knot of Henry (Image 11).
The FDLT will angle slightly downward as it approaches the midfoot. The FDLT is
cephalad to the FHLT, proximal to the intersection of the tendons. Performing tiny
TAX slides (cephalad and plantar) will individually focus on each of these tendons
since tendon crossing creates anisotropy. The FDLT eventually inserts on the base
of the distal phalanges 2, 3, 4, and 5.
rotocol Image 12 (Optional): Flexor Hallucis Longus Tendon

P
Starting at the Tarsal Tunnel, Longitudinal
Again, go back to the TT view from Protocol Image 7. The FHLT or its muscle may
be seen deep to the TN; it may appear mostly hypoechoic if there is a preponderance
of muscle. A hyperechoic structure deep to the neurovascular bundle is likely the
emerging tendon near the myotendinous junction. Verify that this is, in fact, the
FHLT by manually dorsiflexing the large toe.
Center the probe on the FHLT in TAX and rotate it 90° to visualize the FHLT in
LAX. The FHLT may be challenging to visualize. Repeated passive flexion and
dorsiflexion of the great toe during the examination will help with visualization. The
FHLT curves around a shallow groove in the medial posterior aspect of the talus
342 14 Medial Ankle
(between the medial and lateral talar tubercles). It then courses under the plantar
surface of the ST of the calcaneus. It continues through the midfoot Knot of Henry
(Protocol Image 10b), then between the medial and lateral sesamoids, finally insert-
ing on the plantar surface of the distal phalanx of the large toe.
Protocol Image 13: Distal Tibial Nerve, Transverse (Fig. 14.17)
Go back to Protocol Image 7 to visualize the TN in TAX with a high-frequency

probe. If there is a question as to the identity of the TN, tilt the probe to look for
anisotropy and perform a proximal TAX slide to follow the TN proximal to the
TT. Further, confirm the TN’s identity by rotating the probe 90° to view the TN in
LAX to verify its “tram track” echotexture. Once the TN has been identified, follow
the nerve in TAX to the distal TT. Curve the probe around the retrocalcaneal groove.
The proximal probe tip touches the inferior MM, and the distal end is aimed toward
the direction of the heel. As the probe moves distally, the TN descends deep to the
posterior tibial artery and veins.
Continuing a TAX slide distally will demonstrate the TN splitting into two plan-
tar branches, the MPN and the LPN. The MPN is the most anterior of these two
branches’ structures; however, both the MPN and the LPN run anteriorly. The ICN,
or Baxter’s nerve, branches off either the distal TN or the LPN. The ICN is located
posterior to the LPN and, importantly, lies posterior to the vascular bundle. The ICN
is a mixed sensory and motor nerve that innervates the abductor digit minimi muscle
and may mimic plantar fasciitis if entrapped [9, 45]. It is only 1–2 mm in diameter
and may be challenging to visualize. To verify that the ICN has been identified in

13: Distal Tibial Nerve,
transverse
References 343
TAX, rotate the transducer 90° to the LAX view to visualize a tram-track pattern
descending to the sole. Yet another branch, the MCN, stems from the TN, usually
proximal to the TT, and runs posteriorly to the other nerve branches to innervate the
medial calcaneus. To avoid confusing the MCN with the ICN, note again that the
ICN tends to be posterior to the vascular bundle. In contrast, the MCN resides in a
more posterior location.
Complete Medial Ankle Ultrasound Checklist
⎕ Protocol Image 1: Anterior tibiotalar ligament, longitudinal
⎕ Protocol Image 2: Posterior tibiotalar ligament, longitudinal
⎕ Protocol Image 3: Tibiocalcaneal ligament, longitudinal
⎕ Protocol Image 4: Tibiospring ligament, longitudinal
⎕ Protocol Image 5: Tibionavicular ligament, longitudinal
⎕ Protocol Image 6: Spring ligament complex, longitudinal
⎕ Protocol Image 7: Tarsal tunnel tendons at medial malleolus,
transverse ± Doppler
⎕ Protocol Image 8: Tibialis posterior tendon at sustentaculum tali, transverse
⎕ Protocol Image 9: Tibialis posterior tendon navicular insertion, longitudinal
⎕ Protocol Image 10: Flexor digitorum longus tendon at sustentaculum tali,
longitudinal
⎕ Protocol Image 11: Knot of Henry, longitudinal
⎕ Protocol Image 12 (Optional): Flexor hallucis longus tendon starting at the tarsal
tunnel, longitudinal
⎕ Protocol Image 13: Distal tibial nerve, transverse
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Chapter 15
Forefoot and Toes

1. Pain in the forefoot
2. Soft tissue mass in the forefoot
3. Paresthesia in the forefoot
1. Could the patient have intermetatarsal bursitis or Morton’s neuroma?
2. Is there evidence for rheumatoid arthritis (RA), gout, or osteoarthritis?
3. Is there a plantar plate tear?
4. Is there evidence of a foreign body or a metatarsal fracture?
5. If there is a mass, what is the cause?
Basic Anatomy
We include the metatarsals as part of the forefoot, although some authors define the
forefoot as the anatomic region distal to the metatarsals. Please see Figs. 15.1a, b for
an illustration of bony anatomy and the course and insertions of the flexor and
extensor tendons. The fibular and tibial sesamoids are ovoid bones located plantar
to the first metatarsal head. The flexor hallucis longus tendon (FHLT) runs between
them to insert on the base of the distal phalanx [1]. The sesamoids are contained
within the tendons of the flexor hallucis brevis (FHB) and form part of the plantar
(volar) plate (PP). The sesamoids, the plantar plate, and the FHB tendon share a
common connection to the proximal phalanx. The sesamoids elevate the metatarsal
(MT) head off the ground and help bear weight.
States Government.

Switzerland AG 2023
348 15 Forefoot and Toes
Fig. 15.1 (a) Bony anatomy of the forefoot (b) Tendons of the forefoot simplified
The PP is a flexible fibrocartilaginous structure that rests on the plantar surface

of the cartilage of the MT head. It is attached to the collateral ligaments and the
plantar fascia. It originates from the MT neck and inserts into the plantar aspect of
the proximal phalanx (P1). The flexor tendon abuts the plantar surface of the PP. The
PP limits the dorsiflexion of the P1, while the collateral ligaments constrain vertical
and horizontal P1 movement.
Clinical Comments
The causes of forefoot pain are numerous and include plantar plate (PP) tears, joint
disorders, stress fractures, osteonecrosis, Morton’s neuroma, bursitis, tenosynovitis,
and cyst formation [2]. Start the forefoot examination with a detailed clinical evalu-
ation and weight-bearing radiographs to better display defects [3, 4]. If necessary,
the painful area is assessed with ultrasound (US). Observe for pain exacerbated by
transducer pressure. High-frequency transducers are necessary due to the superficial
location of forefoot structures.
Plantar Plate Tear (Fig. 15.2)
On US, with the probe positioned on the plantar surface in longitudinal (LAX), the
PP appears as a curved, mildly grainy hyperechoic structure hugging the
anechoic or hypoechoic plantar cartilage of the MT head [2]. A normal triangular
hyperechoic area at the distal PP may represent extra collagen fibers at the distal PP
insertion. The bulk of PP tears occur at the second metatarsophalangeal joint (MTPJ)
due to excess mechanical overload resulting from a preexisting hallux valgus defor-
mity [5]. A hallux valgus deformity affects the first MTPJ, resulting in the first toe's
lateral deviation and the first MT bone's medial deviation.
Although the second MTPJ is the site of most PP tears, such tears may occur in
other digits [2, 6, 7]. Other causes of mechanical overload leading to PP tears
include anatomic variance of the first and second toes (congenital or acquired),
wearing narrow, high-heeled shoes that chronically hyperextend the lesser MTPJs,
and PP trauma that may occur in sports [2].
There are typical features of a sizeable plantar plate tear [2, 4, 8, 9]:
1. A synovial effusion may be present.
2. There may be sonographic evidence of focal tears at the distal attachments to the
proximal phalanx; these appear as ill-defined hypoechoic irregular defects.
3. Tears often occur at the second MTPJ, involve the lateral distal PP insertion, and
then spread medially and proximally. Ultimately, the PP flattens and attenuates,
becoming imperceptible on US.
4. If the PP tear progresses from a partial-thickness tear to a full-thickness tear,
there may be a proximal retraction of the PP.
Fig. 15.2 Plantar plate normal and complete tear
5. The effusion becomes more evident as it communicates with the dorsal surface
of the joint through the torn PP.
6. The deterioration of the PP leads to the flexor tendon directly touching the plan-
tar cartilage that covers the MT head. A tenosynovial effusion surrounding the
contiguous flexor tendon may appear on US as a hypoechoic halo in TAX.
7. The absence of a functional PP results in MTPJ instability, forefoot dysfunction,
and deformity (second toe splaying, hyperextension, and perhaps even overlap-
ping the first toe) with localized pain.
8. In addition to flexor tendon subluxation and/or tenosynovitis, other US findings
may include a plantar cartilage interface sign, P1 enthesophytes, bony avulsion,
MTPJ synovitis, and pericapsular fibrosis.
Additional dynamic views enhance tear visualization and exaggerate MTPJ sublux-
ation if present [2]. Abnormalities found on static images should also be verified
with transverse (TAX) views and Doppler, the latter being used to evaluate for
hyperemia associated with a recent tear. Two static and two dynamic views are rec-
ommended [4].
Masses of the Forefoot
Forefoot masses may present as painless or painful lumps or be incidental findings

on US or magnetic resonance imaging (MRI). Such masses may also occur in more
proximal locations in the foot. The lesions can often be accurately characterized by
their site, symptom association, and relationship to nearby structures such as nerves
and blood vessels. Always perform a Doppler examination and measure the size of
the lesions. In addition to US, further elucidation may require an MRI. Although a
biopsy may be necessary, US can follow some lesions sequentially to quantitate
enlargement over time.
Morton’s Neuroma
The superficial and deep intermetatarsal ligaments run transversely, connecting the
MT heads [4]. Along the bottom of the foot and between these layers runs the com-
mon plantar digital nerve, which divides into the interdigital nerves near the MT
head. On the dorsal aspect of the intermetatarsal ligament lie the intermetatarsal
bursae. The interdigital nerve in the third interspace (between the toe digits 3 and 4)
is less mobile when compared to the other interdigital nerves [4]. This relatively
fixed position may render this interdigital nerve less able to absorb mechanical
stress and, hence, more prone to injury.
Due to chronic compression against the deep, transverse intermetatarsal liga-
ment, this nerve may develop scarring (fibrosis) and swelling, resulting in a neu-
roma termed Morton’s neuroma. This is the most frequent mass in the forefoot [4,
10, 11]. Causes of chronic entrapment or compression of this nerve include recur-
rent trauma, particularly from high-heeled shoes, and repeated dorsiflexion of the
toes [4]. A Morton’s neuroma may cause local excruciating pain, numbness, or par-
esthesia, perhaps radiating to adjacent toes. Patients liken the pain to “walking on a
marble” [11]. Symptoms are aggravated by walking and improve with rest [12].
Morton’s neuroma usually occurs between the third and fourth toes at the third web
space [13].
Ultrasound can accurately detect Morton’s neuroma and confirm a clinical diag-
nosis [12, 14, 15]. The ultrasonic appearance of Morton’s neuroma is that of a
hypoechoic, anechoic, or heterogeneous fusiform (ovoid) mass. In the sagittal
(LAX) plane, US reveals a normal-sized fibrillar nerve to be continuous with the
neuroma [12]. At the level of the MT heads, normal interdigital nerves measure
1–2 mm in diameter. Most symptomatic neuromas are greater than 5 mm in diam-
eter; however, neuroma size does not necessarily correlate with symptoms [16]. If
Morton’s neuroma is accompanied by intermetatarsal bursitis, this is referred to as
a “neuroma-bursal complex” [13]. Dynamic US may differentiate an IMB from
Morton’s neuroma (see section “Forefoot Bursae”, below).
Ultrasound will also help guide local injections to treat Morton’s neuroma via a
dorsal approach [4, 17]. It is suggested that the area around the neuroma be injected
along with any nearby bursa showing signs of inflammation. One study described a
failure rate of only 15% with direct neuroma injection of corticosteroids [18]. The
larger the neuroma, the less chance there is for injection success; however, there was
no absolute size cutoff above which injection failure could be predicted. Since US
detects the exact location and size of Morton’s neuroma, it also helps guide sur-
gery [4].
Forefoot Bursae
The two types of forefoot bursae, submetatarsal and intermetatarsal, are visible on
US [19, 20]. Submetatarsal (adventitious) bursitis (SMB) is secondary to chronic
overload of the MT heads, whereas intermetatarsal bursitis (IMB) may be associ-
ated with inflammatory arthropathy or Morton’s neuroma [4]. Pain underneath the
MT heads, particularly involving the first and fifth MT heads, is the typical history
of a SMB [11]. On US, the SMB is hypoechoic and compressible within the plantar
fat pad, superficial to the flexor tendon. In contrast, the IMB is located between the
toes, on the dorsal aspect of the deep intermetatarsal ligament [21].
Clinically, an IMB presents with a painful forefoot lump-like sensation, intensi-
fied with walking, and possibly associated with paresthesia, mimicking Morton’s
neuroma [11]. On US, an IMB is centrally located between the MT heads and has
thickened hyperechoic walls filled with an anechoic or hypoechoic fluid [4]. Local
pressure may cause the internal swirling of fluid, confirming its liquid nature. There
may occasionally be internal Doppler activity. Bursae are compressible, which
helps differentiate them from peripheral solid masses such as Morton’s neuroma
and pericapsular fibrosis associated with plantar plate injury [11].
Dynamic US may differentiate an IMB from Morton’s neuroma: place the probe
in LAX on the dorsum of the interdigital webbing and exert upward thumb pressure
from the plantar surface [4]. This maneuver shifts the neuroma in a dorsal direction
and the IMB in a posterior (proximal) direction. However, as described above, a
MN often has a concomitant IMB appearing on US as a large, complex, heteroge-
neous mass [12, 13]. It has been suggested that compression of the plantar nerve by
an enlarged IMB may cause Morton’s neuroma [11]. In practice, it may be challeng-
ing to sonographically distinguish Morton’s neuroma from an IMB, particularly if
the neuroma itself has an anechoic appearance.
Mucoid Cyst
Also known as digital mucous cysts, mucous pseudocysts, or myxoid cysts, these
pearly colored benign cysts are associated with osteoarthritis. Mucoid cysts may
sometimes be confused with ganglia and synovial cysts and occur near the proximal
nail fold and distal interphalangeal joint. These periarticular cystic lesions have a
fibrous wall, are filled with gelatinous material, and may communicate with the
joint cavity or tendon [4]. Most often asymptomatic, these cysts compress sensitive
structures, including nerves, producing pain when walking. On US, a mucoid cyst
appears as a well-defined hypoechoic to anechoic mass adjacent to a joint; however,

hypervascular changes may be noted if septae are present.
Ganglia
These are common benign, gelatinous-filled cystic masses that may communicate
with nearby joints or tendon sheaths [22]. Ganglia appear on US as a uni- or multi-
locular anechoic or hypoechoic lesion with posterior acoustic enhancement and
occasionally a stalk communicating with a tendon sheath or joint [11]. There may
be internal septations, but no Doppler flow. If a ganglion is located between the
metatarsals, it is challenging to differentiate this from an IMB on US. Although
often called a “synovial cyst,” the ganglion cyst lacks an actual synovial lining [23].
Synovial Cyst
These are synovial-lined periarticular fluid collections associated with joint arthrop-
athy, which causes an effusion [24]. Synovial cysts communicate with the abnormal
joint and may function as “drainage reservoirs” for excessive joint effusion in the
setting of arthropathy [25]. Again, the synovial cyst contains synovial fluid, whereas
the ganglion cyst is filled with gelatinous material. With its periarticular location
and communication with a joint, the synovial cyst may easily be confused with a
ganglion cyst.
Rheumatoid Nodules and Pannus
Rheumatoid nodules are granulomas with areas of central necrosis [24]. A history
of RA is often elicited. The nodules, usually adjacent to bone, sonographically dem-
onstrate slightly blurred edges with a mixed to hypoechoic echotexture [26]. There
may be a central hypoechoic area, perhaps due to necrosis. The nodules can be
mildly compressible, but lack posterior shadowing and Doppler activity. Rheumatoid
pannus may also may present as a soft tissue mass in the foot [11]. On US, the pan-
nus appears as hypoechoic synovial thickening within the joint capsule and may
demonstrate Doppler activity.
Callus
This is a superficial thickening of the soft tissue secondary to mechanical pressure

[24]. The typical location is the forefoot submetatarsal soft tissues. These are com-
mon and benign, but may ulcerate, particularly in diabetic patients.
Epidermoid Cyst or Implantation Dermoid
These occur due to the traumatic implantation of epidermal tissue into the dermis,
forming a cyst containing viable epidermal cells that continue to produce keratin,
filling the cyst [11]. Ultrasound reveals these lesions to be well-defined, solid, and
hypoechoic, with variable internal echogenic debris and posterior acoustic enhance-
ment. No Doppler signal is noted.
Inflammatory Granuloma
Retained foreign bodies provoke an immune response that may culminate in the for-
mation of a granuloma. Pain, swelling, and a sinus tract to the skin may be present.
Microorganisms introduced along with the foreign body may cause an abscess,
which, on US, is well-defined and ranges from hypoechoic to hyperechoic with pos-
terior acoustic enhancement [22]. Internal septations may be seen. Transducer com-
pression may reveal Doppler activity in the surrounding area, but not within the
abscess itself.
Ultrasound detects the foreign body and the secondary inflammatory response.
Sonography may provide helpful information about the composition of the foreign
body. If a granuloma forms, US may reveal a surrounding hypoechoic halo with pos-
terior acoustic enhancement. There may or may not be a history of puncture
wounds [4].
See section “Foreign Bodies”, below.
Gouty Tophus
Extensive collections of uric acid may form tophi, which are periarticular solid
masses [11]. Ultrasound reveals a central heterogeneous hyperechogenicity that
may be surrounded by a thin hypoechoic halo. The first MTPJ is a common area to
develop gouty tophi, but tophi may occur in other joints in the foot and, if in a plan-
tar location, may result in the sensation of walking “on a lump.”
Other evidence raising suspicion of a mass being a tophus includes a definitive
history of gouty arthropathy, hyperuricemia, and other US findings such as synovi-
tis, joint effusion, bony erosion (particularly with overhanging edges), or a double
contour sign superficially coating hyaline cartilage. Multiple, hyperechoic uric acid
foci may produce a “snowstorm” appearance on US. These foci are microtophi.
Note that tophi may occur nearly anywhere in the foot and may result in multiple
extensive soft tissue masses, perhaps associated with bony destruction from pres-
sure erosion [24].
Lipoma
Lipomas are benign aggregates of mature fat cells, often elliptical and well-defined,
with the most prominent dimension parallel to the skin [22]. Echogenicity is vari-
able, with no internal Doppler activity. The diagnosis of lipoma, strongly suggested
by US, is confirmed by MRI.
Plantar Fibromatosis (Ledderhose’s Disease)
Benign plantar fascia fibroblastic proliferation occurs in the mid-foot but may
extend more distally to the plantar fascia of the forefoot and toes [22]. Patients usu-
ally present with either pain or a lump on the sole [27]. Ultrasound reveals nodular,
fusiform, hypoechoic, or mixed echogenic masses in the middle or distal plantar
fascia, sometimes demonstrating Doppler activity [22, 24]. Sonographic findings
are often strongly suggestive or diagnostic of plantar fibromatosis, especially if the
condition is bilateral. Plantar fibromatosis may occasionally become aggressive and
surround skeletal muscle [11].
Pigmented Villonodular Synovitis
Also known as a giant cell tumor, pigmented villonodular synovitis (PVNS) is a

benign proliferation of synovial tissue that may affect the ankle joint or tendon
sheaths [4, 24, 28, 29]. It presents in a diffuse or nodular form. The nodular form
primarily affects distal tendon sheaths, appearing sonographically as a homoge-
neous, hypoechoic, well-defined solid mass bordering the tendon. There may also
be Doppler activity [29]. Ultrasound may demonstrate the relationship to adjacent
structures, pressure erosions of bone, or local recurrence after surgical excision.
However, since the appearance of PVNS on US is nonspecific, an MRI is necessary
for a more definitive diagnosis [4]. Although PVNS is described as benign, there is
a 14% recurrence rate after excision [24].
Benign Nerve Sheath Tumors: Schwannoma and Neurofibroma
These benign tumors of peripheral nerves appear on US as hypoechoic to heter-

oechoic, fusiform, well-marginated masses found along the course of a peripheral
nerve [4]. There may be internal Doppler activity. Neurofibromas are not encapsu-
lated and may be infiltrative; schwannomas are encapsulated and may mimic
Morton’s neuromas [11]. Differentiating a schwannoma from a neurofibroma is
often impossible on either US or MR imaging [22].
Glomus Tumor
These benign hamartomas of the neuromyoarterial glomus body may occur in the
fingers or toes [22]. On US, these ovoid masses appear hypoechoic and are sharply
delineated [30]. Color Doppler may delineate vasculature within the lesion, a help-
ful diagnostic sign [31]. Glomus tumors are well-defined on MRI [32].
Other Masses
In addition to the list of masses already considered, additional conditions described

in other sections of this chapter may produce a mass-like structure. These include
pericapsular fibrosis associated with a plantar plate fracture and osteoarthritis. Less
common lesions presenting as a forefoot mass are beyond the scope of this chapter.
These include synovial chondromatosis, soft tissue chondroma, synovial sarcoma,
undifferentiated pleomorphic sarcoma, leiomyosarcoma, clear cell sarcoma, and
subcutaneous granuloma annulare [4, 11, 22, 24].
Foreign Bodies
Plantar puncture wounds may result in foreign body (FB) retention, which predis-
poses to inflammation, infection, and damage to surrounding structures [33].
Radiographs may not detect certain materials, such as wood, plastic, fish bones, and
aluminum. Other FBs may be too small to delineate on radiographs. However, most
FBs are hyperechoic and therefore sonographically discernible.
Glass is radiopaque and therefore detectable on both plain radiographs and
US scans [34]. In the case of a retained pencil tip, the linear graphite center is radi-
opaque, and thus detectable on radiographs; however, the surrounding wood is
radiolucent. Wooden foreign bodies as small as 2.5 mm in length can be detected
with 87% sensitivity and 97% specificity by US [35].
Accurate sonographic localization of FBs minimizes surgical exploration and
may guide percutaneous removal [34]. In addition, US assesses secondary soft tis-
sue reactions and neurovascular and tendon damage caused by the FB. Foreign bod-
ies in soft tissue are all initially hyperechoic on sonography; however, wooden FBs
may become less echogenic with time [35].
Sonographic artifacts help detect the presence and composition of the FB [34]:
1. Acoustic Shadowing (Figs. 15.3a, b): Objects with a small radius of curvature
or a rough surface (e.g., a wooden toothpick) cause “clean” acoustic shadowing
(crisp, well-defined sharp edges with complete darkening deep to the object).
Objects with a large radius of curvature or a smooth surface (e.g., glass and
metal) produce “dirty” (hazy) shadowing and reverberation artifacts.
2. Reverberation Artifact (Fig. 15.3c) occurs when the transducer is positioned

parallel to the FB surface and thus depends on the orientation of the FB. Therefore,
an expected reverberation artifact for a sewing needle may not be visualized on
US if the probe cannot be placed perfectly parallel to the object.
Table 15.1 summarizes the sonographic findings of a study in which different
types of foreign bodies were experimentally introduced into cadaver feet [34, 35].
Note that the probe should be aligned parallel to the object as much as possible for
oblong objects to produce these telltale artifacts. In vivo, the FB may create edema,
hemorrhage, and later granulation tissue [34]. This results in a hypoechoic halo
which helps to identify the object as being a FB. However, the halo may not be pres-
ent in the first 24 h since it represents an inflammatory response [36].
A hypervascular response may be demonstrated with Doppler positivity due to
inflammation or infection [37]. Ultimately, a granuloma may be caused by a retained
FB with clinical evidence of swelling, tenderness, or a sinus tract [11]. Ultrasound
and MRI may both demonstrate a FB and surrounding reactive changes. In addition
to US and MRI, other modalities that can detect the FBs include fluoroscopy and
CT. See section “Inflammatory Granuloma”, above.
a b c
Fig. 15.3 (a) Clean acoustic shadowing with foreign bodies (b) Dirty acoustic shadowing with
foreign bodies (c) Reverberation artifact with foreign bodies
Table 15.1 Summary of Acoustic shadowing Reverberation

foreign body ultrasound
Steel None ++
findings in cadaver feet
[33, 34] BB shot pellet None ++
Glass Dirty +
Sewing needle Dirty +/++
Stone Dirty +
Plastic Clean None
Wooden toothpick Clean None
Pencil fragments Clean None
Tendon Pathology
The pathology of extensor and flexor tendons most often occurs proximal to the
forefoot. Tendon injury in the forefoot may be a result of direct trauma, gout, or
rheumatoid arthritis, although this is relatively rare [38]. Distal tendon tears, either
partial or complete, are detectable by US [4]. A dynamic examination differentiates
a partial tear from a complete tear. A complete tear will demonstrate separation of
the tendon stumps if viewed in LAX by passively flexing or extending the toes or
forefoot.
Arthritis
Forefoot arthropathy often involves the MTPJs, but the interphalangeal joints may
also be involved. Do not mistake the normal first MTPJ physiologic fluid in the
recess for an effusion. Recall that the average bone-joint capsule distance for the
first MTPJ is 1.7 mm [39]. Also, bear in mind that the synovial recess reflects more
proximally than distally.
Osteoarthritis
The first MTPJ is the most common location for degenerative forefoot change; the
diagnosis is best made radiographically [4]. Osteophytes may be noted on US at the
dorsal aspect of the MT head, appearing as hyperechoic protrusions. There may be
some degree of synovial effusion and hypertrophy, but rarely is power Doppler (PD)
activity present.
The foot is often overlooked when evaluating RA. Synovial hypertrophy (pannus)
and cartilage and bone erosion of the MTPJs may be evident [4]. Synovitis appears
as a hypoechoic thickening of the synovium within the recess, which may or may
not contain Doppler activity [40]. The fifth MT head may be the earliest area where
rheumatoid erosion is noted; fifth MT head erosions are 85% specific for RA [41,
42]. Bone erosion appears as an interruption in the hyperechoic cortex, with a small
hyperechoic area appearing as a step off beneath the main level of the cortex surface
[4]. In addition, thinning or interruption of the hypoechoic/anechoic cartilage cover-
ing the bony cortex may be seen. Ultrasound has proven to be a reliable technique
for detecting early RA erosions [43]. Ultrasound-guided injections into RA-afflicted
joints of the foot improve accuracy [4].
Gout
Gouty arthropathy has a predilection for the first metatarsophalangeal joint and the
foot dorsum. Please see Chap. 24 and Gouty Tophus in Clinical Comments above
for more information.
Psoriatic Arthritis
Psoriatic arthritis may involve the toes, including the MTPJs and interphalangeal
joints. Ultrasound reveals synovitis, bone erosion, and enthesitis at tendon inser-
tions [44]. Gout may mimic psoriatic arthritis and vice versa [45]. Ultrasound is
beneficial in differentiating the two.
Bone Disorders
Metatarsal Fracture (Fig. 15.4)
Metatarsal stress fractures often occur in regular military recruits, runners, dancers,
and gymnasts [11]. In addition, insufficiency fractures may occur with everyday
stress on pathologically weak bones [46]. It is essential to diagnose MT fractures
early to avoid progression to a complete fracture, delayed or poor healing, and non-
union [47, 48]. However, plain radiographs have low sensitivity for the diagnosis of
early MT fractures; they may be normal initially and only weeks later demonstrate
changes indicating that a fracture had previously occurred [4, 11, 47, 49].
It is noteworthy that even follow-up radiographs may remain normal [50].
Ultrasound may diagnose early stress fractures of the MT bones even when conven-
tional radiographs are unremarkable [4, 11, 49, 51]. Ultrasound is 83% sensitive and
76% specific for the early diagnosis of MT stress fractures [47].
The US signs of a MT fracture [4, 11, 49–51]:
Fig. 15.4 Metatarsal

fracture
1. Periosteal reaction: periosteal thickening or elevation, Doppler activity indicat-

ing hypervascularity, a minute fluid collection along the bony cortex, focal soft
tissue edema
2. Surrounding soft tissue edema
3. Hematoma (hypoechoic fluid collection)
4. Discontinuities (breaks) in the hyperechoic cortex
5. Bony callus formation later: thickened hyperechoic cortex
MRI is the gold standard for diagnosing MT fractures [47]. A bone scan (scintigra-
phy) may identify occult stress fractures, but requires 24–36 h to become positive
[11, 47, 48].
A proposed algorithm for evaluating suspected MT fractures [47]:
1. Radiographs (oblique view) improve diagnostic accuracy [52]
2. Ultrasound
3. MRI, if available
4. Bone scan, if there is still a question of a fracture
An abnormal bone scan requires a confirmatory imaging procedure such as a CT or
MRI targeting the abnormality; this is important to exclude a bone condition differ-
ent from a fracture, such as a bony neoplasm. When performing US for MT fracture
evaluation, apply gentle transducer pressure over the painful area. Start in LAX
orientation, scanning the entire width of the MT. Use TAX views to complete the
exam and confirm suspected pathology.
Pitfalls
1. Always complete a detailed history and physical examination, followed by

radiographs (if necessary), when evaluating foot pain.
2. Despite myriad causes of forefoot discomfort, common conditions are common
and should be considered first, as directed by the clinical picture. This includes
osteoarthritis, Morton’s neuroma, plantar plate tear, bursitis, stress fracture,
gout, and RA.
3. Do not forget to perform dynamic views when evaluating for plantar plate tears.
4. Forefoot masses are usually benign but need delineation. At the very least, these
need to be followed sequentially for changes in size or shape.
5. Do not forget to perform dynamic maneuvers when evaluating Morton’s
neuroma.
6. Do not neglect to distinguish submetatarsal from intermetatarsal bursitis.
7. Remember to look for confirmatory information when considering gouty tophi.
This includes a clinical history consistent with gout, hyperuricemia, and radio-
graphic evidence of bony erosion with overhanging bone. There is often addi-
tional sonographic evidence of uric acid deposition, namely a double contour
sign, which may be present in the forefoot or other body locations.
Method 361
8. Regarding FBs, obtain a history of the FB composition, examine scout radio-

graphs, and look for a puncture wound. Realize that the FB may be remote
from the puncture wound and may have broken up within the soft tissue. In
addition, try to align the transducer parallel to the FB based on its radiographic
location. Use a sterile field for your US examination to avoid introducing bac-
teria into an open puncture wound. Artifacts associated with the FB help ver-
ify the composition. Look for sonographic signs of an inflammatory response.
9. Remember that RA may initially present in the foot. The earliest detectable ero-
sion of bone may be in the fifth MT head, an area sonographically accessible.
Do not depend on plain radiographs alone to rule out bony erosions in this area
since US is more sensitive at detecting bony erosion.
10. Oblique radiographs increase the detection rate of MT fractures. However, do
not depend on radiographs to rule out a MT fracture. Ultrasound may diagnose
early MT stress fractures with normal radiographs. If the US is negative and a
stress fracture is still suspected, a bone scan or possibly an MRI should be
performed.
Method
Examine the forefoot dorsum with a supine patient and the foot flat on the table [4].
Plantar evaluation is performed with the leg stretched out, exposing the plantar sur-
face of the foot. The foot may dangle off the table to facilitate dynamic maneuvers.
The lateral and medial aspects of the forefoot may also be evaluated. Remember to
do Doppler studies to look for hyperemia. Extensor tendons are thin, hyperechoic
fibrillar structures that can be identified at the anterior ankle and followed to their
distal insertions. Flexion-extension of the toes facilitates tendon identification and
evaluates the integrity of the tendons and plantar plates. Likewise, US can follow
flexor tendons to the distal insertion into the distal phalanx.
Evaluate the cortical aspect of the metatarsals, which is usually hyperechoic,
continuous, and regular [53]. Perform transverse and LAX imaging of the dorsal
and plantar aspects of the MTPJs [4]. For the first and fifth MTPJs, the medial and
lateral views are accessible for inspection as well. The synovial recess of the MTPJs
does not typically contain fluid; however, sometimes, a normal first MTP may dem-
onstrate a small effusion. The cartilage of the distal MT head may be assessed on the
dorsal and plantar surfaces.
The interphalangeal joints are challenging to evaluate due to their small size.
Intermetatarsal spaces can be examined with the probe in both dorsal and plantar
positions and in both TAX and LAX planes. The fifth MT head may demonstrate
RA bony erosion imperceptible on plain radiographs. Inspect the dorsal, lateral, and
plantar aspects of the fifth MT head if RA is suspected. The plantar forefoot often
requires a lower frequency due to the presence of dense soft tissue through which
the US beam needs to penetrate.

1: Dorsal first
metatarsophalangeal joint,
Doppler
rotocol Image 1: Dorsal First Metatarsophalangeal Joint,

P
With the foot flat on the exam table, place the transducer in LAX across the dorsum
of the first MTPJ, looking for the hyperechoic MT head and P1; the joint space is
defined between these two bones. Use a liberal amount of transmission gel. Evaluate
the cartilage and the joint recess to look for effusion, cartilage/bone erosion, cal-
cium deposition, gouty tophi, and double contour sign of uric acid deposition on the
cartilage surface.
Next, passively flex the toe to examine the distal cartilage surface and the exten-
sor tendon. An interface reflex on the dorsum of the cartilage implies a smooth,
intact cartilage surface. Synovial effusion will distend the joint recess distally and,
to a greater extent, proximally. For the first MTPJ, the mean bone-to-joint capsule
Method 363
distance is 1.7 mm, with an additional 0.9 mm representing one standard deviation
[39]. Thus, values larger than 2.6 mm imply abnormal capsular distension.
If bony erosion is suspected, then perform a TAX slide around the first MT head
from dorsal to plantar, confirming a putative erosion in TAX (orthogonal) views.
Turn on the PD to look for hyperemia. Look at the insertion of the extensor tendon
along the distal bony phalanx to evaluate for active enthesitis. This requires a high-
frequency transducer.
rotocol Image 2: Dorsal First Metatarsophalangeal Joint,

P
Rotate the probe 90° and perform a distal TAX slide starting at the MT head and
moving over the joint space to the P1. Reverse the movement if necessary. Look for
erosion, crystal deposits, and hyperemia, confirming prior LAX view findings.
rotocol Image 3: Plantar First Metatarsophalangeal Joint,

P
Longitudinal ± Power Doppler + Dynamic (Fig. 15.7)
Stretch the leg out and place the probe in LAX orientation over the plantar first
MTP. Increasing the depth as needed and lowering the frequency will help identify
the joint space and PP. The latter appears typically as an echogenic, homogeneous

2: Dorsal first
transverse ± power
Doppler

3: Plantar first
Doppler + dynamic
curvilinear structure hugging the anechoic or hypoechoic cartilage of the metatarsal

head [54]. A PP tear will have a hypoechoic or heterogeneous defect and sometimes
be detectable only with passive toe dorsiflexion, so passively flex and extend the toe
to verify the integrity of the PP and the flexor tendon. Turn on the PD to evaluate for
hyperemia. Do not mistake an interface reflex superficial to the MT head cartilage
for a DCS.
(See Protocol Images 6a–c for more details on imaging of suspected plantar
plate tears.)
rotocol Image 4: Plantar First Metatarsophalangeal Joint,

P
Transverse ± Power Doppler ± Dynamic Exam (Fig. 15.8)
Rotate the probe 90° and perform a distal TAX slide starting at the MT head and
moving over the joint space to the P1. Reverse the movement if necessary. Look for
erosion, crystal deposits, and hyperemia, confirming prior LAX view findings. Note
the two sesamoids, the tibial (medial) and fibular (lateral). Examine the sesamoids
in both TAX and LAX views if clinically indicated. The oval structure between the
sesamoids is the FHLT in TAX, and the small bone deep to the sesamoids located
centrally is the first MT. The dynamic examination may be repeated if there are
concerning findings in Protocol Image 3.
Method 365

4: Plantar first
transverse ± power
Doppler ± dynamic exam
rotocol Image 5: Dorsal Fifth Metatarsophalangeal Joint,

P
Longitudinal ± Power Doppler + Dynamic
Place the small footprint probe in an LAX configuration on the dorsal surface of the
fifth MTPJ. Evaluate the fifth MT head for erosion and examine the joint for cal-
cium and uric acid deposits. Passively flex and extend the toe to examine the distal
extensor tendon. Slowly move the probe in a TAX slide to reach the lateral aspect of
the joint, focusing on the MT head and the joint space. Continue to curve the probe
in a TAX slide around the fifth MT head, looking for bone erosion. Passively
flex and extend the toe to examine the distal flexor tendon. Confirm any putative
erosions in the TAX view. Remember that fifth-MT head erosions are 85% specific
for RA [42].
rotocol Images 6a–c (Optional): Evaluation of a Suspected

P
Metatarsophalangeal Plantar Plate Tear
These images may be applied to any toe suspected of having a plantar plate tear.
rotocol Image 6a (Optional): Plantar Plate,

P
Place the probe in LAX over the plantar surface of the MTPJ of concern to visualize
the MT head with covering cartilage, the proximal phalanx, and the curved, slightly
hyperechoic PP superficial to the anechoic or hypoechoic cartilage. A lower fre-
quency might be necessary. Also, note the fibrillar flexor tendon location and if it
directly abuts the MT head cartilage, as would occur with severe PP damage (the PP
normally separates the flexor tendon from the MT head cartilage). Manually dorsi-
flexing the toe may increase tension on the PP and improve visualization. Look for
discontinuity in the PP, which might indicate a tear. Start at the lateral portion of the
PP and perform a slow medial TAX slide, focusing on the distal PP insertion, the
most common location for tears [2]. Be aware that US cannot assess the proximal
insertion of the PP on the MT neck. Turn on PD to assess for hyperemia.
rotocol Image 6b (Optional): Plantar Plate,

P
Rotate the probe 90° to look at the MTPJ in TAX. Use this view to confirm PP tears
by looking for a halo surrounding the flexor tendon (tenosynovial fluid) or an abnor-
mal migration of the flexor tendon to touch the MT head cartilage if the PP is

6b (Optional): Plantar
plate, transverse ± power
Doppler
Method 367
substantially damaged. This view will also portray the eccentric location of pericap-
sular fibrosis, which may be associated with a PP tear [2]. Perform a slow TAX slide
from distal to proximal, focusing on the PP.
rotocol Image 6c (Optional): Dorsal Metatarsophalangeal

P
Joint, Longitudinal + Dynamic
Next, move the probe to the dorsal aspect of the MTPJ, place it in LAX (sagittal
plane), and observe for dorsal subluxation of the proximal phalanx, which might
indicate a full-thickness PP tear. Use the free hand to dorsiflex the toe to better
delineate a PP tear by making the PP tauter. In the case of a full-thickness PP tear,
this maneuver may exaggerate dorsal subluxation of the proximal phalanx, as noted
by increased space between the proximal phalanx and the MT head. Next, place the
free hand thumb on the plantar surface of P1 and exert upward pressure, which
might further displace P1 dorsally should a full-thickness PP tear exist. Observe for
a joint effusion, which may be associated with a PP tear.
rotocol Image 7: Morton’s Neuroma and Intermetatarsal

P
Bursa Evaluation, Dorsal, Longitudinal + Dynamic (Fig. 15.10)
A small footprint, high-frequency probe is placed in TAX over the dorsum of the
interdigital webbing, typically interspace number three, when evaluating for
Morton’s neuroma. Once the honeycomb echotexture of the interdigital nerve is
located, slowly rotate the transducer 90° to visualize the nerve in its longitudinal
orientation.
At the level of the MT heads, normal interdigital nerves measure 1–2 mm in
diameter [16]. Thus, identifying a normal interdigital nerve may be challenging.

7: Morton’s neuroma and
intermetatarsal bursa
evaluation, dorsal,
longitudinal + dynamic
Using a high-frequency transducer (at least 16 MHz) along with the zoom function
(if available) on the US machine will enhance the visualization of this small nerve.
You may see an enlarged interdigital nerve, consistent with Morton’s neuroma. If
detected, a normal-sized interdigital nerve leading into the neuroma helps corrobo-
rate the diagnosis.
Morton’s neuroma may have an accompanying IMB. The free thumb of the
examiner presses upward from the plantar surface. This maneuver decreases the
thickness of the soft tissue and shifts the neuroma dorsally, enhancing visualization.
Furthermore, an IMB will be shifted posteriorly with this maneuver.
See the section “Forefoot Bursae and Morton’s Neuroma”, above for more
information.
rotocol Image 8: Morton’s Neuroma and Intermetatarsal

P
Bursa Evaluation, Plantar, Transverse + Dynamic Exam
(Fig. 15.11)
The high-frequency probe is placed in TAX along the plantar aspect of the painful
interdigital space [12]. The examiner’s free hand compresses the MT heads together.
A Morton’s neuroma will be displaced in a plantar direction, perhaps associated
with a “click” and the reproduction of pain. This has been described as the sono-
graphic Mulder sign [16].

8: Morton’s neuroma and
intermetatarsal bursa
evaluation, plantar,
transverse + dynamic exam
Method 369
rotocol Image 9 (Optional): Evaluation

P
for Metatarsal Fracture
When performing a US examination for an MT fracture, use minimal transducer

pressure over the painful area. Start in LAX orientation, slowly scanning the entire
width of the MT with gentle TAX slides. Use TAX views to complete the exam and
confirm suspected pathology. Use PD to look for further evidence of a periosteal
reaction. Record additional pertinent images as Protocol Images 9a, 9b, etc. See
the section “Metatarsal Fracture”, above for more information.
Protocol Image 10 (Optional): Evaluation for a Foreign Body
After taking a pertinent history, review the radiographs. Plastic, aluminum, and
wooden objects may not be appreciated on plain films. Locate the maximal point of
pain or swelling and the point of entrance. Sterilize the area and perform the US
exam with sterile gel and a probe cover to avoid introducing bacteria into a puncture
wound. Center the probe on this area and slowly rotate and search in 360° since the
object and attendant artifacts, if linear, will be best visualized parallel to the probe.
Perform the exam methodically using both TAX and LAX views as well as views
in between due to orientation issues with the foreign body. Verify all findings with
orthogonal views. Look for the echogenicity of the foreign body, specifically poste-
rior acoustic shadowing and reverberation artifacts. Secondary swelling, granula-
tion tissue, or pus may cause a hypoechoic rim or halo. Do not forget to use Color
or power Doppler to evaluate for hypervascularity. Refer to Table 15.1 and the
“Clinical Comments” section on foreign body artifacts to determine if a visualized
structure has sonographic characteristics compatible with the FB composition
expected from the patient history. The FB may also be somewhat remote from the
entrance wound. Be aware that multiple foreign bodies may be present, and a single
foreign body may have broken into two or more fragments.
Complete Forefoot/Toes Ultrasonic Examination Checklist
□ Protocol Image 1: Dorsal first metatarsophalangeal joint, longitudi-
nal ± power Doppler
□ Protocol Image 2: Dorsal first metatarsophalangeal joint, trans-
□ Protocol Image 3: Plantar first metatarsophalangeal joint, longitudinal ± power
Doppler + dynamic
□ Protocol Image 4: Plantar first metatarsophalangeal joint, transverse ± power
Doppler ± dynamic exam
□ Protocol Image 5: Dorsal fifth metatarsophalangeal joint, longitudinal ± power

Doppler + dynamic
□ Protocol Image 6a (optional): Plantar plate, longitudinal ± power Doppler
□ Protocol Image 6b (optional): Plantar plate, transverse ± power Doppler
□ Protocol Image 6c (optional): Dorsal metatarsophalangeal joint,
□ Protocol Image 7: Morton’s neuroma and intermetatarsal bursa evaluation, dor-
sal, longitudinal + dynamic
□ Protocol Image 8: Morton’s neuroma and intermetatarsal bursa evaluation, plan-
tar, transverse + dynamic exam
□ Protocol Image 9 (optional): Evaluation for metatarsal fracture
□ Protocol Image 10 (optional): Evaluation for a foreign body
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Chapter 16
Anterior Knee

Evaluation or assessment of:
1. Possible suprapatellar recess knee effusion
2. Quadriceps tendon architecture
3. Patellar tendon architecture
4. Hoffa’s fat pad
5. Femoral trochlear cartilage
6. Medial and lateral patellar retinacula
7. Prepatellar bursa, infrapatellar bursae, or pes anserine bursa
8. Inflammatory arthritis
9. Enthesitis
10. Presence of plicae
11. Patella
1. Is there evidence of a suprapatellar knee effusion?
2. If there are structural changes, does the pathology align with the symptoms?
3. If there is evidence of inflammatory arthritis, are there specific findings that
point to the etiology (e.g., double contour sign or tophus)?
4. If there is evidence of bursitis, is the bursitis inflammatory?
5. What is the next step for treatment?
6. Is tendon pain caused by an inflammatory or degenerative process?
States Government.

Switzerland AG 2023
374 16 Anterior Knee
Basic Anatomy
Bony Anatomy
The bones of the anterior knee are illustrated in Fig. 16.1.
Soft Tissues
Tendons and Muscles (Fig. 16.2)
Quadriceps Tendons
The three layers of the quadriceps tendon, from superficial to deep, are the rectus
femoris, the vastus medialis/lateralis, and the vastus intermedius [1]. Look for signs
of tendinosis at the insertion of the quadriceps tendon onto the superior patella, but
this may be mimicked by insertional anisotropy.
Patellar Tendon
Called by some the patellar ligament, the patellar tendon connects the distal ante-
rior patella to a bony prominence on the anterior tibia, the tibial tubercle (or
tuberosity).
Fig. 16.1 Anterior knee

bony anatomy
Basic Anatomy 375
Fig. 16.2 Simplified

anterior knee soft tissue
anatomy
Bursae (Fig. 16.3)
Suprapatellar Recess
The suprapatellar recess (bursa or pouch), or joint recess, is a channel that tracks
proximally from beneath the patella. The recess may contain synovial fluid, syno-
vial hypertrophy, synovitis, loose bodies, plicae, or a combination. The recess com-
municates with and is proximal to the knee joint.
Prepatellar Bursa
This superficial bursa lies anterior to the bony patella and is only evident when
pathologically distended.
Infrapatellar Bursae
At the quadriceps tendon insertion, there are two infrapatellar bursae, the superfi-
cial and the deep. A small amount of fluid in the deep infrapatellar bursa is common.
Pes Anserine Bursa
The pes anserine bursa (PAB) is located near the attachment of the gracilis, sarto-
rius, and semitendinosus tendons to the anteromedial border of the tibia [2].
Fig. 16.3 Anterior knee

bursae
Fat Pads
Just posterior (deep) to the quadriceps tendon are two hyperechoic structures, the
quadriceps (or suprapatellar) and prefemoral fat pads (Fig. 16.3). The suprapatel-
lar recess courses between the two fat pads; fat pad separation is enhanced with
suprapatellar recess distension. The infrapatellar (Hoffa’s) fat pad lies deep in the
patellar tendon; it serves as a shock absorber for the patellar tendon and helps to
nourish and repair contiguous structures [3].
Plica
Occasionally, a suprapatellar synovial plica may divide the recess into two distinct
compartments, connecting the two fat pads [4]. Such a plica is typically not patho-
logic or relevant. However, medication injected into the suprapatellar recess may
not reach the knee joint if an obstructing plica is present. Plicae may evade sono-
graphic detection, obscured by the bony patella.
Ligaments and Retinacula (Fig. 16.4)
The medial and lateral retinacula are fibrous tissues that tether the patella to
underlying soft tissue and bone. The medial patellofemoral ligament (MPFL),
located within the medial retinaculum, attaches the patella to the femur, thus inhibit-
ing lateral patella displacement [5].
Clinical Comments
Effusion
A suprapatellar recess effusion will be seen just deep to the quadriceps tendon as a
fluid-filled distention separating the prefemoral and quadriceps fat pads. The joint
effusion may appear anechoic or heterogeneously hypoechoic depending on the
nature of the fluid [6]. In addition to the suprapatellar recess, effusions may be iden-
tified laterally or medially to the patella in the parapatellar recesses. A simple syno-
vial fluid effusion is displaceable with probe compression but lacks a Doppler
signal [7].
Synovitis
In contrast to synovial fluid, synovial hypertrophy may be appreciated as nondis-

placeable and poorly compressible [7]. Synovial hypertrophy appears as hyper-
echoic tissue or has a mixed hyperechoic and hypoechoic signal occasionally with
synovial fronds. Synovial hypertrophy may or may not reveal a Doppler signal [7, 8].
Fig. 16.4 Ligaments and

retinacula of the
anterior knee
Loose Bodies
Loose bodies may appear as hyperechoic, rounded forms. Additionally, in the same
joint or bursa, there may be simultaneous evidence of a mixture of simple effusion,
synovial hypertrophy, and synovitis.
Tendon Damage
Quadriceps and Patellar Tendons
The quadriceps and patellar tendons can plainly exhibit tendinosis and partial- or full-
thickness tears [6, 9]. Again, the classic sonographic signs of tendinosis are loss of
fibrillar pattern, thickening, hypoechoic areas, and small anechoic clefts due to intra-
substance tearing (and perhaps calcium deposits) [10]. Note that power Doppler (PD)
activity may be present, but realize that this may be neovascularization as a response
to tendon injury rather than a sign of inflammation [11]. Tophaceous gout deposits can
also be seen intratendinously in the distal quadriceps tendon, with a predilection for
the patellar tendon [12, 13]. These deposits occasionally exhibit a hypoechoic rim.
Enthesopathy
The enthesis, or insertion of the tendon or ligament into the bone, can be a site of
inflammatory processes known as enthesitis [14]. This is often due to spondyloar-
thritis, such as psoriatic arthritis or ankylosing spondylitis. Enthesopathy, a more
general term to encompass all pathological abnormalities of an enthesis, can be seen
due to overuse, microtrauma, advanced age, and even the metabolic syndrome [15,
16]. Findings suggesting enthesopathy include neovascularization, bursitis, cortical
abnormalities, enthesophytes, and calcium deposition.
In adolescents, bony irregularity of the patellar tendon distally at the tibial inser-
tion may indicate Osgood-Schlatter disease, whereas bony irregularity at the patel-
lar insertion suggests Sinding-Larsen-Johansson syndrome [17]. The patellar tendon
in “jumper’s knee” may exhibit tendinosis, severe loss of fibrillar echotexture, and
tendon swelling. In most cases, this occurs primarily just distal to the patella. The
abnormal tendon may demonstrate PD activity. There may also be a bony irregular-
ity at the insertion of the patella [17].
Bursitis
Bursitis may be found in the suprapatellar, prepatellar, infrapatellar, or pes anser-

ine bursae [6]. For bursal evaluation, including the suprapatellar recess, a light
touch of the probe avoids artificial compression. Bursitis may also affect the
Pitfalls 379
superficial or deep infrapatellar bursae. However, a small amount of fluid in the

deep infrapatellar bursa is often normal. Similar to the prepatellar bursa, the PAB
is only detected on ultrasound with bursal distention, typically caused by
inflammation.
(Please see Chap. 19 for more information.)
Cartilage Damage
The femoral trochlear cartilage can be assessed for thinning, as seen in osteoarthritis
[18]. Loss of thickness and irregularity of the superficial chondral surface indicate
osteoarthritis [19]. Hyperechoic enhancement at the superficial margin of the hya-
line cartilage can be seen with monosodium urate deposition in gout (a double con-
tour sign). In contrast, hyperechoic enhancement, or spots within the hyaline
cartilage, can be seen with calcium pyrophosphate dihydrate deposition [20].
However, patients with advanced osteoarthritis may have difficulty maximally flex-
ing their knees to obtain this view.
Ligament Damage
The MPFL prevents lateral patellar displacement and may be damaged in acute
lateral patella dislocation. Sonographic evaluation of MPFL tears after acute lateral
patellar dislocation showed diagnostic accuracy comparable to that of magnetic
resonance imaging [21].
Fat Pad Damage
In response to repeated excessive stress, the infrapatellar (Hoffa’s) fat pad may
become inflamed and eventually fibrotic. Ultrasound may reveal hypoechoic thick-
ening, fatty architecture changes, and ultimately hyperechoic fibrous tissue. There
may be PD activity as well. Hoffa’s fat pad may also become impinged between the
patellar tendon and the patella, termed infrapatellar fat pad impingement or Hoffa’s
syndrome [3].
Pitfalls
1. Use a rolled towel under the knee, since knee flexion at 30° is the most sensitive
position to detect effusion [22].
2. Be mindful of anisotropy mimicking tendon pathology.
3. Maintain light probe pressure or float the transducer to avoid inadvertent com-
pression of effusions or bursae.
4. Don’t mistake a physiologic amount of fluid in the suprapatellar recess or the
deep infrapatellar bursa for a pathologic effusion.
5. Positive PD activity does not equate to inflammation. It means neovasculariza-
tion, which may or may not be due to inflammation. Neovascularization may
also occur with a chronic injury, such as tendinosis.
6. Do not confuse a normal variant, a bipartite patella, with a patellar fracture.
Obtain a radiograph to confirm this.
7. Complete tears of the quadriceps or patellar tendon are apparent clinically.
However, always do dynamic exams to expose partial tears if suspected.
Method
The patient is positioned supine with the leg resting comfortably at approximately
30° of flexion. A small pillow or rolled towel beneath the knee is recommended for
comfort. A knee or medium-depth preset is suggested to visualize the femur as the
bottommost structure.
Protocol Image 1: Quadriceps Tendon, Longitudinal (Fig. 16.5)
Place the probe on the long axis (LAX) to the midline of the knee with the probe
marker, or fin, in a proximal position. The distal end of the probe should touch the
proximal patella. The quadriceps tendon is seen in LAX, with the tendon fibrils

1: Quadriceps tendon,
longitudinal
Method 381
creating a paintbrush-like pattern. Move the transducer medially and laterally to

evaluate the entire quadriceps tendon. If an anechoic cleft in the quadriceps tendon
is detected, add a dynamic exam with knee flexion and extension to see if the fissure
enlarges upon stretching.
rotocol Image 2: Quadriceps Tendon, Synovial Fluid

P
Expression, Longitudinal ± Power Doppler (Fig. 16.6)
While keeping the suprapatellar recess in sonographic view, milk the joint upward
by taking a free hand and placing the distal patella tip between the webbing of your
first two fingers. Exert firm pressure superiorly and downward to push synovial fluid
from the parapatellar recesses into the suprapatellar recess. If an obstructing plica is
present, the proximal displacement of fluid can cause bulging of the plica, known as
a “sail sign” [23]. Be sure to evaluate the quadriceps insertion into the patella and
the suprapatellar recess with PD.
rotocol Image 3: Medial and Lateral Parapatellar Recesses,

P
Straighten the knee to enhance fluid in the parapatellar recesses. Move the probe
medially and laterally and look at the recesses with and without manual squeezing
of the infrapatellar area.

synovial fluid expression,
Doppler

3: Medial and lateral
parapatellar recesses,
rotocol Image 4: Quadriceps Tendon, Transverse ± Power

P
Doppler (Fig. 16.8)
Return to the initial position in Protocol Image 1. Identify the quadriceps tendon in
LAX and rotate the probe 90° to see the oval-shaped quadriceps tendon in the trans-
verse axis (TAX). Tilting the probe to create anisotropy can help with tendon iden-
tification. Perform distal and proximal TAX slides to examine the insertion on the
patella and the four contributing muscles. These muscles are the rectus femoris,
vastus medialis, vastus lateralis, and vastus intermedius.
Protocol Image 5: Femoral Cartilage, Transverse (Fig. 16.9)
Have the patient bend the knee to at least 100° and place the probe perpendicular to
the examination table, just proximal to the tip of the patella. Move the probe in
medial and lateral directions to see the hyperechoic bone of the distal anterior femur
covered with anechoic or hypoechoic cartilage. Remember, you are not looking at a
joint but at cartilage residing within the joint. Observe cartilage thickness and any
irregularities at the superficial surface. In the absence of pathological changes, the
cartilage is thicker in the central portion. Also, look for calcium deposits within the
cartilage (chondrocalcinosis) and monosodium urate deposition on the superficial
surface of the cartilage (double contour sign).
Method 383

transverse ± power
Doppler

5: Femoral cartilage,
transverse
Protocol Image 6: Patella, Transverse (Fig. 16.10)
Now, extend the knee and apply copious transmission gel to the patella, sufficient to
float the transducer. You should see an utterly anechoic region above the skin to
indicate that no probe pressure disrupts the view. Gently perform TAX slides over
the entire patella to examine the bony contour and look for the presence of a prepa-
tellar bursa. This bursa becomes visible only when pathologically distended.

6: Patella, transverse
Evaluate for distension of fluid on probe compression (simple effusion), PD activ-

ity, and hyperechoic areas, the latter suggesting a hematoma with clotted blood.
This bursa does not communicate with the knee joint; however, if it is distended,
consider infection and perform aspiration. A complete superior to inferior scan of
the patella may reveal bony “valleys,” which could be from a fracture but more com-
monly indicate a normal variant, a bipartite patella. A radiograph will differentiate
these two entities.
rotocol Image 7: Lateral Patellar Retinaculum, Transverse +

P
Dynamic ± Power Doppler (Fig. 16.11)
Now move the probe laterally off of the mid-patella while maintaining TAX orienta-
tion. The lateral patellar retinaculum (LPR) should be visible as a horizontal, elon-
gated, hyperechoic, fibrillar structure arising from the patella. Perform small
proximal and distal TAX slides to fully examine the retinaculum. If a retinaculum
tear is suspected, evaluate dynamically with knee flexion and extension. PD imag-
ing in this region may reveal the lateral genicular artery.
rotocol Image 8: Medial Patellar Retinaculum, Medial

P
Patellofemoral Ligament, Transverse + Dynamic ± Power
Now move the probe in a medial LAX slide and center it on the medial patellar reti-
naculum (MPR), a structure with a similar echotexture and horizontal orientation as
the LPR. The probe should bridge the medial patella and the distal femur. From the
lateral aspect of the patella, use two fingers of your free hand to push the lateral edge
of the patella medially and posteriorly. This dynamic maneuver tilts the medial
Method 385

7: Lateral patellar
retinaculum, transverse +
dynamic ± power Doppler

8: Medial patellar
retinaculum, medial
patellofemoral ligament,
transverse + dynamic ±
power Doppler
patella anteriorly to expose more of the cartilage on the underside of the patella and
may better demonstrate the MPFL. The MPFL originates at the adductor tubercle of
the femur. It is a superficial thickening of the MPR and may or may not be seen as
a distinct structure. A dynamic maneuver that flexes and extends the knee assists in
evaluating hidden tears of the MPFL. Use PD to locate the medial genicular artery
as well.
rotocol Image 9: Patellar Tendon, Longitudinal ± Power

P
Next, bend the knee to 90°, place the probe just distal to the patella, and rotate it 90°
to LAX to look at the patellar tendon. The proximal portion of the transducer should
rest on the distal end of the patella. Continually sweep the probe (TAX slides) later-
ally and medially as you move the probe distally to thoroughly examine the distal
patellar tendon, Hoffa’s fat pad (deep to the patellar tendon), and the superficial and
deep infrapatellar bursae, both located at the distal patellar tendon.
Hypoechoic areas may be noted within the tendon, indicating tendinosis, which
may be asymptomatic in athletes. Dramatic proximal patellar tendinosis may indi-
cate “jumper’s knee.” However, this finding may suggest Sinding-Larsen-Johansson
syndrome or pediatric patellar tendinosis in a child or adolescent. At the more distal
attachment of the patella tendon to the tibial tubercle, evidence of tendinosis, cal-
cium deposition, irregular bone, PD activity, and an enlarged infrapatellar bursa
may be signs of Osgood-Schlatter disease.
This tendon’s length often exceeds the size of the transducer, necessitating an
extended field of view or simply capturing images of the proximal and distal inser-
tions. Straighten the knee and use PD to examine the proximal and distal attach-
ments. If neovascularization is present, determine if it is within the tendon
(tendinosis) or at the tendon insertion (enthesitis), as seen in inflammatory arthritis.
Fig. 16.13 Protocol Image 9: Patellar tendon, longitudinal ± power Doppler

Method 387
Protocol Image 10: Patellar Tendon, Transverse (Fig. 16.14)
Next, rotate the probe 90° to examine the patellar tendon in transverse view and
perform proximal and distal TAX slides. The tendon should be thin and
oval-shaped.
Complete Anterior Knee Ultrasonic Examination Checklist
⎕ Protocol Image 1: Quadriceps tendon, longitudinal
⎕ Protocol Image 2: Quadriceps tendon, synovial fluid expression, longitudinal ±
power Doppler
⎕ Protocol Image 3: Medial and lateral suprapatellar recesses, longitudinal + dynamic
⎕ Protocol Image 4: Quadriceps tendon, transverse ± power Doppler
⎕ Protocol Image 5: Femoral cartilage, transverse
⎕ Protocol Image 6: Patella, transverse
⎕Protocol Image 7: Lateral patellar retinaculum, transverse + dynamic ±
power Doppler
⎕ Protocol Image 8: Medial patellar retinaculum, medial patellofemoral ligament,
transverse + dynamic ± power Doppler
⎕ Protocol Image 9: Patellar tendon, longitudinal ± power Doppler
⎕ Protocol Image 10: Patellar tendon, transverse.

10: Patellar tendon,
transverse
References
1. De Maeseneer M, Marcelis S, Boulet C, Kichouh M, Shahabpour M, de Mey J, et al. Ultrasound

of the knee with emphasis on the detailed anatomy of anterior, medial, and lateral structures.
Skelet Radiol. 2014;43(8):1025–39.
2. Toktas H, Dundar U, Adar S, Solak O, Ulasli AM. Ultrasonographic assessment of pes anseri-
nus tendon and pes anserinus tendinitis bursitis syndrome in patients with knee osteoarthritis.
Mod Rheumatol. 2015;25(1):128–33.
3. Lapègue F, Sans N, Brun C, Bakouche S, Brucher N, Cambon Z, et al. Imaging of traumatic
injury and impingement of anterior knee fat. Diagn Interv Imaging. 2016;97(7–8):789–807.
4. Liu YW, Skalski MR, Patel DB, White EA, Tomasian A, Matcuk GR Jr. The anterior knee:
normal variants, common pathologies, and diagnostic pitfalls on MRI. Skelet Radiol.
2018;47(8):1069–86.
5. Starok M, Lenchik L, Trudell D, Resnick D. Normal patellar retinaculum: MR and sono-
graphic imaging with cadaveric correlation. AJR Am J Roentgenol. 1997;168(6):1493–9.
7. Wakefield RJ, Balint PV, Szkudlarek M, Filippucci E, Backhaus M, D’Agostino MA, et al.
Musculoskeletal ultrasound including definitions for ultrasonographic pathology. J Rheumatol.
2005;32(12):2485–7.
9. La S, Fessell DP, Femino JE, Jacobson JA, Jamadar D, Hayes C. Sonography of partial-thickness
quadriceps tendon tears with surgical correlation. J Ultrasound Med. 2003;22(12):1323–9.
quiz 30-1
10. Rasmussen OS. Sonography of tendons. Scand J Med Sci Sports. 2000;10(6):360–4.
11. Ackermann PW, Renström P. Tendinopathy in sport. Sports Health. 2012;4(3):193–201.
12. de Ávila FE, Sandim GB, Mitraud SAV, Kubota ES, Ferrari AJL, Fernandes ARC. Sonographic
description and classification of tendinous involvement in relation to tophi in chronic topha-
ceous gout. Insights Imaging. 2010;1(3):143–8.
13. Girish G, Glazebrook KN, Jacobson JA. Advanced imaging in gout. Am J Roentgenol.
2013;201(3):515–25.
14. D’Agostino MA, Terslev L. Imaging evaluation of the entheses: ultrasonography, MRI, and
scoring of evaluation. Rheum Dis Clin. 2016;42(4):679–93.
16. Abate M, Di Carlo L, Salini V, Schiavone C. Metabolic syndrome associated to non-
inflammatory Achilles enthesopathy. Clin Rheumatol. 2014;33(10):1517–22.
17. Carr JC, Hanly S, Griffin J, Gibney R. Sonography of the patellar tendon and adjacent struc-
tures in pediatric and adult patients. AJR Am J Roentgenol. 2001;176(6):1535–9.
18. Naredo E, Acebes C, Moller I, Canillas F, de Agustin JJ, de Miguel E, et al. Ultrasound validity
in the measurement of knee cartilage thickness. Ann Rheum Dis. 2009;68(8):1322–7.
19. Minagawa H, Wong KH. Musculoskeletal ultrasound: echo anatomy & scan technique:
Amazon Digital Services. Tokyo, Japan, Ohmsha Publishing; 2017.
20. Filippucci E, Gutierrez M, Georgescu D, Salaffi F, Grassi W. Hyaline cartilage involvement
in patients with gout and calcium pyrophosphate deposition disease. An ultrasound study.
Osteoarthr Cartil. 2009;17(2):178–81.
21. Zhang GY, Zheng L, Ding HY, Li EM, Sun BS, Shi H. Evaluation of medial patellofemoral
ligament tears after acute lateral patellar dislocation: comparison of high-frequency ultrasound
and MR. Eur Radiol. 2015;25(1):274–81.
References 389
22. Mandl P, Brossard M, Aegerter P, Backhaus M, Bruyn GA, Chary-Valckenaere I, et al.

Ultrasound evaluation of fluid in knee recesses at varying degrees of flexion. Arthritis Care
Res (Hoboken). 2012;64(5):773–9.
23. Bianchi S, Martinoli C. Ultrasound of the musculoskeletal system. New York, NY: Springer,
Berlin, Heidelberg; 2007.
Chapter 17
Posterior Knee

Evaluation or assessment of:
1. Posterior knee pain
2. Baker’s or popliteal cyst (PC)
3. Popliteal vasculature
4. Tibial, sciatic, and common peroneal nerves
5. Posterior cruciate ligament
1. Is there evidence of a PC?
(a) Does the PC communicate with the knee joint?
(b) Is the PC intact or ruptured?
(c) Is the PC complex or simple?
(d) Is synovitis or synovial hypertrophy present?
2. Are the tendons or other structures normal in appearance?
(a) If abnormal, does the pathology align with the symptoms?
3. Does the popliteal vasculature appear normal?
(a) Is a popliteal aneurysm or pseudoaneurysm present?
(b) Is a popliteal deep venous thrombosis (DVT) present?
4. Is there evidence of injury, entrapment, or an intraneural ganglion involving
the nerves?
5. What is the cause of the posterior knee pain?
States Government.

Switzerland AG 2023
392 17 Posterior Knee
Necessary Basic Anatomy: Posterior Knee
See Fig. 17.1 for the location of the bones, posterior distal femoral cartilage, liga-
ments, and menisci. Some people have a calcified accessory sesamoid bone, the
fabella. The soft tissues of the posterior knee (Fig. 17.2) comprise medial, central,
and lateral zones. From medial to lateral, the structures of interest include the sarto-
rius, gracilis, semitendinosus (ST), semimembranosus (SM), gastrocnemius-
semimembranosus bursa (GSB), medial head gastrocnemius (MHG), tibial nerve
(TN), popliteal vein (PV), and artery (PA), and lateral head of the gastrocnemius
(LHG). The mnemonic “Sergeant Grace Stopped Smiling, But Major Nelson, Very
Amused, Laughed” may help to remember the order of these structures.
Muscles and Tendons
The pes anserine (or anserinus) tendons are the sartorius, gracilis, and ST, memo-
rialized by “Say Grace before Tea.” Before these tendons insert into the anterome-
dial knee, they pass through the posteromedial corner of the knee. At this level, the
sartorius is still a muscle rather than a tendon. Likewise, the bulk of the MHG is
muscular, with only the medial tip being tendinous. The ST is superficial to, and
almost appears to be a roof or tent over, the GSB. A mnemonic is that the ST is a
tent over the bursa. The lateral and medial gastrocnemius muscles ascend to
insert upon the lateral femoral condyle (LFC) and medial femoral condyle (MFC),
respectively.
Fig. 17.1 Bones and

ligaments of the posterior
knee simplified
Necessary Basic Anatomy: Posterior Knee 393
Fig. 17.2 Soft tissues of

the posterior knee
simplified
Bursae
The GSB, located between the tendons of the SM and MHG, communicates with
the healthy native knee joint in 40–54% of people [1]. The GSB is named for its
location between the MHG and the SM tendon. The pes anserine bursa lies deep
to the pes anserine tendons at the anteromedial proximal tibia. It is only visible
when distended.
Ligaments
The anterior and posterior cruciate ligaments (ACL and PCL) attach the tibia to the
femur [2]. While technically ultrasound-accessible, these ligaments are better evalu-
ated on magnetic resonance imaging (MRI).
Menisci
The posterior aspects of the medial and lateral menisci may also be visible on ultra-
sound (US) but are more fully evaluated by MRI.
Nerves
The three nerves that are visualized posteriorly are the tibial, sciatic, and common
peroneal. In the distal posterior thigh, the sciatic nerve bifurcates into the tibial and
common peroneal nerves. The TN follows the PA and PV posteriorly, while the
fibular or common peroneal nerve (CPN) moves laterally to wrap around the poste-
rior fibular neck.
Blood Vessels
The main blood vessels in this region are the PA and the PV, which are easy to iden-
tify on US with CF and using vein compression maneuvers.
Cartilage
Often overlooked, the posterior distal femoral condyles have a sizeable cartilage
surface approachable by US.
Clinical Comments
Bursitis
Popliteal Cyst
The GSB may enlarge into a PC, a common pathologic entity first described in 1877
by W. Morant Baker [3]. Most PCs are secondary cysts due to the production of
excess synovial fluid in the knee in response to underlying intraarticular pathologies
Ligament Damage 395
such as meniscal tears, articular cartilage lesions, or inflammatory or noninflamma-

tory joint diseases [4]. Synovial fluid may flow to the cyst via a communicating
channel [1, 5].
Popliteal cysts often present as asymptomatic swelling in the popliteal fossa with
or without posterior knee pain; however, continued enlargement of the PC may
result in rupture [6]. The clinical signs of a ruptured cyst may mimic deep-vein
thrombosis or cellulitis [7]. A PC should be viewed in two planes to determine if a
rupture has occurred [8]. The PC may or may not communicate with the knee joint.
When the bursa enlarges to become a PC, US can determine if communication with
the joint is present since a connection to the joint may be closed in extension but is
open with knee flexion [9]. First, look for a connecting stalk, and then passively flex
and extend the knee to see if the fluid-filled channel size increases in flexion, thereby
indicating a conduit between the GSB and the knee joint.
Ultrasound-guided aspiration and steroid injection may be considered if the PC
is thought to be a pain generator, but the cyst may return unless the principal cause
is addressed. The PC, being a synovial-lined structure, can also become inflamed
and distended due to an underlying inflammatory arthropathy such as rheumatoid
arthritis (RA) [6]. This is defined as primary GSB enlargement and may be seen in
the setting of a noncommunicating GSB. A PC may also arise after total knee
arthroplasty and may be primary or secondary, the latter with a communicating
channel to the prosthesis.
Other cyst-like masses that may be confused with a PC are PA aneurysms or pseu-
doaneurysms. Popliteal artery aneurysms are uncommon but account for up to 70%
of peripheral artery aneurysms [10]. These often occur in older men with significant
cardiovascular disease [11]. There is some controversy regarding the size of a popli-
teal artery aneurysm that requires intervention, but a diameter of 2 cm is considered
a possible threshold [12]. Unlike a true aneurysm, where the weakened vessel wall
dilates abnormally, a pseudoaneurysm is caused by damage to the vessel wall, pro-
ducing a hematoma surrounding the damaged vessel [13]. Swirling flow can be
appreciated on the color Doppler as a “yin-yang” configuration [14]. Remember to
turn on the color Doppler when evaluating any structure that looks like a PC.
Pes Anserine Bursitis
Ligament Damage
The ACL and PCL can be visualized on US, albeit incompletely. MRI remains the
gold standard for assessing these structures [8]. A uniformly hypoechoic PCL is
considered normal, whereas a torn PCL shows heterogeneous hypoechogenicity
and is often thicker than normal [15]. Avulsion fractures at the tibial insertion may
also be visible [16].
Nerve Damage
Entrapment of the CPN due to compression or stretching against the fibular neck
represents the most common cause of lower extremity neuropathy [17]. Triggers
include repetitive trauma (runners), habitual leg crossing, proximal fibula fracture,
and rapid weight loss [18]. After knee replacement and perhaps associated with
prosthetic overhang, the CPN may enlarge due to repetitive knee bending, causing
compression or trauma. This CPN dysfunction may cause localized knee pain with
or without radiating paresthesia [19]. The diagnosis is made by measuring the cross-
sectional area (CSA) of the involved CPN and comparing it with the contralateral
CPN. The diagnosis can be verified with electrophysiologic studies. Using a CPN
cutoff of a CSA of 10.9 mm2, US diagnostic sensitivity was 90%, with a specificity
of 69% for CPN neuropathy at the fibular head (FH) [20].
Intraneural ganglia can also cause lower extremity neuropathy [21]. In patients
with knee osteoarthritis, synovial fluid may track down from the tibiofibular joint
along the epineural sheath of a branch of the CPN, potentially compressing the
CPN. This can result in knee pain, paresthesia, and even foot drop [18]. This fluid
collection may also track proximally to the sciatic nerve and down the TN. This is
an unusual ganglion since it involves a nerve sheath, whereas most other ganglia
originate from joints and tendon sheaths.
Another potential source of compression of the CPN at the posterior knee is the
peroneus longus muscle. After winding around the posterolateral aspect of the fibu-
lar neck, the CPN dives between the peroneus longus muscle and the FH, described
as the peroneal or fibular tunnel. CPN compression may occur here [22].
Blood Vessel Pathology
Although not a pulsatile mass, DVT of the PV may also be appreciated [8]. A visible
thrombus (an echogenic mass within the lumen of the vein) or lack of compressibility
is considered diagnostic of a DVT [23]. However, it is essential to note that a complete
diagnostic point-of-care DVT examination requires a comprehensive evaluation start-
ing at the common femoral vein [24]. A PC can also be mimicked by a soft tissue
injury [9]. However, in contrast to a PC, soft tissue swelling does not originate between
the MHG and SM tendons or connect to the joint cavity. Again, a popliteal artery
aneurysm and a pseudoaneurysm may each mimic a PC. See Popliteal Cyst, above.
Fabella Pathology
Another cause of posterolateral knee pain is the fabella. The fabella, a small “bean-
like” structure in the proximal LHG tendon, is a sesamoid bone that articulates with
the LFC cartilage [25]. The fabella may normally be absent or present and may or
may not be calcified. It is calcified in 10–30% of the general population [26]. If
Method 397
present but noncalcified, it may mimic a tear of the LHG. If present and calcified, it
is a hyperechoic bony semicircle and may mimic a bony avulsion. Since the anterior
face of the fabella communicates with the cartilage, it may develop osteoarthritis
[9]. The fabella may also cause mechanical compression neuropathy of the CPN [25].
Cartilage Damage
Ultrasound enables visualization of the posterior femoral cartilage. This may dem-
onstrate signs of degeneration (loss of cartilage surface sharpness or cartilage thin-
ning), chondrocalcinosis, or the double contour sign of uric acid deposition [27].
Meniscal Damage
Ultrasound enables inspection of the posterolateral and posteromedial menisci. For

details on meniscal pathology, please see the Lateral and Medial Knee chapters.
Pitfalls
1. Don’t attempt an examination with an externally rotated leg. Instead, have the
patient lie prone.
2. Anisotropy of the semimembranosus or MHG tendons may mimic a PC.
3. A noncalcified fabella may be hypoechoic, mimicking an LHG muscle tear on US.
4. Always attempt to trace the origin of a PC to the GSB and perhaps to the knee
joint itself. A dynamic exam with knee flexion and extension may help deter-
mine if the GSB truly communicates with the joint.
5. Determine if a PC is primary or secondary, since this will influence treatment.
6. If you see a possible PC, turn on the color flow Doppler since a popliteal aneu-
rysm or pseudoaneurysm may mimic a PC.
7. The PCL and the menisci are best evaluated with MRI rather than US.
8. Evaluate the PV for a thrombus in the popliteal fossa, but a dedicated venous
duplex study best evaluates venous thrombosis.
9. The insertion of the distal semimembranosus tendon on the tibia mimics a para-
meniscal cyst of the medial meniscus (MM) due to anisotropy.
10. A hypoechoic cleft in the lateral meniscus (LM) may be due to the popliteus
tendon sheath mimicking a meniscal tear.
Method
Begin with the patient in the prone position. The FH may be marked for reference.
Use mid-frequency settings.
rotocol Image 1: Medial Femoral Condyle, Transverse

P
(Fig. 17.3)
Place the probe in a medial position on the posterior knee in the transverse axis
(TAX) (near the knee crease) and visualize the hyperechoic distal MFC. Directly
superficial to the MFC is the hyperechoic SM tendon. Just lateral to the SM tendon
is the hypoechoic MHG muscle and its hyperechoic tendon. Next, move the probe
to center the image on the triangular-shaped MHG muscle and tendon. The tendon
is the medial and superior apex of the muscle and may be hypo- or hyperechoic.
Again, medial to the MHG tendon is the SM tendon.
Between the two tendons is the GSB, where the neck of a PC occurs; the bursa
hugs the MHG tendon. Normally, this bursa contains minimal fluid and is challeng-
ing to detect if not distended. Knee flexion opens the channel to the joint cavity and
may help demonstrate the stalk. A trick to locating the GSB is to perform a dynamic
longitudinal axis (LAX) slide to see the crossing of the MHG muscle and tendon
with the SM tendon. Recall that the MHG tendon inserts on the femur and the SM
tendon inserts on the posterior tibia.
If a PC is identified, separate images (labeled 1a, 1b, etc.) should be obtained in
multiple planes to look for rupture and whether or not the PC tracks to the posterior
knee joint. If present, the connection to the joint closes in extension and opens with

1: Medial femoral condyle,
transverse
Method 399
knee flexion [9]. Passively flex and extend the knee to see if the PC channel to the
posterior knee joint is more visible in flexion, thus establishing a conduit to the knee
joint. Observe the presence of synovial fluid, debris, synovial septations, synovitis,
and PD signals within the PC. Measure the cyst’s size in two dimensions. A rup-
tured PC may be painful, and hypoechoic fluid will move into the surrounding
soft tissue.
rotocol Image 2: Medial Femoral Condylar Cartilage,

P
Increase the depth if needed to visualize the posterior one-third of the articular car-
tilage of the MFC in TAX. Look for cortical defects. With the probe in TAX, have
the patient very slowly flex the knee to 100° and scan the cartilage superiorly and
inferiorly to look for evidence of cartilage degeneration or crystal disease.
rotocol Image 3: Medial Femoral Condylar Cartilage,

P
Extend the knee and rotate the probe 90° into LAX to view the articular cartilage.
Do a TAX slide from medial to lateral to fully evaluate the posteromedial articular
cartilage.

2: Medial femoral condylar
cartilage, transverse

3: Medial femoral condylar
cartilage, longitudinal
rotocol Image 4: Lateral Femoral Condylar

P
Cartilage, Transverse
Now, rotate the probe 90° back to TAX. A lateral LAX slide will bring the LFC into
view. Now perform the same dynamic scan as in Protocol Image 3 to examine the
posterior femoral cartilage more fully.
rotocol Image 5: Lateral Femoral Condylar

P
Cartilage, Longitudinal
Extend the knee and rotate the probe 90° for a LAX view of the articular cartilage.
Do a slight TAX slide from medial to lateral to thoroughly scan the cartilage.
rotocol Image 6: Neurovascular Bundle, Transverse + Color

P
Doppler (Fig. 17.6)
Next, with the probe still in the LAX position, perform a medial TAX slide to the
center of the popliteal fossa. Rotate the probe 90° into TAX to visualize the PA, PV,
and TN. Remember, from superficial to deep are the nerve, vein, and artery. Color
Doppler identifies vascular structures and examines vessel pathology.
Method 401

6: Neurovascular bundle,
transverse + color Doppler
rotocol Image 7: Neurovascular Bundle, Transverse + Color

P
Doppler + Sonocompression (Fig. 17.7)
Superficial to the PA is the PV. The patient can flex the knee approximately 30° to
fill the vein. Probe pressure will collapse a normal PV vein and verify a lack of
thrombosis. Again, color Doppler can help identify the vessels.
Protocol Image 8: Sciatic Nerve, Transverse (Fig. 17.8)
The honeycombed TN in TAX is located superficially and laterally to the PV. With
the probe in TAX, follow the TN with a proximal TAX slide to the large sciatic
nerve before bifurcation into the TN and CPN.
Protocol Image 9: Common Peroneal Nerve, Transverse (Fig. 17.9)
Next, still in TAX, center the probe on the CPN in a cross-sectional view and fol-
low the CPN distally in a TAX slide as it courses more laterally down to the
FH. The FH is seen as a hyperechoic “hill.” The CPN in TAX is best seen medially
Fig. 17.7 Protocol Image 7: Neurovascular bundle, transverse + color Doppler + sonocompression

8: Sciatic nerve, transverse
to the FH and has a rounded or ovoid honeycomb structure. Tilt the probe back and
forth to utilize anisotropy to help identify the CPN, which is often isoechoic with
adjacent soft tissue. If there is a question about CPN dysfunction, measure the
CSA and compare it with the contralateral side. Please see the Clinical Comments
for further discussion.
Method 403

9: Common peroneal
nerve, transverse
Alternatively, take the foreleg, bend the knee 15°, and place the ankle on its con-
tralateral counterpart. This externally rotates the hip and the entire knee. Take the
probe in TAX and scan the proximal FH, looking for the bony linear diagonal cor-
tex. The CPN candidate is located just medially to this bony cortex. Move the probe
distally and watch the CPN move laterally in an oblique path, superficial to and
across the fibular neck, thus identifying the CPN. The CPN then dives beneath the
FH of the peroneus longus muscle, also seen in TAX. This maneuver is akin to what
we use when identifying the median nerve in the wrist by exploiting the distal ana-
tomic course of the CPN.
To obtain a longitudinal view of the CPN, rotate the probe 90°. This view is chal-
lenging. You may see anechoic fluid tracking along the CPN epineural sheath, con-
sistent with an intraneural ganglion. This view may demonstrate the peroneal longus
muscle compressing the CPN as the nerve dives deep into this tendon; the CPN may
swell proximal to the point of compression.
rotocol Image 10: Biceps Femoris Tendon, Longitudinal

P
(Fig. 17.10)
Maintain the probe in LAX with respect to the femur, placing the distal end on the
FH. The FH has a diagonal, hyperechoic cortex. The fibrillar biceps femoris tendon
(BFT) is the product of the long and short heads of the biceps tendon and inserts into
the FH. Verify that this is the BFT by moving the probe proximally to see the transi-
tion to muscle.

10: Biceps femoris tendon,
longitudinal
rotocol Image 11: Posterior Horn of the Lateral Meniscus,

P
Still in LAX, deep to the BFT, locate the curved bony LFC and, more distally, the
proximal tibia. The triangular posterior horn of the LM is between these two bones.
Perform a lateral TAX slide to evaluate the posterior horn. Remember that US can
only penetrate the more superficial portion of the meniscus, so deeper meniscal
pathology will not be appreciated. MRI is the gold standard for meniscal evaluation.
A potential pitfall is to conclude that a hypoechoic cleft in the LM is a tear
since this may be mimicked by the popliteus tendon sheath [28]. Another pitfall is
to assume that a vertical cleft through the LM is a tear since this may be fibrous
tissue [29]. On the femur in the popliteus groove, the popliteus tendon may appear
as a hypoechoic structure due to anisotropy and can be mistaken for a paramenis-
cal cyst. A trick is passively flexing and extending the knee, a maneuver to bring
the meniscus into focus and enlarge a structure that you might think is a parame-
niscal cyst. This positioning lends itself to performing varus stress views of the
knee to look for possible meniscal extrusion. The patient’s leg may be prone or in
external hip rotation, better exposing the posterolateral meniscus. When applying
this technique, keeping the probe LAX to the tibia, not the femur, is essential.
Method 405

11: Posterior horn of the
lateral meniscus,
longitudinal
rotocol Image 12: Posterior Horn of the Medial Meniscus,

P
A medial TAX transverse slide to the posteromedial knee will visualize the posterior
horn of the MM. You may see a hypoechoic round area distal to the MM, just super-
ficially at the proximal tibia. This anisotropic insertion of the distal semimembrano-
sus tendon on the tibia may mimic a parameniscal cyst. Tilting the probe will cause
the hyperechoic tendon insertion to appear.
Protocol Image 13 (Optional): Fabella (Fig. 17.13)
Still in LAX, perform a lateral TAX slide toward the FH to visualize the LFC and
the LHG. You may see a variant, a small bony hyperechoic “bean-like” structure
embedded in the proximal LHG tendon. If the radiograph reveals a calcified fabella,
this will be detectable on US. If there is a hypoechoic area within the LHG tendon,
this may be a noncalcified fabella. Please see Fabella Pathology in the clinical com-
ments above.

12: Posterior horn of the
medial meniscus,
longitudinal

13 (optional): Fabella
References 407
Complete Posterior Knee Ultrasonic Examination Checklist

⎕ Protocol Image 1: Medial femoral condyle, transverse
⎕ Protocol Image 2: Medial femoral condylar cartilage, transverse
⎕ Protocol Image 3: Medial femoral condylar cartilage, longitudinal
⎕ Protocol Image 4: Lateral femoral condylar cartilage, transverse
⎕ Protocol Image 5: Lateral femoral condylar cartilage, longitudinal
⎕ Protocol Image 6: Neurovascular bundle, transverse + color Doppler
⎕Protocol Image 7: Neurovascular bundle, transverse + color Doppler +
sonocompression
⎕ Protocol Image 8: Sciatic nerve, transverse
⎕ Protocol Image 9: Common peroneal nerve, transverse
⎕ Protocol Image 10: Biceps femoris tendon, longitudinal
⎕ Protocol Image 11: Posterior horn of the lateral meniscus, longitudinal
⎕ Protocol Image 12: Posterior horn of the medial meniscus, longitudinal
⎕ Protocol Image 13 (optional): Fabella.
References
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Chapter 18
Lateral Knee

Evaluation or assessment of soft tissue structures, that may be responsible for knee
pain or dysfunction.
1. Is the iliotibial band (ITB) normal in appearance?
(a) Is there evidence of bursitis deep to the ITB?
2. Are the tendons and ligaments normal in appearance?
(b) If abnormal, is the pathology caused by an inflammatory or degenerative
process?
3. Is there evidence of a meniscal tear?
(a) Is a parameniscal cyst present?
(b) Is meniscal extrusion present?
4. Is the common peroneal nerve normal in appearance?
States Government.

Switzerland AG 2023
410 18 Lateral Knee
Basic Anatomy
The iliotibial band (ITB), sometimes called the iliotibial tract, is a complex fibrous
connective tissue structure that originates on the iliac crest and has contributions
from the gluteus maximus and tensor fascia lata muscles [1]. The ITB inserts onto
Gerdy’s tubercle (GT) on the anterolateral aspect of the tibia (Fig. 18.1) but has
other attachment sites more proximally, including the intermuscular septum and
supracondylar femoral tubercle [2, 3]. The ITB transfers forces from the hip to the
knee while stabilizing the lateral knee [4].
The anterolateral ligament (ALL) is a thin ligament that inserts on the tibia
halfway between the GT and the fibular head (FH). It attaches to the lateral femoral
epicondyle (LFE). At knee flexion of 90°, the ALL resists internal rotation
(Fig. 18.2). Deep to the ALL is the lateral inferior geniculate artery (LIGA), which
is an important landmark to verify the identity of the ALL as well as test its integrity.
Just posterior to the ITB and the ALL is the lateral collateral ligament (LCL). The
LCL originates at the distal femur and attaches to the lateral femoral head. It is one
of several lateral knee stabilizers.
Deep to the LCL runs the popliteus tendon, which inserts just proximal to the
LFE in the popliteus groove. This is an unusual tendon since it runs deep to a liga-
ment. The popliteus muscle is flat and lies deep to the plantar and gastrocnemius
Fig. 18.1 Distal

Iliotibial band
Fig. 18.2 Ligamentous

anatomy of the lateral knee
simplified
muscles. It connects the posterior tibia to the external aspect of the lateral femoral
condyle (LFC).
The lateral meniscus (LM) is a semicircular fibrocartilaginous “shock absorber”
located between the lateral articulation of the tibia and femur. The outer aspect can
be sonographically inspected and appears as a hyperechoic triangular structure deep
to the LCL, separating the femur from the tibia. The biceps femoris tendon (BFT)
and LCL share a common distal attachment at the lateral FH, with the BFT located
posterior to the LCL.
The common peroneal (fibular) nerve (CPN) is the most posterior structure in
the lateral knee and is found just posterior to the BFT. Sonographically, the nerve is
best visualized transverse (TAX) to the FH [5]. The nerve curves anteriorly around
the lateral fibular neck and then splits into the superficial and peroneal nerves.
Clinical Comments
Iliotibial Band Syndrome
Repetitive knee flexion and extension, such as running and cycling, may cause the
ITB to scrape against the LFE [4]. This may produce iliotibial band syndrome
(ITBS) (“runner’s knee”), a common overuse injury. Pain on the lateral aspect of the
knee occurs during physical activity and worsens during the initial 25–30° of knee
flexion [4, 6]. Predisposing factors include knee varus deformity, leg length discrep-
ancy, and weak hip abductors [4]. Generally considered a friction syndrome due to
overuse, alternative etiologies include compression of fat and connective tissue
deep to the ITT or chronic inflammation of the IT bursa [7–9].
412 18 Lateral Knee
On ultrasound (US), the normal ITB in longitudinal (LAX) reveals a linear fibril-
lar structure that inserts onto GT [10]. The adventitial iliotibial bursa is located
between the ITB and the LFE [4]. With ITBS, US may reveal soft tissue edema or a
distinct fluid collection between the ITB and LFE. Thickening of the ITB is an
inconsistent finding [4]. The LFE may display cortical irregularities [9].
Reproduction of pain with sonopalpation over the involved area is diagnostically
helpful. A pitfall is to mistake normal lateral recess synovial fluid for adventitial
bursitis [11]. In TAX over the LFE, the ITB can be dynamically evaluated for snap-
ping during flexion and extension of the knee [12]. Some authors maintain that the
ITB movement is actually an illusion created by changing tension in the anterior
and posterior fibers of the ITB [7]. If so, this implies that the ITBS may be more of
a compression syndrome than a true friction syndrome [13]. However, a different
study affirmed ITB movement using US [14].
The ITB may undergo partial and full-thickness tears [15]. Sonography
reveals hypoechogenicity and thickening with fluid surrounding a partial tear.
Full-thickness tears show fiber disruption [15]. Finally, distal ITB tendinopathy,
an entity separate from ITBS, may occur at or near the GT insertion and appears
on US as thickening and/or hypoechogenicity compared with the contralateral
knee [16]. Such tendinopathy may be due to knee prosthesis impingement or
abnormal varus or valgus stress on the ITB due to knee osteoarthritis. Pain may
be localized to the insertion or be perceived along the lateral thigh. Using US
guidance, a fluid collection deep to the ITB can be aspirated and injected for
treatment, and a positive therapeutic response favors the diagnosis of ITBS [4,
17, 18].
Anterolateral Ligament
This thin ligament, whose existence was first suspected in 1879, has recently been
rediscovered and found to be present in 97% of the population in cadaver studies
[19, 20]. In one study, US was 100% sensitive in detecting the ALL [21]. The ante-
rior cruciate ligament (ACL) is the primary stabilizer of the internal rotation of the
knee. The ALL also stabilizes internal knee rotation. Since tears of the ALL may
occur with an ACL tear, it is essential to evaluate for a concomitant ALL tear if an
ACL tear is suspected [22]. Ultrasound detection of ALL tears is at least as accurate
as magnetic resonance imaging (MRI).
Lateral Collateral Ligament
The LCL of the knee is the primary stabilizer to counter varus instability [23]. On
US, the normal LCL appears hyperechoic and fibrillar. Injuries to the LCL include
partial or complete tears as well as soft tissue or bony avulsions, the latter most
commonly occurring at the FH attachment [24]. On US, pathology ranges from
Lateral Meniscus 413
ligament thickening, heterogeneity, or a wavy pattern, to complete ligament disrup-

tion or even avulsion of the LCL from the fibula [9].
There are several pitfalls in the sonographic evaluation of the LCL. Valgus knee
angulation slackens the LCL, producing a wavy, anisotropic appearance that mim-
ics injury. Another trap is to mistake the anisotropy of the dual insertion of the LCL
and the BFT on the FH for LCL enthesopathy or BFT tendinosis [9]. A third pitfall
is to mistake decreased echogenicity of the proximal LCL for pathology in the
absence of lateral knee symptoms [25]. This normal sonographic finding most likely
relates to connective tissue mucin. It is unusual to have an isolated LCL injury since
it is but one of the several lateral knee stabilizers [9]. Therefore, further evaluation
for concomitant soft tissue damage should be considered if LCL injury is detected.
Lateral Meniscus
To accurately evaluate the entire LM, MRI is the best choice; however, specific find-
ings on US may indicate pathology [9]. On US, the ordinary LM is hyperechoic and
triangular-shaped. Degeneration of the LM appears as meniscal heterogeneity with
possible extrusion and fragmentation [9]. The knee menisci, positioned between the
femoral and tibial components, protect knee cartilage from excessive wear and tear
[26]. Meniscal tears may accelerate knee osteoarthritis and are associated with
meniscal extrusion [9]. Tears may appear as focal anechoic or hypoechoic defects
extending to the meniscal surfaces.
One study comparing US to MRI to detect meniscal tears revealed only 64%
specificity for US [27]. The medial and lateral menisci posterior horns yielded the
best specificity of 100% and 94%, respectively. However, sensitivity levels were
only 63 and 75%, respectively. Furthermore, US cannot detect bucket-handle tears
due to the beam’s inability to penetrate the meniscus [27].
Meniscal (parameniscal) cysts may present as palpable, sometimes painful,
masses along the knee joint [28]. The cyst on US is anechoic or hypoechoic and may
contain septa or debris. Ultrasound is 94% accurate for detecting parameniscal cysts
[28]. An underlying meniscal tear is associated with 90% of LM cysts, making the
latter a bellwether finding. If a meniscal cyst is detected, knee flexion may enhance
its prominence [29]. A complex meniscal cyst may mimic a solid mass; however,
continuity with the meniscus argues in favor of a cyst [15]. Transducer compression
may demonstrate a connection in which the cyst partially empties its contents via a
connecting tract with the meniscus.
Meniscal extrusion is described as the displacement of meniscal tissue beyond
the tibial margin [30]. In addition to meniscal tears, the degree of meniscal extru-
sion is affected by age, body weight, knee alignment, cartilage damage, and the
presence of osteoarthritis [26, 31]. The MRI is the gold standard for assessing
meniscal extrusion [32]. Meniscal extrusion on MRI is defined as >3 mm [33].
Ultrasound reliably measures LM extrusion but tends to overestimate extrusion by
about 1.1 mm compared to MRI [26]. However, the same study demonstrated an
overlap of values of LM extrusion in normal and abnormal subjects.
414 18 Lateral Knee
Biceps Femoris Tendon
The BFT may develop tendinosis, noted as thickening and hypoechogenicity at the
conjoined tendon with the LCL, where both insert on the FH [9]. However, to reiter-
ate the pitfall previously described for the LCL, the dual insertion of the LCL and
the BFT on the FH may give a false impression of heteroechogenicity and swelling,
thus mimicking enthesopathy of the LCL and tendinosis of the BFT. Tears of the
BFT have been reported to occur more often at the distal myotendinous junction [9].
Common Peroneal Nerve
Peroneal neuropathy may cause lateral foreleg paresthesia and foot weakness. The
CPN is found just posterior to the BFT. Due to its proximity to the FH, the CPN is
prone to direct injury [9]. It is also subject to entrapment, neoplasms, and intraneu-
ronal ganglia. The nerve may develop hypoechoic swelling proximal to the point of
compression from the entrapment [9]. Repetitive injury from an overhanging pros-
thetic knee component may also cause neuropathy [14].
Pitfalls
1. Use a 12 MHz or higher transducer since the region of interest is superficial.

2. Accurately mark three bony landmarks: the LFE, the GT, and the FH. The FH
is more posterior than most people think.
3. Remember, when evaluating the LCL, valgus knee angulation slackens this
ligament, producing a wavy appearance with anisotropy that may mimic injury.
A pillow between the knees moderates valgus knee angulation, thus reducing
artifacts.
4. Do not mistake the lateral recess synovial fluid or synovial hypertrophy for
adventitial bursitis associated with ITBS.
5. Do not mistake the dual insertion of the LCL and the BFT on the FH for enthe-
sopathy or tendinosis since this may give a false impression of hypoecho-
genicity and swelling.
6. Do not mistake decreased echogenicity of the proximal LCL for pathology
without lateral knee symptoms; this is a normal sonographic finding.
7. Since the LCL is only one of several lateral knee stabilizers, further evaluation
for concomitant soft tissue damage should be undertaken if an LCL injury is
detected.
8. While some meniscal tears may be visible sonographically, MRI remains the
gold standard to confirm and evaluate for bucket-handle tears since the latter
remain invisible to US.
Method 415
9. Look for telltale signs of meniscal damage, such as a meniscal cyst or extrusion.
10. If a meniscal cyst is detected, knee flexion may enhance its prominence, and
transducer compression may partly empty the cyst, thus demonstrating a tract
leading to the meniscus.
11. Minimize the anisotropy of the lateral knee stabilizing ligaments by examining
them when taut. The LCL is tight when the knee is extended, whereas the ALL
is taut when the knee is flexed 90° and the foot is internally rotated.
Method
The patient is in the lateral decubitus position with a bolster under the knee; the knee
is bent 10–20°. An alternative position is to have the supine patient internally rotate
the hip and flex the knee [9]. Mark off GT, the bony prominence on the anterolateral
tibia just distal to the patella. This should not be confused with the FH at the same
level, which is posterolateral. Mark off the FH and LFE as well (Fig. 18.3).
rotocol Image 1: Iliotibial Band, Longitudinal + Dynamic

P
(Fig. 18.4)
With the transducer in LAX with respect to the femur, place the distal end on GT, a
brightly hyperechoic bone with a gentle proximal slope. Rotate the proximal end
posterolaterally until you see hyperechoic ITB fibers inserted onto GT. The ITB
courses over the underlying LFE; look for sonographic signs related to ITBS and
distal tendinopathy. Deep to the ITB, just proximal to the knee joint, you may see
the ITB bursa, which is more apparent when ITB bursitis is present. See Clinical
Comments for more information.
An alternative method to visualize the ITB is to view the patellar tendon in LAX
and then perform a lateral TAX slide to visualize the ITB extending from GT [9].
Fig. 18.3 Lateral knee

topographic landmarks
416 18 Lateral Knee

1: Iliotibial band,
Note that with this method, the transducer is initially positioned parallel to the tibial
axis, so you will need to rotate the proximal end of the probe in a posterolateral
direction.
rotocol Image 2 (Optional): Iliotibial Band, Transverse +

P
Dynamic (Fig. 18.5)
At GT, rotate the transducer 90° to examine the ITB in TAX view to confirm any
pathology found on the LAX or if you suspect ITBS with or without snapping.
Slowly move the probe in a proximal TAX slide to thoroughly explore the ITB in a
cross-section. If considering ITBS, try to identify an adventitial iliotibial bursa or
simply soft tissue swelling between the ITB and the LFE. There may or may not be
ITB thickening or LFE cortical irregularity. Sonopalpitory pain is diagnostically
useful. Do not mistake the normal lateral recess synovial fluid for adventitial bursi-
tis [11]. At the LFE, have the patient slowly bend the knee to see if the ITB snaps
over the LFE. At 30° of flexion, the ITB is said to move from anterior to posterior
over the LFE. This can be evaluated in a supine or standing position [34]. Be aware
that some authors maintain that the ITB movement is only an illusion created by
changing tension in the anterior and posterior fibers of the ITB [7]. See Clinical
Comments, Iliotibial Band Syndrome.
rotocol Images 3a/b: Lateral Collateral Ligament,

P
The knee is bent at 10°. Rotate the probe 90° back to a longitudinal orientation,
place the distal end on the FH, and aim the proximal end toward the LFE to visual-
ize the fibrillar LCL. You may visualize the hyperechoic bone between the femur
Method 417

2 (optional): Iliotibial
band, transverse + dynamic
Fig. 18.6 Protocol Images 3a/b: Lateral collateral ligament, longitudinal + dynamic
and the FH; this is the tibia. Perform a proximal LAX slide and scrutinize the entire
LCL. Separate images can be saved for the proximal (Protocol Image 3a) and distal
attachments (Protocol Image 3b).
A valgus knee deformity may slacken the LCL, creating anisotropy with a wavy
appearance of the LCL, thus mimicking injury [9]. If this is present, a pillow
between the knees will somewhat correct the valgus angulation [35]. Normal
418 18 Lateral Knee
anisotropy can be diminished by fully extending the knee to increase tension on the
ligament, thereby improving LCL damage assessment [29]. Deep to the LCL is the
popliteus tendon origin at the popliteus groove or sulcus of the femur. This sulcus is
at the distal LFC. Tilt the probe to counteract anisotropy since this may mimic a
cystic mass otherwise. To place dynamic varus stress on the LCL in the lateral decu-
bitus position, place a block under the knee so that the foreleg is suspended. Press
down on the foreleg to look at the integrity of the LCL and note any joint space
widening.
Protocol Image 4: Lateral Meniscus, Longitudinal (Fig. 18.7)
Next, focus on the structures deep to the LCL. Between the distal femur and the
tibia lie the femorotibial joint and the triangular, hyperechoic LM. Tilt the probe in
either direction to enhance LM visualization.
The hypoechoic or anechoic areas on each side of the LM are the cartilage of the
tibia and femur. If a meniscal cyst is suspected, flex the knee to enhance its promi-
nence and apply transducer pressure to see if the putative cyst connects to the LM
and partially empties its contents. Focusing on the LM, perform a TAX slide poste-
riorly, continually tilting the probe back and forth to optimize visualization.
To evaluate for meniscal extrusion, capture the image of the LM and the poplit-
eus groove. Draw a horizontal line along the tibial surface, extending proximally
just past the middle of the LM. Measure the distance between this line and the most
superficial protrusion of the LM in millimeters (Fig. 18.8). This is an unloaded
(non-weight-bearing) view. One study protocol suggests examining the patient in a
standing bipedal, weight-bearing (loaded) view with the knee bent in 10° flexion

4: Lateral meniscus,
longitudinal
Method 419
Fig. 18.8 Lateral meniscus extrusion measurement
[26]. This requires marking the transducer position with a ballpoint pen when supine
so that the identical probe position can be duplicated in the standing position. Make
sure there is no tibial rotation in the supine or standing examination.
rotocol Image 5: Biceps Femoris Tendon, Longitudinal

P
(Fig. 18.9)
With the patient supine or in lateral decubitus, the knee is bent to 10° and the hip is
internally rotated. Affix the distal end of the transducer to the posterolateral edge of
the FH, which appears as a hyperechoic diagonal line. Rotate the proximal trans-
ducer end posteriorly to parallel the femoral axis to visualize the BFT in a LAX
view. The myotendinous junction is seen proximally and is deep to the tendon. Note
that the LCL and the BFT both insert into the FH; this dual insertion produces
hypoechogenicity, mimicking enthesopathy.
420 18 Lateral Knee

5: Biceps femoris tendon,
longitudinal
rotocol Image 6: Common Peroneal Nerve, Transverse

P
(Fig. 18.10)
At the insertion of the BFT on the FH, rotate the probe 90° to look for the CPN. The
CPN, located posterior to the FH, is a rounded/ovoid honeycomb structure. Tilt the
probe back and forth to utilize anisotropy to help identify the CPN, which is often
isoechoic with adjacent soft tissue. This may be challenging. Measure the cross-
sectional area (CSA) of the CPN and compare it with the contralateral side. If the CSA
is enlarged on one side or is greater than 10 mm2, this may indicate CPN swelling.
An alternative method of finding the CPN:
With the patient in a prone position, bend the knee 15° and place the ankle on the
contralateral ankle, thus externally rotating the hip. With the probe in TAX, identify
the proximal FH by its hyperechoic linear diagonal cortex. In cross-section, the
CPN is just medial to the straight bony cortex of the FH. Move the probe distally and
watch the CPN move in an oblique path, superficial to and then lateral to the fibular
neck, thus identifying the CPN. The CPN then dives beneath one of the heads of the
peroneus longus muscle, also seen in TAX. This maneuver exploits the anatomic
course of the CPN, akin to the method of identifying the median nerve in the wrist.
rotocol Image 7: Common Peroneal Nerve, Longitudinal

P
(Fig. 18.11)
Once the CPN is identified in TAX, rotate the probe 90° to evaluate the nerve in
LAX, remembering its oblique path as described above. In this view, there may be
anechoic fluid tracking along the CPN epineural sheath, consistent with an intraneu-
ral ganglion. This view may also demonstrate the peroneus longus tendon com-
pressing the CPN as the nerve dives deep to this tendon to hug the fibular neck.
Again, the CPN may swell proximal to compression.
Method 421

6: Common peroneal
nerve, transverse

7: Common peroneal
nerve, longitudinal
rotocol Image 8 (Optional): Anterolateral Ligament,

P
Return the transducer to the position in Protocol Image 1 of the ITB. Next, flex the
knee to 90° and internally rotate the knee by slightly inverting the foot [19]. From
GT, perform a posterolateral TAX slide to a point halfway between GT and the FH
to visualize the distal ALL insertion point onto the tibia. If you reach the FH, you
have gone too far. Once the ALL insertion point is seen, rotate the proximal end of
the probe slightly posteriorly to visualize the full ligament in LAX and its insertion
onto the LFE. Deep to the ligament is the popliteus groove and the LM [19]. Turn
422 18 Lateral Knee
Fig. 18.12 Protocol Image 8 (Optional): Anterolateral ligament, longitudinal + dynamic
the PD on to locate the LIGA in cross-section deep to the ALL [21]. Since the ALL
and the LIGA are closely related, the presence of the LIGA helps confirm that the
nearby thin linear structure is the ALL. To dynamically demonstrate the integrity of
the ALL, turn on PD and further internally rotate the foot to increase tension on this
ligament [21]. This rotation should impede the blood flow to the LIGA if the ALL
is intact.
Complete Lateral Knee Ultrasonic Examination Checklist
□ Protocol Image 1: Iliotibial band, longitudinal + dynamic
□ Protocol Image 2 (optional): Iliotibial band, transverse, + dynamic
□ Protocol Images 3a/b: Lateral collateral ligament, longitudinal + dynamic
□ Protocol Image 4: Lateral meniscus, longitudinal
□ Protocol Image 5: Biceps femoris tendon, longitudinal
□ Protocol Image 6: Common peroneal nerve, transverse
□ Protocol Image 7: Common peroneal nerve, longitudinal
□ Protocol Image 8 (optional): Anterolateral ligament, longitudinal ± power Doppler
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26. Winkler PW, Csapo R, Wierer G, Hepperger C, Heinzle B, Imhoff AB, et al. Sonographic
evaluation of lateral meniscal extrusion: implementation and validation. Arch Orthop Trauma
Surg. 2021;141(2):271–81.
27. Unlu EN, Ustuner E, Saylisoy S, Yilmaz O, Ozcan H, Erden I. The role of ultrasound in the
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424 18 Lateral Knee
28. Rutten MJ, Collins JM, van Kampen A, Jager GJ. Meniscal cysts: detection with high-
resolution sonography. AJR Am J Roentgenol. 1998;171(2):491–6.
29. Bianchi E, Martinoli C. Knee. Ultrasound of the musculoskeletal system. Springer; 2007.
p. 637–744.
30. Masouros SD, McDermott ID, Amis AA, Bull AM. Biomechanics of the meniscus-meniscal
ligament construct of the knee. Knee Surg Sports Traumatol Arthrosc. 2008;16(12):1121–32.
31. Crema MD, Roemer FW, Felson DT, Englund M, Wang K, Jarraya M, et al. Factors associated
with meniscal extrusion in knees with or at risk for osteoarthritis: the Multicenter Osteoarthritis
study. Radiology. 2012;264(2):494–503.
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symptom relationship with wide-area ultrasound scanning of knee osteoarthritis. Sci Rep.
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2013;32(7):1199–206.
35. Jacobson J. Knee ultrasound. Fundamentals of musculoskeletal ultrasound. Philadelphia, PA:
Elsevier; 2018. p. 284–327.
Chapter 19
Medial Knee

Evaluation or assessment of the following:
1. Medial (tibial) collateral ligament
2. Medial meniscus
3. Pes anserine tendon insertion
4. Pes anserine bursa
5. Snapping pes anserine tendons
1. Are the tendons and ligaments normal in appearance?
(b) If abnormal, is the pathology caused by an inflammatory or degenerative
process?
2. Is there evidence of a meniscal tear?
(a) Is a parameniscal cyst present?
(b) Is meniscal extrusion present?
3. Is there evidence for pes anserine bursitis?
4. Is there evidence for snapping pes anserine tendons?
States Government.

Switzerland AG 2023
426 19 Medial Knee
Basic Anatomy (Fig. 19.1)
The medial collateral ligament (MCL), also known as the tibial collateral liga-
ment, traverses from the medial femoral epicondyle (MFE) to the proximal tibia
[1]. It resists valgus stress on the knee. The MCL has superficial and deep fibers,
also known as anterior and posterior bands. A third, even deeper layer consists of
the meniscofemoral and meniscotibial ligaments, the latter known as the coronary
ligament. On ultrasound (US), the superficial layer is hyperechoic, and the deeper
layer is hypoechoic. The even deeper meniscofemoral and meniscotibial ligaments
are more hyperechoic. This trilaminate structure evokes a sandwich cookie, but with
inverse coloration. The deeper layers may be increasingly difficult to visualize on
US. Between the superficial and deep bands of the MCL lies the MCL bursa.
The medial meniscus (MM), a crescent-shaped fibrocartilage between the fem-
oral condyle and tibial plateau, functions as a shock absorber. The meniscotibial
ligaments attach the MM to the tibia. In contrast to the lateral meniscus, the MM is
fused to the collateral ligament via meniscofemoral and via the meniscotibial liga-
ments [1].
Pes Anserine Tendons and Bursa
The pes anserine tendons (sartorius, gracilis, and semitendinosus) cross superfi-
cially at an oblique angle to the distal MCL along their way to the proximal antero-
medial tibia. The three pes anserine tendons (PATs) from anterior to posterior [2]:

medial knee anatomy
Pes Anserine Tendons and Bursa 427
1. Sartorius
This superficial, flat muscle runs obliquely from the anterior superior iliac spine
across the anterior thigh to the medial tibial tubercle. “Sartor” is Latin for tailor; the
sartorius muscle is the longest in the body and evokes a tailor’s tape measure.
2. Gracilis
This thin muscle runs along the medial thigh, deep to the adductor longus and
magnus, from the pubic symphysis to the medial tibial tubercle. “Gracilis” is
Latin for thin, slender, and svelte.
3. Semitendinosus
This superficial muscle in the posterior medial thigh runs from the ischial
tuberosity to insert on the medial tibial tubercle. The semitendinosus name
reminds us that the distal free tendon comprises about 25% of the length of the
entire muscle-tendon unit.
The tendons are mnemonically recalled by “Say Grace before Tea” [3]. An alter-
native mnemonic is “SGT” or “sergeant.” The pes anserinus (Latin for “goose foot”)
is the joining of the three tendons that are superficial to the MCL and inserted into
the anteromedial proximal tibia just distal to the insertion of the MCL [3]. The ten-
dons splay out at their insertion, suggesting the shape of a goosefoot [4]. Our favor-
ite mnemonic is “Silly Goose Tendons,” which evokes both the tendon names and
insertional configuration (Fig. 19.2).
Fig. 19.2 Pes anserine

tendons
428 19 Medial Knee
The pes anserine (anserinus) bursa (PAB) is sandwiched between the deeper
MCL and the more superficial PATs at the anteromedial border of the tibia [5]. This
bursa is undetectable unless it is pathologically distended due to inflammation [4].
Clinical Comments
Medial Collateral Ligament
Valgus stress or twisting knee injuries are the leading cause of MCL injuries, most
often occurring in sports participants such as soccer players and skiers [3, 6].
Ultrasound had 94% accuracy in one small series for MCL injury detection [7].
The most common locations for MCL tears are the proximal portion of the super-
ficial MCL and the meniscofemoral ligaments; bony avulsion of the proximal inser-
tion may occur for either layer [6]. Sonographic findings of MCL injury are
ligamentous thickening and heterogeneous hypoechogenicity [3, 7]. Ligamentous
thickening implies damage and is defined as greater than 6 mm at the femoral
attachment or greater than 3.6 mm at the tibial attachment. Injury may also be
inferred from loss of the fibular echotexture when the ligament is taut (knee
extended) [3].
The grading of a ligamentous sprain may also be suggested by the sonographic
appearance [8, 9]:
1. Grade 1 (mild): ligamentous stretching without fiber disruption but with associ-
ated edema indicated by adjacent hypoechoic or anechoic fluid.
2. Grade 2 (moderate, partial thickness tear): abnormal focal hypoechogenicity,
possibly with the edematous changes as in Grade 1.
3. Grade 3 (severe, full-thickness tear): complete disruption of the ligament
fibers and possibly retraction; there may be hemorrhage and surrounding edema-
tous change.
Valgus stress with dynamic US has also been proposed to define injury grade
depending upon the degree of joint space widening [3, 7]:
1. <5 mm: Grade 1 injury
2. 5–10 mm: Grade 2 injury
3. >10 mm: Grade 3 injury.
However, variations in ordinary medial joint spaces under valgus stress may overlap
with grade 1 and 2 parameters above [10]. In addition, be aware that the male gen-
der, advancing age, and 30 degrees of knee flexion are all associated with increased
medial knee joint space. The Pellegrini-Stieda sign is calcification of the proximal
MCL seen on radiographs, indicating prior or chronic MCL injury [3]. Such cal-
cium deposits may also be seen on US as hyperechoic echogenicity within the prox-
imal MCL [6, 8]. If there is a concern for MCL sprain, compare the MCL echotexture
Medial Meniscus 429
and joint space width of the affected knee with the normal contralateral knee. The
MCL echotexture should be examined in full knee extension while the joint space is
evaluated in 30-degree flexion under valgus stress.
Medial Collateral Ligament Bursitis
The bursa between the superficial and deep MCL layers may become inflamed and
produce medial joint line pain on palpation or valgus stress [11]. Lidocaine injec-
tions may be both diagnostic and therapeutic. Ultrasound may be used to guide the
injection of the bursa [12]. Causes of MCL bursitis include rheumatoid arthritis,
genu valgus, direct trauma, pes planus, osteophytes, and activities such as riding a
horse or motorcycle [13]. The latter two pursuits generate friction in the medial
aspect of the knee.
Medial Meniscus
Ultrasound may detect meniscal abnormalities but, by itself, is insufficient to diag-

nose meniscal tears [14]. Magnetic resonance imaging (MRI) is the gold standard
imaging modality for detecting meniscal pathology [15]. Evaluation of the menis-
cus by US is limited by a lack of visualization of the entire meniscus, particularly
the inner margins [14]. The knee menisci, positioned between the femoral and tibial
components, protect knee cartilage from excessive wear and tear [16]. Consequently,
meniscal damage may encourage the development of osteoarthritis.
On US, the normal MM is hyperechoic and triangular-shaped [3]. Meniscal
degeneration appears on US as a heterogeneous echotexture with possible frag-
mentation and extrusion. Medial meniscal tears may arise as focal anechoic or
hypoechoic defects extending to the meniscal surface [3]. Using high-frequency
transducers (12 or 14 MHz), sensitivity and specificity for sonographic detection of
meniscal tears have been reported as 85 and 86% in one study and 88 and 85% in
another [15, 17]. Varus stress may enhance visualization of a meniscal tear [18].
A meniscal (parameniscal) cyst may present as a palpable, sometimes painful,
mass along the knee joint [19]. The cyst on US is anechoic or hypoechoic and may
contain septa or debris. Ultrasound is 94% accurate for detecting parameniscal cysts
[19]. An underlying meniscal tear is often, but not always, associated with a menis-
cal cyst. Thus, sonographic identification of a meniscal cyst should heighten suspi-
cion of an underlying meniscal tear. If a meniscal cyst is detected, knee flexion may
enhance its prominence [6]. A complex meniscal cyst may mimic a solid mass;
however, continuity with the meniscus favors a cyst [18]. Linkage is demonstrated
when transducer compression causes the cyst to empty its contents via a tract con-
nected to the meniscus.
430 19 Medial Knee
Meniscal extrusion (ME) is described as the displacement of meniscal tissue

beyond the tibial margin [20]. Meniscal extrusion, also known as subluxation, is
associated with meniscal tears and osteoarthritis [21, 22]. MRI is considered the
gold standard for the assessment of ME [21–23]. Meniscal extrusion is detectable
by US; the degree of ME is affected by age, body weight, knee alignment (varus
deformity for medial ME), cartilage damage, and the presence of osteoarthritis
[21, 24].
When compared with MRI results, US had excellent sensitivity (95–96%) and
reasonable specificity (70–82%) for the detection of ME [22]. A study of primarily
medial menisci suggests that MRI-delineated ME greater than 2 mm often indicates
an underlying meniscal tear confirmed by arthroscopy [25]. Medial meniscal extru-
sion (MME) may displace the MCL. One interesting study describes that 61% of
patients with knee pain and radiographic osteoarthritis had MME coupled with
MCL displacement [24]. This held true for patients with milder degrees of radio-
graphic joint space narrowing. This suggests but does not prove that MME and
MCL displacement may be pain generators in some patients with knee osteoarthri-
tis. It is unclear if the MME contributes to radiographic medial joint space narrow-
ing or vice-versa.
Pes Anserine Tendons and Bursitis
Pes anserine bursitis is associated with obesity, osteoarthritis, MM tear, direct knee
trauma, overuse, obesity, valgus knee deformity, pes planus, and type 2 diabetes [4,
26–28]. Symptoms of PAB include local pain, swelling, and tenderness at the
anteromedial knee, approximately 5–7 cm below the joint line [4, 29]. The pain is
exacerbated by arising from a seated position or using stairs.
Bursitis appears as anechoic fluid deep to the pes anserine tendons with thicken-
ing and decreased echogenicity of the tendons [3]. The distended oblong bursa is
sandwiched between the PAT and the deeper MCL [4]. Ultrasound-guided injection
of the PAB is more accurate than blind injection [30, 31]. It is important to remem-
ber that PAB is only one reason for proximal tibial anterior and anteromedial knee
pain. Other causes, depending on the clinical setting, include MM tear, proximal
medial tibial fracture or osteonecrosis, saphenous nerve compression or damage,
and snapping pes anserine tendons [32–36].
Snapping Pes Anserine Tendons
Snapping pes anserine tendons (gracilis or semitendinosus) over the medial femur
or tibia during active knee flexion or extension may cause extra-articular knee snap-
ping and pain [35, 36]. The snapping may be audible and visible in the medial distal
hamstring area [35]. This condition has been described in athletes or associated with
Pitfalls 431
trauma, overuse, tumors, and postoperative changes. Structural etiologies of snap-

ping pes anserine tendons include bony protuberance, unstable pes tendons due to
deficient accessory bands or ligamentous laxity following trauma, and chronic over-
load of the anterior knee [37]. Dynamic US of the involved area of the posterior
medial knee is diagnostic [35, 37]. Ultrasound-guided corticosteroid and anesthetic
injections may assist in diagnosis [35].
Infrapatellar Branch of the Saphenous Nerve Damage
The infrapatellar branch of the saphenous nerve (IPBSN) is a terminal sensory

branch that innervates the anteromedial knee. Injury may occur from surgical inci-
sion or retraction, sports injury, direct trauma such as in a motor vehicle accident, or
entrapment neuropathy between the sartorius tendon and the MFE [32]. Symptoms
include acute or chronic anterior knee pain, stiffness, dysesthesia, numbness, abnor-
mal gait, swelling, and warmth; the latter two symptoms mimic complex regional
pain syndrome [32, 34]. Pain may be poorly localized and exacerbated by knee
flexion [34]. A positive Tinel’s sign over the involved nerve may be diagnostically
helpful [32].
High-resolution US (15–22 MHz) correctly identifies the IPBSN in 86–100%
and demonstrates hypoechoic neural thickening described as a neuroma [33].
Ultrasound may visualize the causative condition, such as fibrous scar tissue or
surgical fixation [32]. Diagnostic sensory nerve conduction studies have also been
suggested [34]. Treatment options include ultrasound-guided injection, radiofre-
quency ablation, or neuroma excision [32, 34].
Pitfalls
1. To avoid mistaking a meniscal cyst for a solid mass, apply probe pressure to
establish a connection with the meniscus since the cyst may empty some of its
contents via a tract to the meniscus.
2. The Pellegrini-Stieda sign is radiographically or sonographically detected MCL
calcification indicating prior or chronic MCL injury.
3. If there is a concern for MCL sprain, sonographically compare the MCL
echotexture and joint space width of the affected and the normal contralateral
knee. Due to variations in normal medial joint spaces under valgus stress, there
may be an overlap of grade 1 and 2 parameters. In addition, the male gender and
advanced age are associated with increased medial knee joint space width.
4. The MCL echotexture should be examined in full knee extension, while the
joint space is best evaluated in 30-degree flexion and under valgus stress.
5. Ultrasound may detect abnormalities in the MM but is insufficient as a stand-
alone imaging technique to diagnose meniscal tears. MRI is the gold standard.
432 19 Medial Knee
6. When evaluating sources of knee pain, consider that MME or MCL displace-
ment may be pain generators in some patients with knee osteoarthritis.
7. It is unclear if the MME contributes to radiographic medial joint space narrow-
ing or vice versa.
8. Ultrasound-guided injection of the PAB is more accurate and effective.
9. Do not misinterpret the insertion of the semimembranosus tendon in its bony
groove (sulcus) on the tibia for a parameniscal cyst. Tilting the probe to coun-
teract anisotropy will reveal the hyperechoic tendon.
10. Pes anserine bursitis is only one cause of proximal anteromedial knee pain.
Depending on the clinical setting, other reasons include MM tear, proximal
medial tibial fracture or osteonecrosis, saphenous nerve compression or dam-
age, and snapping pes anserine tendons.
Method
The patient is recumbent with the knee flexed to about 20–30 degrees using a bolster
or rolled-up towel. The hip should be comfortably externally rotated, allowing full
access to the medial knee. With a ballpoint pen, mark off the palpable protruding
MFE, which is about 3 cm superior to the joint line. A trick to verify the location of
the MFE is to slowly scan the medial femur in transverse axis (TAX) with a TAX
slide until you see a hyperechoic triangular protrusion, which is the MFE [38]. Also,
mark off the joint line by palpation. The evaluation of the medial patellar retinacu-
lum and the medial patellofemoral ligament is described in Chap. 16.
rotocol Image 1: Medial Collateral Ligament, Longitudinal +

P
dynamic (Fig. 19.3)
The MCL stretches from the MFE to the medial tibia in a slightly oblique path.
Align the probe with the femur, placing the proximal end on the MFE. The probe is
in the coronal plane of the femur. Rotate the distal transducer end posteriorly toward
the examination table about 20–30 degrees until you see the MCL, a hyperechoic
band overlying the V-shaped joint space. The long axis of the probe should lie some-
where between the femoral and tibial long axes. Note that the bony tibial portion of
the knee joint is slightly more superficial than the femoral section.
To best delineate the MCL, tilt the probe back and forth, performing slight TAX
slides anteriorly and posteriorly to look at the margins of the MCL; anisotropy will
demarcate it from other soft tissue structures. Evaluate the layers of the MCL. Please
see Basic Anatomy above for more details. The deeper layers are challenging to
visualize. Between the superficial and deep bands of the MCL, the MCL bursa may
be visible. Perform longitudinal axis (LAX) slides to examine the proximal
Method 433
Fig. 19.3 Protocol Image 1: Medial collateral ligament, longitudinal + dynamic
insertion of the MCL on the MFE and the distal insertion on the tibia about 5 cm
distal to the joint line. If anisotropy is significant, the knee can be placed into full
extension to reduce artifacts by increasing MCL tautness.
To examine the MCL’s integrity, apply valgus stress to a knee at 20–30-degree
flexion by pushing the foreleg in a lateral direction; a damaged MCL may permit
joint space widening [3, 7, 24]. In a fully extended knee, look for MME against the
MCL, possibly displacing the MCL. If necessary, rotate the transducer 90 degrees
to visualize the MCL in TAX view. Identify the MCL in cross-section by tilting the
transducer since the anisotropy of the ligament will help define the margins of this
band-like oblong structure. The TAX view may verify any damage suspected from
the LAX images. The entire length of the MCL, from the femur to the tibia, should
be carefully scanned to look for pathology that may have been overlooked on the
LAX scan.
434 19 Medial Knee
Protocol Image 2: Medial Meniscus, longitudinal (Fig. 19.4)
Stretch and elevate the leg by gently placing the calf on a yoga block. Return the
probe to the coronal position in Protocol Image 1, that is, the LAX view of the
MCL. Focus on the triangular-shaped hyperechoic MM. Tilting the probe one way
Fig. 19.4 Protocol Image 2: Medial meniscus, longitudinal

Method 435
and then the other will aid visualization. Perform a slow TAX slide posteriorly to
see the posterior horn of the MM, tilting the probe back and forth to sharpen the
view at each stage. Look for meniscal degeneration, tears, cysts, or extrusion. Do
not misinterpret the insertion of the semimembranosus tendon in its groove at the
tibia as a parameniscal cyst. Tilting the probe to counteract anisotropy will reveal
the hyperechoic tendon and avoid this pitfall.
rotocol Image 3 (Optional): Medial Meniscal Extrusion

P
Measurement, Longitudinal
Look for MME, which is the protrusion of the MM beyond the tibial bone. If pres-
ent, also note the displacement of the MCL. To quantitate MM extrusion, draw a
line across the external edge of the medial tibial plateau. Measure the height of any
protrusion of the meniscus superficial to this line [22]. See Clinical Comments
above for more information.
Protocol Image 4: Pes Anserine Tendons, transverse (Fig. 19.5)
Perform a distal LAX slide to center the probe on the distal MCL insertion on the
medial tibia. This is about 5–6 cm distal to the joint line. Rotate the distal probe
10–20 degrees medially toward the anterior tibia to look for the PATs in TAX. Just
superficial to the MCL insertion, look for three subtle hyperechoic “hills”: the pes
anserine tendons (sartorius, gracilis, and semitendinosus) in transverse view, on
their way to their insertion points slightly distal and anterior to the MCL insertion,
the tibia. This may require tilting the probe in both directions to use anisotropy to
delineate these tendons in cross-section.

4: Pes anserine tendons,
transverse
436 19 Medial Knee
Fig. 19.6 Pes anserine

bursitis
The PAB, sandwiched between the MCL and the PATs, is typically detected only
when filled with anechoic fluid, such as when bursitis is present (Fig. 19.6). Slight
TAX slides in either direction may help to detect the PAB, which will appear as an
oblong anechoic fluid collection. Verify the PAB in an orthogonal view. The inferior
medial genicular artery may be seen by using the PD; it is deep to the MCL inser-
tion, resting on the tibial cortex. If an injection is contemplated, rotate the trans-
ducer to best define the PAB and survey the area with PD to avoid damaging the
genicular artery.
Turn the probe 90-degrees if needed for an orthogonal view of the pes anserine
tendons. The tendon complex may appear as a single entity in this position; moving
the probe in a TAX slide posteriorly may help to demarcate individual tendons as
they are followed proximally [3].
Complete Medial Knee Ultrasonic Examination Checklist
□ Protocol Image 1: Medial collateral ligament, longitudinal, + dynamic
□ Protocol Image 2: Medial meniscus, longitudinal
□
Protocol Image 3 (optional): Medial meniscal extrusion measurement,
longitudinal
□ Protocol Image 4: Pes anserine tendons, transverse
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Chapter 20
Anterior Hip

1. Anterior hip and groin pain
2. Anterior thigh pain
3. Paresthesia of the lateral thigh
1. Is the anterior hip pain referred from the lumbosacral spine or pelvis?
2. Is the anterior hip pain coming from the femur, the hip joint, or the labrum?
3. If the hip pain is from the joint, is it due to an inflammatory or structural problem?
4. Is the cause of the pain greater trochanteric pain syndrome? If so, what is the
specific underlying pathology?
5. Is anterolateral thigh paresthesia due to meralgia paresthetica?
Basic Anatomy
Bones (Fig. 20.1)
Bony landmarks and protuberances pertinent to US examination are depicted. Note

that the femoral neck angles inward about 30–45° from the axis of the femur.
Labrum (Fig. 20.2)
The fibrocartilaginous labrum along the acetabulum’s circumference augments the

contact area with the femoral head (FH). On ultrasound (US), the labrum appears as
a hypo- or hyperechoic triangular-shaped structure between the acetabulum and FH.
States Government.
Switzerland AG 2023
440 20 Anterior Hip
Fig. 20.1 Bony anatomy

of the hip
Fig. 20.2 Hip labrum

Ligaments 441
Ligaments
The three ligaments reinforcing the hip joint all end with “femoral “and start with
the pelvic origin: ischiofemoral, pubofemoral, and iliofemoral. Another ligament,
the inguinal ligament (IL), runs diagonally from the anterior superior iliac spine
(ASIS) to the pubic tubercle (Fig. 20.3). Structures deep to the IL, from lateral to
Fig. 20.3 Inguinal ligament + neurovascular bundle

442 20 Anterior Hip
medial, are the lateral femoral cutaneous nerve (LFCN), the iliacus muscle, the
femoral nerve/artery/vein, the psoas major, and the pectineus muscle. A mnemonic
for these structures deep to the IL is “Lifelong Itinerant Nomads Are Very Private
People.”
Neurovascular Bundle
Lateral to medial, find the femoral nerve, artery, or vein (or “NAV”). Another mne-
monic is “NAVEL” by adding the more medial “empty space” and then lymphatics.
Anterior Hip (Joint) Recess
The anterior hip recess (AHR) (Fig. 20.4a) is distal to the hip joint and lies along the
femoral neck (FN). The hyperechoic joint capsule starts at the acetabulum and spans
distally to a bony femoral ridge called the intertrochanteric line. The intertrochan-
teric line is at the junction of the FN and shaft and stretches between the lesser and
greater trochanters. The AHR is formed by two layers of the joint capsule: the deep
and the superficial. Distally, the anterior (superficial) layer folds back to become the
posterior (deep) layer.
The distal portion of the iliofemoral ligament (IFL) is just superficial to the
AHR. Thus, the AHR is “sandwiched” between the FN and the IFL. An effusion, if
present, is located between the two layers of the joint recess and distends the joint
capsule, spreading the anterior and posterior layers apart (Fig. 20.4b). A normal
AHR on US gives the appearance of a snake, while a distended AHR is reminiscent
of the shape of a whale.
a b
Fig. 20.4 (a) Anterior joint recess. (b) Anterior hip effusion
Hip Joint
The hip joint, or femoroacetabular joint (FAJ), is comprised of the femoral head
(FH) (the ball) and the acetabulum (socket). The labrum lines the edge of the ace-
tabulum. Superficial to the FH are the iliopsoas tendon (IPT) and muscle (IPM).
Iliopsoas Muscle, Tendon, and Bursa
The IPM-IPT unit, formed from the merger of the psoas major muscle and iliacus,
crosses the FAJ and the FH to insert medially on the lesser trochanter (LT) to func-
tion as a hip flexor. The iliopsoas bursa (IPB) is deep to the IPM and medial to the
IBT. The IPB is usually invisible when not distended and may typically contain
some synovial fluid in about 15% of normals due to communication with the
FAJ [1].
Tensor Fascia Lata and Sartorius
The ASIS is the origin of the tensor fascia lata (TFL) and the sartorius. The sarto-
rius, the longest muscle in the body, crosses the anterior thigh to insert posteromedi-
ally at the knee. The TFL contributes anterior fibers to the iliotibial band, thus
stabilizing the knee with walking and running.
Rectus Femoris
The rectus femoris (RF) is one of the four quadriceps muscles. It has two heads: the
direct head originates from the anterior inferior iliac spine (AIIS); the indirect head
stems from the iliac bone at the lateral edge of the acetabulum. The RF flexes the hip
and extends the knee. At the juncture of the indirect and direct heads, the interdigita-
tion of the tendon fibers creates anisotropy, which can mimic an RF tendon tear.
Clinical Comments
A dynamic US examination of the hip may be extraordinarily helpful [2].

444 20 Anterior Hip
Joint Effusion and Synovitis
The AHR at the FN is the best location to visualize an effusion and synovitis [2].
When a hip effusion is present, synovial fluid often pools in the AHR (Fig. 20.4b).
The AHR allows access to the FAJ and is thus commonly aspirated and injected. In
the longitudinal axis (LAX) view on US, measure the distance from the joint cap-
sule to the FN; an effusion is suspected if the space is >7 mm or if there is a >1 mm
difference between the two hips [3]. Often, no fluid is normally present [4]. However,
internal rotation of the leg may cause bulging of the normal joint capsule, falsely
mimicking an effusion [2]. The transverse axis (TAX) view should confirm an effu-
sion detected in LAX.
The AHR may appear hypoechoic or hyperechoic, depending on anisotropy and
patient body habitus. Recess widening may be due to a joint effusion or synovial
hypertrophy [2]. Distention of the AHR by an effusion may be anechoic, isoechoic,
or hypoechoic, depending on the composition of synovial fluid. Doppler activity
might indicate synovial hypertrophy but is not always diagnostic. However, Doppler
activity may also occur with an infection. If an infection is a consideration, aspira-
tion is always required to confirm an effusion and establish its nature [2]. If initial
aspiration yields no fluid, lavage of the AHR and repeat aspiration may increase the
yield for infected synovial fluid by 25% [5]. Synovial hypertrophy in the AHR may
be due to inflammatory polyarthropathy, pigmented villonodular synovitis, synovial
chondromatosis, and amyloid deposition [2, 6]. The sonographic finding of AHR
distension by itself is not diagnostic of hip effusion in native and prosthetic hips;
aspiration is necessary for confirmation [7].
Ultrasound can also detect a noncommunicating soft-tissue fluid collection that
might be an adjacent abscess. Never aspirate the anterior recess through such a fluid
collection since this might seed the joint/prosthesis with bacteria [7].
Iliopsoas Bursitis
The IPB is usually located medially to the iliopsoas tendon and deep to the muscle.
Together, this iliopsoas complex passes over the ilium [2]. The nondistended IPB is
usually undetectable [8]. Fifteen percent of normal people will have communication
between the IPB and the FAJ, although this percentage increases after arthroplasty
and with inflammatory arthritis [9]. With IPB distension, attempt to verify commu-
nication between the IPB and the FAJ since IPB distention may be due to a chronic
hip problem causing excess synovial fluid. This communication may be seen in the
TAX view, medial to the FH near the psoas major tendon [2].
Distention of the IPB may be due to synovial fluid or synovitis, possibly with
positive power Doppler (PD). Absent direct hip joint pathology, IPB distension
from synovitis may be due to an underlying inflammatory arthropathy such as gout
or rheumatoid arthritis, infection, trauma, or overuse [10–12]. However, the IPB
Postsurgical Hip 445
may be distended asymptomatically. Concomitant iliopsoas bursitis and tendinitis

often occur due to proximity; this is described as iliopsoas syndrome [10].
Be aware that IPB enlargement may typically occur after hip arthroplasty; how-
ever, aspiration is necessary if an infection is suspected [13]. Infection is suggested
by transducer-induced pain or PD activity. A distended IPB may extend anteriorly,
anterolaterally, and even proximally into the abdomen, mimicking a psoas
abscess [2].
Labrum Abnormalities
The anterior labrum is the most common site for labral tears and is the portion of the
hip labrum best visualized by US [14]. Labral hypo- or heteroechogenicity suggests
degeneration, but a well-defined anechoic cleft indicates a labral tear [15].
Ultrasound is 82% sensitive but only 60% specific for labral tear detection, making
the MR arthrogram the premier modality for delineating labral pathology [15].
Femoral acetabular impingement (FAI) with hip flexion and internal rotation
may cause a labrum tear [16]. This is typically a cam-type impingement whose pres-
ence may be inferred from plain radiographs. A bony protuberance or irregularity of
the anterior superior femoral head-neck junction may impinge on the hyaline carti-
lage and labrum, causing a tear [16]. Impingement on the labrum may be dynami-
cally visualized by US; however, US is unreliable as a screening tool for FAI [17].
A paralabral cyst, contiguous to the labrum, also implies a labral tear [18].
Postsurgical Hip
To delineate pain after total hip replacement, an US examination is recommended as

the next step after radiographs [19]. Causes of hip pain after arthroplasty include
infection, iliopsoas bursitis or impingement, prosthesis loosening, arthroplasty par-
ticle disease, trochanteric bursitis (possibly septic), abductor tendon insufficiency,
incision site infection, hematoma, seroma, and heterotopic ossification [19]. The
prosthetic cup, FH, and femoral shaft may all exhibit reverberation artifacts, whereas
normal bone demonstrates acoustic shadowing [20]. A hypoechogenic area that is
superficial to the FN is a common finding after hip replacement and should not be
misinterpreted as pathologic [21].
Since the native joint capsule may have been resected with surgery, a poorly
demarcated pseudocapsule may form over the prosthesis neck. The pseudocapsule
may distend, but the degree of distention does not accurately predict the presence or
absence of an effusion [7]. The suggested threshold for pseudocapsule enlargement
indicative of a septic prosthesis varies from 3.2 mm to 10 mm [13]. Detection of
effusion after hip arthroplasty may be highly challenging, and a lack of AHR or
pseudocapsule distension on US does not rule out an effusion [7, 19]. An effusion
446 20 Anterior Hip
may be loculated, so when you suspect a fluid collection, also evaluate the soft tis-
sue superficial to the lateral and posterior FN [2].
In addition to possible infection, joint effusion may be aseptic, such as in particle
disease and joint loosening [19]. Particle disease is a granulomatous reaction to
polyethylene or polymethylmethacrylate debris and may cause periprosthetic oste-
olysis and a soft tissue mass called a pseudotumor [19]. Also, consider the iliopsoas
tendon and bursal impingement directly upon the anterior femoral component or
acetabular cup as a sources of pain.
Additionally, evaluate the gluteal tendons for abnormalities, particularly if the
arthroplasty was inserted via the anterolateral approach since the abductor tendons
are manipulated with this approach [19]. Iliotibial band abnormalities may also be
due to the lateral surgical approach or friction over the GT [19]. Ultrasound may
detect tendinosis or tears. Heterotopic bone, occurring in approximately 6% of total
hip arthroplasties, may cause pain or decreased range of motion in the hip replace-
ment [19, 22]. Ultrasound will detect heterotopic bone as hyperechoic ossifications
with posterior acoustic shadowing [19].
Tendon and Muscle Abnormalities
The RF may experience a tear at the origin of the direct or indirect heads [23].
However, tears of the RF most commonly occur in the muscle belly, or myotendi-
nous junction, and less often at the tendon origin itself. The RF crosses two joints
and is the most frequently injured quadriceps muscle or tendon [24]. The direct and
indirect heads of the RF, the IPT, and the sartorius origin may exhibit sonographic
signs of tendinosis or a frank tendon tear. Tears of any of these muscles may also be
sonographically detectable, appearing as a loss of normal muscle echotexture, per-
haps associated with a hypoechoic hematoma [24]. Later, an organized hematoma
may have a hyperechoic appearance [24].
Snapping Hip Syndrome
Extra-Articular Medial
Just medial to the AIIS are the lateral and medial iliacus muscles. The medial iliacus
muscle normally interposes between the psoas major tendon (PMT) and the iliopec-
tineal eminence when the leg is in a frog-leg or FABER position (hip flexion, abduc-
tion, and external rotation). In some individuals, this muscle becomes transiently
entrapped so that straightening the leg abruptly releases the ensnared muscle later-
ally, causing the PMT to forcibly snap against the iliopectineal eminence [2, 25, 26].
Diabetic Muscle Infarction 447
This is the frog-leg test for medial extra-articular snapping hip syndrome. However,
such entrapment and release may be asymptomatic.
Remember that even though some sources describe this as the IPT snapping, the
PMT does the snapping since the iliopsoas muscle and tendon have not yet formed
in this location. However, the IPT may impinge and snap upon a protruding acetabu-
lar component of a total hip arthroplasty [27].
Extra-Articular Lateral
The ITB or the gluteus maximus snaps anteriorly over the GT with hip flexion.
Intra-Articular: Femoroacetabular Impingement
This, the least common form of snapping hip, is due to hip capsule injuries such as
loose bodies in the synovial folds, a torn acetabular labrum, synovial chondromato-
sis, or recurrent hip dislocation/subluxation [28].
See Labrum Abnormalities, above.
Calcific Tendinosis
Calcific tendinosis, primarily calcium hydroxyapatite deposition, may also occur in

several hip tendons, including the RF, gluteus maximus, and gluteus medius ten-
dons. Ultrasound reveals hyperechoic foci, perhaps with posterior acoustic shadow-
ing and increased Doppler flow [29]. This may be a source of pain.
Diabetic Muscle Infarction
Diabetic muscle infarction may occur in the calf and, less commonly, in the thigh.
The cause is suspected to be vascular occlusive disease in the setting of longstand-
ing diabetes [30]. A differential diagnosis includes soft tissue infection. Muscle
infarcts are well-marginated, hypoechoic intramuscular lesions with internal linear
structures felt to be muscle fibers. In contrast to an abscess, a muscle infarct lacks
fluid swirling with transducer pressure [30].
448 20 Anterior Hip
Meralgia Paresthetica
Meralgia paresthetica (MP) may occur when the LFCN is compressed as it courses
deep to the IL, just medial to the ASIS (Fig. 20.5) [31]. Symptoms of LFCN
impingement include paresthesia, numbness, burning, dysesthesia, and pain in an
oval shape along the long axis of the anterolateral thigh [31]. Symptoms may
worsen with prolonged walking and standing. Known causes of MP are leg length
discrepancy, weight gain, tight belts or clothing, prolonged standing or hyperex-
tension of the leg or trunk, trauma, and pelvic tumors [31]. The diagnosis is often
made on clinical grounds since the electrophysiologic study of this nerve is chal-
lenging. Ultrasound may demonstrate a hypoechoic, swollen LFCN near the lat-
eral aspect of the inguinal ligament, particularly when compared to the
contralateral, unaffected side [31]. Sonopalpation over the affected nerve may
reproduce symptoms. Treatment is conservative but may require injection under
the ligament near the nerve; US guidance markedly improves injection effi-
cacy [32].
Inguinal Lymph Nodes
Inguinal lymph nodes are a common finding. Normal lymph nodes sonographically
have an oval appearance with a hypoechoic cortex and a hyperechoic hilum [2]. On
short-axis, asymptomatic inguinal lymph node measurements range from 2.1 to
Fig. 20.5 Meralgia

paresthetica mnemonic
Method 449
13.6 mm [33]. Be aware that average-size inguinal lymph nodes may still be malig-
nant, and enlarged reactive lymph nodes may be benign [2]. Sonographic features
that imply possible malignancy include enlargement with a round or asymmetric
shape, absence of normal echogenic hilum, nonuniform cortical thickness, and a
peripheral blood flow pattern [2, 34]. A biopsy is often required if uncertainty exists,
depending on the clinical setting.
Pitfalls
1. When imaging the AHR, position the transducer perpendicular to the recess
since anisotropy may cause the hyperechoic recess layers to appear hypoechoic,
thus mimicking an effusion [2].
2. Be aware that internal hip rotation may produce AHR bulging, simulating disten-
tion [2].
3. The sonographic delineation of a hip effusion is inaccurate for both native and
prosthetic hips. Aspiration is mandatory to confirm an effusion and determine its
nature [7].
4. Never aspirate the AHR through a fluid collection since the latter might be
infected and seed the joint or prosthesis with bacteria [7].
5. Sonographic evaluation of hip arthroplasty has several potential pitfalls:
(a) An effusion may be loculated; thus, US evaluation for an effusion over the
lateral and posterior FN should also be performed [2].
(b) Hip arthroplasty makes it difficult to detect a small joint effusion [7].
(c) Consider the complications of hip arthroplasty, such as particle disease and
pseudotumor formation [35].
6. For medial extra-articular hip snapping, the psoas major tendon (not the ilio-
psoas tendon) snaps against the iliopectineal eminence.
7. A small size of an inguinal lymph node is not assurance that it is benign; like-
wise, a large nodal size does not mean malignancy.
8. A hypoechoic area in the direct head of the RF may be due to anisotropy from
the interdigitation of the indirect head tendon fibers, thereby mimicking a ten-
don tear.
Method
The patient is recumbent with the foot in a slight external rotation of about 15°.
Palpate and mark the bony prominences of the AIIS and the ASIS. Most patients
require a curvilinear probe with the lower frequency; however, a linear probe may
be used in thin patients. When a linear probe is used, lower the frequency and use
the virtual convex setting to widen the field of view.
450 20 Anterior Hip
rotocol Image 1: Femoral Head and Neck, Anterior Hip (Joint)

P
Recess, Longitudinal (Fig. 20.6)
Place the probe in LAX orientation, aligned with the long axis of the femoral shaft,
proximal to the FAJ. Perform a proximal LAX slide to visualize the femoral neck
and head. Toggle and rock the probe to sharpen the hyperechoic FN and FH image,
which resembles a staff with a hooked end. The goal is to image the AHR crisply;
this requires aiming the cephalad end of the probe toward the umbilicus and varying
the transducer angle anywhere between 10 and 45°. Perform a further proximal
LAX slide to see part of the FAJ. Performing tiny TAX slides in either direction will
help to delineate the AHR better. Look at the curved FH, the smaller curved hyper-
echoic acetabulum, and the slightly hyperechoic/hypoechoic anterior acetabular
labrum between these two bones.
Just superficial to the labrum is the IFL, and just superficial to that is the IPT,
which extends distally. Tendinosis of the IPT may be represented by hypoecho-
genicity, swelling, and loss of fibrillar echotexture. The IPB lies medially to the IPT
and remains invisible when not distended.
Look for the hyperechoic joint capsule, which starts at the acetabulum and spans
the FN distally to the bony femoral ridge, the intertrochanteric line. The hypoechoic
AHR is “sandwiched” between the FN bony cortex and the IFL. The AHR is com-
prised of two layers within the joint capsule: the deep and the superficial. An effu-
sion, if present, is located between the two layers of the AHR and may distend the
capsule. Measure the distance from the joint capsule to the FN; an effusion is

1: Femoral head and neck,
anterior hip (joint) recess,
longitudinal
Method 451
diagnosed if the space is >7 mm or if there is a >1 mm difference in this measure-

ment between the two hips [3].
Perform a slight TAX slide in each direction to evaluate the full extent of the
AHR. A small amount of joint fluid may be physiologic. A pitfall is that if the foot
is internally rotated, the AHR may bulge, mimicking an effusion. Another pitfall is
misinterpreting an effusion as normal postoperative changes after hip arthroplasty.
rotocol Image 2: Femoral Head, Iliopsoas, Transverse

P
(Fig. 20.7)
Next, center the image over the FH, and then rotate the probe to a horizontal posi-
tion. In the example image of the right anterior hip, the finned end of the transducer
is on the left side (lateral). This view evaluates the iliopsoas muscle and tendon in
cross-section as it crosses the medial aspect of the FAJ. Focus on the hyperechoic
FH, which should have a thin covering of anechoic hyaline cartilage. The IPT is a
hyperechoic structure that is just deep to the IPM. Superficial to the IPT, you may
see the cross-section of the iliopsoas bursa, if distended, containing
anechoic or hypoechoic synovial fluid or synovitis. In addition to the iliopsoas mus-
cle, the sartorius and the rectus femoris muscles can also be viewed in cross-section.
This image verifies the putative pathology seen in the LAX view.

2: Femoral head, iliopsoas,
transverse
452 20 Anterior Hip
Protocol Image 3: Anterior Labrum, Longitudinal (Fig. 20.8)
Rotate the transducer approximately 90° to a near-vertical position, with the finned
end being more cephalad (proximal). Angle the finned end medially by about 10°.
If the probe is over the FAJ, the bony hyperechoic acetabulum will be on the left
side of the screen and the FH on the right side. Just superficial to the FH is the
anechoic joint cartilage, and just superficial to that is the hypoechoic labrum, which
attaches to the acetabulum. From deep to shallow, the IFL, the IPT, and the iliopsoas
muscle are three concentric, longitudinal layers.
Focus on the labrum, the slightly hyper- or hypoechoic tissue between the ace-
tabulum and the humeral head, and perform TAX slides medially and laterally to
evaluate the anterior labrum for tears, cysts, and calcium deposition. Also, examine
the hyaline cartilage covering the FH. The acetabular labrum may be challenging to
visualize in many normal patients. Switching to a linear probe for a thin patient may
enhance visualization.

3: Anterior labrum,
longitudinal
Method 453
rotocol Image 4: Neurovascular Structures, Transverse ±

P
Doppler (Fig. 20.9)
Next, go back to the transducer position in Protocol Image 2 and perform a medial
LAX slide to see the neurovascular structures. Turn on Color Flow Doppler to aid
identification of the femoral artery and vein. Alternatively, transducer pressure will
collapse the vein, thus distinguishing it from the artery. Angling the medial end of
the transducer approximately 20° in a caudal direction may enhance visualization.
Lateral to medial, find the femoral nerve, artery, or vein or “NAV.”
rotocol Image 5: Anterior Inferior Iliac Spine, Transverse

P
(Fig. 20.10)
The AIIS is the “home base” bony protuberance that will lead to the next few
images. Again, go back to the transducer position for Protocol Image 2. Find the
AIIS by performing a proximal (cephalad) TAX slide until you see the hyperechoic

4: Femoral Neurovascular
structures, transverse ±
Doppler
454 20 Anterior Hip

5: Anterior inferior iliac
spine, transverse
curved “hill,” which is the AIIS. Look for the distinct anechoic acoustic shadowing
deep to the AIIS. The AIIS shape is also reminiscent of a comet with a dark tail. Do
not confuse the AIIs with the ASIS, which is also a hyperechoic curved “hill” but is
more cephalad and lateral to the AIIS.
rotocol Image 6: Iliacus and Psoas Major Muscles, Transverse

P
± Dynamic (Fig. 20.11)
Next, perform a medial LAX slide to view the iliacus and psoas major muscles.
These muscles will more distally form the iliopsoas muscle and tendon. You will
need to angle the medial aspect of the probe about 30–45° in a caudal direction to
view the hyperechoic iliopectineal eminence. If you suspect medial extra-articular
snapping hip syndrome, perform the dynamic test (frog-leg test) by having the
patient abduct and externally rotate the hip, followed by straightening the leg, to see
if there is a painful snapping of the PMT against the iliopectineal eminence. See
Clinical Comments, Extra-articular Medial Snapping Hip Syndrome, above for
more information.
Method 455
Fig. 20.11 Protocol Image 6: Iliacus and psoas major muscles, transverse ± dynamic
rotocol Image 7: Anterior Inferior Iliac Spine, Direct Head

P
of the Rectus Femoris, Longitudinal (Fig. 20.12)
Next, return to the view from Protocol Image 5 (AIIS TAX). Center the transducer
on the AIIS and slowly rotate it 90° to see the origin of the direct head of the RF in
456 20 Anterior Hip

7: Anterior inferior iliac
spine, direct head of the
rectus femoris, longitudinal
LAX at the AIIS. Within the hyperechoic tendon, there may be a hypoechoic area,
which is the union of the direct and indirect heads of the RF. This does not represent
tendinopathy or a tendon tear. The origin of the indirect head is the lateral aspect of
the superior acetabular ridge. Look for tears of the RF tendon, although most RF
tears occur in the muscle belly, myotendinous junction, and tendon origin [23].
rotocol Image 8 (Optional): Lateral Femoral Cutaneous

P
Nerve, Transverse
Next, rotate the probe back to TAX and place it over the AIIS again (protocol image
5). Move the transducer further cephalad to see a slightly more lateral bony promi-
nence, the ASIS, which has a similar but more robust appearance than the
AIIS. Similar to the AIIS, the ASIS is a broad hill or comet-shaped formation with
posterior acoustic shadowing causing an anechoic appearance deep to the hyper-
echoic curved bony cortex. The ASIS is the origin of the TFL (laterally) and the
sartorius (medially).
The ASIS is also the origin of the IL and is a landmark for the nearby LFCN. From
the TAX position, rotate the medial probe end downward about 30–45°, aiming for
the bony pubic tubercle. This highlights the lateral aspect of the hyperechoic linear
IL and the LFCN. To locate the LFCN sonographically, look for ovoid hypo-
or hyperechoic fascicles of the LFCN, which in most people are just deep to the
junction of the IL and next to the ASIS. A linear transducer is beneficial in this more
superficial location. Entrapment of the LFCN at the attachment of the IL to the
ASIS causes proximal nerve swelling and the symptoms of meralgia paresthetica.
Method 457
The normal LFCN may be challenging to visualize. The image example compares a
normal with an abnormal LFCN in a person who suffers from meralgia paresthetica
(Fig. 20.13a, b).
Helpful hints [31]:
(a) Use a high-frequency linear probe since the nerve is relatively small.
(b) Perform small TAX slides in cephalad and caudal directions to visualize the
nerve, which sometimes passes superficially to, deep to, or even through the
IL. Sometimes it is visualized as two fascicles that bifurcate distally.
(c) Compare the LFCN cross-sectional area to the contralateral, presumably unaf-
fected side.
(d) Look for swelling and hypoechogenicity proximal to the compression area,
similar to other nerves in tight fibro-osseous canals, such as the median nerve in
the carpal tunnel.
(e) Sonopalpation may reproduce the symptoms of meralgia paresthetica.
Fig. 20.13 Lateral femoral cutaneous nerve, transverse (a) Normal nerve on the left side (b)
Enlarged, abnormal nerve on the right side
458 20 Anterior Hip
rotocol Image 9 (Optional): Rectus Femoris, Vastus

P
Muscles, Transverse
Return to the AIIS in TAX (Image 5), perform a TAX slide distally toward the knee,
and see the vastus intermedius deep to the RF. Perform medial and lateral LAX
slides to view these muscles fully. More distally, the vastus medialis (VM) and late-
ralis (VL) muscles join the RF and the deeper vastus intermedius (VI) to form the
quadriceps tendon. These are the four muscles, or quadriceps, of the anterior thigh.
Look for tears, contusions, edema, hematomas, and myositis ossificans. Turn the
probe 90° for an orthogonal view (LAX) to verify any pathologic findings.
rotocol Image 10 (Optional): Sartorius and Tensor Fascia

P
Latae Origins, Longitudinal
Next, at the ASIS, center the probe in TAX at the medial slope of the ASIS and
rotate it 90° to LAX to see the tendon origin of the sartorius. The sartorius muscle
gently angles anteriorly and superficially across the thigh to reach the medial knee.
The tensor fascia latae (TFL) originates from the lateral border of the ASIS and
continues distally to form the anterior fibers of the iliotibial band (ITB).
(See Chap. 22 for further details and images.)
Protocol Image 11 (Optional): Sartorius, Transverse
At the ASIS, center the probe on the sartorius and then rotate it to the TAX view.
Maintaining the oval-shaped sartorius muscle in the center of the image, slowly
move caudally in a TAX slide to identify these three contiguous muscles: the sarto-
rius, the rectus femoris, and the iliopsoas. Distal to the AIIS, the image in Fig. 20.7,
Protocol Image 2, emerges. From this view, if necessary, the sartorius muscle can
be followed distally in TAX for evaluation.
Complete Anterior Hip Ultrasonic Examination Checklist
□ Protocol Image 1: Femoral head and neck, anterior joint recess, longitudinal
□ Protocol Image 2: Femoral head, iliopsoas, transverse
□ Protocol Image 3: Anterior labrum, longitudinal
□ Protocol Image 4: Neurovascular structures, transverse ± Doppler
□ Protocol Image 5: Anterior inferior iliac spine, transverse
□ Protocol Image 6: Iliacus and Psoas Major muscles, transverse ± dynamic
□ Protocol Image 7: Anterior inferior iliac spine, direct head of the rectus femoris,
longitudinal
□ Protocol Image 8 (optional): Lateral femoral cutaneous nerve, transverse
References 459
□ Protocol Image 9 (optional): Rectus femoris, vastus muscles, transverse

□ Protocol Image 10 (optional): Sartorius and tensor fascia latae origins,
longitudinal
□ Protocol Image 11 (optional): Sartorius, transverse
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5. Kung JW, Yablon C, Huang ES, Hennessey H, Wu JS. Clinical and radiologic predictive fac-
tors of septic hip arthritis. AJR Am J Roentgenol. 2012;199(4):868–72.
6. Pai VR, van Holsbeeck M. Synovial osteochondromatosis of the hip: role of sonography. J Clin
Ultrasound. 1995;23(3):199–203.
7. Weybright PN, Jacobson JA, Murry KH, Lin J, Fessell DP, Jamadar DA, et al. Limited effec-
tiveness of sonography in revealing hip joint effusion: preliminary results in 21 adult patients
with native and postoperative hips. AJR Am J Roentgenol. 2003;181(1):215–8.
8. Lin Y-T, Wang T-G. Ultrasonographic examination of the adult hip. J Med Ultrasound.
2012;20:201–9.
9. Wunderbaldinger P, Bremer C, Schellenberger E, Cejna M, Turetschek K, Kainberger
F. Imaging features of iliopsoas bursitis. Eur Radiol. 2002;12(2):409–15.
10. Corvino A, Venetucci P, Caruso M, Tarulli FR, Carpiniello M, Pane F, et al. Iliopsoas bursitis:
the role of diagnostic imaging in detection, differential diagnosis and treatment. Radiol Case
Rep. 2020;15(11):2149–52.
11. Toohey AK, LaSalle TL, Martinez S, Polisson RP. Iliopsoas bursitis: clinical features, radio-
graphic findings, and disease associations. Semin Arthritis Rheum. 1990;20(1):41–7.
12. Johnston CA, Wiley JP, Lindsay DM, Wiseman DA. Iliopsoas bursitis and tendinitis. A review.
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13. Douis H, Dunlop DJ, Pearson AM, O’Hara JN, James SL. The role of ultrasound in the
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Chapter 21
Posterior Hip

1. Posterior hip/thigh pain
2. Hip dysfunction
3. Evaluation for piriformis syndrome
4. Guidance for sacroiliac injections

1. Is the cause of the pain ischial bursitis or a torn hamstring muscle?
2. Is sciatica-type pain due to piriformis syndrome?
Anatomy
Posterior Pelvic Bones (Fig. 21.1)
Deep Posterior Pelvic Muscles (Fig. 21.2a)
The external (lateral) rotator muscles, from superior to inferior, are the Piriformis,
Superior gemellus, Obturator internus, Inferior gemellus, and Quadratus femoris [1].
A mnemonic for the external rotator muscles is “Pear Sits On Indigo Quilt”
(Fig. 21.2b).
States Government.

Switzerland AG 2023
462 21 Posterior Hip
Fig. 21.1 Posterior hip

bony anatomy
a b
Fig. 21.2 (a) Deep posterior pelvic muscles (b): Deep posterior pelvic muscles mnemonic
Posterior Thigh Muscles (Fig. 21.3)
A way to remember the location of the hamstring muscles in the thigh is that the
long head of the biceps femoris muscle (LHBFM) is lateral. The semitendinosus
muscle (STM) is medial to the LHBFM and has a long, thin distal tendon, hence the
Anatomy 463
name “semitendinosus.” The LHBFM and the STM share a common (conjoined)
tendon on the ischial tuberosity (IT) [2]. This conjoined tendon (CT) is sometimes
called the biceps femoris-semitendinosus tendon. The semimembranosus muscle
(SMM) also originates from the IT, just anterior (deep) to and slightly lateral to the
CT. The SMM runs deep to the STM.
Fig. 21.3 Left posterior

thigh muscles
Clinical Comments
Sacroiliac Joint
The sacroiliac joint (SIJ) is sonographically accessible. However, insufficient evi-

dence supports using ultrasound (US) to diagnose sacroiliitis in spondyloarthropa-
thy [3]. By contrast, US is useful for guiding SIJ injections. Injection of the lower
(caudal) portion of the SIJ is preferred since this is the synovial component of the
joint [4]. In contrast, the upper portion is fibrous (ligamentous) and not a true diar-
throdial joint. Successful SIJ injection occurred in 60% of patients in one study, and
with practice, it improved to 93.5% [5]. Another study compared US-guided versus
fluoroscopy-guided sacroiliac intra-articular injections and demonstrated success
rates of 87% with US compared with 98% with fluoroscopy [6].
Hamstring Injury
Hamstring injuries frequently occur in athletes at the proximal myotendinous junc-

tion [7, 8]. The biceps femoris is the most commonly injured hamstring muscle.
Other locations of hamstring injury include avulsion injury at the IT, the proximal
tendons, the distal tendon (particularly the semitendinosus), and at the myofascial
junction proximal to the fusion of the short and long heads of the biceps femoris [7,
8]. Damage may be from acute or chronic overexertion, most commonly due to
proximal tendinopathy, in particular the SMM in runners [7, 8]. Hamstring injuries
may be graded 1–3: grade 1 demonstrates no distinct muscle tear, while grade 3 is a
complete tear that affects function, perhaps with a noticeable gap. This grading
system was developed using magnetic resonance imaging (MRI) [9].
When assessing a potential hamstring muscle injury, begin with plain radio-
graphs. These are often normal, although an IT avulsion may be evident. The next
step is an MRI, which will readily diagnose an IT avulsion, an important finding
since surgical treatment is the most effective treatment [10]. Additionally, the MRI
will assess the hamstring injury’s location, size, and extent.
Ultrasound has also been shown to help assess hamstring injuries [11]. Ultrasound
may demonstrate tendon damage such as tendinopathy, peritendinous fluid, fibrillar
pattern disruption, localized edema, and intrasubstance anechoic clefts [12].
Sonographic signs of muscle tears include hyperechoic muscle fibers at ruptured
ends, hematoma, hypoechoic muscle echotexture, fascial disruption, and muscle
edema [13].
Limitations of US in assessing hamstring injuries include imperfect visualization
of tendon origin injuries and assessment of re-injuries due to soft tissue scarring. In
addition, US may not detect milder muscle strains, particularly in larger patients
[11]. MRI is more sensitive than US in detecting tendinopathy, peritendinous fluid,
and ischial tuberosity avulsion. An MRI is suggested to be performed within the
first 24 hours of an injury; US is most useful after 72 hours and for follow-up [11].
Pitfalls 465
Poor prognostic indicators are proximal tendon injuries, grade 3 injuries, and
tears near the IT [8, 14]. The recurrence rate of hamstring muscle injuries is approx-
imately 20% [7, 9, 14]. With posterior thigh pain and a nondiagnostic MRI, consider
referred pain from the lumbosacral spine, fascial injury, and gluteal trigger points [8].
Piriformis Syndrome
The sciatic nerve (SN) may be compromised as it emerges between the piriformis
and obturator internus muscles. Resultant buttock pain with sciatica mimics lumbar
radiculopathy and is termed piriformis syndrome [15, 16]. Ultrasound may reveal a
hypoechoic, swollen piriformis muscle on the symptomatic side compared with the
unaffected side [15, 17]. The SN may be compressed due to piriformis hypertrophy,
spasm, inflammation, or an anatomic variant [15].
Since electrophysiologic studies in this deep location may be unhelpful, piri-
formis syndrome is a diagnosis of exclusion made mainly by ruling out lumbar
radiculopathy [18]. Treatment is a corticosteroid injection into the fascial plane
between the piriformis and the more superficial gluteus maximus muscles. One
study comparing fluoroscopic and sonographic cadaveric injections of pirifor-
mis muscles revealed 95% accuracy with ultrasound-guided injection but only
30% accuracy with fluoroscopically-guided injection [19]. This result attests to
the ability of US to delineate fascial planes in this location. Be aware that the
SN runs deep to the piriformis muscle in 89%, through the muscle in nearly 9%,
and superficial to the piriformis muscle in 2–3% [20]. Thus, it is essential to
identify the SN before the injection since it may lie at or near the intended
injection site.
Ischiogluteal Bursitis
Ischiogluteal bursitis is also known as “weaver’s bottom” since prolonged sitting is

a causative factor [21]. An enlarged ischiogluteal bursa can be detected on MRI
[22]. However, US may likewise demonstrate anechoic fluid in the ischiogluteal
bursa adjacent to the IT [17]. An ultrasound-guided ischial bursal injection is tech-
nically feasible and may help avoid SN damage [15, 23].
Pitfalls
1. Do not neglect to perform radiographs to look for bony changes such as an IT

avulsion.
2. Use an MRI to assess hamstring injuries within the first 24 hours of the injury.
Ultrasound is helpful for follow-up.
3. In treating piriformis syndrome, use US guidance to inject between the fascial

plane of the piriformis muscle and the gluteus maximus muscle. Take care to
avoid injecting the SN, recalling that the nerve is not always located deep to the
piriformis muscle.
4. Use US to guide ischial bursal injections; visualizing the SN will avoid injury.
Method
Review radiographs for bony changes, such as an IT avulsion. The patient is prone.
Use a linear probe (perhaps with virtual convex at a lower frequency), although
many require a curvilinear probe to increase depth acquisition. A pillow beneath the
abdomen will assist in comfort and decrease lumbar lordosis. Topographically, the
PSIS is seen as a skin dimple. Mark off the PSIS on each side. Confirm all sono-
graphic findings with orthogonal views. Depending on the patient’s body habitus,
image acquisition may be challenging.
rotocol Image 1: Cephalad Sacroiliac Joint, Transverse

P
(Fig. 21.4)
With the transducer in TAX orientation to the femoral shaft, place the lateral probe
end on the hyperechoic hill-like PSIS and look for the hyperechoic sacrum medially
near the base of the ilium. Between these two bones is the SIJ.

1: Cephalad sacroiliac
joint, transverse
Method 467
rotocol Image 2: Caudal Sacroiliac Joint, Transverse

P
(Fig. 21.5)
Next, with the probe still in TAX orientation, perform a TAX slide in a caudal direc-
tion to image the lower SIJ. As you move the transducer in a caudal direction, note
that the height of the ilium decreases and the SIJ narrows.
rotocol Image 3: Piriformis, Longitudinal ± Dynamic

P
(Fig. 21.6)
A curvilinear probe may be required to visualize the piriformis muscle connecting

the sacrum to the GT. With the probe still in the same TAX orientation and anchored
to the sacrum, rotate the lateral end in a downward (caudal) direction to see the GT’s
hyperechoic superior/posterior aspect. This requires approximately 40° of angula-
tion plus some fine-tuning by tilting the transducer to visualize the piriformis tendon
insertion on the GT. The hypoechoic, longitudinal piriformis muscle is medial. The
gluteus maximus muscle is superficial to the piriformis muscle. The two muscles
are separated by a longitudinal hyperechoic fascial plane, a common injection target
for treating piriformis syndrome.
A dynamic maneuver to assist in identifying the piriformis is to have the patient
bend the knee. At the same time, the examiner passively rotates the hip internally and
externally by directing the foreleg to the left and then to the right, like a windshield
wiper. Since the piriformis muscle connects the GT to the sacrum, external hip rota-
tion will cause the piriformis muscle to stretch out, thus confirming its identity and

2: Caudal sacroiliac joint,
transverse
Fig. 21.6 Protocol Image 3: Piriformis, longitudinal ± dynamic
enhancing visualization. The honeycombed SN may be found more medially, just

deep to the piriformis muscle, although, in some individuals, it penetrates directly
through this muscle. Occasionally, the SN runs superficial to the piriformis.
Protocol Image 4 (Optional): Gluteal Muscles, Transverse
By slowly moving the transducer caudally in TAX, the five posterior pelvic muscles
can also be identified if necessary. Recall the external rotator muscles, from supe-
rior (cepahlad) to inferior (caudal): piriformis, superior gemellus, obturator inter-
nus, inferior gemellus, quadratus femoris. Remember that each muscle lies deep to
the gluteus maximus. A detailed sonographic evaluation of these muscles can be
found elsewhere [24].
Method 469
rotocol Image 5: Ischial Tuberosity, Hamstring Muscles,

P
Next, place the transducer in the TAX position, just cephalad to the gluteal fold. The
medial end of the probe should visualize the curved, hyperechoic, bony IT. The IT
is the origin of the hamstrings and may be palpable in many people. The ischial
bursa lies between the hamstring tendons and the gluteus maximus; the bursa may
become more prominent when inflamed or distended.
Protocol Image 6: Conjoined Tendon, Longitudinal (Fig. 21.8)
Next, center the probe on the CT and rotate 90° to visualize the CT in LAX orienta-
tion. The transducer is vertical. The semimembranosus tendon insertion may be
seen deep to the CT.
rotocol Image 7: Semimembranosus Tendon, Longitudinal

P
(Fig. 21.9)
Perform a slight lateral TAX slide with the transducer tilted, aiming towards the
midline, to visualize the insertional origin of the SMT on the IT. The SMT is seen
at a slightly deeper level than the CT.

5: Ischial tuberosity,
hamstring muscles,
transverse
Fig. 21.8 Protocol Image 6: Conjoined tendon, longitudinal

7: Semimembranosus
tendon, longitudinal
Method 471

7: Sciatic nerve,
longitudinal
Protocol Image 8: Sciatic Nerve, Longitudinal (Fig. 21.10)
Perform yet another lateral TAX slide with the transducer parallel to the long axis
of the thigh. The transducer slides off the bony hyperechoic IT; the SN should be
visible in the LAX view. Look for the emergence of the typical tram track appear-
ance of the large SN in the LAX view. If you do not visualize the SN, rotate the
transducer 90° to identify the SN in the TAX view.
Complete Posterior Hip Ultrasonic Examination Checklist
□ Protocol Image 1: Cephalad sacroiliac joint, transverse
□ Protocol Image 2: Caudal sacroiliac joint, transverse
□ Protocol Image 3: Piriformis, longitudinal ± dynamic
□ Protocol Image 4 (optional): Gluteal muscles, transverse
□ Protocol Image 5: Ischial Tuberosity, hamstring muscles, transverse
□ Protocol Image 6: Conjoined tendon ± semimembranosus, longitudinal
□ Protocol Image 7: Semimembranosus tendon, longitudinal
□ Protocol Image 8: Sciatic nerve, longitudinal
References
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2012;199(3):525–33.
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clinical benefits and pitfalls - a review of the current literature. Open Access J Sports Med.
2017;8:167–70.
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variant analyzed by magnetic resonance imaging. J Clin Imaging Sci. 2018;8:6.
19. Finnoff JT, Hurdle MF, Smith J. Accuracy of ultrasound-guided versus fluoroscopically
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Chapter 22
Lateral Hip

1. Lateral hip pain
2. Swelling of the lateral hip

1. Is the cause of the pain greater trochanteric pain syndrome (GTPS), snapping
iliotibial band (ITB), tensor fascia latae (TFL) tendinopathy, or another soft tis-
sue structural problem? If so, what is the specific underlying pathology?
2. If the ultrasound (US) exam of the lateral hip soft tissue is unremarkable, could
the lateral hip pain be referred from the lumbosacral spine, the femur, the hip
joint, the labrum, or the lateral femoral cutaneous nerve?
Basic Anatomy
The greater trochanter (GT) is a bony protuberance of the proximal posterolateral

femur (Fig. 22.1). The ITB is a longitudinal fibrous band that originates from the
topmost external iliac crest and runs along the lateral aspect of the thigh superficial
to the GT, finally inserting on Gerdy’s tubercle of the tibia (Fig. 22.2). It receives
fibers from two muscles: anteriorly from the TFL and posteriorly from the gluteus
maximus (Gmax) [1]. These muscular contributions enable ITB tension, thus stabi-
lizing the knee with ambulation.
States Government.

Switzerland AG 2023
474 22 Lateral Hip

lateral hip bony anatomy
Fig. 22.2 Iliotibial band

Basic Anatomy 475
The Gmax originates from the posterior external iliac bone and inserts into the
posterior ITB (as noted above) and the gluteal (femoral) tubercle, distal to the GT
(Fig. 22.3). The gluteus minimus (Gmin) and gluteus medius (Gmed) muscles both
originate from the external posterior iliac bone, with the Gmin being the deeper of
the two. The Gmin flexes, abducts, and medially rotates the thigh depending on the
hip position. The Gmed extends and abducts the thigh. The Gmin inserts on the
anterior facet (AF) of the GT, while the Gmed inserts on the lateral (LF) and supero-
posterior facets of the GT (Fig. 22.4).
A mnemonic for these two insertions is “Aunt Minnie Loves Mead.”
Anterior facet: Gluteus minimus; Lateral facet: Gluteus medius.
A mnemonic for the five soft tissue structures of the lateral hip (gluteus minimus,
gluteus medius, gluteus maximus, iliotibial band, and tensor fascia latae) is as
follows:
“Minimal meditation maximally improves tension.”
It is easy to remember the names and locations of the bursae surrounding the
GT. Each bursa has the prefix “sub” before the name of the muscle and is located

muscular anatomy of the
posterior hip
476 22 Lateral Hip
Fig. 22.4 Simplified tendon insertions on the lateral greater trochanter
deep to the respective tendon or muscle near its insertion: subgluteus minimus, sub-
gluteus medius, and subgluteus maximus bursae.
Again, note that the Gmax inserts along the posterior portion of the ITB and the
bony gluteal tubercle (distal to the GT) and not on the GT. Also note that the sub-
gluteus maximus bursa (the true trochanteric bursa) separates the Gmax muscle
from the posterior facet (PF) and, if distended, may extend between the Gmed ten-
don and the ITB [2]. What was previously referred to as “trochanteric bursitis” is
now called GTPS since this entity is only sometimes associated with true subgluteus
maximus bursitis [3].
Clinical Comments
Greater Trochanteric Pain Syndrome
In this condition, the patient complains of pain or tenderness at the posterolateral

hip over the GT [3]. A putative cause of GTPS is repetitive friction between the ITB
and the GT, causing microtrauma to the gluteal tendons at their GT insertions [4, 5].
Ultrasound helps evaluate the abductor tendons and bursae at the GT and has the
advantage of sonopalpation, which directs the clinician to the painful area [6, 7].
Gluteus medius tendinopathy may manifest sonographically as hypoechogenicity
with focal swelling and initially preserved fibrillar echotexture [8–10].
Partial-thickness tears are represented as focal anechoic areas with loss of
fibrillar echotexture [8]. With tendon damage, hyperechoic calcification may
occur at tendon insertion sites [11]. Complete tears may demonstrate a retracted
tendon with anechoic fluid accumulation and a bare GT [12]. Bursal distension
of the subgluteal bursae of the Gmed and the Gmin may be seen deep to each
respective tendon as hypoechoic fluid collections just proximal to the insertion
on the GT. The subgluteal bursa of the Gmax, the true trochanteric bursa, is
located deep to the Gmax muscle and ITB, superficial to the lateral and posterior
facets of the GT [13].
A large retrospective study in patients with GTPS revealed the most common
sonographic finding to be Gmed or Gmin tendinosis, followed by ITB thickening
[3]. Isolated bursitis was the least common finding. The Gmax tendon or underlying
subgluteus maximus bursa (the “true trochanteric bursa”) is not commonly involved
in GTPS [3]. In summation, friction from the ITB may cause local microtrauma of
the abductor tendons and may be the leading cause of GTPS [9, 10]. However, be
aware that gluteal tendinosis or bursitis may be present asymptomatically [14].
Perhaps impingement of the ITB against the Gmed and Gmin is the cause of many
cases of GTPS; this would be analogous to shoulder rotator cuff impingement by
the acromion [9, 15]. Another school of thought is that the bursal distension noted
in GTPS may be secondary to a gluteal tendon abnormality, similar to the fluid
accumulation in subacromial-subdeltoid bursitis associated with a rotator cuff tear
in the shoulder [16].
Predisposing conditions to the GTPS include an external snapping hip, blunt
trauma to the hip, iatrogenic injury during hip arthroplasty, increased age, obesity,
osteoarthritis of the knee or hip, low back pain, and leg length discrepancy [10]. The
differential diagnosis of lateral hip pain includes osteoarthritis, avascular necrosis
of the femoral head, labral tears, femoral acetabular impingement, femoral neck
stress fractures, loose bodies, radiation from lumbar stenosis, and meralgia pares-
thetica (lateral femoral cutaneous neuropathy). It is controversial whether cortical
bone irregularity at the GT is helpful with the diagnosis of GTPS or not [10].
Radiographic imaging is best used to recognize alternative sources of pain such as
osteoarthritis, avascular necrosis, lumbar spondylosis, and femoral acetabular
impingement [10].
Magnetic resonance imaging (MRI) is still the gold standard for evaluating
GTPS, with a sensitivity/specificity of 93/92% for diagnosing abductor tendon tears
[10]. Sonographic sensitivity has been described as 79%. Therefore, US is a less
reliable diagnostic modality, and MRI is necessary before considering surgical
intervention.
Treatment is conservative, including nonsteroidal anti-inflammatory medica-
tions, physical therapy, and attention to remediable risk factors such as leg length
discrepancy, obesity, and contributing knee, hip, and foot disorders [4]. Local injec-
tion can be performed with US guidance, but debate persists about injecting corti-
costeroids versus platelet-rich plasma since corticosteroids may potentially weaken
damaged tendons. Low-energy shock wave therapy has been used as well. Surgery
is often the last resort [4].
478 22 Lateral Hip
Tendinosis and Tendon Tears
The gluteus minimus and medius tendons may also be abnormal at their respective
trochanteric insertions, ranging from tendinosis to tendon tears. Tendinosis is evi-
dent by thickening (swelling) and hypoechoic loss of fibrillar echotexture. Partial or
full-thickness tears may be noted as well. Comparison with the contralateral (pre-
sumably unaffected) side may be helpful. Again, pain at the GT is more likely from
a gluteal tendon abnormality than true bursitis.
The gold standard for the diagnosis of abductor tendon pathology is
MRI. However, one study reports US to be highly sensitive for detecting Gmed
tendon pathology (tendinosis, partial-or full-thickness tear), albeit with a tendency
to incorrectly overstate some normal tendons as being damaged [17]. However, the
same study revealed that MRI tended to understate the presence of tendon pathol-
ogy. Both imaging techniques poorly differentiate tendinosis from partial-and full-
thickness tears [17]. Despite the improved resolution of modern US machines,
deep-lying structures such as the gluteal tendons may not be sharply delineated.
Given the strengths and weaknesses of US and MRI modalities, our practice for
uncertain diagnoses has been to follow-up US examinations with an MRI or MR
arthrogram to confirm gluteal pathology suggested by US and to evaluate the hip
further since other conditions may mimic GTPS. Such conditions include degenera-
tive change, avascular necrosis, labrum tears, and femoral acetabular impingement.
napping Iliotibial Band and External Lateral Snapping

S
Hip Syndrome
When the thigh is flexed (with the hip in adduction), the ITB normally glides ante-
riorly over the GT [13]. This is logical since the distal ITB is tethered to the proxi-
mal anterior tibia at Gerdy’s tubercle. External lateral snapping hip (ELSH) is
described as intermittent impingement of the ITB (or the anterior Gmax or the TFL)
over the GT; this may be painful or painless. The patient may experience a clicking
or popping sensation [13]. As the hip moves back into extension, there may be a
similar impediment to the movement of the ITB.
Static US may reveal the ITB to be thickened and hypoechoic [11]. Bursal disten-
sion may also be involved [13]. Evaluate for ELSH dynamically with the patient stand-
ing or lying in a lateral decubitus position. The hip is extended and then slowly flexed.
The transducer is placed in TAX over the GT, and the ITB is identified. The ITB (or
Gmax) may catch over the GT and abruptly lurch anteriorly during flexion [11].
The snapping sensation may be best demonstrated with the patient standing
[13]. Pain is postulated to be from secondary tendinopathy and bursitis due to
repetitive snapping. Again, painless snapping may be present and considered nor-
mal. Predisposing conditions for ELSH include athletic activities such as ballet
dancing, variant body structures affecting biomechanics, femoral osteochondroma,
Tensor Fascia Latae Tendinopathy 479
and postoperative changes [13]. Dynamic US is the best technique to demonstrate

this pathologic entity [18].
Morel-Lavallee Lesion
Morel-Lavallee (M-L) lesions occur when blunt, soft tissue trauma causes shearing
between the subcutaneous tissue and superficial muscle fascial layers, creating a
space that fills with serosanguineous fluid and necrotic fat [13, 19, 20]. This lesion
often results from an injury sustained in football, baseball, or skiing [21]. Eventually,
localized inflammation produces a fibrous pseudocapsule, which may result in per-
sistent or recurrent fluid collection [19].
The most common locations are near the GT and the anterior proximal thigh, and
M-L lesions may be associated with pelvic fractures [13]. Acutely, the patient pres-
ents with an enlarged, painful mass with decreased cutaneous sensation [22].
Alternatively, the M-L lesion may initially be clinically inapparent, growing slowly
without pain, thus mimicking a soft tissue tumor [13]. An acute M-L lesion on US
may demonstrate heterogeneous hyperechogenicity due to debris such as necrotic
lobules and irregular margins [19].
The US picture, although variable, evolves with time into a compressible,
homogeneous lesion with well-defined, smooth margins containing
anechoic or hypoechoic fluid and no power Doppler activity [19]. However,
rebleeding within a chronic lesion may alter the sonographic appearance.
Diagnosing M-L lesions as early as possible is essential to avoid chronic pain and
a potential space for infection [19].
Tensor Fascia Latae Tendinopathy
Anterior groin pain in athletes may be associated with tendon injuries, hernias, avul-
sion injuries, referred pain, or tumors [23]. Injury to the TFL has increasingly
become recognized as a cause of anterior groin pain in athletes and is sonographi-
cally detectable; point tenderness may correlate with pathology [24]. It is postulated
that recurrent microtrauma damages the TFL.
Sonographic signs of tendinopathy include enlargement of the TFL, focal areas
of hypoechogenicity, and linear or other anechoic areas. Anechoic regions are
assumed to be intrasubstance tears [24]. Tendinopathy may be at or proximal to the
insertion [25]. A sonographic comparison with the presumably unaffected contralat-
eral side is suggested [24].
A TFL tear in the muscle belly may mimic GTPS and be sonographically visible
[26]. Treatment for TFL injuries includes rest, massage, nonsteroidal anti-
inflammatory medications, corticosteroid injections, surgery, and, more recently,
tendon fenestration with platelet-rich plasma injections [24, 27].
480 22 Lateral Hip
Bursal Abnormalities
The three gluteal bursae may or may not be distended with GTPS. Bursal distention
may be secondary to tendinopathy or primary, perhaps associated with an underly-
ing inflammatory condition such as rheumatoid arthritis. Bursal fluid is typically
anechoic but may also be hypoechoic, particularly if there is associated synovial
hypertrophy.
Proximal Iliotibial Band Syndrome
Not to be confused with snapping ITB syndrome or distal “ITB syndrome,” proxi-
mal ITB syndrome has been described most often in athletes as causing localized
pain at the iliac crest due to enthesopathy, presumably from chronic repetitive
microtrauma of the ITB at or near its insertion [28]. Proximal ITB syndrome is
either uncommon or uncommonly recognized, occurs more frequently in females,
and may be due to overuse, trauma, or degenerative change [5]. Pain increases with
physical activity and may mimic hip and GT-related conditions [26]. The imaging
modality most often used to define this enthesopathy is MRI [26, 28]. Sonographic
findings are that of a thickened (swollen) hypoechoic ITB at the IT and crest, par-
ticularly in comparison with the normal contralateral side [13].
Pitfalls
1. When describing pain in the GT area, the designation “GTPS” is used rather than
the outdated “trochanteric bursitis.”
2. Do not unquestionably accept US or MRI findings regarding the Gmed tendon at
the GT. Ultrasound tends to overreport, while MR may underreport Gmed
pathology [17].
3. Likewise, US and MRI may poorly distinguish tendinosis, partial thickness
tears, and full-thickness tears of the Gmed tendon at the GT [17].
4. Don’t forget to consider using a combination of US and MR modalities to define
the cause of lateral hip pain since MRI will additionally delineate other hip
pathologies mimicking GTPS.
5. Be aware that treatment paradigms for GTPS are evolving, including injection
protocols and the products being injected.
6. Don’t forget to consider TFL and proximal ITB pathology as causes of pain
proximal to the hip.
Method 481
Method
The patient is in a lateral decubitus position, lying on the unaffected side. Palpate
the bony prominence, the GT at the posterolateral hip, and mark this area with a
ballpoint pen. Use a curvilinear probe since the lower frequency is necessary to
achieve adequate depth. The linear transducer (with a virtual convex setting and a
lower frequency) will suffice for some thin patients to visualize the GT.
Protocol Image 1: Greater Trochanter, Transverse (Fig. 22.5)
Place the probe in the transverse axis (TAX) over the GT and look for the sharp
hyperechoic bony peak that separates the AF and LF. The AF is closer to the anterior
thigh. Look at the tendon cross-sectional insertions in TAX of the Gmin on the AF
and the Gmed on the LF. One or even both of these tendons may be poorly seen due
to anisotropy. In cross-section, the ITB is the thin, curved, hyperechoic structure
superficial to the tendons and muscles. The ITB is delineated as the patient slowly
extends and flexes the hip to demonstrate the movement of the ITB from posterior
to anterior with hip flexion.

1: Greater trochanter,
transverse
482 22 Lateral Hip
rotocol Image 2: Gluteus Minimus Insertion, Anterior Facet,

P
Perform a longitudinal axis (LAX) slide anteriorly to center the probe on the AF in
TAX orientation. Visualize the hyperechoic Gmin (in cross-section) inserted into
the LF. This may require slight rotation and tilting of the transducer. Then, rotate the
probe 90° to look for the insertion of Gmin on the AF in LAX.
To best view the Gmin insertion, rotate the cephalad end of the probe anteriorly
about 20–30° (aiming the cephalad end of the transducer in the direction of the
umbilicus). Also, tilt the probe about 10–20° to direct the US beam posteriorly to
sharpen visualization of the tendon insertion. The insertion on the AF should look
like an elongated “bird’s beak.” Using time-gain control to focus on the area may be
very helpful. The ITB is superficial to the Gmed muscle, which itself is superficial
to the Gmin. Look for a subgluteus minimus bursa deep to the Gmin, as well as
tendinopathy and frank tendon tears.
rotocol Image 3: Gluteus Medius Insertion, Lateral Facet,

P
longitudinal (Fig. 22.7)
Next, perform a TAX slide in the posterolateral direction to the LF and then rotate
the cephalad aspect of the probe about 20–30° (from the midline) toward the but-
tocks. Tilt the probe about 10–20° to aim the US beam anteriorly. Look at the

2: Gluteus minimus
insertion, anterior facet,
longitudinal
Method 483

3: Gluteus medius
insertion, lateral facet,
longitudinal
anterior fibers of the Gmed as it inserts on the LF in LAX in yet another “bird’s
beak” configuration. The ITB is superficial to the tendon. Again, ensure the probe is
perpendicular to the facet by slightly tilting and rocking the transducer to optimally
visualize the tendon insertion. Look for fluid deep to the Gmed tendon, representing
a subgluteus medius bursa. The ITB will be seen as a hyperechoic band superficial
to the Gmed.
rotocol Image 4: Gluteus Medius Insertion, Superoposterior

P
Facet, Longitudinal (Fig. 22.8)
Next, perform a slight TAX slide in a posterolateral direction to see the insertion of
the posterior fibers of the Gmed on the superior portion of the posterior facet (PF).
This view will reveal the more superficial ITB and, if present, a distended Gmax
bursa superficial to the Gmed. The Gmax bursa is the true trochanteric bursa. The
trochanteric bursa, when distended, may spread laterally to become sandwiched
between the Gmed tendon and the overlying ITB.
484 22 Lateral Hip

4: Gluteus medius
insertion, superoposterior
facet, longitudinal
rotocol Image 5: Proximal Iliotibial Band, longitudinal

P
(Fig. 22.9)
If clinically indicated, evaluate the TFL by locating the anterior superior iliac spine
(ASIS) in TAX orientation. The ASIS is a curvilinear hyperechoic bony protuber-
ance most easily located from an anterior approach. The ASIS appears as a broad
hill or comet-shaped formation with posterior acoustic shadowing causing an
anechoic appearance deep to the hyperechoic curved bony cortex.
Center the probe on the posterior slope of the ASIS and then rotate the trans-
ducer 90° to visualize in LAX the fibrillar hyperechoic echotexture of the common
origin of the TFL and the ITB. The TFL muscle is deeper. The fibers of the TFL
merge into the anterior portion of the ITB.
rotocol Image 6: Iliotibial Band, Transverse + Longitudinal

P
(Fig. 22.10)
Place the transducer in TAX orientation across the GT. The ITB is easily identified
dynamically. As the patient slowly extends and flexes the hip, the ITB moves from
posterior to anterior; the examiner may evaluate for a snapping ITB over the
GT. Moving the probe in a cephalad TAX slide will demonstrate the more proximal
Method 485

5: Proximal iliotibial band,
longitudinal
ITB. When the iliac crest is reached, the transducer can be rotated 90° to the LAX
orientation. Then, TAX slides can be done anteriorly and posteriorly on the iliac
crest to evaluate the ITB origin, including the iliac tubercle, which has a slight bony
prominence.
rotocol Image 7 (Optional): Iliotibial Band, Transverse

P
+ Dynamic
The patient should stand to be evaluated for an external snapping hip at the
GT. Return to the GT and turn the probe to TAX (Protocol Image 6). Have the
patient move the hip from extension to flexion while the hip is in adduction. Look
for the ITB (or the TFL or Gmax) suddenly skipping from posterior to anterior over
the GT (which may or may not be painful). The ITB may be thickened from repeti-
tive trauma. Use only mild transducer pressure and feel for a snapping sensation
through the probe. The ITB moves anteriorly because it is anchored distally at
Gerdy’s tubercle of the tibia.
486 22 Lateral Hip

6: Iliotibial band,
transverse + longitudinal
(See Clinical Comments: Snapping iliotibial band (ITB) or external (extraarticu-

lar) lateral snapping hip syndrome (ELSH).)
Complete Lateral Hip Ultrasonic Examination Checklist
□ Protocol Image 1: Greater trochanter, transverse
□ Protocol Image 2 Gluteus minimus insertion, anterior facet, longitudinal
□ Protocol Image 3: Gluteus medius insertion, lateral facet, longitudinal
□ Protocol Image 4: Gluteus medius insertion, superoposterior facet, longitudinal
□ Protocol Image 5: Proximal iliotibial band, longitudinal
□ Protocol Image 6: Iliotibial band, transverse + longitudinal
□ Protocol Image 7 (optional): Iliotibial band, transverse + dynamic
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Chapter 23
Medial Hip

1. Medial thigh pain
2. Groin pain

1. What is the cause of groin or thigh pain? Is it athletic pubalgia, adductor tendi-
nopathy, muscle strain, or “thigh splints?”
2. Is an additional imaging modality different from ultrasound necessary to confirm
the cause of pain, such as with an inguinal hernia or femoroacetabular
impingement?
Basic Anatomy
Bones (Fig. 23.1)
Muscles (Fig. 23.2)
Five adductor muscles originate from the pubic bone; all but the gracilis insert on
the femur. The adductor muscles are arranged in three layers. The anterior (superfi-
cial) layer is composed of the pectineus, adductor longus (AL), and gracilis. The
more posterior middle layer is the adductor brevis (AB), and the most posterior
deep layer is the adductor magnus (AM). Thus, a mnemonic to remember the adduc-
tor muscles from anterior to posterior is “Patty’s Legs Got Big Muscles.”
States Government.

Switzerland AG 2023
490 23 Medial Hip
The AL originates from the body of the pubis near the pubic tubercle; the AB
originates from the body of the pubis and inferior pubic ramus; and the AM origi-
nates from the inferior pubic ramus and ischial tuberosity.
Fig. 23.1 Focused bony

anatomy of the medial hip
Fig. 23.2 Muscular anatomy of the medial hip

Tendinosis and Partial-Thickness Tears 491
Clinical Comments
Athletic Pubalgia
Sports-related injuries may result in groin pain. Athletic pubalgia (sports or sports-
man’s hernia) is a general term describing conditions from a variety of causes,
including tears of the (abdominal) conjoined tendon (common aponeurosis of the
internal abdominal oblique and transverse abdominis muscles) or other soft tissue
injuries in this area [1]. The AL and the rectus abdominis share a common aponeu-
rosis anterior (superficial) to the pubic bone, and both attach to the pubic symphysis
[2]. The putative precipitating injury is physical activity-related trauma to the com-
mon aponeurosis of the rectus abdominis and AL [3]. Participation in tennis, hockey,
and football is often a factor.
Symptoms include unilateral groin pain at rest and during exercise. There is
often a preceding episode of acute tearing sensation in this location [3]. Pain may be
reproduced with resisted hip abduction and sit-ups. Point tenderness may be noted
at the pubic attachments of the rectus abdominis and AL. Ultrasound (US) may
reveal enthesopathy, tendinosis, or a complete or partial tear of the common apo-
neurosis [3]. Magnetic resonance imaging (MRI) may reveal reactive bony changes
at the symphysis pubis, including bone marrow edema. Some patients may have
inflammation of the pubic bone, termed osteitis pubis [3].
Tendinosis and Partial-Thickness Tears
Adductor tendinopathy and tears (partial or complete) may also occur separately
from the common aponeurosis of the rectus abdominis and AL. These may be pre-
cipitated by an acute event or chronic overuse [3]. Acute tears of the AL muscle may
occur in football players and present with pain in the upper medial thigh, worsened
by resisted hip adduction. Adductor injuries typically occur with forced hip hyper-
adduction during contraction of the adductor muscle group [4]. The AL and gracilis
are most commonly affected by tendinopathy [5].
Ultrasound may reveal hypoechoic thickening of the tendon compared to the
asymptomatic side [6]. Ultrasound findings may include insertional enthesopathy
and possibly hyperemia detected by Doppler [7]. Pain due to sonopalpation may
also be present. Intratendinous tears may be seen as anechoic clefts [7]. Tendon
rupture is suspected if the muscle is retracted. Bony avulsion may occur with
tendon rupture, particularly in adolescents [7]. Magnetic resonance imaging is
more sensitive than US for detecting low-grade injuries and chronic abductor
tendinopathy [5].
492 23 Medial Hip
Muscle Strain
The AL and gracilis may also be subject to muscle strain. An MRI with contrast is
the best modality to visualize a deep adductor muscle tear.
Adductor Insertion Avulsion Syndrome
At the adductor insertion onto the posteromedial femur, chronic repetitive stress
trauma has been termed “thigh splints” [8, 9]. This may result in periostitis and
stress fractures. It occurs in cheerleading, soccer, hockey, and football participants,
as well as military recruits. Symptoms occurring after physical activity include pain
in the groin, hip, and thigh, which may be improved with rest [8, 9]. There may be
a palpable mass due to periostitis. Radiographs may be normal or show periosteal
proliferation or even a stress fracture. Magnetic resonance imaging and nuclear
bone scans have proven diagnostically helpful [8, 9]. Ultrasound may show cortical
irregularity, localized insertional hypoechogenicity, hyperemia on power Doppler
(PD), and pain reproduction with sonopalpation over the affected area of the poste-
rior medial femur. Differential diagnoses include articular hip disease, femoral
stress fracture, infection, and neoplasm [8, 9].
Other Sources of Pain
These may include inguinal hernia and femoroacetabular impingement [10]. This
Manual does not cover the evaluation of inguinal hernias, but information about
femoroacetabular impingement is found in Chap. 20. Clinicians treating athletes
frequently utilize ultrasound for point-of-care determination of injury type and
severity.
Method
The patient’s leg should be in the “frog leg” position (abduct and externally rotate
the hip, and bend the knee). The curvilinear (low frequency) probe is usually neces-
sary, but a linear transducer with an extended field of view (i.e., virtual convex) may
be beneficial for very thin subjects. Once identified in orthogonal views, each medial
thigh muscle can be visualized along a short axis from proximal to distal.
Method 493
rotocol Image 1: 6 cm Distal to the Superior Pubic Ramus,

P
Fig. 23.3 Protocol Image 1: 6 cm distal to the superior pubic ramus, transverse
494 23 Medial Hip
The origin of the muscles topographically creates a discernible triangle at the medial
thigh. Place the transducer on this triangle in the transverse axis (TAX) position.
The posteromedial end of the transducer should be angled in a caudal direction of
about 35 degrees, which should parallel the superior pubic ramus.
Move the probe cephalad (TAX slide) until the hyperechoic pubic bone is seen,
and then, maintaining the same angle, move the transducer in a TAX slide caudally
about 6 cm. Visualize the three adductor muscles, from superficial to deep: the AL,
the AB, and the AM. The gracilis is just posterior to the AL. The vastus medialis
(VM) is anterior to the AL at about the same depth as the AB. Use copious gel,
particularly with a curvilinear probe, to preserve contact with the skin. This may
also require exerting some downward pressure on the transducer.
Perform TAX slides as necessary to scan the area of complaint and note any pain
from sonopalpation. Sonographically-detectable injuries include enthesopathy, ten-
dinosis, complete or partial tears, bony avulsion, muscle tears, muscle or tendon
retraction, cortical irregularity, and hyperemia on Doppler. (See Clinical Comments
above for specific pathology.)
Protocol Image 2: Adductor Insertions, longitudinal (Fig. 23.4)
Rotate the probe 90 degrees to visualize the insertion of the adductor muscles in the
longitudinal axis (LAX). The transducer should bisect the topographic triangle.
Move the transducer in TAX slides medially and laterally along the curved hyper-
echoic superior pubic ramus until you see the hill-like most prominent portion
medially; this is the pubic tubercle.
The probe is now in LAX orientation with respect to the adductor tendon inser-
tions. The origins of the AL and the deeper AB near the pubic tubercle give a con-
joined tendon appearance, although the tendons have different origins [3].
The LAX view allows confirmation of putative pathology noted on TAX imaging.
Complete Medial Hip Ultrasonic Examination Checklist
□ Protocol Image 1: Protocol Image 1: 6 cm distal to the superior pubic ramus,
transverse
□ Protocol Image 2: Adductor insertions, longitudinal
Method 495
Fig. 23.4 Protocol Image 2: Adductor insertions, longitudinal

496 23 Medial Hip
References
1. Omar IM, Zoga AC, Kavanagh EC, Koulouris G, Bergin D, Gopez AG, et al. Athletic pub-
algia and "sports hernia": optimal MR imaging technique and findings. Radiographics.
2008;28(5):1415–38.
2. Morley N, Grant T, Blount K, Omar I. Sonographic evaluation of athletic pubalgia. Skelet
Radiol. 2016;45(5):689–99.
2018;38(3):867–89.
4. Rizio L 3rd, Salvo JP, Schürhoff MR, Uribe JW. Adductor longus rupture in professional
football players: acute repair with suture anchors: a report of two cases. Am J Sports Med.
2004;32(1):243–5.
5. Robinson P, Barron DA, Parsons W, Grainger AJ, Schilders EM, O’Connor PJ. Adductor-
related groin pain in athletes: correlation of MR imaging with clinical findings. Skelet Radiol.
2004;33(8):451–7.
2012;20:201–9.
7. Pesquer L, Reboul G, Silvestre A, Poussange N, Meyer P, Dallaudière B. Imaging of adductor-
related groin pain. Diagn Interv Imaging. 2015;96(9):861–9.
8. Weaver JS, Jacobson JA, Jamadar DA, Hayes CW. Sonographic findings of adductor inser-
tion avulsion syndrome with magnetic resonance imaging correlation. J Ultrasound Med.
2003;22(4):403–7.
9. Sofka CM, Marx R, Adler RS. Utility of sonography for the diagnosis of adductor avulsion
injury (“thigh splints”). J Ultrasound Med. 2006;25(7):913–6.
10. Naal FD, Dalla Riva F, Wuerz TH, Dubs B, Leunig M. Sonographic prevalence of groin her-
nias and adductor tendinopathy in patients with femoroacetabular impingement. Am J Sports
Med. 2015;43(9):2146–51.
Chapter 24
Crystalline Disease
Our primary focus is on two crystals: monosodium urate (MSU) [which may cause
gout] and calcium pyrophosphate dihydrate (CPP) [which may cause CPPD deposi-
tion disease, or CPPD disease, for short]. In the past, CPPD disease has been referred
to as pseudogout [1]. Refer to OMERACT definitions of ultrasound (US) pathology
for MSU and CPPD crystals in other sections: Getting Started, Crystal Disease,
and Hand Arthropathy, as well as Reference 1 [2]. Please refer to additional refer-
ences for a clinical review of gout and CPPD [3].
1. Evaluate for the possibility of gout or acute CPPD disease arthritis causing joint
inflammation, particularly acute monoarthritis.
2. Evaluate the possibility of chronic gout or CPPD disease causing structural
changes in joints as well as bone erosion.
3. Evaluate for the presence of MSU crystals and tophi in patients with
hyperuricemia.
4. Evaluate for CPP crystals in patients with polyarthropathy who have associated
conditions such as aggressive osteoarthritis, hyperparathyroidism, hemochroma-
tosis, hypomagnesemia, hypophosphatasia, or hypothyroidism [4].
5. To detect a small effusion or bursitis for injection or aspiration.

1. Is crystal disease the primary cause of acute or chronic arthropathy?
2. Is crystal disease mimicking another inflammatory arthritis, such as rheumatoid
or psoriatic arthritis?
3. Is crystal disease a concurrent cause of polyarthropathy along with another
condition?
States Government.

Switzerland AG 2023
498 24 Crystalline Disease
4. Is crystal disease present, active, or inactive and contributing to structural

changes or patient discomfort?
5. Are CPP or MSU crystals present but simply “innocent bystanders” in a patient
with polyarthritis?
Clinical Comments
High-frequency US excels in the evaluation of gout and CPPD. There are similari-
ties between these two conditions [1, 5].
1. Both may mimic other forms of arthritis in any joint, including small joints.
2. Each may have three phases: acute (severe inflammation), intercritical (clinically
quiescent), and chronic.
3. Both may deposit crystals in joints and soft tissue but may NOT be causing any
clinical problems.
4. Both tend to cause joint inflammation in a monoarticular pattern, less often oli-
goarticular (2–4 joints), but occasionally polyarticular.
5. Ultrasound may be supportive of one or the other diagnosis by demonstrating
distinct patterns consistent with the diagnosis.
6. Both require joint aspiration and rapid synovial fluid analysis for a definitive
diagnosis.
7. Gout and CPPD disease each have predilections for certain joints, although over-
lap may occur.
(a) Gout: First metatarsophalangeal joint (MTPJ), midfoot, ankle, and knee
(b) CPPD disease: Knee and wrist
Gout
The most valuable US sign of gout is the double contour sign (DCS) (Fig. 24.1).
DCS occurs when MSU crystals deposit on the external surface of cartilage, form-
ing a band [2]. On US, the DCS is a hyperechoic layer, continuous or discontinuous,
nearly as thick as the underlying bony cortex, and does not change with different
insonation angles. A DCS may cover any cartilage surface but favors the first MTPJ,
the tibiotalar joint, and the distal femoral cartilage [6]. The other helpful sono-
graphic signs of MSU crystals are tophi and MSU aggregates.
Tophi are hyperechoic and are either oval or amorphous (Fig. 24.2) [2]. They
vary in size and echogenicity and may have an acoustic shadow. There may also be
a hypoechoic halo surrounding the tophus. Tophi are often present within joint cap-
sules and other soft tissues such as bursae, tendons, and soft tissue surrounding
joints and tendons, but they may occur anywhere. MSU aggregates are small
hyperechoic foci found in synovial fluid, synovium, and other soft tissues, usually
Gout 499
Fig. 24.1 Double contour sign with illustration
Fig. 24.2 Tophus
without acoustic shadowing and exhibiting no change with insonation angle [2].
MSU aggregates mimic “sugar clumps” or “snowstorm” patterns. In the proper
clinical setting, MSU cloudy areas, or “snowstorms,” along with synovial hypertro-
phy and power Doppler (PD) activity, argue for acute gout.
A positive DCS is listed as a criterion for gout classification [7]. Regarding the
use of sonography for treatment decisions, US findings do not directly influence
treatment decisions for gout. When considering gout treatment, the presence of a
DCS alone is not a sufficient reason for treatment with uric acid-lowering therapy
[8]. However, since the DCS may help establish the diagnosis of gout, US plays a
vital role in determining which patients are under consideration for treatment.
Chronic gout may cause bony erosion, an abnormal discontinuity of the smooth
cortex of the bone that should be verified in two planes. Gout may also demonstrate
color or PD activity in joints, bursae, and tendons [9, 10]. In the future, US may play
a more significant role in gout treatment. Sequential sonographic follow-up of the
DCS and tophi may help monitor treatment efficacy and adherence since US
changes occur as early as 3 months after urate level normalization [11, 12].
Furthermore, patients with asymptomatic hyperuricemia may demonstrate tophi,
MSU aggregates, joint capsule swelling (with or without PD activity), and bone
erosion. Current gout guidelines do not address such subclinical activity, but this
will undoubtedly be the subject of future investigation [13–16].
Calcium Pyrophosphate Deposition Disease
For CPP crystals, the sonographic sign is calcium deposition within cartilage (hya-
line and fibrocartilage) (Figs. 24.3 and 24.4). CPP crystals appear as hyperechoic
discontinuous or continuous areas of varying size, which may cause an acoustic
shadow if sufficiently large or dense [2]. This calcification may occur within any
cartilage but, in particular, is noted in the distal anterior femoral cartilage, medial
and lateral menisci, and the triangular fibrocartilage of the wrist. In the distal femo-
ral cartilage, linear CPP crystal deposition may resemble a sandwich cookie.
Fig. 24.3 Calcium

deposition in hyaline
cartilage
Sonographic Overlap 501
Fig. 24.4 Calcium

deposition in fibrocartilage
Calcium deposition may also occur in tendons, ligaments, and entheses. Cartilage
calcification may be seen on radiographs, but US is a more sensitive detector of soft
tissue calcium [17]. The finding of CPP crystal aggregates on US, particularly in
cartilage, is considered to be corroborative but not diagnostic for CPPD disease [1,
4]. Thus, similar to gout, the sonographic findings of CPP crystals do not direct
therapeutic decisions.
Be aware that other causes of soft tissue calcium deposition may mimic CPP
crystals on US. The domain of CPPD disease is primarily within the cartilage. Still,
other causes or conditions associated with cartilage calcification (with or without
CPPD disease) include hyperparathyroidism, hemochromatosis, gout, Wilson’s dis-
ease, ochronosis, hypophosphatasia, hypothyroidism, and hypomagnesemia [18]. In
addition, there are causes of soft tissue calcification NOT in cartilage: dystrophic
calcification, calcinosis cutis, and basic calcium phosphate. One variety of basic
calcium phosphate is hydroxyapatite deposition.
Hydroxyapatite deposition disease (HADD) may cause calcium deposits in the
shoulder and other tendons and joints [19]. HADD deposits are not typically in
cartilage, occur most often in middle-aged females, and are of unclear origin. There
are several HADD stages: pre-calcific, formative, resorptive, and post-calcific [20,
21]. The resorptive, or “slurry,” stage is the most inflammatory, but many individu-
als are asymptomatic. Although typically asymptomatic, HADD may cause struc-
tural damage in the shoulder, such as rotator cuff tears, glenohumeral joint
narrowing, and bone destruction [22]. The destructive change of HADD has been
called Milwaukee shoulder syndrome. More detailed reviews of HADD beyond the
scope of this manual are available [23, 24].
Sonographic Overlap
One location of potential sonographic confusion is the dorsal metacarpophalangeal

joint (MCPJ). Chronic CPPD disease may cause cartilage destruction, resulting in
structural changes mimicking an erosive polyarthropathy such as rheumatoid arthri-
tis [25]. However, CPPD crystals may be seen within the MCPJ cartilage if
sufficient cartilage remains. In addition, a DCS on the MCPJ cartilage surface may
also be seen in patients with longstanding polyarticular gout.
To further complicate matters, on the surface of smooth, intact MCPJ cartilage,
one may find the interface reflex (IR) artifact. An IR is easily differentiated from a
DCS since the fragile IR line disappears with the change of the insonation angle
[26]. The IR will move along the cartilage surface as you passively flex the finger at
the MCPJ and is only present when the probe is 90 degrees to a particular section of
the cartilage. Also, the IR is not nearly as thick as the DCS.
Pitfalls
1. According to the 2015 gout classification criteria, the ultrasonic finding of DCS
is counted if the DCS is found in an inflamed joint or a different joint if that
joint was previously symptomatic.
2. There is increased sensitivity for the detection of a DCS by looking at contra-
lateral and noninflamed joints. However, for the DCS to count towards a gout
classification, the joint must be currently or previously symptomatic.
3. Always remember that infection or other causes of arthritis may concurrently
be present with crystal disease. It is critical to examine synovial fluid whenever
possible, not just for the presence of crystal disease but also for infection.
4. Be careful when looking at joints where an IR may mimic a DCS.
5. When looking for calcium deposits, be aware that not all calcium deposits may
be from CPPD.
6. When looking at the triangular fibrocartilage and knee menisci, be mindful that
the bulk of calcium deposition may appear superficial since deeper portions of
the structures can be hypoechoic from acoustic shadowing artifacts.
7. DCS and MSU aggregates may be found in patients without gout or even with
normal uric acid levels [27].
8. Consider that some hyperuricemic patients may have subclinical activity, which
may be delineated as synovitis by PD or by the presence of bone erosion.
9. Since US is more sensitive at detecting calcium deposition and bone erosion
than radiographs, do not rely solely on radiographs to exclude these
conditions.
10. Ultrasound demonstration of CPPD crystals at the knee is an accurate tool com-
pared to surgical histopathologic evaluation as the gold standard [28].
Method
The following protocol is a general crystalline US examination. It will need to be

customized based on the clinical suspicion of gout or CPPD disease. It is essential
to evaluate asymptomatic and contralateral joints since crystal deposition may be
present in joints that are not inflamed. Ask the patient which joints have ever been
Method 503

1a: Dorsal 1st
Doppler
inflamed, and focus on those joints. Capture an additional PD view of the joint or
structure for almost every image listed below.
rotocol Image 1a: Dorsal First Metatarsophalangeal Joint,

P
The patient is seated and semi-upright. On the affected side, the hip should be par-
tially flexed and the inferior heel in contact with the examination table. The first toe
should be in a neutral position, flat on the exam table. Position the probe in a longi-
tudinal axis (LAX) orientation using a high-frequency preset. The joint should be
still when evaluated with PD to avoid motion artifacts.
Center the probe over the first MTPJ. Evaluate the distal metatarsal (MT) head
and proximal phalanx for bone erosion. Turn on the PD to look for active soft tissue
inflammation. Note the anechoic or hypoechoic cartilage overlying the MT head
and look for a hyperechoic coating on the surface of the cartilage, which may indi-
cate a DCS. Remember that an IR accentuated by synovial fluid in the dorsal recess
may mimic a DCS. Again, the IR is hyperechoic but not nearly as thick as the DCS,
and the IR will change dramatically with the angle of insonation in contradistinction
to the DCS [10, 26]. Examine the dorsal recess for distention, crystal aggregates,
and tophi. Examine the bony surface of the MT neck.
rotocol Image 1b: Medial First Metatarsophalangeal Joint,

P
Have the patient externally rotate the hip, keeping the knee flexed into a “frog-
leg” position. This fully exposes the medial and plantar first MTPJ. Perform a
medial transverse axis (TAX) slide to reach the medial MTPJ. Repeat the

1b: Medial 1st
Doppler
examination described in Image 1A, including using PD to look for active soft
tissue inflammation. Again, the joint should be supported to avoid motion arti-
facts with PD.
rotocol Image 1c: Plantar First Metatarsophalangeal Joint,

P
Slide the probe (still in LAX orientation) to the plantar surface of the first MTPJ to
evaluate the structures previously described. The plantar MTPJ is a common site for
an IR, so probe movements varying the insonation angle help distinguish between
an IR and a DCS. Use PD to look for active soft tissue inflammation.
rotocol Image 2: Tibiotalar Joint, Longitudinal ± Power

P
Doppler (Fig. 24.8)
The patient’s foot is flat on the examination table, or the leg is extended with a
cushion beneath the calf to expose the anterior ankle. Set the preset for “ankle”
and place the probe on the dorsum of the foot in LAX. Locate the hyperechoic
tibia and the more distal talus, with the joint space in between. The cartilage
surface of the proximal talus is another location to look for a DCS. The tibiotalar
joint may exhibit distention with synovitis and possible PD activity. Slide the
probe to the medial and lateral aspects of the tibiotalar joint to better encompass
the entire joint.
Method 505

1c: Plantar 1st
Doppler

2: Tibiotalar joint,
Doppler
rotocol Image 3: Achilles Tendon, Longitudinal ± Power

P
Doppler (Fig. 24.9)
The patient is prone with a bolster underneath the anterior ankle. The foot hangs off
the table to enable passive manipulation. With the probe in LAX, visualize the cal-
caneus, and then focus on the more proximal Achilles tendon. Look for tophaceous
deposits or MSU aggregates within and surrounding the tendon (Fig. 24.2). Also,
look for calcium deposits within the tendon. Power Doppler may be noted within or
surrounding the tendon and in the subcutaneous calcaneal and retrocalcaneal bur-
sae. The PD activity may correlate with visible MSU or CPPD crystals. Look at the
enthesis to see if MSU or CPP crystal deposits may be associated with PD activity.
Manually flex and extend the ankle, but remember that PD activity diminishes with
increased tension on the Achilles tendon [29].

3: Achilles tendon,
Doppler
rotocol Image 4: Distal Anterior Femoral Cartilage, Transverse

P
± Power Doppler (Fig. 24.10)
The patient is semi-upright or supine, and the knee should be maximally flexed. Place
a linear probe with a mid-depth setting in TAX orientation across the femoral notch.
The transducer should be perpendicular to the table. Move the examination proxi-
mally until the femoral notch appears, represented as a hypoechoic “V-shaped” struc-
ture. Tilt the probe in one direction and then the other while moving it medially and
laterally to delineate the distal femoral cartilage. Note that this is NOT the joint space
itself but simply the articular cartilage covering about one-third of the anterior femur.
Look at the cartilage thickness, clarity, and for any CPP crystals within the cartilage.
Also, examine the superficial surface of the cartilage for a DCS. Again, DCS thick-
ness rivals that of the femoral cortex and persists with different insonation angles.
Protocol Image 5: Medial Meniscus, Longitudinal (Fig. 24.11)
The patient extends the knee, and a bolster is placed behind the knee to bend it to
approximately 30 degrees. Rotate the probe to an LAX orientation and place it
medially to the distal half of the patella. Slowly move the transducer posteriorly
with a TAX slide until the joint space emerges. Tilt the probe to clarify the triangu-
lar, slightly hyperechoic medial meniscus. Also, fix the proximal end of the trans-
ducer and slightly rotate the distal portion in either an anterior or posterior direction
while tilting the probe in either direction to sharpen the image of the medial menis-
cus. The probe can also be moved posteriorly with a TAX slide to examine the
posterior portion of the medial meniscus. Evaluate for calcium deposits within the
medial meniscus and the medial collateral ligament. The deeper part of the medial
Method 507

4: Distal anterior femoral
cartilage, transverse ±
power Doppler

5: Medial meniscus,
longitudinal
meniscus may not exhibit as much calcium due to possible acoustic shadowing from
calcium deposition in the superficial portion [30].
Protocol Image 6: Lateral Meniscus, Longitudinal (Fig. 24.12)
With the knee in the same position as in Protocol Image 5, place the probe in LAX
orientation just lateral to the distal half of the patella. Slowly perform a TAX slide
posteriorly until the joint space is recognized; center the joint space in the field. Tilt
the transducer back and forth to identify a sharp image of the lateral meniscus,
which is also hyperechoic and triangular. Fixing the proximal portion of the probe
and fanning the distal portion anteriorly or posteriorly while slightly tilting in both

6: Lateral meniscus,
longitudinal

7: Triangular fibrocartilage
complex, longitudinal ±
power Doppler
directions will help optimize the image. Again, look for calcifications within the
meniscus and the lateral collateral ligament. The probe can be moved posteriorly
with a TAX slide to look at the posterior portion of the lateral meniscus.
rotocol Image 7: Triangular Fibrocartilage Complex,

P
With the patient’s hand lying prone and in slight radial flexion, place the high-
frequency probe at the ulnar aspect of the wrist in an LAX orientation. One end of
the transducer is on the curved, hyperechoic distal ulna, and the other is on the
Method 509
triquetrum, thus encompassing the TFCC. Radial flexion uncovers the triangular
fibrocartilage, which is adherent to the distal ulna. Distal to the articular disc is the
meniscal homolog, and superficial is the extensor carpi ulnaris tendon. Evaluate the
triangular fibrocartilage complex for CPP crystals. If significant superficial calcium
deposition is present, you may not be able to visualize deeper calcium deposits due
to an acoustic shadowing artifact [30]. The triangular fibrocartilage complex is typi-
cally the province of CPPD rather than MSU crystals. Look for PD activity, which
may indicate acute CPPD disease arthritis.
rotocol Image 8a: Dorsal Second Metacarpophalangeal Joint,

P
With the hand prone on a flat surface, place the high-frequency probe in LAX ori-
entation over the second MCPJ. Evaluate the metacarpal head (MCH) for erosions,
but do not mistake the normal indentation at the base of the MCH for a true erosion.
Look at the hypoechoic or anechoic cartilage covering the MCH. On the cartilage
surface, there may be a DCS whose appearance persists despite any change in the
insonation angle. The DCS is typically as thick as the underlying cortex. Within the
cartilage, there may be chondrocalcinosis associated with CPPD. There may be
damage to the cartilage due to chronic CPPD disease or other polyarthropathies. On
the cartilage surface, there may be an IR that can mimic a DCS. The IR changes
dramatically with any change in insonation angle and is thin and fragile compared
to the robust DCS. By gently grasping the patient’s fingers and bending the MCPJ,
the examiner may demonstrate the extent of the dorsal cartilage covering the
MCH. Evaluate the joint capsule for grayscale enlargement and turn on the PD to
look for acute synovitis.

8a: Dorsal 2nd
Doppler

8b: Dorsal 3rd
Doppler
rotocol Image 8b: Dorsal Third Metacarpophalangeal Joint,

P
Repeat the same evaluation as for the second MCPJ.

Crystalline Arthritis Ultrasonic Examination Checklist
□ Protocol Image 1a: Dorsal first metatarsophalangeal joint, longitudinal ±
power Doppler
□ Protocol Image 1b: Medial first metatarsophalangeal joint, longitudinal ±
power Doppler
□ Protocol Image 1c: Planter first metatarsophalangeal joint, longitudinal ±
power Doppler
□ Protocol Image 2: Tibiotalar joint, longitudinal ± power Doppler
□ Protocol Image 3: Achilles tendon, longitudinal ± power Doppler
□ Protocol Image 4: Distal anterior femoral cartilage, transverse ± power Doppler
□ Protocol Image 5: Medial meniscus, longitudinal
□ Protocol Image 6: Lateral meniscus, longitudinal
□ Protocol Image 7: Triangular fibrocartilage complex, longitudinal ± power Doppler
□ Protocol Image 8a: Dorsal second metacarpophalangeal joint, longitudinal ±
power Doppler
□ Protocol Image 8b: Dorsal third metacarpophalangeal joint, longitudinal ±
power Doppler
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20. Goller SS, Hesse N, Dürr HR, Ricke J, Schmitt R. Hydroxyapatite deposition disease of the
wrist with intraosseous migration to the lunate bone. Skelet Radiol. 2021;50(9):1909–13.
21. Hongsmatip P, Cheng KY, Kim C, Lawrence DA, Rivera R, Smitaman E. Calcium hydroxy-
apatite deposition disease: imaging features and presentations mimicking other pathologies.
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22. Merolla G, Bhat MG, Paladini P, Porcellini G. Complications of calcific tendinitis of the shoul-
der: a concise review. J Orthop Traumatol. 2015;16(3):175–83.
23. Garcia GM, McCord GC, Kumar R. Hydroxyapatite crystal deposition disease. Semin
24. Beckmann NM. Calcium apatite deposition disease: diagnosis and treatment. Radiol Res
Pract. 2016;2016:4801474.
25. Ivory D, Velázquez CR. The forgotten crystal arthritis: calcium pyrophosphate deposition. Mo
Med. 2012;109(1):64–8.
26. Lai K-L, Chiu Y-M. Role of ultrasonography in diagnosing gouty arthritis. J Med Ultrasound.
2011;19(1):7–13.
27. Abhishek A, Courtney P, Jenkins W, Sandoval-Plata G, Jones AC, Zhang W, et al. Brief report:
monosodium urate monohydrate crystal deposits are common in asymptomatic sons of patients
with gout: the sons of gout study. Arthritis Rheumatol. 2018;70(11):1847–52.
28. Filippou G, Scanu A, Adinolfi A, Toscano C, Gambera D, Largo R, et al. Criterion validity
of ultrasound in the identification of calcium pyrophosphate crystal deposits at the knee: an
OMERACT ultrasound study. Ann Rheum Dis. 2021;80(2):261–7.
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in the diagnosis of calcium pyrophosphate dihydrate deposition disease. A systematic litera-
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Chapter 25
Enthesopathy

1. Suspicion of enthesitis
2. Pain at an enthesis
1. Is there a systemic process causing enthesitis?
2. What precisely is causing pain near an enthesis?
3. Is the pain near or at an enthesis due to a localized problem rather than a sys-
temic one?
Clinical Comments
The enthesis is the insertional point for attachment to bone of tendons, ligaments,
fascia, muscles, and joint capsules [1]. OMERACT defines enthesitis as hypoechoic
or thickened insertion of the tendon <2 mm from bony surfaces, which may exhibit
a Doppler signal if active and may show erosions [2, 3]. Enthesophytes and calcifi-
cations may be signs of structural damage.
Enthesitis is predominantly the domain of spondyloarthropathy (SpA), particu-
larly psoriatic arthritis (PsA) [4]. Differentiating seronegative rheumatoid arthritis
(RA) from PsA is a challenge compounded by the fact that approximately 15% of
patients with PsA exhibit no psoriasis before the arthritis presentation [5]. In patients
with seronegative peripheral polyarthritis, sonographic confirmation of enthesitis
supports the diagnosis of PsA.
States Government.

Switzerland AG 2023
514 25 Enthesopathy
Recall that SpA in adults classically includes ankylosing spondylitis (AS), PsA,
reactive arthritis, and enteropathic arthritis (the latter associated with inflammatory
bowel disease). These four types may overlap and, more recently, may be classified
as axial and/or peripheral SpA [6]. In this newer classification system, enthesitis is
a prominent criterion for diagnosing both peripheral and axial SpA [6]. However,
this system is based on clinical enthesitis detection without the aid of ultrasound
(US) or other imaging modalities.
Bear in mind that enthesis involvement is not the exclusive realm of SpA. It
may also be less commonly associated with RA, gout, other crystal diseases, sar-
coidosis, juvenile idiopathic arthritis, diffuse idiopathic skeletal hyperostosis
(DISH), and osteoarthritis (OA). Almost any enthesis can be evaluated sonographi-
cally, and the US exam should be tailored to the symptoms and clinical suspicion of
systemic disease. The more common sonographically accessible areas for tendon
enthesis evaluation include the following [7]:
1. Achilles tendon insertion on the calcaneus
2. Plantar fascia insertion on the calcaneus
3. Patellar tendon insertions on the patella and tibial tuberosity
4. Quadriceps tendon insertion on the patella
5. Common extensor tendon insertion on the lateral elbow epicondyle
6. Common flexor tendon insertion on the medial elbow epicondyle
7. Triceps tendon insertion on the olecranon
8. Supraspinatus tendon insertion on the greater tuberosity
9. Flexor and extensor tendons insertions on the phalanges of the hand and foot
10. Tibialis anterior tendon insertion on the medial cuneiform and first metatarsal
The enthesis and the surrounding structures (fibrocartilage, bursae, fat pad, adja-
cent bone, and fascia) are termed the enthesis organ, whose function is to dissipate
repetitive physical stress [4, 8]. Mechanical problems can also affect the enthesis,
including repetitive injury [1, 9, 10]. Such repetitive mechanical forces may trigger
an inflammatory response, leading to localized inflammation [1]. Adjacent to the
site of enthesitis, the bone may develop spurs, and eventually, there may be destruc-
tion of superficial fibrocartilage, vascular invasion (neovascularization), and inflam-
matory cell infiltration. In addition to the enthesis being a site of repetitive
mechanical stress and localized inflammation, an underlying systemic inflamma-
tory process may reveal itself in this location.
Enthesitis is clinically underdiagnosed by physical examination [1]. Clinical
methods to score enthesopathy include the Manders enthesis index (MEI) and the
Maastricht ankylosing spondylitis enthesitis score (MASES) [11, 12]. Both scoring
systems lack accuracy and depend on the examiner physically exerting direct pres-
sure over an enthesis to elicit pain. One study looked at clinical assessment using
MASES compared to US as the gold standard. Depending on the specific MASES
enthesis site, the physical examination had a sensitivity and specificity of 71.4–87%
and 47.4–75%, respectively [13].
Plain radiographs may show late chronic bony changes (enthesophytes, new
bone formation, bony irregularity) and likewise lack sensitivity [1, 14, 15].
Conversely, magnetic resonance imaging (MRI) is quite helpful in detecting enthesi-
tis but remains cost-prohibitive [1, 15]. Compared with physical examination, US is
very sensitive for detecting enthesitis, particularly subclinical enthesitis [4, 16, 17].
Ultrasound is diagnostically accurate and helpful for early the diagnosis of SpA,
notably PsA [15, 18]. Neovascularization (as demonstrated by the Doppler signal)
of the enthesis provides good predictive value for diagnosing SpA [19]. It is also
suggested that US be used when monitoring response to treatment since changes
with treatment have been sonographically demonstrated [17, 20, 21]. Despite
advances, there is no current gold standard modality for enthesitis detection [15,
22]. Trials are ongoing to determine the best modality and scoring system to moni-
tor the treatment of enthesitis in PsA [15].
Ultrasound is emerging as the preferred method of enthesitis identification due
to its sensitivity (subclinical enthesitis), functional evaluation (Doppler activity),
morphologic delineation (including new bone formation), and low cost [4].
Enthesitis reportedly occurs in 35–50% of PsA patients, a more frequent rate than
in RA, AS, and OA. However, one study demonstrated that although enthesitis with
power Doppler (PD) activity occurs more frequently with PsA and psoriasis, it may
also be present in patients with fibromyalgia [23]. On the other hand, the higher the
number of US-documented enthesitis sites, the greater the likelihood of PsA being
the correct diagnosis rather than fibromyalgia [23, 24].
A scoring system for enthesitis has been developed using a 0–3 grading
system [3]:
• Grayscale (GS) (Fig. 25.1):
Grade 0 = normal
Grade 1 = hypoechogenicity (loss of fibrillar pattern)
Grade 2 = hypoechogenicity + thickening + calcifications/enthesophytes
Grade 3 = Grade 2 features + bone erosions
• Power Doppler (Fig. 25.2):
Grade 0 = no PD signal
Grade 1 = <2 punctate signals
Grade 2 = 2–4 punctate signals or 1 confluent signal
Grade 3 = >4 punctate signals or >1 confluent signal
Current efforts are being made to study, refine, and validate an enthesitis scoring
system [25].
A more recently proposed enthesitis scoring system identified six entheseal sites
that effectively differentiated patients with PsA from normal: proximal and distal
insertions of the patella tendon, Achilles tendon, plantar fascia, common extensor
tendon, and supraspinatus tendon [26]. The elements and grading of this scoring
system are as follows:
516 25 Enthesopathy
Fig. 25.1 Grayscale enthesitis scoring
Fig. 25.2 Power Doppler enthesitis scoring

Pitfalls 517
• GS:
Hypoechogenicity: 0 (absent), 1 (present)
Tendon/ligament thickening: 0 (absent), 1 (present)
Bone erosion: 0 (absent), 1 (present)
“Fluffy” bone irregularities: 0 (absent), 1 (present)
Enthesophytes: 0 (absent), 1 (small) 2 (medium) 3 (large)
Calcifications within the tendon/ligament: 0 (absent), 1 (present)
Bursitis: 0 (absent), 1 (present)
• PD:
The Doppler signal within 2 mm of the bony cortex is arbitrarily evaluated,
although there may be a PD signal within 2–5 mm of cortical bone. Power
Doppler grading is 0 (absent), 1 (mild), 2 (moderate), and 3 (severe).
pecial Clinical Consideration: Inflammatory

S
Arthritis Differentiation
Differentiating seronegative early rheumatoid arthritis (ERA) from PsA is challeng-

ing, particularly in patients without overt psoriasis. Ultrasound may be revealing
since enthesitis is a key feature of PsA [14, 27, 28]. Do not neglect sonographic
evaluation for enthesitis, particularly in the fingers of such patients since this may
tip the diagnostic scale.
Specific US findings supporting a diagnosis present in PsA [29]:
1. At the metacarpophalangeal joint, extensor tendon paratenonitis was 2.5% in
ERA vs. 54.1% in early PsA.
2. At the finger proximal interphalangeal joint, enthesitis of the central slip did not
occur with ERA but only in PsA.
Dactylitis, which is diffuse swelling of a finger or toe (“sausage digit”), most often
occurs in SpA and, in particular, PsA; however, it may also be present in sarcoid, gout,
syphilis, tuberculosis, and sickle cell disease [30]. Additionally, digits in patients with
RA may sometimes demonstrate diffuse swelling. Patients who display dactylitis, distal
interphalangeal joint pain, or fingernail changes merit a diligent search for enthesitis
[31]. If clinical evaluation reveals nail disease compatible with psoriasis (such as pitting,
onycholysis, and subungual hyperkeratosis), perform an US examination of the extensor
tendon enthesis at the distal phalanx. Since the nail root fascia is an extension of the
extensor tendon, nail disease in PsA is associated with enthesitis [32–34].
Pitfalls
1. A gentle examiner’s touch is needed to prevent dampening of the Doppler sig-

nal. The joint should be in a relaxed, neutral position since putting tension on
the tendon (or ligament) at the enthesis might diminish PD activity [35].
518 25 Enthesopathy
2. Any US-accessible enthesis can be inspected, even those not included in this
suggested protocol. The more superficial the enthesis, the better for sonographic
evaluation. Always perform an US exam of any painful area that contains an
enthesis.
3. Again, be aware that enthesitis occurs mainly with SpA (and particularly PsA)
but also with other conditions such as RA, sarcoidosis, and possibly fibromyal-
gia. Put this information into proper clinical context if your sonographic
examination documents enthesitis with positive PD activity. A sonographic
demonstration of enthesitis supports a SpA diagnosis but is not pathognomonic.
4. Evaluation of the hands for enthesitis also bypasses the pitfall of having
increased PD activity in weight-bearing entheses, particularly in patients with a
high BMI [29].
5. For the fingers and toes, use a high-definition probe set at a minimum of
16 MHz to look at the extensor and flexor entheses.
6. Do not neglect sonographic evaluation for enthesitis in the hands or feet if
symptoms or signs are present, since this may tip the diagnostic scale.
7. Since nail disease in PsA is associated with enthesitis, clinical findings of nail
pitting or thickening should prompt meticulous sonographic assessment of the
extensor tendon enthesis at the distal phalanges of the hands and feet.
8. Grade enthesitis according to a scoring system and devote adequate time when
pursuing PD activity. However, looking at the contralateral side may detect
subclinical enthesitis in the presence of systemic disease.
9. In practice, US is best used to confirm a clinical impression of enthesitis and to
detect subclinical enthesitis. Ultrasound by itself is not diagnostic.
10. If an inferior calcaneal enthesophyte is noted, examine a plain radiograph; an
indistinct margin or “fluffy” periostitis may indicate SpA, as described in one
study of PsA [36].
11. Plantar fasciitis may cause PF swelling (>4 mm), loss of fibrillar echotexture,
cortical irregularities, and PD activity proximally at the calcaneal insertion
[37]. These sonographic features technically meet the enthesitis criteria.
However, enthesitis found in other body areas argues for the presence of a sys-
temic condition.
Method
The enthesopathy protocol below is merely a suggestion and should be tailored to

the particular patient. Select one of the scoring systems described in Clinical
Comments. Often, we are requested to distinguish PsA from normal; the GRAPPA
US Working Group Study influenced our site selection based on its success in this
clinical situation [26]. We note disagreement in the literature regarding naming the
patellar tendon vs. ligament. For consistency, we use the term patellar tendon in
this Manual.
Method 519
When scanning the width of a tendon or ligament with PD, (a) use light probe
pressure, (b) give sufficient time for a PD signal to register an accurate PD signal,
and (c) make certain the tendon or ligament is not too taut. Protocol Images describe
the longitudinal axis (LAX) evaluation with respect to tendons or fascia; however,
the examiner should confirm GS and PD abnormalities in orthogonal views. Perform
slow transverse axis (TAX) slides for both longitudinal and short-axis views for
both GS and PD. Evaluate the enthesis in GS with the highest possible frequency
and note any hypoechoic or thickened insertion of the tendon <2 mm from bony
surfaces, bony enthesophytes, or erosions. Then turn on PD to look for activity.
High-frequency transducers enhance the detection of PD activity. Use a minimal
Pulse Repetition Frequency (PRF) that does not produce excess noise in surround-
ing tissue. The protocol image examples are scanned with PD; however, initial GS
evaluation will better elucidate echotexture and structural detail.
Set the presets as necessary for the region of interest.
rotocol Image 1: Achilles Tendon at the Calcaneal Insertion,

P
If able, the patient should be prone with the foot in slight dorsiflexion and hanging
off the table. Place the probe in LAX with the distal end over the superior posterior
calcaneus to see the insertion of the Achilles tendon (AT). Move the transducer lat-
erally and medially to encompass the entire width of this flat tendon. The approxi-
mately 1 cm-long insertion point is typically hypoechoic or anechoic due to
the anisotropy of AT fibers. A heel-to-toe maneuver of the probe and slight foot
dorsiflexion may diminish anisotropy at the calcaneal insertion. Look for AT tears,
swelling, hypoechogenicity, calcifications, MSU aggregates, or tophi adjacent to or
within the AT. Look for bony posterior calcaneal erosion; a hyperechoic protrusion
might be an enthesophyte.

1: Achilles tendon at
calcaneal insertion,
Doppler
520 25 Enthesopathy
After examining using GS ultrasound, turn on the PD at the insertion. Recall that
extreme dorsiflexion stretches the AT, thus enhancing the normal fibrillar echotex-
ture at the cost of a diminished PD signal. Rather than a tenosynovium, the AT has
a paratenon, best seen posteriorly.
rotocol Image 2: Plantar Fascia Insertion at the Calcaneus,

P
Place the probe in LAX at the center of the inferior calcaneus, and slowly move the
transducer medially and laterally to examine the full extent of the fibrillar plantar
fascia (PF). Manually dorsiflexing the ankle may clarify the PF image. Using a
lower frequency and time-gain control enhances this deeper image. Probe tilting
and using a heel-to-toe maneuver (with plenty of transmission gel) diminish anisot-
ropy, which might mimic insertional tearing or enthesitis.
Note that the PF will typically lose fibrillar definition near the calcaneal inser-
tion; however, if there is no attendant PF thickening, this is normal [38]. The PF
is usually 3-4 mm thick near the calcaneal insertion [39]. Measure the PF thickness
to look for thickening >4 mm, which may indicate plantar fasciitis, a mimic of
enthesitis. Look for more distal PF thickening to confirm plantar fasciitis. The find-
ing of enthesitis in other body areas favors a systemic disease. Positive PD activity
may be from SpA but may occur with the more acute phase of plantar fasciitis [40].
The ankle should not be maximally dorsiflexed since this may ablate PD activity.

2: Plantar fascia insertion
at calcaneus, longitudinal ±
power Doppler
Method 521
rotocol Image 3: Tibialis Anterior Tendon Insertion,

P
The patient is recumbent with the foot placed flat on the examination table, expos-
ing the foot dorsum. Place the probe in TAX, centered on the tibialis anterior tendon
(TAT) on the medial aspect of the dorsal foot. Turn the probe 90° into LAX. Move
the transducer distally in an LAX slide, shifting it slightly laterally and medially as
you go to see the complete TAT in LAX. As you look at the talus from proximal to
distal, you will sequentially visualize the tibiotalar joint, the talar dome, the talar
neck, the talar head, and finally, the talonavicular joint. Continue to move the probe
in LAX distally, following the TAT. The joint distal to the navicular is the naviculo-
cuneiform joint. Technically, you are looking at the navicular-medial cuneiform
joint. Continue to move the probe distally, following the TAT, to see its insertion on
the distal medial cuneiform and the base of the first metatarsal.
rotocol Image 4: Patellar Tendon at the Distal Patella,

P
The patient is recumbent with a bolster placed against the popliteal fossa to achieve
30-degree knee flexion [26]. Place the probe in LAX over the distal patella and the
proximal insertion of the patella tendon. Tilt and rock the transducer to enhance the
image of the tendon at the insertion. Sweep the probe in slow TAX slides medially
and then laterally to scrutinize for swelling, hypoechogenicity, and enthesophytes.

3: Tibialis anterior tendon
insertion, longitudinal ±
power Doppler
522 25 Enthesopathy

4: Patellar Tendon at distal
patella, longitudinal ±
power Doppler

5: Patellar tendon at
proximal tibia, longitudinal
± power Doppler
rotocol Image 5: Patellar Tendon at the Proximal Tibia,

P
Next, perform an LAX slide distally, following the fibrillar patellar tendon to the
insertion on the curved bony insertion point, the tibial tuberosity. Again, enhance
the image if needed by slightly tilting or rocking the probe. Sweep the probe slowly
medially and then laterally to scrutinize for tendon swelling, hypoechogenicity, and
enthesophytes. Be aware that bony irregularity at the tibial tuberosity may be from
Osgood-Schlatter disease.
Method 523
rotocol Image 6: Quadriceps Tendon at the Proximal Patella ±

P
Place the probe in LAX at the midline of the knee with the distal end of the probe
over the proximal patella. The quadriceps tendon is seen in LAX, with the tendon
fibrils creating a paintbrush-like pattern. Be sure to move the probe medially and
laterally to evaluate the entire quadriceps tendon insertion on the patella.
rotocol Image 7: Common Extensor Tendon at the Lateral

P
Epicondyle, Longitudinal ± Power Doppler (Fig. 25.9)
The patient is recumbent, resting the arm comfortably with a pronated forearm on
the abdomen. The elbow is bent at 90° [26]. Place the proximal end of the probe in
LAX on the lateral epicondyle. It may be a bit more posterior than you think. Look
for the hyperechoic gentle slope of the lateral epicondyle, the more superficial fibril-
lar common extensor tendon (CET), and possible cortical irregularities and entheso-
phytes. Near the enthesis, look for loss of fibrillar echotexture/hypoechogenicity
and swelling that may indicate enthesitis.
The lateral collateral ligament (LCL), also called the radial collateral ligament
(RCL), is deep to the CET. The LCL is usually challenging to differentiate from the
CET. The LCL extends distally to the annular ligament, which is the hyperechoic
structure just superficial to the radial head; the CET more distally becomes muscle
[41]. Once the CET and LCL are visualized, sweep the probe medially and laterally
to encompass the full width of their insertions. Remember, the LCL also inserts on
the lateral epicondyle and may be subject to enthesitis.

6: Quadriceps tendon at
proximal patella ± power
Doppler
524 25 Enthesopathy
Fig. 25.9 Protocol Image 7: Common extensor tendon at lateral epicondyle, longitudinal ±
power Doppler
rotocol Image 8: Common Flexor Tendon at the Medial

P
Epicondyle, Longitudinal ± Power Doppler (Fig. 25.10)
Palpate the medial epicondyle (ME) and place the probe in LAX over the joint along
the anterior medial elbow to visualize the humeroulnar joint (HUJ). See the bony
hyperechoic curved “ski-slope“of the ME leading down the curved valley, the coro-
noid recess, and then a smaller “hill,” the trochlea of the humerus. Look at the com-
mon flexor tendon (CFT), its muscle, and the insertion on the ME. Elbow extension
enhances CFT visualization. Deep to the CFT and muscles is the ulnar collateral
ligament’s anterior bundle, which we refer to simply as the UCL. To delineate the
separation of the CFT from the UCL, look at the more hypoechoic CFT muscle just
superficial to the ligament. In elbow extension, the UCL is hypoechoic. Flexing the
elbow to 90° will create tension in the UCL, enhancing echotexture visualization.
Look at the enthesis of the CFT and the UCL on the ME for evidence of enthesopa-
thy, muscle tears, and bony avulsions. Compare this image to the (unaffected) con-
tralateral side if needed.
Method 525
Fig. 25.10 Protocol Image 8: Common flexor tendon at medial epicondyle, longitudinal ±
power Doppler
rotocol Image 9: Triceps Tendon Insertion on Olecranon

P
Process ± Power Doppler (Fig. 25.11)
The patient is recumbent with the hand placed over the umbilicus, elbow flexed at
90°, and pointed downward at least 45°. Place the transducer in LAX along the edge
of the olecranon process to visualize the bird’s beak configuration of the distal tri-
ceps tendon (DTT) insertion on the bony olecranon. Use adequate gel, and perform
heel-to-toe maneuvers in either direction to sharply visualize the “birds-beak” inser-
tion of the distal triceps tendon onto the olecranon process. Tilt the probe to decrease
anisotropy. Small medial and lateral TAX slides help evaluate the full extent of the
DTT. Slightly extend the elbow to avoid extreme tension on the tendon, which may
ablate PD activity.
526 25 Enthesopathy

9: Triceps tendon insertion
on olecranon process ±
power Doppler

10: Supraspinatus Tendon
at greater tuberosity,
Doppler
rotocol Image 10: Supraspinatus Tendon at Greater

P
Tuberosity, Longitudinal ± Power Doppler (Fig. 25.12)
The patient internally rotates the shoulder by placing the hand into the ipsilateral
back pocket. This is the modified Crass position, an excellent position to search for
enthesitis [26]. Find the supraspinatus tendon (SST) insertion by placing the probe
in TAX over the biceps tendon’s round or oval long head (LHBT) in the bicipital
groove. Rotate one end of the transducer toward the middle of the clavicle to visual-
ize as much of the LHBT in LAX as possible. Then move the probe laterally to see
the large “bird’s beak” of the fibrillar SST inserted on the greater tuberosity (GT).
Method 527
This is the distal anterior portion of the SST at the insertion on the superior facet
(SF) of the GT.
The hyperechoic bony SF is concave, with the distal portion of the concavity
being somewhat elongated and flattened. Focus on the insertion by alternatively
performing heel-to-toe and tilting probe maneuvers. At the insertion of the anterior
part of SST on the superior facet, there is a very thin hypoechoic line due to the
downward curve of the distal SST fibers, causing anisotropy. This is not a tendon
tear or enthesopathy.
Next, perform a TAX slide posteriorly to look at the middle facet (MF) and the
posterior SST while the probe remains in the LAX orientation. Here, the bird’s beak
configuration is smaller and sharper, and the MF is flatter. A hypoechoic area of the
SST near the insertion on the GT is due to anisotropy from the interdigitation of the
insertional fibers of the infraspinatus tendon (IST) coming from a different direc-
tion. Do not mistake this for a tear or tendinosis. Again, perform all the probe
maneuvers necessary to minimize anisotropy and evaluate the enthesis. Be aware
that the SST is about 2.5 cm wide, and you must scan this wide enthesis [42].
rotocol Image 11: Extensor Tendon Insertion on Hand

P
and Feet Phalanges, Longitudinal ± Power Doppler (Fig. 25.13)
Evaluate fingers or toes that are symptomatic with pain, stiffness, and swelling,
particularly those digits demonstrating dactylitis, distal interphalangeal joint pain,
or fingernail changes (such as pitting, subungual hyperkeratosis, or onycholysis).
The patient’s hand or foot rests on a flat surface, exposing the dorsal surface.
Place the highest-frequency probe available (at least 16 MHz) on the dorsum of the
distal phalanx using sufficient transmission gel. Adjust the PRF downward to
enhance the detection of Doppler signals but avoid excess Doppler “noise.” Note the
normal reverberation effect produced by the fingernail or toenail. Look for PD activ-
ity on the distal phalanx’s hyperechoic bone, where the extensor tendon’s fibers are
inserted. Any Doppler signal deep to the bone is an artifact and should be dis-
counted. A Doppler signal not in the distribution of the tendon insertion may be due
to normal blood vessels and should not be interpreted as active enthesitis. Recall
that while the extensor tendon inserts on the bony distal phalanx, some fibers extend
superficially to form the fingernail bed matrix.
rotocol Image 12: Flexor Tendon Insertion on the Hand

P
and Feet Phalanges, Longitudinal ± Power Doppler (Fig. 25.14)
The hand is placed palm up, or the foot is placed in a neutral position, exposing the
toes’ undersurface. Place a small footprint probe (with a frequency of at least
16 MHz) in LAX over the flexor surface of the distal phalanx to evaluate the inser-
tional fibers of the flexor tendon. Small TAX slides in the ulnar and radial directions
528 25 Enthesopathy
Fig. 25.13 Protocol Image 11: Extensor tendon insertion on hand and foot phalanges, longitudinal
± power Doppler
Fig. 25.14 Protocol Image 12: Flexor tendon insertion on hand and feet phalanges, longitudinal ±
power Doppler
References 529
enhance the search for PD activity indicative of active enthesitis. Remember, a light
touch and abundant transmission gel are mandatory.
Enthesis Ultrasonic Examination Checklist
□ Image 1: Achilles tendon at the calcaneal insertion, longitudinal ± power Doppler
□ Image 2: Plantar fascia insertion at the calcaneus, longitudinal ± power Doppler
□ Image 3 Tibialis anterior tendon insertion, longitudinal ± power Doppler
□ Image 4 Patellar tendon at the distal patella, longitudinal ± power Doppler
□ Image 5 Patellar tendon at the proximal tibia, longitudinal ± power Doppler
□ Image 6 Quadriceps tendon at the proximal patella ± power Doppler
□ Image 7 Common extensor tendon at the lateral epicondyle, longitudinal ±
power Doppler
□ Image 8. Common flexor tendon at the medial epicondyle, longitudinal ±
power Doppler
□ Image 9. Triceps tendon insertion on olecranon process ± power Doppler
□ Image 10. Supraspinatus Tendon at greater tuberosity, longitudinal ±
power Doppler
□ Image 11. Extensor tendon insertion on hand and feet phalanges, longitudinal ±
power Doppler
□ Image 12. Flexor tendon insertion on the hand and feet phalanges, longitudinal ±
power Doppler
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tis in spondyloarthritis by ultrasound: results of a Delphi process and of a reliability reading
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Index
A extensor digitorum longus, transverse

Accessory muscles, 124 +/- power Doppler, 269–270, 275
Accessory soleus muscle, 280 extensor hallucis longus at insertion on 1st
Achilles tendon, 284, 514 phalanx, transverse +/- power
Acoustic enhancement, 20 Doppler, 274, 275
Acoustic shadowing, 19, 356 extensor hallucis longus over tibiotalar
Acromioclavicular joint (ACJ), 207, 211, 218, joint, longitudinal +/- power
224, 228, 233, 234 Doppler, 272–273, 275
Adductor insertion avulsion syndrome, 492 ligaments, 258
Adductor tendinopathy and tears (partial/ masses and cysts, 263–265
complete), 491 muscles, 259
Adhesive capsulitis (AC), 207, 218 osteochondritis dissecans, 266–267
Angling movements, 7 soft tissue structures, 257
Anisotropy, 4, 19 subcutaneous tissue, 265–266
Ankylosing spondylitis (AS), 514 talonavicular joint, longitudinal +/- power
Annular ligament (AL), 180, 183–185, 187 Doppler, 271–272, 275
Anterior ankle impingement syndrome tendons, 258
(AAIS), 266, 271 tibialis anterior tendon at medial cuneiform
Anterior ankle pain insertion, longitudinal +/- power
anterior ankle impingement syndrome, 266 Doppler, 273, 275
anterior retinacula, 260 tibialis anterior tendon at medial cuneiform
anterior tibiotalar joint, 260–261 insertion, transverse +/- power
basic anatomy, 255–257 Doppler, 274, 275
disadvantages, 267 tibialis anterior tendon at
extensor digitorum longus at insertion on naviculocuneiform joint,
digits 2-5, longitudinal +/- power longitudinal +/- power Doppler,
Doppler, 274, 275 273, 275
extensor digitorum longus at tibiotalar tibialis anterior tendon + extensor hallucis
joint, longitudinal +/- power longus, transverse +/- power
Doppler, 274, 275 Doppler, 268–269, 275
extensor digitorum longus insertion on the tibiotalar joint, dorsalis pedis artery,
base of digits 2-5, transverse +/- longitudinal +/- power Doppler,
power Doppler, 275 270–272, 274, 275
© This is a U.S. government work and not under copyright protection in the 533
U.S.; foreign copyright protection may apply 2023
https://doi.org/10.1007/978-3-031-37416-6
534 Index
Anterior cruciate ligament (ACL), 412 Anterior hip recess (AHR), 442
Anterior drawer test, 304 Anterior inferior iliac spine, direct head of the
Anterior elbow rectus femoris,
anterior distal humeral cartilage radial, longitudinal, 455–456
transverse +/- power doppler, 164 Anterior inferior tibiofibular ligament
anterior distal humeral cartilage radial, (AITiFL), 258, 300
transverse +/- power Anterior knee
Doppler, 160–161 bones, 374
anterior distal humeral cartilage ulnar, bursitis, 378
transverse, 156–157, 164 cartilage damage, 379
anterior distal humerus, transverse effusion, 377
+/- power Doppler, 155–156, 164 enthesopathy, 378
anterior humeroradial joint, longitudinal, fat pad
158–159, 164 anatomy, 376
anterior humeroulnar joint, longitudinal, damage, 379
157–158, 164 femoral cartilage, transverse, 382, 387
anterior joint recess, 149 infrapatellar bursae anatomy, 375
biceps tendon, longitudinal, 162–164 lateral patellar retinaculum, transverse,
bicipitoradial bursitis, 152–153 384, 387
bones, 147 loose bodies, 378
brachial artery, 150 medial and lateral parapatellar recess,
cartilage/bone erosion, 151 381, 387
crystal disease, 151 medial and lateral retinacula, 377
distal biceps tendon insertion, medial patellar retinaculum, 384, 387
longitudinal, 163–164 medial patellofemoral ligament
distal biceps tendon pathology, 151–152 anatomy, 377
effusion, 151 damage, 379
fracture, 151 transverse, 384, 387
joints, 148 patellar tendon
loose bodies, 151 anatomy, 374
median nerve, transverse +/- longitudinal damage, 378
+/- power Doppler, 159–160, 164 longitudinal view, 386, 387
posterior interosseus nerve at Arcade of transverse view, 387
Frohse, transverse +/- longitudinal, patella, transverse, 384, 387
161–162, 164 pes anserine bursa, 375
radial nerve pathology, 154 plica, 376
synovitis, 151 prepatellar bursa, 375
Anterior hip and groin pain, 439 quadriceps tendon
anterior labrum, 445 anatomy, 374
arthroplasty, 445 damage, 378
bones, 439 longitudinal, 380, 381, 387
extra-articular lateral, 447 transverse axis, 382, 387
extra-articular medial, 446–447 suprapatellar recess, 375
fibrocartilaginous labrum, 439 synovitis, 377
inferior iliac spine, transverse, 453–454 Anterior labrum, 445
intra-articular, 447 Anterior retinacula (AR), 260
joint effusion, 446 Anterior superior iliac spine (ASIS), 456
labrum, longitudinal, 452 Anterior talofibular ligament (ATaFL), 258,
lateral femoral cutaneous nerve, 300, 310
transverse, 456–458 Anterolateral ligament (ALL), 410
ligaments, 441 Anterosuperior impingement, 211, 212
neurovascular structures, 453 Artifacts, 19–21
pseudocapsule, 445
Index 535
Athletic pubalgia (sports or sportsman’s Concomitant iliopsoas bursitis and

hernia), 491 tendinitis, 445
Atrophy, 259 Conjoined tendon, longitudinal, 469
Attenuation, 4 Cortical irregularity, 213
Crystal deposition
CPPD, 122–123
B gout, 121, 122
Baseball finger, see Mallet finger Crystalline disease, 262, 283
Bassett’s ligament, 300, 304 Achilles tendon, longitudinal ± power
Benign nerve sheath tumors, 355 Doppler, 505–506
Biceps femoris tendon (BFT), 411, distal anterior femoral cartilage, transverse
414, 419–420 ± power Doppler, 506
Biceps pulley system, 210, 218, 230 distal metatarsal (MT) head and proximal
Biceps tendon phalanx for bone erosion, 503
acromial impingement, 223 dorsal 1st metatarsophalangeal joint,
entrapment, 223 longitudinal ± power Doppler, 503
instability, 222 dorsal 2nd metacarpophalangeal joint,
subacromial-subdeltoid bursa, 224 longitudinal ± power
tears, 221 Doppler, 509–510
tendinosis, 221 dorsal 3rd metacarpophalangeal joint,
tenosynovitis, 222 longitudinal ± power Doppler, 510
Bicipitoradial bursitis, 152–153 lateral meniscus, longitudinal, 507–508
B mode scanning, 4 medial 1st metatarsophalangeal joint,
Bone erosion, 117 longitudinal ± power
Bony spurs (enthesophytes), 283 Doppler, 503–504
Boxer’s knuckle, 84 medial meniscus, longitudinal, 506–507
Bursitis, 18, 217, 378, 430, 480 plantar 1st metatarsophalangeal joint,
longitudinal ± power Doppler, 504
tibiotalar joint, longitudinal ± power
C Doppler, 504–505
Calcaneofibular ligament (CFL), 300 triangular fibrocartilage complex,
Calcific tendinosis, 447 longitudinal ± power
Calcium deposits, 18, 285 Doppler, 508–509
Calcium hydroxyapatite deposition, 447 US examination, 502
Calcium pyrophosphate deposition crystals in Cubital (bicipitoradial) bursitis, 153
tendons, 17
Calcium pyrophosphate deposition disease
(CPPD), 54, 70, 112, 122, 123, 127, D
128, 262, 500, 501 Dactylitis, 517
Capitellum osteochondritis dissecans (COCD), Deep posterior pelvic muscles, 461
169, 170 Deltoid herniation sign, 215
Carpal tunnel syndrome (CTS), 29–32, 37 De Quervain's stenosing tenosynovitis (dQT),
Cartilage, 13, 16, 18, 116, 117 50, 51, 55, 56, 59, 60
Caudal sacroiliac joint, transverse, 467 Diabetic muscle infarction, 447
Central slip injury, 83 Diffuse idiopathic skeletal hyperostosis
Cephalad sacroiliac joint, transverse, 466–467 (DISH), 514
Chronic gout, 499 Distal intersection syndrome, 52
Combined pain-localizing and dynamic Distal triceps tendon (DTT), 169, 170, 172
sonopalpation, 9 Doppler imaging, 3, 6, 17
Common peroneal (fibular) nerve (CPN), Dorsal metacarpophalangeal joint (MCPJ),
411, 414 114, 501
Complete tear, 16, 215 Dorsal radiocarpal and intercarpal joint
Compression, 9 synovitis, 114–115
536 Index
Dorsal wrist tenosynovitis, 55

carpal bones, 46–47 TFCC/calcium deposition, 54
clinical comments, 50–55 3rd extensor compartment at distal
de Quervain’s tenosynovitis, 50–51 intersection, transverse, 64, 72
disadvantages, 55, 56 3rd extensor compartment at distal
distal radioulnar joint at distal radius, intersection, transverse + power
transverse +/- power Doppler, 64, 72
Doppler, 67, 72 3rd extensor compartment at distal radius,
extensor compartments, 48, 49 transverse, 63–64, 72
fifth compartment tenosynovitis, 53 triangular fibrocartilage complex,
1st and 2nd extensor compartments at longitudinal, radial deviation wrist,
proximal intersection, transverse, 69–70, 72
60–62, 71 wrist joints, 47
1st and 2nd extensor compartments at Double contour sign (DCS), 498
proximal intersection, transverse + Dupuytren's disease, 88
power Doppler, 62, 72 Dynamic movements, 7–9
1st extensor compartment at distal radius, Dynamic sonopalpation, 9
transverse, 58–59, 71
1st extensor compartment at distal radius,
transverse + power Doppler, 60, 71 E
1st extensor compartment at scaphoid, Early rheumatoid arthritis (ERA), 517
transverse, 57–58, 71 Echogenicity, 4
1st extensor compartment at scaphoid, Echotexture, 4
transverse + power Doppler, Enteropathic arthritis, 514
57–58, 71 Enthesitis, 17, 110–112, 119–121, 127, 128,
4th and 5th extensor compartments at 132, 218, 513–515
distal radius, transverse, 66–67, 72 Enthesopathy, 284, 286
fourth compartment tenosynovitis, 52 Achilles tendon at the calcaneal insertion,
ganglia, 54 longitudinal ± power
intersection syndrome, 51–52 Doppler, 519–520
Lister's tubercle, 47–48 clinical assessment, 514
radiocarpal and intercarpal joints, extensor tendon at the lateral epicondyle,
longitudinal +/- power longitudinal ± power Doppler, 523
Doppler, 71–72 extensor tendon insertion on hand and feet
radiocarpal joint at scaphoid and trapezoid, phalanges, longitudinal ± power
longitudinal +/- power Doppler, 527
Doppler, 70–72 flexor tendon insertion on the hand and feet
scapholunate joint, transverse +/- stress phalanges, longitudinal ± power
view, 65–66, 72 Doppler, 527–529
scapholunate ligament tear, 53 functional evaluation (Doppler
2nd extensor compartment at distal radius, activity), 515
transverse, 62–63, 72 medial epicondyle, 524
2nd extensor compartment at distal radius, morphologic delineation, 515
transverse + power Doppler, 63, 72 neovascularization, 515
6th compartment tenosynovitis, 53 patellar tendon at the distal patella,
6th extensor compartment at distal ulna, longitudinal ± power
longitudinal, 69, 72 Doppler, 521–522
6th extensor compartment at distal ulna, patellar tendon at the proximal tibia,
transverse + dynamic exam, longitudinal ± power
67–68, 72 Doppler, 522–523
soft tissue structures, 49–50 peripheral and axial SpA, 514
superficial branch of the radial nerve, 55 plantar fascia insertion at the calcaneus,
superficial radial nerve, 50 longitudinal ± power Doppler, 520
Index 537
power Doppler (PD) activity, 515 dorsal middle phalanx, transverse +/-
protocol, 518 longitudinal, 97, 105
quadriceps tendon at the proximal patella ± dorsal proximal interphalangeal joint,
power Doppler, 523 longitudinal +/- power
repetitive mechanical forces, 514 Doppler +/- transverse, 96–97,
scoring system, 515 105
sensitivity (subclinical enthesitis), 515 dorsal proximal phalanx, transverse +/-
ski-slope, 524 power Doppler +/-
supraspinatus tendon at greater tuberosity, longitudinal, 96, 105
longitudinal ± power extensor hood, 82
Doppler, 526–527 extensor tendons, 79
tibialis anterior tendon insertion, first digit, 82
longitudinal ± power Doppler, 521 flexor tendon enthesis, longitudinal +
triceps tendon insertion on olecranon power Doppler, 103, 106
process ± power Doppler, 525–526 flexor tendons, 80
Epidermoid cyst/implantation dermoid, 353 lateral aspect
Erosion, 261 first carpometacarpal joint
Excessive synovial fluid, 18 osteoarthritis, 91
Extensor hood (EH), 82, 84, 96 rheumatoid arthritis, 91
Extensor retinaculum (ER), 49 ulnar collateral ligament, 89
Extensor tendons (ETs), 79, 83 ulnar digital neuroma, 91
External lateral snapping hip syndrome, 478 pathology by location, 83–91
pulleys, 81
radial aspect of the first carpometacarpal
F joint, longitudinal +/-power
Femoral head and neck, anterior hip (joint) Doppler, 104–106
recess, longitudinal, 450–451 ulnar aspect of the 1st
Femoral head, iliopsoas, transverse, 451–452 metacarpophalangeal joint,
Femoroacetabular impingement, 445, 447 longitudinal +/- transverse,
Femoroacetabular joint (FAJ), 443 103–104, 106
Fibrocartilaginous labrum, 439 volar aspect
Fibromyalgia, 515 Dupuytren's disease, 88
Fifth compartment tenosynovitis, 53 flexor tendon injury, 84
Fingers ganglion cysts, 88
anatomy, 78–82 glomus tumors, 89
clinical comments, 82–92 jersey finger, 85
dorsal aspect rock climber finger, 86
Boxer’s knuckle, 84 tenosynovial giant cell tumors, 89
central slip injury, 83 tenosynovitis, 85
extensor tendon tears, 83 transection neuromas, 88
mallet finger, 83 trigger finger, 85
paratenonitis, 84 volar plate injuries, 86, 88
dorsal distal interphalangeal joint, volar distal interphalangeal joint,
longitudinal +/- transverse, 98, 105 longitudinal +/- transverse,
dorsal distal phalanx extensor tendon 102–103, 106
insertion longitudinal + power volar middle phalanx, longitudinal +/-
Doppler, 98–99, 106 transverse, 102, 106
dorsal metacarpophalangeal joint, volar plates, 82
extension + flexion, longitudinal volar proximal interphalangeal joint,
+/- power Doppler, 93–95, 105 longitudinal +/- transverse,
dorsal metacarpophalangeal joint, 101–102, 106
transverse, +/- power Doppler, volar proximal phalanx, longitudinal +/-
95–96, 105 transverse, 99–101, 106
538 Index
First carpometacarpal joint osteoarthritis, 91 Gerdy’s tubercle (GT), 410

Flat-tire sign, 215 Glenohumeral joint (GHJ), 207, 209, 211, 214,
Flexor and extensor tendons insertions, 514 215, 218, 221–225, 227, 228, 230,
Flexor digitorum brevis tendinosis, 288 232, 241, 245
Flexor retinaculum dysfunction, 331 Glenoid labrum, 225
Flexor tendons (FTs), 80, 81, 84, 88 Glomus tumor, 89, 126, 355
Flexor tenosynovitis, 85 Gluteal bursae, 480
Focal/incomplete full-thickness tears, 214 Gluteal muscles, transverse, 468
Foot pain "Golfer's elbow, 192
anatomy, 347, 349 Gout, 120–123, 127, 128, 358, 498
arthritis, 358, 359 Gouty tophus, 264
benign nerve sheath tumors, 355 Gracilis, 427
bone disorders, 359, 360 GRAPPA US Working Group Study, 518
callus, 353 Grayscale ultrasound, 6
dorsal 1st metatarsophalangeal joint, 367 Greater trochanteric pain syndrome, 476–477
longitudinal, 361, 362, 369
transverse, 363, 369
dorsal 5th metatarsophalangeal joint, H
longitudinal, 364, 367, 369 Haglund's deformity, 283
epidermoid cyst/implantation dermoid, 353 Hamstring injuries, 464
flexion-extension, 361 Hand arthropathies
forefoot bursae, 352 accessory muscles, 124
foreign body (FB), 356, 357, 369 bone erosion, 117
ganglia, 353 calcium pyrophosphate deposition
glomus tumor, 355 disease, 127
gouty tophus, 354 cartilage erosion, 116, 117
inflammatory granuloma, 354 crystal deposition
intermetatarsal bursa evaluation, 367–369 CPPD, 122–123
lipomas, 354 gout, 121, 122
metatarsal fracture, 368, 369 diagnosis, 110
Morton’s neuroma, 351, 352, 367–369 disease progression, 110
mucoid cysts, 352 distal ulna, longitudinal +/- power Doppler,
plantar fibromatosis, 355 134–135, 139
plantar 1st metatarsophalangeal joint dorsal distal 2nd phalanx extensor tendon
longitudinal, 363, 369 insertion, longitudinal +/- power
transverse, 364, 369 Doppler, 139
plantar plate dorsal distal 3rd phalanx extensor tendon
longitudinal, 365, 369 insertion, longitudinal +/- power
tear, 349, 350 Doppler, 133, 139
transverse, 366, 369 dorsal 2nd metacarpophalangeal joint,
PVNS, 355 longitudinal +/- power Doppler,
rheumatoid nodules, 353 131, 139
rheumatoid pannus, 353 dorsal 2nd proximal interphalangeal joint,
synovial cysts, 353 longitudinal +/- power Doppler,
tendon pathology, 357 132, 139
Forefoot bursae, 352 dorsal 3rd metacarpophalangeal joint,
Foreleg calcification, 259 longitudinal +/- power Doppler,
Fourth compartment tenosynovitis, 52 133, 139
Frequency, 2–4 dorsal 3rd proximal interphalangeal joint,
longitudinal +/- power Doppler,
133, 139
G dorsal 5th metacarpophalangeal joint,
Ganglia, 54–56 longitudinal +/- power Doppler,
Ganglion cyst, 18, 88, 110, 123, 131, 263 134, 139
Index 539
dorsal radiocarpal joint, intercarpal joint, volar wrist, transverse +/- power Doppler,
longitudinal +/- power Doppler, 136, 139
130–131, 139 Hemangiomas, 125
enthesitis, 119–121 Hematomas, 124
flexor tendon enthesis, longitudinal + Hip joint, 443
power Doppler, 138–139 Hydroxyapatite, 220, 223
ganglion cysts, 123 Hydroxyapatite deposition disease
gout, 127 (HADD), 501
joints, 109 Hyperechoic deposits of CPPD, 18
lupus, 127
masses, 123
osteoarthritis, 127 I
paratenonitis, 119 Iliacus and psoas major muscles, 454–455
prognosis, 110 Iliopsoas bursa (IPB), 443–445
rheumatoid arthritis, 127 Iliopsoas syndrome, 445
specific ultrasound findings, 128 Iliopsoas tendon (IPT), 443
spondyloarthropathy, 127 Iliopsoas tendon muscle (IPM), 443
synovitis Iliotibial band (ITB), 410, 446, 458
combined scoring system, 113 Iliotibial band syndrome (ITBS), 411, 412
dorsal metacarpophalangeal joint Impingement syndrome, 212
synovitis, 114 Infectious arthritis, 262
dorsal radiocarpal and intercarpal Inferior calcaneal spurs (enthesophytes), 287
joint synovitis, 114–115 Inferior peroneal retinaculum (IPR), 303
grayscale grading, 112 Inflammatory arthritis differentiation, 517
power Doppler grading, 113 Inflammatory granuloma, 354
practical synovitis grading, 113 Infrapatellar branch of the saphenous nerve
ultrasound, 110–112 (IPBSN), 431
tenosynovitis, 118 Infraspinatus tendon tears (IST), 208, 209,
traumatic disorders 212, 216–219, 227, 238,
foreign bodies, 124 241, 243–245
hematomas, 124 Inguinal lymph nodes, 448
tendon tear, 124 Instability, 222
treatment, 110 Integrity of Achilles tendon repair, 285
tumors, pseudotumors, lumps and Interface reflex (IR) artifact, 20, 502
bumps, 125–126 Intermetatarsal bursitis (IMB), 352
ulnocarpal joint, longitudinal +/- Internal impingement, see Posterosuperior
power Doppler, 135–136, impingement syndrome
139 Interosseous membrane (IOM), 300
volar 2nd metacarpophalangeal joint, Intra-articular bodies, 262
longitudinal +/- power Doppler, Ischiogluteal bursitis, 465
136–137, 139
volar 2nd proximal interphalangeal joint,
longitudinal +/- power J
Doppler, 137–139 Jersey finger, 85
volar 3rd metacarpophalangeal joint, Joint effusion, 168, 260, 444
longitudinal +/- power Doppler, Juvenile idiopathic arthritis, 514
138, 139
volar 3rd proximal interphalangeal joint,
longitudinal +/- power Doppler, K
138, 139 Kager’s fat pad (KFP), 280
540 Index
L ligaments, 180, 181

Lateral ankle pain radial head, transverse + dynamic, 186–187
accessory anterior inferior tibiofibular Lateral epicondylitis, 180–182
ligament, longitudinal, 312, 319 Lateral hip
anatomy gluteus medius insertion, lateral facet,
bones, 299 longitudinal, 482–483
ligament, 300 gluteus medius insertion, superoposterior
muscles and tendons, 301, 302 facet, longitudinal, 483–484
retinacula, 302 gluteus minimus and medius tendons, 477
anterior inferior tibiofibular ligament, gluteus minimus insertion, anterior facet,
longitudinal, 311, 312, 318 longitudinal, 482
anterior talofibular ligament, longitudinal, Gmax, 475
310, 311, 318 greater trochanter, 473, 481–482
calcaneofibular ligament, longitudinal, iliotibial band, transverse +
313, 319 dynamic, 485–486
crystalline disease, 308 iliotibial band, transverse +
distal interosseous membrane, 312, 319 longitudinal, 484–485
high ankle ligament injury, 304, 305 proximal iliotibial band, longitudinal, 484
ligament laxity, 303 Lateral knee
low ankle ligament injury, 304 anterolateral ligament, longitudinal ±
mechanical joint instability, 303 power Doppler, 421–422
peroneal tendons biceps femoris tendon, 419–420
at lateral malleolus, 314, 316, 319 iliotibial band, longitudinal +
at peroneal tubercle, 317, 319 dynamic, 415–416
at supramalleolar region, 314, 319 iliotibial band, transverse + dynamic, 416
peroneus brevis tendon insertion, lateral collateral ligament, longitudinal +
longitudinal, 318, 319 dynamic, 416–418
peroneus longus tendon distal to peroneal lateral femoral condyle, 411
tubercle, longitudinal, 318, 319 lateral meniscus, longitudinal, 418–419
peroneus quartus at lateral malleolus, meniscal extrusion, 418
316, 319 peroneal nerve
POPS, 308 longitudinal, 420–421
retinacula injury, 306, 308 transverse, 420
sinus tarsi, 313, 319 valgus knee deformity, 417
STS, 308 Lateral meniscus (LM), 411, 413
tendon injury, 305, 306 Lateral ulnar collateral ligament (LUCL), 180,
ultrasound, 303, 304 181, 185, 412, 413
variants, 309 Ledderhose’s disease, 355
Lateral (or radial) collateral ligament (LCL), Ligaments, 10, 16–17
180, 181, 183, 184, 186, 410, 523 Lipomas, 125, 354
Lateral elbow pain Lister's tubercle (LT), 47, 52, 57, 62,
bones, 177–178, 182 63, 65, 66
common extensor tendon origin, Longitudinal axis (LAX), 4, 5, 7, 11
longitudinal +/- power Doppler, 187 Loose bodies, 18
disadvantages, 182 Lupus, 127, 261
humeroradial joint, longitudinal +
dynamic, 185–187
joints, 179–180, 182 M
lateral collateral ligament, longitudinal, Maastricht ankylosing spondylitis enthesitis
184–185, 187 score (MASES), 514
lateral epicondylitis, 181 Mallet finger, 83
lateral ulnar collateral ligament, Manders enthesis index (MEI), 514
longitudinal, 185, 187 Master Knot of Henry, 331
Index 541
Medial ankle pain at medial epicondyle, transverse,

anatomy, 325 dynamic exam, active flexion,
anterior tibiotalar ligament, longitudinal, 201, 204
333, 343 at medial epicondyle, transverse,
bone, 323 dynamic exam, passive flexion,
deltoid ligament, 324, 325, 328, 329 199–200, 204
distal tibial nerve, transverse, 342, 343 at medial epicondyle, transverse,
flexor digitorum longus tendon, 326, 330, dynamic exam, resisted flexion, 204
339, 343 at medial epicondyle, transverse +
flexor hallucis longus tendon, 326, measurement, 204
330, 341–343 in true cubital tunnel, longitudinal,
flexor retinaculum (FR), 328, 331 203, 204
intersection syndrome, 331 in true cubital tunnel,
Knot of Henry, longitudinal, 341, 343 transverse, 201–204
os trigonum variant, 330 proximal to the medial epicondyle, 204
posterior tibiotalar ligament, longitudinal, Medial epicondylitis, 192
334, 343 Medial femoral epicondyle (MFE) to the
rheumatoid arthritis, 331 proximal tibia, 426
spondyloarthritis, 331 Medial hip
spring ligament, 325, 329, 336, 343 adductor insertion onto the posteromedial
tarsal tunnel, 327, 331, 332, 337, 338, femur, 492
343 adductor insertions, longitudinal, 494
tibialis posterior tendon, 325, 326, adductor muscles, 489
329, 330 AL and gracilis, 492
navicular insertion, longitudinal, bony avulsion, 491
338, 343 distal to the superior pubic ramus,
sustentaculum tali, transverse, 338, 343 transverse, 493–494
tibiocalcaneal ligament, longitudinal, inguinal hernia and femoroacetabular
334, 343 impingement, 492
tibionavicular ligament, longitudinal, Medial knee
336, 343 medial collateral ligament, longitudinal +
tibiospring ligament, longitudinal, 335, 343 dynamic, 432–433
Medial collateral ligament (MCL), 426, medial meniscal extrusion measurement,
428, 429 longitudinal, 435
Medial elbow pain, 192 medial meniscus, longitudinal, 434–435
disadvantages, 194–195 pes anserine tendons, transverse, 435–436
medial epicondyle and common flexor Medial meniscus (MM), 426, 429
tendon, 190 Meniscal (parameniscal) cyst, 413, 429
medial epicondyle, longitudinal, extension Meniscal degeneration, 429
+/- power Doppler, 196–197, 204 Meniscal extrusion (ME), 413, 430
medial epicondyle, longitudinal, flexion Meniscofemoral and meniscotibial
+/- power Doppler, 197, 204 ligaments, 426
medial epicondyle, valgus maneuver, Meralgia paresthetica (MP), 448
longitudinal, 204 Metatarsal stress fractures, 359, 360
posteromedial elbow, 191 Mirror-image artifacts, 19
snapping triceps, 194 Monosodium urate (MSU) crystals,
snapping ulnar nerve, 194 17, 18, 498
sonographic anatomy, 191–192 Morel-Lavallee (M-L) lesions, 479
ulnar collateral ligament, 190 Morton’s neuroma, 351, 352, 367–369
ulnar nerve Mucoid cysts, 352
entrapment, 192 Muscle, 11, 17, 259
in forearm, transverse, 203–204 Musculoskeletal ultrasound (MSUS), 1–4, 6,
instability, 194 19, 21–23
542 Index
N humeroradial joint, 169

Nerves, 11, 15–16, 263–264 joint effusion, 168
Neurofibromas, 125, 355 olecranon bursa, 170
Neuromas, 126 olecranon process, longitudinal, 174–175
Normal tissues, echogenic features, 9–15 posterior humeroradial joint, longitudinal
+/- power Doppler, 174, 175
posterior joint recess, longitudinal +/-
O power Doppler, 171, 175
Olecranon bursa, 170 posterior joint recess, transverse,
Osborne's fascia, 191, 193, 198 172–173, 175
Osborne's ligament, 191–193, 198, 201, 203 triceps brachii, 169–170
Os peroneum (OP), 306 ulnar nerve compression, 170
Osteoarthritis (OA), 126–128, 261, 358, 514 Posterior hip/thigh pain, 461
Osteochondritis dissecans (OCD), 266, 267 Posterior/inferior heel pain
Osteophytes, 117, 122, 126 Achilles tendon
Os trigonum syndrome, 330 dynamic scan, longitudinal,
Outcomes Measures in Rheumatology 290–291, 295
(OMERACT), 15, 513 enthesis, longitudinal + power Doppler,
291, 295
longitudinal +/- power Doppler,
P 289–290, 295
Painful OP syndrome (POPS), 308 transverse +/- power Doppler,
Pain-localizing sonopalpation, 9 291–292, 295
Palmar fibromatosis, 88 bony anatomy, 280–283
Paratenon, 13, 17 disadvantages, 288
Paratenonitis, 17, 84, 91, 95, 119, 127, 285 inferior heel anatomy, 282–283
Partial articular side tear (PASTA), 213, 216 plantar fascia origin
Partial-thickness or incomplete tears, 213, 214 longitudinal, 292–295
Peroneal neuropathy, 414 longitudinal + power Doppler, 294–295
Peroneus brevis tendon (PBT), 301, 302, 305 thickness measurement, longitudinal,
Peroneus longus tendon (PLT), 301, 306 294, 295
Peroneus quartus muscle (PQM), 309 posterior heel anatomy, 280
Peroneus quartus tendon (PQT), 301 posterior tibiotalar recess, longitudinal +/-
Pes anserine (anserinus) bursa (PAB), 428, 430 power Doppler, 292, 295
Pes anserine tendons (PATs), 426, potential ultrasound findings, 283–288
428, 435–436 proximal/posterior calf anatomy, 280–282
Pigmented villonodular synovitis (PVNS), 355 Posterior inferior tibiofibular ligaments
Piriformis syndrome, 465, 467–468 (PITiFL), 300
Plantar fascia insertion, 514 Posterior knee pain
Plantar fasciitis, 286 anatomy, 392–394
Plantar fibromatosis, 287, 355 biceps femoris tendon, longitudinal,
Plantaris tendon (PT), 280, 285 403, 407
Polyarthropathy, 110, 119, 123 blood vessel pathology, 396
Popliteal cyst (PC), 394, 395 cartilage damage, 397
Popliteus tendon, 410 fabella, 396, 405, 407
Posterior acoustic enhancement, 20 lateral femoral condylar cartilage
Posterior acoustic shadowing, 19 longitudinal, 400, 407
Posterior elbow transverse, 400, 407
anatomy, 167 ligament damage, 395
distal triceps tendon, longitudinal +/- medial femoral condylar cartilage
power Doppler, 172, 175 longitudinal, 399, 407
distal trochlea and capitellum, transverse, 398, 399, 407
transverse, 173–175 meniscal damage, 397
Index 543
nerve damage, 396 subcoracoid impingement, 212

neurovascular bundle, transverse, 400, Rotator cuff interval (RCI), 209–211, 216,
401, 407 218, 229, 236, 237, 240
peroneal nerve, transverse, 401, 403, 407 Rotator cuff muscle atrophy, 219
popliteal cyst, 394, 395 Rotator cuff tear, 212–213, 215–217, 222, 224,
posterior horn of the lateral meniscus, 227, 230
longitudinal, 404, 407
posterior horn of the medial meniscus,
longitudinal, 405, 407 S
sciatic nerve, transverse, 401, 407 Sacroiliac joint (SIJ), 464
Posterior pelvis, 461 Sail sign, 381
Posterior talofibular ligaments (PTaFL), 300 Sarcoidosis, 262
Posterior thigh muscles, 463 Sartorius, 427, 458–459
Posterosuperior impingement syndrome, 212 Scapholunate ligament (SLL), 49, 50, 53,
Postoperative arthroplasty, 219–220 54, 56, 65
Postoperative rotator cuff repair, 219 Schwannomas, 125, 355
Postsurgical hip, 445–446 Sciatic nerve (SN), 465, 471
Power Doppler activity, 285 Semimembranosus tendon,
Probe (transducer), 3–7, 9, 11, 13–16, longitudinal, 469–471
18, 20, 22 Semitendinosus muscle (STM), 427, 462
Pronator teres syndrome, 153, 159 Shoulder pain
Proximal iliotibial band syndrome (Proximal acromioclavicular joint, 224, 233–234,
ITB syndrome), 480 246
Proximal intersection syndrome (PIS), 51, 60 adhesive capsulitis, 218
Proximal tendon injury, 465 biceps tendon, 221
Pseudoaneurysms, 125 acromial impingement, 223
Pseudogout, 497 entrapment, 223
Psoriatic arthritis, 359 instability, 222
Pulse repetition frequency (PRF), 519 tears, 221
tendinosis, 221
tenosynovitis, 222
R bony shoulder architecture, 207
Radial collateral ligament (RCL), 523 bursitis, 217
Radial flexion, 509 calcium, 220
Radial nerve pathology, 154 complete tear, 215
Reactive arthritis, 514 Crass vs. modified Crass, 229
Rectus femoris (RF), 443, 458 disadvantages, 227–228
Regenerative medicine, 1 dynamic evaluation, 218
Region-of-interest (ROI), 2, 4, 7, 9, 16, 22 enthesitis, 218
Repetitive knee flexion and extension, 411 fluid accumulation, 209
Retrocalcaneal bursitis, 280, 285 focal/incomplete full-thickness tears, 214
Reverberation, 19, 356 glenohumeral joint, 218, 225–226
“Reverse shoulder” prosthesis, 219 glenoid labrum, 225
Rheumatoid arthritis (RA), 51, 53, 54, 56, 67, inflammatory disease, 226
91, 127, 226, 255, 258, 261–263, infraspinatus and teres minor muscles,
267, 284, 331, 358 TAX, 246–247
Rheumatoid nodules, 126 infraspinatus tendon and muscle, proximal,
Rock climber finger, 86 longitudinal, 242–243, 247
Rotator cable (RC), 209, 240 infraspinatus tendon, distal, longitudinal,
Rotator cuff impingement 243–244, 247
anterosuperior impingement, 211, 212 infraspinatus tendon tears, 217
posterosuperior impingement long head biceps tendon, longitudinal
syndrome, 212 +/- power Doppler, 231–232, 246
544 Index
Shoulder pain (cont.) Snapping triceps syndrome, 170, 194

long head biceps tendon, transverse +/- Snapping ulnar nerve, 194
power Doppler, 230–231, 246 Sonopalpation, 9
partial-thickness/incomplete tears, Spondyloarthropathy (SpA), 119–121, 127,
213, 214 128, 192, 194, 261, 331
posterior glenohumeral joint, longitudinal, Sports-related injuries, 491
internal + external rotation +/- Sternoclavicular and costochondral joints,
power Doppler, 244–245, 247 225
postoperative arthroplasty, 219–220 Subacromial-subdeltoid bursa, 223–224
postoperative rotator cuff repair, 219 Subcoracoid impingement, 212
rotator cuff impingement Subcutaneous calcaneal bursa, 280, 285
anterosuperior impingement, 211, 212 Submetatarsal (adventitious) bursitis
posterosuperior impingement (SMB), 352
syndrome, 212 Subscapularis tendon tears (SSCT), 208, 209,
subcoracoid impingement, 212 212, 216–218, 222, 223, 227,
rotator cuff muscle atrophy, 219 230–233, 237
rotator interval, modified Crass position, Superficial radial nerve (SRN), 50, 55–59,
236–237, 247 62
shoulder soft tissue, 207 Superior peroneal retinaculum (SPR), 302
spinoglenoid notch, longitudinal + power Supraspinatus tendon tears (SST), 208, 209,
Doppler, 245–247 211, 212, 215–224, 226–230,
sternoclavicular and costochondral 234–241, 514
joints, 225 Synovial cysts, 353
subacromial-subdeltoid bursa, 223–224 Synovial fluid, 14
subscapularis tendon, longitudinal + Synovial hypertrophy in the AHR, 444
dynamic view, 232–233, 246 Synovial tissue, 13
subscapularis tendon tears, 216 Synovitis, 18, 149, 151, 218, 260, 261,
subscapularis tendon, transverse, 233, 246 264–265, 444
suprascapular nerve, 226 combined scoring system, 113
supraspinatus tendon, 216 dorsal metacarpophalangeal joint
anterior, transverse, 240–241, 247 synovitis, 114
coracoacromial ligament, longitudinal dorsal radiocarpal and intercarpal joint
+ dynamic view, 247 synovitis, 114–115
distal acromion, longitudinal + grayscale grading, 112
dynamic view, 234–236, 247 power Doppler grading, 113
distal anterior, longitudinal +/- power practical synovitis grading, 113
Doppler, 237–238, 247 ultrasound, 110–112
distal posterior, longitudinal +/- power Systemic sclerosis, 261
Doppler, 238–239, 247
posterior, transverse, 241–242, 247
proximal anterior, longitudinal +/- T
power Doppler, 240, 247 Tarsal tunnel syndrome (TTS), 331, 332
proximal posterior, longitudinal +/- Tendinopathy, 479
power Doppler, 239–240, 247 Tendinosis, 17, 217, 221, 228, 258, 259, 262,
synovitis, 218 284, 477, 478
tendinosis, 217 Tendons, 9, 13, 16–17
teres minor tendon, 217, 244, 247 enthesis evaluation, 514
Sinus tarsi syndrome (STS), 308 and muscle abnormalities, 446
Sisyphus's boulder, 198 tears, 477, 478
Snapping hip syndrome, 446–447 Tennis elbow, see Lateral epicondylitis
Snapping iliotibial band, 478 Tennis leg, 285
Snapping pes anserine tendons (gracilis or Tenosynovial effusion, 222
semitendinosus), 430, 431 Tenosynovial giant cell tumors, 89, 125
Index 545
Tenosynovitis, 17, 51–53, 55, 109–111, Volar wrist

118–119, 122–124, 127–129, 131, basic anatomy, 27–29
136, 222, 258, 263 carpal tunnel syndrome, 29, 31
Tenosynovium, 13 distal Guyon's canal, transverse, 40, 42
Tensor fascia lata (TFL), 443, 479 forearm, 12 cm proximal to wrist crease,
Teres minor tendon tears, 217 transverse, 34, 41
Tibialis anterior muscle atrophy, 259 median nerve, longitudinal +/- power
Tibialis anterior tendon insertion, 514 Doppler, 38, 41
Tibiotalar arthritis, 261 median nerve, proximal carpal tunnel,
Time–gain controls (TGC), 3 transverse, cross-sectional area
Tophi, 498 measurement, 36–37, 41
Total shoulder replacements (TSR), 219 median nerve, 12 cm proximal to wrist
Transection neuromas, 88 crease, transverse, cross-sectional
Transverse axis (TAX), 4, 5, 7, 11 area measurement, 34–35, 41
Traumatic disorders mid-wrist, transverse, 33–34, 41
foreign bodies, 124 proximal carpal tunnel, transverse, 35–36
hematomas, 124 proximal carpal tunnel, transverse + power
tendon tear, 124 Doppler, 37, 41
Triangular fibrocartilage complex (TFCC), 49, proximal Guyon's canal, transverse, 40, 42
50, 53–56, 69 proximal Guyon's canal, transverse +
Triceps tendon insertion, 514 power Doppler, 39–41
Trigger finger, 85 ulnar artery at Guyon’s canal, longitudinal
+ power Doppler, 41, 42
ulnar aspect, transverse, 32, 41
U ulnar nerve at Guyon’s canal,
Ulnar collateral ligament (UCL), 89–92, 103, longitudinal, 41–42
104, 189–192, 195–197 ulnar nerve damage, 31
Ulnar digital neuroma, 91
Ulnar nerve (UN), 31, 170, 192, 201
Ulnar nerve instability (UNI), 194 W
Ultrasound machine, 2, 3, 19, 20, 22 "Weaver’s bottom", 465
Wrist compartments, 48
V
Valgus stress/twisting knee injuries, 428 X
Volar plates, 82, 86, 88 Xanthomas, 285, 288

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Mark H.

ISBN 978-3-031-37415-9 ISBN 978-3-031-37416-6 (eBook)

Paper in this product is recyclable.

Doctors Greenberg, Day, and Alradawi have created a first-of-its-kind book on

Professor of Medicine and Past Dean Richard A. Hoppmann, MD,

While teaching musculoskeletal ultrasound, we observed that students learned best

Columbia, SC, USA Mark H. Greenberg

1 Introduction/Getting Started������������������������������������������������������������������ 1

5 Hand Arthropathies �������������������������������������������������������������������������������� 109

12 Posterior Ankle and Heel������������������������������������������������������������������������ 279

18 Lateral Knee �������������������������������������������������������������������������������������������� 409

Inguinal Lymph Nodes���������������������������������������������������������������������������� 448

Suliman Alradawi (Illustrator) Department of Medicine, Division of

Why Learn Musculoskeletal Ultrasound?

Why a Protocol-Driven Approach?

Protocol-driven examinations improve the efficiency of ultrasound (US) examina-

The Goals of This Manual

This Manual demonstrates MSUS protocols that evaluate conditions commonly

The Ultrasound Machine

in centimeters on the ultrasound viewscreen. Lower frequencies achieve higher

Terms are jargon used to communicate in the US world.

Hyperechoic Isoechoic Hypoechoic Anechoic

Fig. 1.1 Echogenicity

Fig. 1.3 Tendon in

example would be when evaluating the subscapularis tendon, a structure oriented

Fig. 1.4 Avoiding cord tugs

Fig. 1.5 Angling movements. (a) Heel-toe and (b) tilting

Fig. 1.7 Dynamic

Sonopalpation is a technique in which the examiner uses the transducer to delineate

Echogenic Features of Normal Tissues

Bone, being hyperechoic, is the most straightforward structure to visualize since it

Fig. 1.8 Bone

Fig. 1.10 Ligament

Fig. 1.15 Hyaline

Fig. 1.16 Synovial tissue

Fig. 1.17 Tenosynovium

Fig. 1.18 Longitudinal

Sonographic Pathology by Structure

The examiner confirms pathology with images in two perpendicular, or orthogonal,

Erosion: An intra-articular discontinuity of the bone surface visible in two perpen-

Halo sign is a homogeneous, hypoechoic wall thickening of an artery, appearing as

Venous thrombosis may be evident with vein resistance to compression by the

Entrapment: Nerves tend to enlarge proximal to compressions, as may occur when

A true neuroma following nerve injury results from a disorganized attempt to

Fibrocartilage is usually hyperechoic. A hypoechoic cleft may represent a tear.

Tendons and Ligaments

Tendinosis, a degenerative process, is the preferred term over tendonitis or tendi-

Other Pathologic Findings

Excessive synovial fluid is indicated by detecting overabundant, commonly

Artifacts: Friend or Foe?

Fig. 1.19 Reverberation of a therapeutic needle in a practice gel phantom

Fig. 1.21 Acoustic

Organization of the Manual

Limited Versus Complete Protocols

Finished reports should contain standard information that often includes:

1. Brandli L. Benefits of protocol-driven ultrasound exams. Radiol Manag. 2007;29(4):56–9.

18. Martinoli C, Derchi LE, Pastorino C, Bertolotto M, Silvestri E. Analysis of echotexture of

Reasons to Do the Study

© The Author(s), under exclusive license to Springer Nature 27

Columbia, SC, USA Mark H. Greenberg

1 Introduction/Getting Started�� 1

5 Hand Arthropathies �� 109

12 Posterior Ankle and Heel�� 279

18 Lateral Knee �� 409

Inguinal Lymph Nodes�� 448

Why Learn Musculoskeletal Ultrasound?

Why a Protocol-Driven Approach?

The Goals of This Manual

The Ultrasound Machine

Echogenic Features of Normal Tissues

Sonographic Pathology by Structure

Tendons and Ligaments

Other Pathologic Findings

Artifacts: Friend or Foe?

Organization of the Manual

Limited Versus Complete Protocols

Carpal Tunnel Syndrome

Ulnar Nerve Damage

rotocol Image 1: Volar Wrist, Ulnar Aspect, Transverse

Protocol Image 2: Volar Wrist, Mid-Wrist, Transverse (Fig. 2.4)

rotocol Image 3: Forearm, 12 cm Proximal to Wrist Crease,

rotocol Image 4: Median Nerve, 12 cm Proximal to Wrist

rotocol Image 5: Proximal Carpal Tunnel, Transverse

rotocol Image 6: Median Nerve, Proximal Carpal Tunnel,

rotocol Image 7: Proximal Carpal Tunnel, Transverse + Power

rotocol Image 8: Median Nerve, Longitudinal ± Power Doppler

rotocol Image 9: Proximal Guyon’s Canal, Transverse + Power

Protocol Image 10: Proximal Guyon’s Canal, Transverse

Protocol Image 11: Distal Guyon’s Canal, Transverse (Fig. 2.13)

rotocol Image 12: Ulnar Artery at Guyon’s Canal,

rotocol Image 13: Ulnar Nerve at Guyon’s Canal, Longitudinal

Necessary Basic Anatomy

Carpal Bones (Fig. 3.1a, b)

Joints of the Wrist (Fig. 3.2)

Lister’s Tubercle (Fig. 3.2)

Extensor Compartments (Fig. 3.3a)

Soft Tissue Structures

Superficial Radial Nerve

de Quervain’s Tenosynovitis

Scapholunate Ligament Tear

Triangular Fibrocartilage Complex Injury/Calcium Deposition

Superficial Radial Nerve

rotocol Image 1: First Extensor Compartment at Scaphoid,

rotocol Image 2: First Extensor Compartment at Scaphoid,

rotocol Image 3: First Extensor Compartment at Distal Radius,

rotocol Image 4: First Extensor Compartment at Distal Radius,

rotocol Image 5: First and Second Extensor Compartments at

rotocol Image 5a (Optional): First and Second Extensor

rotocol Image 6: Second Extensor Compartment at Distal

rotocol Image 6a (Optional): Second Extensor Compartment at

rotocol Image 7: Third Extensor Compartment at Distal

rotocol Image 8: Third Extensor Compartment at Distal

rotocol Image 8a (Optional): Third Extensor Compartment at