Musculoskeletal Imaging: A Survival Manual [1st ed. 2023] 3031490207, 9783031490200

Table of contents :
About this Book
Contents
About the Authors
Abbreviations
1: Survival
Survival Actions
S-Size Up the Situation
U-Use Your Senses, Undue Haste Makes Waste
R-Remember Who and Where
V-Vanquish Fear and Panic
I-Improvise
V-Value Your Report
A-Act Decisively
Live by Your Wits and Learn Basic Skills
Psychology of Survival
Factors that Can Increase Stress
Take Care of Yourself
Further Reading
2: Reporting and Communication
Report Structure
Key Findings Versus Incidental Findings
Use and Abuse of Classification Systems
Saved Rounds
Further Readings
3: Trauma
Spine
Cervical Spine
Atlanto-Axial Interval
Causes of Atlanto-Axial Widening
Facet Dislocation
Dens Fracture
C1 Ring Fractures (Jefferson Fracture)
Flexion Tear Drop Fracture
Hanged Man’s Fracture
Clay Shoveler’s Fracture
Warning
Thoracic and Lumbar Spine
Compression Fracture
Tips for Assessing Acuity
Burst Fracture
Chance Fracture
Shoulder
Anterior Shoulder Dislocation
Greater Tuberosity Fracture
Scapula Fractures
Acromioclavicular Injury
Stress Injuries of the Distal Clavicle
Chronic Rotator Cuff Pathology
Biceps Dislocation
Sternum and Sternoclavicular Joints
Ribs
Elbow
The Terrible Triad
Olecranon Fracture
Capitellum Fracture
Tendon Injuries
Biceps Tendon Tear
Common Extensor/Flexor Tendon Tear
Forearm
Monteggia Fracture
Galeazzi Fracture
Wrist
Triquetral Fracture
Scaphoid Fracture
Distal Radial Fractures
Pisiform Fracture
Hamate Fracture
Carpal Metacarpal Dislocation
Stress Fracture
Gymnasts
Carpal Dislocations
Hand
Metacarpal Fractures
Phalangeal Injuries
Thumb Ulnar Collateral Ligament Injury
Ultrasound
Foreign Bodies
Tendon Laceration/Tear
Pelvis and Hips
Proximal Femoral Fractures
Sacral Insufficiency Fractures
Pelvic and Obturator Ring Fractures
Diastasis and Dislocations
Knee
Traumatic Arthrotomy
Less Obvious Knee Injuries
Tibial Plateau Fractures
Patella Fractures
Bipartite Patella
Patella Dislocation
Insufficiency Fractures
Stress Fractures
Dislocation
Ankle
Fracture at the Base of the Fifth Metatarsal
Fracture of the Anterior Process of the Calcaneus
Dorsal Capsular Avulsion Fractures
Traumatic Osteochondral Fracture of the Lateral Talar Dome
Fracture of the Lateral Process of the Talus
Fracture at the Origin of the Extensor Digitorum Brevis Muscle
Distal Fibular Fractures
Trimalleolar Fractures
Maisonneuve Fracture
Calcaneal Stress Fracture
Achilles Tendon Injury
Fracture Blisters
Tendon Entrapment
Foot
Fifth Metatarsal Base Fractures in Kids
Lisfranc Injuries
Metatarsal Neck Fractures
Bone Stress Injuries
Toe Fractures
Saved Rounds
Live Fire Exercises
After Action Review
Bibliography
4: Infection
Foundations
Imaging Modalities
Plain Radiography
Computed Tomography
Ultrasound
Nuclear Medicine
Magnetic Resonance Imaging
Osteomyelitis
Pyogenic vs. Nonpyogenic
Pediatric vs. Adult
Acute vs. Chronic
Imaging of Acute Osteomyelitis
Imaging of Chronic Osteomyelitis
Soft Tissues Infection
Necrotizing Fasciitis
Other Soft Tissue Infections
Intra-Articular Infection
Infection of the Spine
Atypical Infections
Saved Rounds
Bibliography
5: Bone Tumors
Periosteal Reaction
The Good
The Bad
The Ugly
Border and Zone of Transition
The Good
The Bad
The Ugly
Age
Alone or in Battalions
Good or Bad?
What to Look for in Making this Judgment?
After Action Review
Refinement
Location
Giant Cell Tumor
Chondroblastoma
Aneurysmal Bone Cyst
Clear Cell Chondrosarcoma
Infection
Unicameral or Simple Bone Cyst
Enchondroma
Chondrosarcoma
Osteochondroma
Osteosarcoma
Infection
Fibrous Dysplasia
Fibroxanthoma (also Called a Non-Ossifying Fibroma)
Metastasis and Myeloma
Round Blue Cell Tumors
Osteofibrous Dysplasia
Adamantinoma
Osteoid Osteoma
The Distal Phalanx
Glomus Tumor
Epidermoid Inclusion Cyst
Matrix
Osteoid
Chondroid
Fluid
Fibrous
Fat
Tumor Mimics
Infection
Brown Tumor
Osteonecrosis
Giant Bone Island
Osteopoikilosis
Osteopathia Striata
Melorheostosis
Polyostotic Lesions
Metastasis and Myeloma
Polyostotic Fibrous Dysplasia
Multiple Enchondroma Syndromes
Infection
Brown Tumors
Langerhans Cell Histiocytosis
Saved Rounds
Live Fire Exercises
After Action Review
Bibliography
6: Orthopedic Hardware
Foundations
Hardware Imaging
Plain Radiography
CT
MRI
Nuclear Medicine
Hardware Complications
Hardware Failure
Displaced Hardware
Perihardware Fracture
Hardware Infection
Specific Complications of Arthroplasty Hardware
Saved Rounds
Bibliography
7: Arthritis
Osteoarthritis
Erosive Osteoarthritis
Inflammatory Arthropathies
Rheumatoid Arthritis
Profile
Target Recognition
Hands/Wrists
Feet/Ankles
Shoulders
Knees
Hips
Elbow
Sacroiliac Joints
Juvenile Idiopathic Arthritis
Profile
Hands/Wrists
Hips and Knees
Ankylosing Spondylitis
Profile
Psoriatic and Reactive Arthritis
Profile
Target Recognition
Enteropathic-Related Arthritis
Profile
Septic Arthritis
Neuropathic Arthropathy
Deposition Arthropathy
Gout
Key Points
Calcium Pyrophosphate Dihydrate Crystal Deposition Disease (CPPD)
Key Points
Amyloid Deposition Arthropathy
Key Points
Hemophilia Arthropathy
Benign Proliferative Processes
Synovial Chondromatosis/Osteochondromatosis
Tenosynovial Giant Cell Tumor
Lipoma Arborescens
Vascular Malformations
Sundries
Calcific Periarthritis (Calcific Tendinopathy)
Systemic Lupus Erythematosus (SLE) and Rhupus
Scleroderma and Mixed Connective Tissue Diseases
Sarcoid
Saved Rounds
Live Fire Exercises
After Action Review
Bibliography
8: Metabolic Disorders
Imaging of Metabolic Disorders
Physiology of Bone
Imaging Modalities
Plain Radiography
Computed Tomography (CT)
Magnetic Resonance Imaging (MRI)
Dual Energy X-ray Absorptiometry (DEXA or DXA)
Osteoporosis
Generalized Osteoporosis
Regional Osteoporosis
Imaging Findings in Osteoporosis
Osteomalacia
Foundations
Causes
Low Dietary Vitamin D
Malabsorption
Hyperparathyroidism
Renal Causes
Findings
Hyperparathyroidism
Foundations
Imaging Findings
Paget Disease
Foundations
Pathophysiology
Imaging Findings
Complications of Paget Disease
Saved Rounds
Acromegaly
Tumoral Calcinosis
Melorheostosis
Osteopoiklosis and Osteopathia Striata
Bibliography
Index

Citation preview

Benjamin Plotkin Bennett L. Davis

Musculoskeletal Imaging A Survival Manual

Musculoskeletal Imaging

Benjamin Plotkin • Bennett L. Davis

Musculoskeletal Imaging A Survival Manual

Benjamin Plotkin Department of Radiology UCLA Health Los Angeles, CA, USA

Bennett L. Davis Radiology and Imaging Consultants An Affiliate of UCHealth Colorado Springs, CO, USA

ISBN 978-3-031-49020-0    ISBN 978-3-031-49021-7 (eBook) https://doi.org/10.1007/978-3-031-49021-7 © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 The anatomic sketches of the cover image is based on 16th century anatomical studies by Leonardo da Vinci This work is subject to copyright. All rights are solely and exclusively licensed by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. The artist for the cover image is Leonardo da Vinci. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland Paper in this product is recyclable.

“Medicine is both timeless and ever changing. While the basic nature of medicine is constant, the means and the methods we use evolve continuously. These changes may be gradual in some cases and drastic in others.” —Adapted from USMC FMFM1

To: Our teachers and mentors. Our friends and family. Our colleagues. Our residents and fellows. To all who have trod the path before us and to all who come after.

About this Book

This book is a guide, a manual, a tool. There is much to learn, and much that no one may formally teach you. Learning may be random and haphazard based on what you encounter, what you read, and who you work with. This book is not a complete treatise or definitive manual of musculoskeletal radiology. There is much that you can investigate independently, and we encourage you to use other sources and get differing perspectives. Through our cumulative years of experience, we believe that what we included and stressed covers the vast majority of what you will need to understand, interpret, and report in regards to musculoskeletal radiographs. Understanding the cases in this book will leave you well trained. It is a manual that we hope contains common, useful, and practical answers to the myriad of confusing cases that you will confront. Some are simple, some are complex, and all require time, dedication, and perseverance. We have chosen to adopt a practical and results-oriented approach, providing information we think will help you survive and thrive in an ever changing and often hectic diagnostic radiology environment. This book is primarily focused on radiographic findings and diagnosis although other modalities are touched upon. It would take another book to thoroughly discuss the musculoskeletal manifestations of MRI and ultrasound. We own any mistakes, errors, or omissions that we have made. We have tried to be as through and disciplined as possible in ensuring that all we have included is correct, practical, and applicable. Where we have failed, the fault is ours and ours alone. We hope you learn and enjoy. Please let us know of any flaws and failures or successes, or suggestions. Respectfully, Benjamin Plotkin B. L. Davis

ix

Contents

1 Survival ������������������������������������������������������������������������������������������    1 Survival Actions ������������������������������������������������������������������������������    1 S-Size Up the Situation����������������������������������������������������������������    1 U-Use Your Senses, Undue Haste Makes Waste��������������������������    2 R-Remember Who and Where ����������������������������������������������������    2 V-Vanquish Fear and Panic����������������������������������������������������������    2 I-Improvise����������������������������������������������������������������������������������    2 V-Value Your Report��������������������������������������������������������������������    2 A-Act Decisively��������������������������������������������������������������������������    3 Live by Your Wits and Learn Basic Skills������������������������������������    3 Psychology of Survival����������������������������������������������������������������    3 Factors that Can Increase Stress��������������������������������������������������    4 Take Care of Yourself������������������������������������������������������������������    4 2 Reporting and Communication����������������������������������������������������    7 Report Structure ������������������������������������������������������������������������������    7 Key Findings Versus Incidental Findings����������������������������������������    8 Use and Abuse of Classification Systems����������������������������������������    9 Saved Rounds����������������������������������������������������������������������������������    9 Further Readings������������������������������������������������������������������������������   10 3 Trauma��������������������������������������������������������������������������������������������   11 Spine������������������������������������������������������������������������������������������������   11 Cervical Spine������������������������������������������������������������������������������   11 Atlanto-Axial Interval������������������������������������������������������������������   12 Causes of Atlanto-Axial Widening����������������������������������������������   12 Facet Dislocation ������������������������������������������������������������������������   12 Dens Fracture ������������������������������������������������������������������������������   14 C1 Ring Fractures (Jefferson Fracture)����������������������������������������   14 Flexion Tear Drop Fracture����������������������������������������������������������   15 Hanged Man’s Fracture����������������������������������������������������������������   15 Clay Shoveler’s Fracture��������������������������������������������������������������   16 Warning����������������������������������������������������������������������������������������   16 Thoracic and Lumbar Spine������������������������������������������������������������   18 Compression Fracture������������������������������������������������������������������   18 Tips for Assessing Acuity������������������������������������������������������������   18 Burst Fracture������������������������������������������������������������������������������   19 Chance Fracture ��������������������������������������������������������������������������   20 xi

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Shoulder ������������������������������������������������������������������������������������������   21 Anterior Shoulder Dislocation ����������������������������������������������������   21 Greater Tuberosity Fracture ��������������������������������������������������������   22 Scapula Fractures ������������������������������������������������������������������������   22 Acromioclavicular Injury������������������������������������������������������������   23 Stress Injuries of the Distal Clavicle��������������������������������������������   23 Chronic Rotator Cuff Pathology��������������������������������������������������   25 Biceps Dislocation ����������������������������������������������������������������������   25 Sternum and Sternoclavicular Joints������������������������������������������������   26 Ribs��������������������������������������������������������������������������������������������������   27 Elbow ����������������������������������������������������������������������������������������������   27 The Terrible Triad������������������������������������������������������������������������   27 Olecranon Fracture����������������������������������������������������������������������   28 Capitellum Fracture ��������������������������������������������������������������������   29 Tendon Injuries����������������������������������������������������������������������������   30 Biceps Tendon Tear����������������������������������������������������������������������   30 Common Extensor/Flexor Tendon Tear ��������������������������������������   31 Forearm��������������������������������������������������������������������������������������������   31 Monteggia Fracture����������������������������������������������������������������������   31 Galeazzi Fracture ������������������������������������������������������������������������   32 Wrist������������������������������������������������������������������������������������������������   32 Triquetral Fracture ����������������������������������������������������������������������   32 Scaphoid Fracture������������������������������������������������������������������������   33 Distal Radial Fractures����������������������������������������������������������������   33 Pisiform Fracture ������������������������������������������������������������������������   34 Hamate Fracture��������������������������������������������������������������������������   35 Carpal Metacarpal Dislocation����������������������������������������������������   36 Stress Fracture������������������������������������������������������������������������������   36 Carpal Dislocations����������������������������������������������������������������������   37 Hand������������������������������������������������������������������������������������������������   40 Metacarpal Fractures��������������������������������������������������������������������   40 Phalangeal Injuries����������������������������������������������������������������������   41 Thumb Ulnar Collateral Ligament Injury������������������������������������   43 Ultrasound������������������������������������������������������������������������������������   43 Foreign Bodies ����������������������������������������������������������������������������   43 Tendon Laceration/Tear ��������������������������������������������������������������   44 Pelvis and Hips��������������������������������������������������������������������������������   44 Proximal Femoral Fractures��������������������������������������������������������   45 Sacral Insufficiency Fractures������������������������������������������������������   50 Pelvic and Obturator Ring Fractures��������������������������������������������   51 Diastasis and Dislocations ����������������������������������������������������������   52 Knee ������������������������������������������������������������������������������������������������   54 Traumatic Arthrotomy������������������������������������������������������������������   55 Less Obvious Knee Injuries ��������������������������������������������������������   55 Tibial Plateau Fractures ��������������������������������������������������������������   58 Patella Fractures��������������������������������������������������������������������������   58 Bipartite Patella����������������������������������������������������������������������������   59 Patella Dislocation ����������������������������������������������������������������������   60

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Insufficiency Fractures����������������������������������������������������������������   61 Stress Fractures����������������������������������������������������������������������������   61 Dislocation ����������������������������������������������������������������������������������   61 Ankle������������������������������������������������������������������������������������������������   63 Fracture at the Base of the Fifth Metatarsal��������������������������������   63 Fracture of the Anterior Process of the Calcaneus����������������������   64 Dorsal Capsular Avulsion Fractures������������������������������������������������   64 Traumatic Osteochondral Fracture of the Lateral Talar Dome����������������������������������������������������������������������   64 Fracture of the Lateral Process of the Talus��������������������������������   65 Fracture at the Origin of the Extensor Digitorum Brevis Muscle������������������������������������������������������������������������������   65 Distal Fibular Fractures����������������������������������������������������������������   65 Trimalleolar Fractures������������������������������������������������������������������   65 Maisonneuve Fracture������������������������������������������������������������������   67 Calcaneal Stress Fracture������������������������������������������������������������   67 Achilles Tendon Injury����������������������������������������������������������������   67 Fracture Blisters ��������������������������������������������������������������������������   67 Tendon Entrapment����������������������������������������������������������������������   67 Foot��������������������������������������������������������������������������������������������������   70 Fifth Metatarsal Base Fractures in Kids��������������������������������������   70 Lisfranc Injuries ��������������������������������������������������������������������������   70 Metatarsal Neck Fractures ����������������������������������������������������������   71 Bone Stress Injuries ��������������������������������������������������������������������   71 Toe Fractures��������������������������������������������������������������������������������   71 Saved Rounds����������������������������������������������������������������������������������   75 Live Fire Exercises��������������������������������������������������������������������������   75 After Action Review������������������������������������������������������������������������   80 Bibliography������������������������������������������������������������������������������������   83 4 Infection������������������������������������������������������������������������������������������   89 Foundations��������������������������������������������������������������������������������������   89 Imaging Modalities��������������������������������������������������������������������������   89 Plain Radiography������������������������������������������������������������������������   89 Computed Tomography����������������������������������������������������������������   89 Ultrasound������������������������������������������������������������������������������������   90 Nuclear Medicine������������������������������������������������������������������������   91 Magnetic Resonance Imaging������������������������������������������������������   91 Osteomyelitis ����������������������������������������������������������������������������������   92 Pyogenic vs. Nonpyogenic����������������������������������������������������������   92 Pediatric vs. Adult������������������������������������������������������������������������   92 Acute vs. Chronic������������������������������������������������������������������������   92 Imaging of Acute Osteomyelitis��������������������������������������������������   92 Imaging of Chronic Osteomyelitis����������������������������������������������   95 Soft Tissues Infection����������������������������������������������������������������������   96 Necrotizing Fasciitis��������������������������������������������������������������������   96 Other Soft Tissue Infections��������������������������������������������������������   96 Intra-Articular Infection������������������������������������������������������������������   97

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Infection of the Spine����������������������������������������������������������������������   98 Atypical Infections��������������������������������������������������������������������������  100 Saved Rounds����������������������������������������������������������������������������������  101 Bibliography������������������������������������������������������������������������������������  101 5 Bone Tumors������������������������������������������������������������������������������������ 103 Periosteal Reaction��������������������������������������������������������������������������  104 The Good ������������������������������������������������������������������������������������  104 The Bad����������������������������������������������������������������������������������������  104 The Ugly��������������������������������������������������������������������������������������  105 Border and Zone of Transition��������������������������������������������������������  106 The Good ������������������������������������������������������������������������������������  107 The Bad����������������������������������������������������������������������������������������  107 The Ugly��������������������������������������������������������������������������������������  108 Age����������������������������������������������������������������������������������������������  108 Alone or in Battalions������������������������������������������������������������������  108 Good or Bad? ����������������������������������������������������������������������������������  109 What to Look for in Making this Judgment? ������������������������������  109 After Action Review������������������������������������������������������������������������  111 Refinement ��������������������������������������������������������������������������������������  111 Location ������������������������������������������������������������������������������������������  111 Giant Cell Tumor ����������������������������������������������������������������������������  114 Chondroblastoma ����������������������������������������������������������������������������  115 Aneurysmal Bone Cyst��������������������������������������������������������������������  116 Clear Cell Chondrosarcoma������������������������������������������������������������  116 Infection ������������������������������������������������������������������������������������������  117 Unicameral or Simple Bone Cyst����������������������������������������������������  118 Enchondroma ����������������������������������������������������������������������������������  118 Chondrosarcoma������������������������������������������������������������������������������  119 Osteochondroma������������������������������������������������������������������������������  119 Osteosarcoma����������������������������������������������������������������������������������  120 Infection ������������������������������������������������������������������������������������������  122 Fibrous Dysplasia����������������������������������������������������������������������������  123 Fibroxanthoma (also Called a Non-­Ossifying Fibroma) ����������������  123 Metastasis and Myeloma������������������������������������������������������������������  124 Round Blue Cell Tumors ����������������������������������������������������������������  125 Osteofibrous Dysplasia��������������������������������������������������������������������  126 Adamantinoma��������������������������������������������������������������������������������  126 Osteoid Osteoma������������������������������������������������������������������������������  126 The Distal Phalanx��������������������������������������������������������������������������  127 Glomus Tumor ����������������������������������������������������������������������������  127 Epidermoid Inclusion Cyst����������������������������������������������������������  128 Matrix������������������������������������������������������������������������������������������  128 Osteoid ����������������������������������������������������������������������������������������  128 Chondroid������������������������������������������������������������������������������������  128 Fluid ��������������������������������������������������������������������������������������������  129 Fibrous ����������������������������������������������������������������������������������������  129 Fat������������������������������������������������������������������������������������������������  129

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Tumor Mimics����������������������������������������������������������������������������������  131 Infection ��������������������������������������������������������������������������������������  131 Brown Tumor ������������������������������������������������������������������������������  131 Osteonecrosis ������������������������������������������������������������������������������  132 Giant Bone Island������������������������������������������������������������������������  133 Osteopoikilosis����������������������������������������������������������������������������  134 Osteopathia Striata ����������������������������������������������������������������������  134 Melorheostosis ����������������������������������������������������������������������������  134 Polyostotic Lesions��������������������������������������������������������������������������  135 Metastasis and Myeloma��������������������������������������������������������������  135 Polyostotic Fibrous Dysplasia�����������������������������������������������������  136 Multiple Enchondroma Syndromes ��������������������������������������������  136 Infection ��������������������������������������������������������������������������������������  136 Brown Tumors������������������������������������������������������������������������������  136 Langerhans Cell Histiocytosis ����������������������������������������������������  137 Saved Rounds������������������������������������������������������������������������������  137 Live Fire Exercises��������������������������������������������������������������������������  139 After Action Review������������������������������������������������������������������������  144 Bibliography������������������������������������������������������������������������������������  145 6 Orthopedic Hardware���������������������������������������������������������������������� 149 Foundations��������������������������������������������������������������������������������������  149 Hardware Imaging ��������������������������������������������������������������������������  149 Plain Radiography������������������������������������������������������������������������  149 CT������������������������������������������������������������������������������������������������  149 MRI����������������������������������������������������������������������������������������������  150 Nuclear Medicine������������������������������������������������������������������������  150 Hardware Complications ����������������������������������������������������������������  150 Hardware Failure��������������������������������������������������������������������������  150 Displaced Hardware��������������������������������������������������������������������  150 Perihardware Fracture������������������������������������������������������������������  150 Hardware Infection����������������������������������������������������������������������  150 Specific Complications of Arthroplasty Hardware����������������������  152 Saved Rounds����������������������������������������������������������������������������������  156 Bibliography������������������������������������������������������������������������������������  157 7 Arthritis�������������������������������������������������������������������������������������������� 159 Osteoarthritis������������������������������������������������������������������������������������  160 Erosive Osteoarthritis������������������������������������������������������������������  161 Inflammatory Arthropathies ������������������������������������������������������������  162 Rheumatoid Arthritis��������������������������������������������������������������������  164 Target Recognition����������������������������������������������������������������������  164 Juvenile Idiopathic Arthritis��������������������������������������������������������  168 Ankylosing Spondylitis����������������������������������������������������������������  168 Psoriatic and Reactive Arthritis����������������������������������������������������  169 Enteropathic-Related Arthritis ����������������������������������������������������  173 Septic Arthritis ��������������������������������������������������������������������������������  177 Neuropathic Arthropathy ����������������������������������������������������������������  179 Deposition Arthropathy��������������������������������������������������������������������  180

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Gout����������������������������������������������������������������������������������������������  180 Calcium Pyrophosphate Dihydrate Crystal Deposition Disease (CPPD)����������������������������������������������������������������������������������������  181 Amyloid Deposition Arthropathy������������������������������������������������  181 Hemophilia Arthropathy������������������������������������������������������������������  184 Benign Proliferative Processes��������������������������������������������������������  185 Synovial Chondromatosis/Osteochondromatosis������������������������  185 Tenosynovial Giant Cell Tumor��������������������������������������������������  185 Lipoma Arborescens��������������������������������������������������������������������  186 Vascular Malformations ��������������������������������������������������������������  186 Sundries��������������������������������������������������������������������������������������������  187 Calcific Periarthritis (Calcific Tendinopathy)������������������������������  187 Systemic Lupus Erythematosus (SLE) and Rhupus��������������������  188 Scleroderma and Mixed Connective Tissue Diseases������������������  189 Sarcoid ����������������������������������������������������������������������������������������  190 Saved Rounds����������������������������������������������������������������������������������  190 Live Fire Exercises��������������������������������������������������������������������������  191 After Action Review������������������������������������������������������������������������  197 Bibliography������������������������������������������������������������������������������������  198 8 Metabolic Disorders������������������������������������������������������������������������ 201 Imaging of Metabolic Disorders������������������������������������������������������  201 Physiology of Bone����������������������������������������������������������������������  201 Imaging Modalities����������������������������������������������������������������������  201 Osteoporosis������������������������������������������������������������������������������������  203 Generalized Osteoporosis������������������������������������������������������������  203 Regional Osteoporosis ����������������������������������������������������������������  203 Imaging Findings in Osteoporosis ����������������������������������������������  203 Osteomalacia������������������������������������������������������������������������������������  205 Foundations����������������������������������������������������������������������������������  205 Causes������������������������������������������������������������������������������������������  205 Findings���������������������������������������������������������������������������������������  206 Hyperparathyroidism ����������������������������������������������������������������������  207 Foundations����������������������������������������������������������������������������������  207 Imaging Findings ������������������������������������������������������������������������  207 Paget Disease ����������������������������������������������������������������������������������  210 Foundations����������������������������������������������������������������������������������  210 Pathophysiology��������������������������������������������������������������������������  211 Imaging Findings ������������������������������������������������������������������������  211 Complications of Paget Disease��������������������������������������������������  212 Saved Rounds����������������������������������������������������������������������������������  213 Acromegaly����������������������������������������������������������������������������������  213 Tumoral Calcinosis����������������������������������������������������������������������  213 Melorheostosis ����������������������������������������������������������������������������  213 Osteopoiklosis and Osteopathia Striata ��������������������������������������  213 Bibliography������������������������������������������������������������������������������������  213 Index��������������������������������������������������������������������������������������������������������   215

About the Authors

Benjamin  Plotkin  is an Associate Clinical Professor of Radiological Sciences at the University of California, Los Angeles. Bennett  L.  Davis  is a Diagnostic Radiologist affiliated with UCHealth in Colorado Springs, Colorado.

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Abbreviations

AC Acromioclavicular ACL Anterior Cruciate Ligament AP Anteroposterior AS Ankylosing Spondylitis AVN Avascular Necrosis BMD Bone Mineral Density BMI Body Mass Index BMT Bone Marrow Transplant BUN Blood Urea Nitrogen CK Creatine Kinase CMC Carpometacarpal CP Cerebral Palsy CR Closed Reduction CRPS Complex Regional Pain Syndrome CT Computed Tomography CTS Carpal Tunnel Syndrome CTS Carpal Tunnel Syndrome CTS Carpal Tunnel Syndrome DDD Degenerative Disc Disease DEXA Dual-Energy X-ray Absorptiometry DIP Distal Interphalangeal joint DJD Degenerative Joint Disease DMARDs Disease-Modifying Antirheumatic Drugs DTR Deep Tendon Reflex DTR Deep Tendon Reflex EMG Electromyography ESR Erythrocyte Sedimentation Rate FHO Femoral Head Ostectomy Fx Fracture GH Glenohumeral HNP Herniated Nucleus Pulposus (Herniated Disc) IM Intramedullary IMN Intramedullary Nailing IP Interphalangeal joint IT Iliotibial (as in IT band)

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IV Intravenous IVD Intervertebral Disc JRA Juvenile Rheumatoid Arthritis LBP Low Back Pain LCL Lateral Collateral Ligament LE Lower Extremity LP Lumbar Puncture LP Lumbar Puncture MCL Medial Collateral Ligament MCP Metacarpophalangeal joint MD Muscular Dystrophy MMF Maxillomandibular Fixation MRI Magnetic Resonance Imaging MS Musculoskeletal MTP Metatarsophalangeal joint MTSS Medial Tibial Stress Syndrome (Shin Splints) NSAIDs Nonsteroidal Anti-inflammatory Drugs OA Osteoarthritis OA Osteoarthritis OP Osteoporosis ORIF Open Reduction and Internal Fixation ORIF Open Reduction Internal Fixation PA Posterior-anterior PA Psoriatic Arthritis PCL Posterior Cruciate Ligament PEMF Pulsed Electromagnetic Field therapy PIP Proximal Interphalangeal joint PMR Polymyalgia Rheumatica PRP Platelet-Rich Plasma PT Physical Therapy RA Rheumatoid Arthritis RF Rheumatoid Factor RICE Rest, Ice, Compression, and Elevation ROM Range of Motion SC Sternoclavicular SCI Spinal Cord Injury SCI Spinal Cord Injury SLAP Superior Labrum from Anterior to Posterior SLE Systemic Lupus Erythematosus SLE Systemic Lupus Erythematosus SLR Straight Leg Raise TBI Traumatic Brain Injury TEN Traction Epiphysiolysis (or Slipped Capital Femoral Epiphysis) THA Total Hip Arthroplasty THR Total Hip Replacement

Abbreviations

Abbreviations

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TKA TKR TMJ UE VCF WB WNL

Total Knee Arthroplasty Total Knee Replacement Temporomandibular joint Upper Extremity Vertebral Compression Fracture Weight Bearing Within Normal Limits

1

Survival

The night is dark. The list is long. You’re all alone. You stare with dread at the screen, if only you knew what to say, where to look, what was that elusive finding you were missing? You can feel the fear and anxiety pulsating within you. You need to survive. Keep reading. You will survive and thrive. All you need to survive is contained within. Survival is a mindset. Survival requires skills and training. There are skills that no one may have taught before. Residency training is based on reading, observing, and learning. You emulate and copy the attendings you work with. But they may not always be teaching you the skills you will need. Hopefully they help you learn the basics, but the basics are not enough. There are skills that no one will teach you. This manual will provide you with those skills. There is a survival mindset.

Survival Actions S-U-R-V-I-V-A-L will be your guide. We will expand upon each letter in the world survival as a first step.

S-Size Up the Situation Take note of your environment. You want to be mentally sharp, aware, and primed for action. Take care of the basics first. –– Size up your surroundings. Optimize your work environment. Keep the temperature cool. Too warm will stupefy you. Turn away distractions. Block out or minimize sounds, sights, and other peripherals that take away from your focus. The focus should be on the images you are evaluating. Close the browser, don’t look at your phone. If there are noises or other people in the room, consider using noise abating ear devices. Concentrate, stay focused. Lapses in attention cause errors. –– Size up your physical and mental condition. Have food and drink near if needed. Caffeine is a performance enhancer and can help. If you’re sick, injured, or hurt, take note, but don’t allow these distractors to intervene with your focus. Push them to the corner of your mind. –– Size up your equipment. Monitors at eye level. Peripheral input devices should be customized and optimized for your individual

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 B. Plotkin, B. L. Davis, Musculoskeletal Imaging, https://doi.org/10.1007/978-3-031-49021-7_1

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1 Survival

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work flow to streamline performance. These tools are there to aid you and help with workflow and efficiency. They should not be a distraction or disruption.

 -Use Your Senses, Undue Haste U Makes Waste –– Your visual sense is what you need to survive. –– Have your checklists ready. –– Where to look first, second, and third. –– What pitfalls, traps, and hazards do you need to be aware of? –– Be thorough in your search pattern and evaluation. Repeat and repeat. With repetition comes speed, but don’t sacrifice steps in your evaluation for the sake of speed. You will make errors. Speed will come naturally with experience, practice, and repetition. –– Be observant! Small details can make a big difference. –– Be observant! There is often more than one finding. –– Be observant! Secondary and tertiary findings may provide you with the definite diagnosis.

R-Remember Who and Where –– Remember who the patient is and the environment in which they present. –– Context matters. –– Context will help guide your search and prime you for what to look for. –– Did the patient just get hit by a truck? Stop perseverating over the appendix! –– Are they a rheumatology patient? Zero in on the joints and any possible arthritis. –– We do not evaluate in a zero-information vacuum (usually). There is additional information available. Use it. –– Check the chart. What does the note say? Do labs or ancillary information help? –– Call up the ordering provider and ask questions, gain situational awareness. A short con-

versation can instantly clarify a murky situation. –– Remember to use all information at your disposal.

V-Vanquish Fear and Panic –– Fear is the mind killer! –– Fear is real. We fear making mistakes. We fear getting sued. We fear looking like an incompetent in the eyes of our colleagues and referring clinicians. –– Fear is real, but don’t let fear overwhelm, overpower, and overawe you. Fear can paralyze you and lead you down the alley you most dread. –– Fear can be an ally. Use it to keep you sharp, to stay focused, but keep it at bay and don’t let it overwhelm you. –– Fear of mistakes is real, but mistakes are going to happen. Everyone makes mistakes. You will make mistakes and miss things, it is inevitable but when you do you must own them, accept them, and learn from them.

I-Improvise –– Sometimes the usual way of working won’t work. Be able to adapt and improvise. –– The ER study is confusing. Go see the patient yourself, talk to him, and examine him. –– Use information on scout images. –– If encountering difficulty with a procedure, try a different approach.

V-Value Your Report –– Radiologists play a crucial role in patient care and diagnosis. –– It is a heavy responsibility. –– Value your observations, they may be critical for your patient’s survival and well-being. –– Value your report. –– Your report shouldn’t be a free form jumbled stream of conscious run on paragraph. Your

Survival Actions

report is a vital component of your job. Take pride in it. Make sure you report is clear, concise, and well organized to effectively communicate the key findings and answer the clinical questions. –– Stress critical findings and be clear in your language to avoid ambiguity and doubt when possible. –– Proof your report before you finalize it to avoid mistakes and transcription errors. Any mistakes are on you, you can’t blame technology or others for your errors.

A-Act Decisively –– Your observations and judgement are often a critical deciding factor in patient management. –– Clinicians and patients rely on you for a clear understanding. This is not always possible, but the majority of the time it is. When it is clear then act with certainty and decisiveness. –– Don’t use ambiguous or vague terminology in your reports. State things in a simple and direct fashion. –– Commit yourself to the diagnosis. If you think there is a finding, then say so. Radiologist have a bad predilection for hedging and indecisive language. Do not pick up this bad trait! You may occasionally be wrong about the finding or its interpretation, but this must not dissuade you from trying to be as decisive as the situation allows.

 ive by Your Wits and Learn Basic L Skills –– To prepare yourself to survive and thrive you must learn the basic skills. –– Basic anatomy is a must. –– Knowledge of common pathologies. –– Know what to look for, and when to look for it. –– Arm yourself with the checklists and search patterns you need for each study.

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–– This survival manual will help you to learn, guide you on the path, and stress the skills you need to survive. Survive and thrive. Read and learn. S—Size up the situation U—Use your senses, undue haste makes waste R—Remember who and where V—Vanquish fear and panic I—Improvise V—Value your report A—Act decisively L—Live by your wits and learn basic skills

Psychology of Survival There is a pattern for surviving and thriving in a high stress environment. Stress is an important factor to be aware of. Stress is inescapable and a part of the job. Stress comes from many factors. There is the stress of having a long list of studies to read. There is the stress of time pressure in which you need to read them. There is the stress that comes from the fear of making a mistake, or a wrong or missed diagnosis. These stressors can be magnified by other factors. Solitude is one factor that can be stressful. If you are alone, or feel that you are alone, then this is often a source for added stress, as the psychological reassurance of colleague is a huge factor. If you have colleagues around, you know you can ask for help, or a second opinion. Even if you never actually take advantage of this, just the knowledge that it is an option is a psychological balm. Other stressors can come from fatigue, which may be the result of inadequate sleep or prolonged hours at work. Lack of adequate energy can contribute to decreased mental focus and increase stress. It is important to be aware of additional factors that can cause stress.

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Factors that Can Increase Stress –– –– –– –– –– –– ––

High work load Pressure to read quickly Fear Solitude Fatigue Poor nutrition Worries outside of work

Do your best to optimize, reduce, or minimize as many of these as possible. Know that it will not be possible to eliminate all stress. You can however use stress to your advantage. Stress can be good. It can spur you to me more alert, more attentive, and more focused. Stress forces you to adapt and deal with the pressure, which if not overwhelming will make you stronger and more capable. Too little stress will make you complacent and lackadaisical. Just make sure that the stressors with you at work are not too overwhelming. Too much stress can lead to errors, indecision, and decreased effectiveness. Learn to wield the double-edged weapon that is stress. DO NOT let stress paralysis you! You must decide, you must be useful, you strive to be right. Don’t be paralyzed by the fear of being wrong. We all make mistakes. Own your mistakes, learn from your mistakes, don’t be afraid of mistakes. Mistakes are part of the journey. Make a plan to keep yourself in optimal physical and mental condition. To survive, you must be strong. You must prepare your mind and body for the trials and tribulations of a stressful night in the reading room. This is not special radiology knowledge or advice, this is a general life goal. To be great at your job and thrive, you must stay in good shape. Your mind is your primary weapon, but do not neglect your body. Mind and body go together, work together, and if one is weak, it will drag the other one down.

Take Care of Yourself –– Eat well –– Physical exercise sharpens your mind and body

–– Don’t stay sedentary. If you can, work standing up, or take exercise breaks throughout the day. Nothing like a few burpees on the the hour to keep you sharp and awake. What they don’t teach you in residency are the soft skills, the non-radiology knowledge that will give you that extra edge to survive and thrive. It takes more than book knowledge to survive. It requires adaptation, curiosity, and using all resources and your disposal. To be the best at your job, to make the great calls, the subtle finds the astute observations you need full immersion. When needed, glean all necessary information from the records and if necessary in person, don’t be afraid to pick up the phone and call. You may learn a critical piece of information not conveyed on the request. Get to know you referring clinicians, create bonds of trust and understanding. These relationships will help. A small clue from your trusted clinical colleague may prevent you overlooking a subtle finding. Develop clear, discrete, and repeatable search patterns. AND USE THEM! Patterns are self-reinforcing, but take discipline to continuously repeat. Get in the habit of approaching the study the same way, each time, over and over. The more you practice this the more ingrained it becomes. Soon it will be second nature. There is the fear of causing injury or death with a bad read, or sending someone to surgery un-necessarily. Some calls are big calls, some are irrelevant. Know which calls matter, which calls will make a drastic change in clinical response. Control what you can control, and accept ambiguity, imperfection, and doubt will always be present. Isolation is hard. Seek friends, ask for help. You’re probably not alone. We are stronger as a team, stronger together. Use your teammates, they can help you. Don’t be afraid to ask for help. Asking for help is not a mark of weakness, but a sign of strength. The more eyes and minds focused on a problem, the more likely they will be right. Fear, guilt, and anxiety are natural emotions. You can’t suppress them, but you can learn to

Further Reading

acknowledge their existence without them degrading your operational capacity. Be realistic about your knowledge. Know what you know, and more importantly know what you don’t know. It is hard to evaluate our weakness and blind spots, but if you can do this you will side step many troubles. Don’t be afraid to say, “I don’t know.” There are always instances where we do not know. This is hard and scary to admit, we don’t like to own up to our shortcomings, but if the life and health of another are at stake, we must put our ego aside and acknowledge the instances where we do not know. At these times, we can suggest alternative possibilities that might aid in a diagnosis and ask for help when we can. Adopt a positive attitude. As Marcus Aurelius told himself (and us)—never find yourself complaining, not even to yourself. Complaining about the ER doc, the technologist, the scanner or the patient moving is not helpful, it is counterproductive and distracting. Focus on what you can control. Focus on being the best radiologist and physician you can be, leave the rest behind. The patient was only able to complete a single sequence in the MR. Good, this is your chance to shine. Instead of giving up and saying the exam is non-diagnostic, look harder. Often there is much you can glean and deduce on a single sequence. It may be enough to provide the answer to the clinical question. There was no history with the scan. Good. This is your opportunity to read through the chart

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and get extra information you might not have gone searching for. Your inner complaints are actually opportunities. Use them. Those around you will notice and feed off of your strength, resilience, and leadership. Don’t let them down. Study. Train. Learn. Repeat. It’s a long road and there is lots to cover. Ready? Advance to contact!

Further Reading

The United States Marine Corps is the source of the cover manual

2

Reporting and Communication

Report Structure Many radiologists in training adopt the reporting structure of an upper classmen very early in their residency. While it is an easy and intuitive answer to one of the first problems faced by a first-year resident, it typically results in only mediocre reports. Often the reports are disjointed and difficult to follow. They slowly improve with time, but it isn’t until either a clinician pointedly identifies deficiencies in a report or the volume of studies to interpret becomes overwhelming that meaningful changes actually occur. Best to get that sorted out as soon as practicable, so here are a few thoughts to hasten the time to improvement. First, there is always some sort of structure to any report. Header information such as the name of the study, the clinical indication, a list of any prior comparison studies, and the basic technique are standard and fairly boilerplate. The body of the report typically follows, and the final impression usually closes the report. Occasionally, the impression section will be the first thing in the report, a nod to the idea that “the impression is for the clinicians, the body of the report is for the other radiologists.” Do what is done at your institution, but unless required to put the impression section at the top, consider that, logically, it should conclude your report.

The real personal style of every radiology report is within the body section. In general, this can assume a free form or structured format. Follow your local practices. If there are no standards, then give good consideration to the following few points: • Don’t bother with structured reports for musculoskeletal plain films or ultrasound. • Musculoskeletal CTs only occasionally benefit from structured reports. • Most musculoskeletal MRI reports are more easily read and more quickly generated in a structured fashion. • Just create a “Findings/Impression” section for fracture follow-up plain films. Regardless of how you document the findings you make, the impression section of the report is what everyone—patients, clinicians, and other radiologists—reads. Invest time developing how you summarize and phrase common findings. Here are a few go-bys. • Avoid restating the findings; you already did that. Call it what it is (e.g. “advanced left knee osteoarthritis,” “massive rotator cuff tear”). • Explicitly detail necessary follow-up of incidental, but clinically important, findings. This is even more true if they are found on advanced

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 B. Plotkin, B. L. Davis, Musculoskeletal Imaging, https://doi.org/10.1007/978-3-031-49021-7_2

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imaging studies and fall outside of the scope of practice of the ordering provider. • For complex studies where you are really pulling together multiple pieces of data and injecting your (ever growing) clinical experience, do not be afraid to use the word “I.” It’s okay to say, “Given the provided clinical history and the abnormal laboratory values, I favor the above-described constellation of imaging findings to represent...” • Document with whom (by name!), how, and when you relayed critical or unexpected findings.

 ey Findings Versus Incidental K Findings Key findings answer the clinical question (if one is asked), provide new insight into the patient’s medical condition, or guide therapy, to include prompting additional imaging studies and guiding targeted laboratory evaluation. In brief, they are the raison d’etre for the study. Some key findings such as gross fractures are straightforward, but many others are far more difficult to recognize in totality. A tiny Segond fracture fragment, for example, strongly suggests ACL injury, and appropriate supportive medical management and MRI are necessary to confirm or exclude this much more serious injury. Failure to do so risks complete ligamentous failure if only a partial tear had occurred, the inability to exclude a concomitant meniscal tear, and ultimately delays treatment. Most providers need little help interpreting simple, but grossly abnormal, plain films. More savvy providers can detect major findings at CT, and surgeons can usually do the same for MRI exams within their subspecialty field. Regardless of a clinical provider’s background, most practicing radiologists will have interpreted more advanced imaging studies within a few years of completing training than senior clinicians will review in their career. Synthesis of the entirety of the patient’s available imaging into a cohesive diagnosis or short differential diagnosis is where radiologists add significant value. Differentiating

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subtle findings of incidental value from those of critical importance (good judgement) is a skill that comes only with time and feedback (experience). To finish the saying, “… and experience comes from bad judgement.” So what to do either early in your career or when faced with an heretofore unseen clinical and imaging situation? Take solace; your final impression does not have to be 100% correct, but it must be 100% reasonable. When in doubt, take a page from the breast imaging playbook and get short interval follow-up. Most fractures will start to show early bony healing changes by about 14 days. Most aggressive tumors will show some sort of imaging change within 4–6 weeks. But what about all of those incidental findings? Well, first are they really incidental or are they small pieces of a large constellation of findings? The answer to this goes back to good judgment. Fortunately, most are truly incidental. The vast majority of these do not change clinical management, and those that do typically do so in an obvious way. For example, a T2 hyperintense pulmonary mass on a shoulder MRI or a heterogeneously T2 hyperintense renal mass on a lumbar spine MRI clearly need further imaging and follow-up. As suggested above, in these situations, the incidental finding needs to be clearly stated within the report’s final impression. Other truly incidental findings such as punctate non-­obstructing renal stones, small fat containing inguinal hernias, and superficial venous varicosities are best described within the report and nothing further. As professional relationships develop over time with common referring providers, it will become clear what can be safely omitted entirely from the report. One final note. Insurance providers and quality metrics (frequently developed in conjunction with the insurance industry) may stipulate that certain incidental findings either be outlined in the impression or that specific follow-up is documented in the report. When starting at a new practice, you should ask if any such requirements exist for the facility. Very few new radiologists take the 15 seconds to ask that question, and the rest that don’t ultimately spend several hours addending reports; a suboptimal use of time to say the least.

Saved Rounds

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 se and Abuse of Classification U Systems

Here are a few classification systems which seem to come up frequently:

The vast majority of medical classification systems (not just imaging-based classifications) are relegated to the dusty pages of old medical libraries, and for good reason. Those that endure are usually easy to remember and provide at least a modest degree of clinical utility. Since most classification systems do neither of these well, they are, thankfully, lost to time. The good news is that you probably never need to classify anything in musculoskeletal imaging. The downside is that you should be familiar with either the most commonly used classification system for a particular entity or the system used by the orthopedic surgeons with whom you work. For musculoskeletal imaging, these classification systems primarily involve fractures. For reporting purposes, specifically naming a particular classification system in your impression has, at best, limited utility, and, at worst, paints the treatment team into a corner, especially if they disagree with you. Why make things harder than they need to be? Familiarity with the details of a given classification system allows you to succulently describe the findings and provide pertinent negatives. For things you encounter continually, the details will become rote. For the rest, there is great reference library of the internet. As an example, the Schatzker classification for tibial plateau fractures defines six different types. The only difference between several classification categories is the degree of fragment displacement with 0.4  cm being the threshold. Your findings section may read, “Pure cleavage type fracture of the lateral tibial plateau with approximately 0.6 cm of articular step off.” While your impression may read, “Depressed lateral tibial plateau fracture.” Just use the classification system to describe and summarize the imaging findings. The orthopedic surgeons can read between the lines and know that you are cognizant of the classification criteria, and they will thank you, albeit quietly, for not putting classification names and numbers on fractures.

• Neer classification of proximal humeral fractures • Rockwood classification of acromioclavicular separation injuries • Mayo classification of olecranon fractures • Schatzker classification of tibial plateau fractures • Weber classification of ankle fractures When in doubt, go back to the basics and describe the findings.

Saved Rounds Three final thoughts. Ultimately, the entire point of the report is to communicate imaging findings so that treatment decisions can be made. Doing so in a cogent, logical, and succent fashion is a significant component of the radiologic “art of medicine.” Your structured reports should be organized in a way that makes sense, and your free form reports should similarly communicate findings in a logical way. You are essentially creating a story arc with everything described in the report supporting your impression. Secondly, formatting matters. What looks good in your dictation software may come out as nearly unreadable garbage after it is posted in the electronic medical record. Judicious use of ALL CAPS allows individual sections of structured reports to be quickly located. Well placed line breaks and paragraph breaks substantially impact the overall appearance of the final report in the electronic record. When is the last time you opened a patient’s EMR record (not PACS) and looked at a report that you authored? Does it reflect the best possible product that you can generate, or does it say something else? Remember, the standard is excellence. Finally, I’ll share the wise words of an English Professor teaching a Technical Writing class to a young aspiring physician. After receiving a mediocre grade on his midterm paper, the

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somewhat disappointed look on the student’s face was noticed by the Professor. He kindly stooped down and said in muffled voice, “If you would have spent more time, it would have been shorter.”

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Further Readings Zinsser W.  On writing well: the classic guide to writing nonfiction. 30th anniversary ed., 7th ed., Rev. Updated. HarperCollins; 2006. Anything by Kipling or Hemmingway

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Trauma

Training is a professional and moral imperative. Time for trauma training. Fired up, fired up. Here we go on the road… Trauma is a big subject. Much of what we see and evaluate in the realm of musculoskeletal imaging is trauma related. From the simple trip and fall, to a plane crash and all between. It’s a big cruel world, filled with lots of sharp, hard and blunt things that can crush, injure, and maim in a myriad of manners. It is impossible to cover every trauma situation that you will encounter. Some will be new and you will be required to adapt and proceed based upon basic principles. Our aim is to give you an overview of the injuries you are likely to encounter in the wild. Stress is placed on key places to focus and pitfalls to avoid. We’re going to start cranially and advance caudally. Semper Gumby! Stay flexible friends.

Spine The spine deserves special concentration and attention to detail in evaluation. Miss a toe fracture—unlikely to have harmful sequelae. Missing a spine injury can be devastating.

In a general consideration, any kind of significant accident or real concern for spine injury should go to cross-section imaging. Radiographs are not sufficient. Radiographs will show you big major injury. Smaller, more subtle, but still significant injuries often are not visible on the radiographs. If there is any doubt, ask for CT or MRI.

Cervical Spine Checklist for Cervical Spine Evaluation

–– –– –– –– –– –– –– ––

C7-T1 junction imaged Anterior spinal line Posterior spinal line Spinal lamina line Spinous process line Pre-vertebral soft tissues Atlanto-axial interval Symmetry between dens and C1 lateral masses –– Vertebral body heights –– Disc spaces –– Lung apices The C7-T1 junction must be imaged for you to consider a radiograph adequate, especially in the setting of trauma.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 B. Plotkin, B. L. Davis, Musculoskeletal Imaging, https://doi.org/10.1007/978-3-031-49021-7_3

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Follow the lines. –– Anterior spinal line (red) This should be a smooth continuous line without break or displacement. Any subluxation (listhesis), either anterior or posterior, is abnormal. Now it is common in degenerative spinal disease to have a little bit of anterior or posterior listhesis. This shouldn’t be ignored, should be mentioned, and may be significant and causing neurological symptoms. In the setting of trauma, it may reflect traumatic ligament injury or a fracture. –– Posterior spinal line (orange) Again, a smooth continuous line. Look for fractures, disruptions, and subluxation –– Spinal lamina line (yellow) This line parallels the posterior aspect of the spine and should be a smooth, slightly curved line. Look for fracture or disruptions in the posterior elements as you observe this line. –– Spinous process line (green) This is a curved asymptotic line that follows the most posterior aspects of the spinous processes. Often the C2 spinous process juts out a bit more and breaks the gentle curve of the line, but do not be alarmed this is normal. Otherwise any major discontinuity or break in the line should raise concern. Again scan for fractures of the spinous processes at this time. –– Pre-vertebral soft tissues (blue) As a general guide, the pre-vertebral soft tissues should be no wider than the adjacent vertebral body. They start out more diminished higher up and increase in prominence along the lower aspect of the cervical spine.

Key Point

Increase in the size of the pre-vertebral soft tissues is often a warning sign that there is other pathology. In the setting of trauma, this may be an occult fracture or ligamentous injury. It could also indicate an infection.

Any abnormal increase or prominence in this region may be a sign of trauma or infection. Figure 3.1 a and b show normal lateral and AP views of the cervical spine.

Atlanto-Axial Interval The distance between the posterior ring of C1, and the anterior cortex of the C2 dens. This measurement should be 2–3 mm in adults. Figure 3.2a In kids, it can be up to 5 mm. There are several potential causes of atlanto-axial widening.

Causes of Atlanto-Axial Widening –– Trauma –– Rheumatoid (or other inflammatory arthopathies) This is caused by the inflammation degrading and destroying the ligaments, which help to stabilize the two bones. –– Down syndrome. Individuals with this genetic profile can have ligamentous laxity and instability causing widening. There are other rarer congenital conditions that can cause this, but Down syndrome is the more common. Figure 3.2b shows abnormal widening of the distance. In this case caused by rheumatoid arthropathy. This is a flexion view, in the neutral view the distance was normal. Atlanto-axial widening may be dynamic and only present in flexion. Flexion and extension views are often critical in spinal evaluation. Trauma can cause atlanto-axial widening and associated ligament disruption Fig. 3.3. Also note the prominence of the pre-vertebral soft tissues from hematoma associated with the injury.

Facet Dislocation Facet dislocation-disruption can be a subtle finding on radiographs Fig. 3.4.

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Spine Fig. 3.1 (a) Normal lateral view of the cervical spine. -Red: anterior spinal line. -Orange: posterior spinal line. -Yellow: spinal lamina line. -Green: spinous process line (note how the C2 spinous process juts out, this is normal). -Blue: pre-vertebral soft tissue line, thinner at top and increasing more distal. (b) Normal AP view of the cervical spine. The midline spinous processes all line up in a nice column

a

s

b

b

Fig. 3.2 (a) Normal atlanto-axial distance. (b) Abnormal widening of the distance (white bar). In this case caused by rheumatoid arthropathy. Figure  3.2a is the neutral view, and Fig. 3.2b is a flexion view, which demonstrates

that the atlanto-axial widening may be only present in flexion. Flexion and extension views are often critical in spinal evaluation to assess for dynamic instability

Note how the finding is near the lower aspect of the image and could easily be overlooked if you are not following your checklist and check-

ing the lines. As you follow the spinal lamina line, you will see there is disruption. Obviously, this is a critical finding and should prompt both

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CT and MRI for further evaluation. MRI to look for cord injury and CT to get a better sense of the bone injury and mal-alignment.

Dens Fracture

Fig. 3.3  Atlanto-axial widening caused by trauma (white bar). There is prominence of the pre-vertebral soft tissues from hematoma (oval)

Dens fractures can be sneaky and subtle and are often difficult to find on radiographs. Remember, when in doubt get a CT or MRI Fig. 3.5a. Some dens fractures of course are visible on radiographs. Flexion and extension views are helpful for assessing instability. Figures 3.5b and c show an unstable dens fracture in a different individual. In the neutral view, the dens fragment is well-aligned with the rest of C2, but in flexion, we can see there is significant anterior displacement.

C1 Ring Fractures (Jefferson Fracture)

Fig. 3.4  Facet dislocation at the C6-C7 level. As you follow the spinal lamina line down you see an abrupt discontinuity and step off at the level of the injury (arrow)

A fracture and disruption of the ring of the C1 (atlas) vertebral body. The open-mouthed dens view of the spine is particularly useful for detection on radiographs. It should be obvious on a CT, where the ring of C1 is broken in more than one location. These injuries are less likely to be associated with neurological injury than others in the cervical spine. The distances between the lateral masses of C1 and the dens should be symmetric, and there shouldn’t be any step off (Fig. 3.6a). The fracture lines are clear on the CT (Fig. 3.6b), the asymmetrical distance between the dens and the ring of C1 is also apparent. Figure 3.6c shows a different individual with a C1 fracture. We can see the same finding on the CT, that correlates with the dens view radiograph finding. There is disruption of the C1 ring in relation to the C2 ring. The C1 ring fragments are displaced laterally.

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Spine

a

b

c

Fig. 3.5 (a) There is a dens fracture (arrow) but this was not visible on the radiographs. CT is far superior for the evaluation of cervical spine injuries. (b) The dens fracture is subtle, but we can see it. (c) The flexion view, which

makes the fracture more apparent and we see how far the more superior dens fragment is displaced in relation to the rest of C2

Flexion Tear Drop Fracture

Hanged Man’s Fracture

This fracture is caused by a hyperflexion injury, which results in a fracture of the anterior and inferior aspect of a cervical vertebral body. The injury results in a small displaced triangular fragment of the vertebral body and is associated with ligamentous injury. Figure 3.7 is a flexion tear drop injury involving the anterior inferior aspect of the C3 vertebral body. There is no alignment abnormality, but because we know this injury is associated with ligamentous damage, an MRI is needed for further evaluation.

Sounds bad. Is bad. The same force exerted on the neck after being dropped with a noose wrapped around you, except in modern times usually the result of high speed injury causing hyperextension of the spine. The injury pattern is characterized by bilateral pars interarticularis fractures of the spine, often associated with traumatic anterolisthesis. The pars injuries may not be clearly visible on initial radiographs, but the anterolisthesis

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a

b

c

Fig. 3.6 (a) The C1 burst fracture can be diagnosed by noting the step off between the base of C1 and C2. The white bars show where the ring of C1 should be, and the arrows show the displacement caused by the fracture. (b) The axial CT shows the fracture lines in both the anterior

and posterior aspects of the C1 ring, as well as widening and asymmetry of the space between the dens and the lateral aspect of the C1 ring (arrow). (c) Coronal CT showing the same finding in a different patient. There is offset of the C1 lateral masses with the ring of C2 (arrows)

should be. Again, CT and often MRI are warranted for better understanding of the full extent of the injury. Here is a hanged man’s injury with pars fractures and traumatic anterolisthesis of C2 in relation to C3 (Figs. 3.8a–c). There is an additional fracture of the anterior superior aspect of the C3 body, reminding us that spine injuries often have multiple and complex components and do not always follow the simple boxes we create for books.

C7. This is a stable non-surgical injury and while painful, is not associated with any neurological complication or spinal cord injury. One of the few spinal injuries that does not necessitate cross-­ section imaging. Figure 3.9 shows a typical example of this injury. A finding that is sneakily on the margin of the image, one that could easily be overlooked if you are not following your pattern and checklist of evaluation. Follow that spinous process line and you will find the injury.

Clay Shoveler’s Fracture

Warning

One of the more benign spinal injuries. This is an avulsion fracture of a spinous process, usually

Be especially vigilant in evaluating spines in individuals with diffuse idiopathic skeletal hyper-

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Spine

ostosis (DISH) and ankylosis of the spine in the setting of inflammatory arthropathy. When the spine is fused or partially fused, it is much more susceptible to injuries, and these injuries can be disastrous. This is a catastrophic set of injuries in an individual with extensive DISH with fusion of the anterior cervical spine (Fig. 3.10).

Key Point

Fused spines in the setting of DISH and ankylosing inflammatory arthropathy are less compliant and especially susceptible to injury. Be very vigilant in your evaluation and CT and or MR are often necessary to fully exclude injury.

Fig. 3.7  Flexion tear drop injury with the displaced fracture fragment at the anterior inferior aspect of the C3 body (arrow)

a

b

c

Fig. 3.8 (a) Pars fracture of C2 (long arrow) with associated anterolisthesis. There is an associated fracture of the C3 vertebral body (short arrow). (b) CT of the same person

showing the anterolisthesis and the small fracture fragment of the anterior C3 body. (c) The axial image from the CT shows the pars fractures more clearly (arrows)

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Thoracic and Lumbar Spine Evaluation of the thoracolumbar spine follows a similar drill to the cervical spine. Things to check: –– Alignment looking for steps offs along the anterior and posterior aspects. –– Vertebral body heights –– Intervertebral disc spaces –– Posterior elements

Compression Fracture

Fig. 3.9  A fractured and displaced C7 spinous process. No helpful arrow, just like in real life. Find the injury!

Probably the most common injury in the thoracolumbar spine. Very common in older individuals with osteopenia, when weakened bone is prone to compress and fracture with little force, but it can also occur with normal bone and higher force injuries. These injuries involve the vertebral body and result in height loss. This can range from mild to severe, with near complete loss of vertebral body height.

Key Point

Look for associated retropulsion, which can cause neurological compromise as it narrows the canal and may impact the cord or nerve roots.

Since these are common injuries, you will encounter them in non-acute settings, and sometimes it can be challenging to tell an old from a more acute injury.

Fig. 3.10  In this individual with extensive DISH and anterior fusion, there are multiple injuries. There is fracture and disruption through C3-C4 intervertebral disc space. There are additional injuries. The long arrow points to a fracture through the dens, the shorter arrow through dislocation and disruption of the spinal alignment with distraction of the posterior elements at the C3-C4 level. Look how narrow the spinal canal is at this level, and be assured there is associated cord injury

Tips for Assessing Acuity –– Comparison films are you friends, look to see if the finding is new. –– Do you see a distinct sharp cortical break? If so this is likely acute. –– Sclerosis and blurring of the margins of the endplate are indicative of a subacute injury.

Thoracic and Lumbar Spine

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–– Old injuries look old, with smooth margins. –– On MRI, acuity is more clear as there will be edema associated with the more acute injuries, which dissipates over time. Figure 3.11 shows an old compression fracture of L1. There is slight retropulsion of the posterior aspect of the body. Although hard to tell for sure, this is the typical appearance of an old injury, we don’t see an acute break in the bone, or sclerosis from healing in a subacute injury.

In acute injuries, look for a sharp cortical break in the endplate. Figure 3.12a shows a compression fracture, more subtle but we can see the slight height loss and disruption of the superior endplate. Figure 3.12b is a few weeks later, where there is early healing sclerosis. A subtle finding, but one that can help to date the injury. On follow-up images be sure to assess for any further collapse of the body and any new or increasing retropulsion or change in spinal alignment. With MRI, it is easier to determine the acuity of the injury. Figure  3.13 shows edema associated with this acute compression fracture. The edema will diminish with time, and be less prominent in the subacute setting and absent in an older injury.

Burst Fracture

Fig. 3.11  L1 compression fracture with severe height loss and slight retropulsion (arrow). This is an old injury, but it can be difficult to tell without comparison images or MRI Fig. 3.12 (a) An acute fracture of the T12 vertebral body with mild height loss and cortical disruption. (b) The follow-up radiograph shows subtle early healing sclerosis three weeks later, as well as increased height loss of the superior endplate

a

A burst fracture is a more complex version of a compression fracture, in which the vertebral body has fractured into multiple fragments, often with significant anterior and posterior displacement. Chances of neurological injury are higher with this injury, and surgery is often needed. If

b

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Fig. 3.13  Bright is bad. The vertebral body compression fracture has height loss and T2 bright edema. Typical of an acute injury

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Fig. 3.15  CT of the same individual, which better images the fracture detail. Please note the retropulsed fragment extending into the spinal canal. MRI is a good idea for evaluation of the spinal canal and nerve roots

you see these, please reach out and speak with the physician or team caring for the patient. This injury requires person to person communication. Figures 3.14 and 3.15 show a burst fracture of the L4 vertebral body. The body is broken into multiple fragments. Another injury that has risk of associated neurological injury and requires urgent communication with the care team.

Chance Fracture

Fig. 3.14  L4 burst fracture with fragmentation of the body and severe height loss

Another bad injury, which is the result of high energy flexion and distraction usually seen in the setting of car crashes. These injuries can be unstable and require surgical intervention. Look for disruption and fractures of the posterior elements. These injuries are often associated with intra-abdominal injury. Look for both the vertebral body fracture and the associated distraction and disruption of the posterior elements, which can cause spinal instability (Fig. 3.16).

Shoulder

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Anterior Shoulder Dislocation

Fig. 3.16  Chance injury with a fracture of the superior endplate of L1 (arrow) and associated distraction injury of the posterior elements (bar). Note the distance and disruption between the spinous processes, which has caused spinal instability and will require surgery

Shoulder

Anterior dislocations are common injuries. The dislocation is usually apparent to just about everyone, including the patient. Look for other injuries associated with the dislocation. Common ones are an impaction fracture of the posterior humeral head, a Hill-Sachs deformity and a fracture of the anterior inferior glenoid—a Bankart injury. Figure 3.17 shows a typical anterior shoulder dislocation. Axillary views (Fig. 3.18) are great for assessing the glenohumeral alignment, as well as looking for Hill-Sachs injuries. These injuries are often more apparent on this view than others. Here’s a quick test for you. Look at the two images (Fig. 3.19a and b) What do you see? Both are dislocated, but which way. You don’t really want to get this wrong on your report, it’s bad form. Write your answers down and hand them to the staff sergeant for evaluation. How did you do? Figure 3.19a is an anterior dislocation, associated with a good-sized Hill-Sachs impaction injury, you can see the posterior humeral head perched against the anterior glenoid and can see why when the dislocation occurs when there is a Hill-Sachs injury. Figure 3.19b is a posterior dislocation. Hopefully you used the coracoid to orient yourself so you knew which way the humerus

On radiographs, at least two distinct orthogonal views are required for the evaluation of injury in any joint, in the shoulder a third view in the form of an axillary of scapula Y view is often useful.

Checklist for Shoulder Radiograph Evaluation

–– –– –– –– ––

Glenohumeral alignment Acromioclavicular distance Tubersosities Joint spaces Soft tissues, especially looking for calcifications –– Adjacent lung

Fig. 3.17  An anterior shoulder dislocation. You can see the Hill-Sachs deformity of the posterior humeral head (arrow)

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was dislocated. Also good to know that the coracoid is always anterior. The coracoid is the lighthouse of the shoulder. It will guide you across rocky shoals. The posterior dislocation is associated with a reverse Hill-Sachs injury and fracture of the anterior humeral head. Check your work on the annotated images (Fig. 3.20a and b).

Greater Tuberosity Fracture Falls and fractures of the greater tuberosity of the humerus are common injuries and are often missed. If the fracture is associated with a humeral neck fracture, it is usually obvious, but isolated greater tuberosity fractures can difficult to spot. That is unless you look (Fig. 3.21)!

Key Point

Isolated greater tuberosity fractures can be sneaky and subtle. Make sure you scrutinize this area well. Sometimes all you will see is the slightest of cortical disruption or irregularity.

Scapula Fractures Fig. 3.18  An axillary view of the shoulder showing a large Hill-Sachs impaction injury of the posterior humeral head. The curved line approximates what the normal counter of the humeral head was before it got bashed in. The coracoid is anterior, a good landmark for orienting yourself. Make sure you can find it

a

Fig. 3.19 (a) Describe the injury. (b) Describe the injury

Scapula fractures are another injury, which can be overlooked. Look at Fig.  3.22a. What is the injury? Hopefully you see it. In real life, this injury was missed. Do better, and learn from the mistakes of others. b

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Shoulder

a

Fig. 3.20 (a) This is a Velpeau view, which is a modified axillary view. We orientate ourself with the coracoid (C) and can see the humeral head has dislocated anteriorly, and is perched on the lip of the anterior glenoid (arrow) causing the Hill-Sachs injury. (b) An axillary view with a posterior dislocation. Again, we orient ourself by finding

b

the coracoid (C) so we know which way is anterior. The humeral head has gone posterior and is perched on the posterior lip of the glenoid causing a large reverse Hill-­ Sachs impaction injury (arrow) of the anterior humeral head. You can see the displaced fracture fragment aligned with the glenoid

vicular and coracoclavicular spaces on a radiograph. You should just be able to eyeball an abnormal widening, but for those of who like measurements, a normal acromioclavicular distance is 5–8 mm and a normal coracoclavicular distance is 10–13 mm. Figure 3.23 shows injury to both ligaments with widening of both the acromioclavicular and coracoclavicular distances. Sometimes views of the asymptomatic side can be a useful internal comparison control for what is normal for that individual. Any asymmetry may indicate injury.

Stress Injuries of the Distal Clavicle Fig. 3.21  An isolated fracture of the greater tuberosity (arrows) All we see is slight cortical disruption from the fracture. There are even more subtle injuries than this example. Stay frosty!

Acromioclavicular Injury Another common injury, often not associated with any fracture. You can diagnose the ligament injuries based on the widening of the acromiocla-

Gunny is happy that you’re getting after it, but take things too far and you might end up with this injury. This is very common, especially in the demographic of those pushing hard at the gym. Over cranking those bench presses in middle age is the typical scenario, but any set of repetitive stress at the acromioclavicular joint can lead to a distal clavicular bone stress injury. Usually they will complain of focal pain at distal clavicle.

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a

b

Fig. 3.22 (a) Make the call! (b) A fracture (long arrow) at the base of the coracoid (C), which was missed. To confuse things, this patient was 14, and there is still an

unfused apophysis (short arrow) in the acromion (A), which could be mistaken for another fracture

Fig. 3.23  Ligamentous injury at the shoulder with widening and disruption of the acromioclavicular joint (AC bar) and widening of the coracoclavicular distance (CC bar). Both these ligaments are torn

Fig. 3.24  Typical appearance of a bone stress injury of the distal clavicle showing resorption and irregularity of the distal clavicle. There is no arthritis, and the acromion is normal

Often the early manifestations on radiograph are subtle and this is another diagnosis that is routinely over-looked. What you need to look for is subtle bone resorption, irregularity, and cyst formation in the distal clavicle, almost always with the absence of any degenerative arthritis on the other side of the joint (Fig. 3.24). On MRI, there will be focal edema in the distal clavicle, and at times, a small, but distinct fracture line (Fig. 3.25). Key Point

Distal clavicle stress injuries are commonly not picked up on the radiograph. Scrutinize this area, and look at the history, as this may help.

Fig. 3.25  MRI of a distal clavicular stress fracture in another gunner. There is marrow edema and irregularity of the distal clavicle with a small, but clear dark fracture line (arrow)

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Shoulder

Chronic Rotator Cuff Pathology Rotator cuff tendinopathy in the forms of tendinopathy and tears is an exceedingly common cause of shoulder pain. While radiographs will never be able to tell you exactly what is wrong with the cuff, we can certainly see that there are problems. We infer the chronic rotator cuff

pathology by observing irregularity at the tendon attachments on the tuberosities of the humerus (Fig.  3.26). This can take various forms: sclerosis, hypertrophy, and cyst formation. If you see this, you can say that there is chronic rotator cuff pathology. When the distance between the superior aspect of the humeral head and the undersurface of the acromion is significantly reduced, you can infer that there are actual tears, which allow the humeral head to ride higher than normal. Acute tears are better evaluated with MRI or ultrasound. On these modalities, we look for focal discontinuity in the tendons, often with a fluid filled gap. Figure 3.27a and b show more acute rotator cuff tears, with a full-thickness full-width tear of the supraspinatus tendon, with the torn tendon retracted to the joint line. There is also a full-­ thickness, full-width tear of the infraspinatus tendon.

Biceps Dislocation Fig. 3.26  Irregularity at the greater tuberosity indicating chronic rotator cuff pathology, although the exact extent of the injury cannot be determined on the radiograph

a

Fig. 3.27 (a) MRI showing a full-thickness full-width tear of the supraspinatus tendon. There is decreased acromiohumeral distance, with the humeral head articulating with the undersurface of the acromion. If you see this as a

Long head biceps dislocation requires MRI or ultrasound for an imaging diagnosis. This can be b

radiographic finding, you can infer that there must be a tear. (b) In the same patient, on the posterior coronal image, we see the full-thickness full-width infraspinatus tear, with the torn and retracted tendon

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another sneaky pitfall on MRI as the dislocated biceps tendon can look like the middle glenohumeral ligament. Make sure you follow the long head of the tendon all the way to its posterior labral attachment. When you see an empty bicipital groove, you should wonder where did that tendon go? Figure 3.28 shows a medially dislocated long head biceps tendon. Note that the bicipital groove is empty, the tendon should run in the groove. This injury is invariably associated with tears of the subscapularis tendon, as some of its fibers run over the biceps tendon, and help to stabilize it within the groove.

Sternum and Sternoclavicular Joints Dislocation at the sternoclavicular joint usually requires significant trauma. This can be very difficult to detect on radiographs and usually requires a CT or MR for full evaluation. Anterior dislocation at the joint is more common and less serious than posterior dislocation. Posterior dislocation can be associated with mediastinal or vascular injury. Medial clavicular fractures are also often overlooked and hard to find on radiographs. Evaluation of the sternoclavicular joints, is better accomplished with CT. Figure 3.29a and b showing a chronic anterior dislocation of the right medial clavicle at the sternoclavicular joint. If you are astute, you will pick up the finding on the radiograph showing sternoclavicular joints which are not symmetric, and the right medial clavicle is superiorly subluxed compared to the left. On CT, the diagnosis should be clear.

Key Point

Fig. 3.28  The long head biceps tendon is dislocated medially (long arrow) It is also not a normal tendon as there is some high signal/tearing within the tendon. The bicipital groove (short arrow) is empty

a

Medial clavicular injuries and sternoclavicular dislocation often require a CT or MRI for adequate diagnosis. These injuries can be hard to see on radiographs.

b

Fig. 3.29 (a) The eagle-eyed observer will detect the asymmetry of the right medial clavicle (arrow). (b) CT scan of the same individual where the anterior dislocation

at the right sternoclavicular joint is now clear. This is an old injury, and there are small old fracture fragments posterior to the right medial clavicle

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Elbow

Ribs

Elbow

Everyone wants to know if they have a rib fracture. It is a painful injury. Radiographs for evaluating rib fractures are notoriously suboptimal, and small fracture can be very difficult to detect. Bigger and severely displaced rib fractures are easier to find. Make sure you look for any associated pneumothorax. Subtle secondary signs such as a pleural effusion, lung contusion or subcutaneous emphysema can be clues that there is a fracture. Look at Fig. 3.30. Can you see the small lateral rib fractures? The pleural effusion and emphysema along the chest wall should make you alert.

When assessing an elbow radiograph for injury, first look for an effusion. The presence of an effusion should make you paranoid that the injury is significant and there may well be a fracture. In the absence of an effusion, it is unlikely that there is an acute fracture. Take a look at Fig. 3.31a. Hopefully you picked up on the big effusion not only on your own, but because we also added helpful arrows. The effusion causes displacement of the anterior and posterior fat pads, which are semi-mobile focal areas of fat which live in the coronal and olecranon fossae. The fluid displaces the fat pad, which allows us to better see or infer an effusion on the radiographs. When you see an effusion this big, keep your head on a swivel. In trauma, there is likely a fracture. Look at Fig. 3.31b. Same patient, PA view. Do you see the subtle cortical step-off of the radial neck? That’s it. That’s all you get. That’s the fracture. Easy to miss if you weren’t alerted by the presence of an effusion. Even if you don’t see a fracture, with an effusion in the setting of trauma it is probably wise to say that there may be an occult radial head or neck fracture. A good bet in adults. In kids, the fracture is more likely to be an occult condylar or supracondylar fracture Figs. 3.32a and b.

Key Point

Look for secondary signs of chest wall injury such as pleural effusion, soft tissue emphysema, or a pneumothorax to alert you to the presence of rib fractures.

Key Point

Elbow effusion in the setting of trauma is a red flag. There is a fracture!

The Terrible Triad

Fig. 3.30  We see a small pleural effusion and emphysema along the lateral chest wall. See if you can spot the fractures

Sounds terrible. Is terrible. The terrible triad is a common elbow injury pattern that has three main components.

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a

b

Fig. 3.31 (a) Big effusion, helpfully outlined by the displaced anterior and posterior fat pads, and of course the arrows. (b) AP view of the same elbow showing the subtle radial neck fracture (arrow) Fig. 3.32 (a) A 10 year old who didn’t tap out it time. See the effusion? Something is definitely wrong with the elbow. (b) On this view, you can see the trans condylar fracture

a

• Dislocation (posterior and lateral) • Radial head fracture • Coronoid process fracture

b

cess fractures. Look for them. Often a CT is needed for better characterization and is also obtained for preoperative planning. Figures 3.33a and b show a typical example. It is hard to tell what fracture fragments come from where, but now you are armed with the knowledge that one is radial head and one is coronoid.

Bad injury because once you break Humpty Dumpty, it is hard to put him back together again. As you can imagine just about every ligament at the elbow gets torn with this injury. The patient often ends up with decreased mobility and post-­ traumatic arthritis.  lecranon Fracture O The dislocation should be obvious, it is helpful to know that the two fractures associated with These are not any problem to identify, but just this injury are the radial head and coronoid pro- know that they exist and are common injuries. In

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Elbow

a

b

Fig. 3.33 (a) Terrible! There is posterior dislocation. The displaced fracture fragments are from the coronoid process (c) and radial head (r). (b) Another view, harder to

make sense of the fractures, but you can see the fracture deformity of the radial head well, and with the orthogonal view know that the dislocation is posterior and lateral

Fig. 3.34 Olecranon fracture, a back of the room diagnosis

Fig. 3.35  A displaced fracture of the capitellum (arrow). This is a less common injury so it is good that you have seen it. Note the effusion

this example, from a direct fall onto the elbow (Fig. 3.34).

Capitellum Fracture This is a less common injury, but one that is likely going to surgery if there is any significant dis-

placement. It is an intra-articular injury so we will see a joint effusion associated with it, and as we know the joint effusion is the sign that something has been injured in the elbow. Figure 3.35 is a typical example of a displaced capitellar fracture, guaranteeing a visit from your friendly orthopedic surgeon.

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Tendon Injuries The goal with this manual is not to provide a complete guide to tendon and ligamentous injuries, but there are times when an MRI may be ordered by an ER doc who really wants to know about a biceps tear at zero dark thirty. So here are two of the more common injuries you might be asked to evaluate. You’re going to need some anatomical knowledge of where things are on MRI, which you can easily look up. The quick and dirty guide to diagnosing these injuries on MRI is to look for a focal gap or discontinuity in the struc-

a

ture, usually associated with surrounding fluid or edema. Bright is bad! Find the bright to stay in the fight.

Biceps Tendon Tear The biceps tendon attaches at the radial tuberosity. Tears can be partial or complete with proximal retraction of the torn tendon. In the acute setting (Fig. 3.36a–c), this is usually pretty easy to see with fluid and edema along the course of the tendon and often with some edema in the muscle belly at the myotendinous junction.

b

c

Fig. 3.36 (a) An acute tear of the biceps tendon (arrow). We are at the level just distal to the myotendinous junction. There is fluid and edema around the tendon and bright edema within the tendon. (b) A little more distal with fluid surrounding the biceps tendon. (c) At the radial

tuberosity insertion, there are still portions of the tendon attaching on the radial tuberosity, but we can see the focal tear just proximal to its insertion (arrow). Even the remnant inserting fibers are abnormal with edema and irregularity

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Forearm

a

b

Fig. 3.37 (a) Completely torn and avulsed common extensor tendon (arrow) with adjacent fluid. (b) The axial image showing the same injury

Common Extensor/Flexor Tendon Tear The common extensor tendon originates from the lateral humeral epicondyle, the common flexor tendon comes from the medial humeral epicondyle. There may a partial or complete tears. Look for focal discontinuity and disruption of the fibers and surrounding edema and fluid in the more acute setting. Figure  3.37a and b show a complete avulsion of the common extensor tendon with the torn fibers displaced along the lateral elbow and a prominent associated fluid pocket. Although outside the scope of this manual, the ligaments along the lateral elbow, which have a close association with the tendon, are also going to be torn. A tear of the common flexor tendon would look similar, just on the medial side.

Forearm The main point to keep in mind about forearm injuries and fractures is that there may be an associated dislocation, either at the wrist or at the elbow. So don’t get cocky just because you found the fracture, make sure you look for any disruption or dislocation at the elbow or wrist. Sometimes this is pretty obvious, other times it can be more subtle, especially disruption at the distal radial ulnar joint.

Fig. 3.38 Displaced fractures of the proximal ulna, which are associated with a dislocation of the radial head. On this lateral view, you can see that there is the loss of the normal articulation between the radial head and the capitellum. This will require surgery

Monteggia Fracture This is a fracture of the proximal ulna associated with a dislocation of the radial head at the elbow. This is a more common injury in kids, but as we see in this case (Fig. 3.38) it can occur in adults.

Key Point

If there is a forearm fracture, look for an associated dislocation at the elbow or wrist.

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32 Fig. 3.39 (a) Fractures of the distal radius and distal ulna associated with dislocation at the distal radial ulnar joint. (b) The lateral view which shows both the degree of displacement of the fractures and associated distal radial ulnar joint disruption

a

Galeazzi Fracture Another fracture dislocation pattern in the forearm. In this setting, there is a distal radial fracture and associated with a disruption or dislocation at the distal radial ulnar joint. This disruption at the distal radial ulnar joint can be more subtle and can be missed. If you see the distal radial fracture, make sure you take a moment to go through your checklist and look at the distal radial ulnar joint. Figure 3.39a and b show a version of this injury. In this case, there is also a fracture of the distal ulna in addition to the distal radial fracture. Which just goes to show that many injuries and diagnosis don’t fit in the nice little boxes and names we create for them, and real life is more complex and messy than textbooks suggest, adapt, and overcome.

Wrist You will encounter many wrist injuries. Fractures of the distal radius, often accompanied by a fracture of the ulnar styloid process are very com-

b

mon. Many of these injuries are obvious and don’t present any diagnostic challenge, but some are more subtle and challenging.

Triquetral Fracture If you don’t know where to look, or what to look for, then you will miss this injury. Triquetral fractures are relatively common and usually the result of a fall. You need to look along the dorsal aspect of the wrist, and they are often only apparent on the lateral view of the wrist. Another reminder, why more than one radiographic view is needed for the proper evaluation of trauma. The displaced dorsal fragment may range from a small speck of bone to larger and more multiple fragments (Fig. 3.40).

Key Point

Look at the dorsal wrist on the lateral view to diagnosis triquetral fractures.

Wrist

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Fig. 3.41  Navicular view of the wrist shows the small mid scaphoid fracture (arrow). Make it your duty to ensure this view is obtained whenever possible

Key Point

A good dedicated navicular view is required to adequately assess for scaphoid injury.

Fig. 3.40  A typical appearance of a triquetral fracture (arrow), which is almost always along the dorsum of the wrist

Scaphoid Fracture Another common injury, usually the result of a fall. Scaphoid fractures come with the potential pitfall that they can be missed or occult on initial radiographic evaluation. One factor that is critical for evaluation of scaphoid injuries is obtaining a good scaphoid/navicular view with the radiographic series. Any suspicion for a scaphoid fracture must have a dedicated scaphoid view. It is perilous to proceed without it. Insist that this additional view is obtained. Even with a complete set of radiographic images, the fracture may still be occult. Evaluation with MRI is required for definitive diagnosis, although often the patient is splinted and treated as if they have a fracture with ­short-­term follow-up imaging to look for signs of the injury as the fracture heals. Accurate diagnosis is important to avoid the risks of osteonecrosis and non-union.

Figure 3.41 shows a typical scaphoid fracture. This is a more subtle example. Figure 3.42 shows the importance of a dedicated navicular view. The image on the left is the standard PA view. Do you see the fracture? If you do, then put down this manual and apply for a change of MOS to sniper school. The fracture is crystal clear on the right with the proper navicular view. You need the navicular view. Figure 3.43 shows what happens when this diagnosis is missed. The mid scaphoid fracture has not healed and is non-united. Additionally, there is the suggestion of osteonecrosis in the proximal pole of the scaphoid which is more sclerotic than the other portion of the bone. Not a good sign.

Distal Radial Fractures Fracture of the distal radius is extremely common. The big displaced ones are obvious to everyone, and your special skills are not required. The more subtle injuries are where you get to stand up and shine. As common as these injuries are, it is also common that they are missed.

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Fig. 3.42  Standard PA view on the left and navicular view on the right. The mid scaphoid fracture is immediately clear on the navicular view, but a very hard diagnosis to make on the PA view

Often the lateral view of the wrist is key in making the diagnosis, as you might be able to pick up on a slight cortical discontinuity or displacement of the dorsal aspect of the distal radius. Look at Fig. 3.45. The distal radial fracture was not clear on the other views. Only on this lateral view, do we see a slight cortical break along the dorsal aspect of the distal radius. This is a subtle finding. Some findings are obvious, not this one. You have to be focused and know where to look in order to make the diagnosis.

Fig. 3.43  Not what we want to see. An old un-united fracture of the mid-scaphoid. There is some sclerosis in the proximal scaphoid pole suggesting osteonecrosis

There are of course classification systems and eponyms of these fractures, but for day-to-day practice, it is not necessary that you know them. They can be easily looked up if needed. As long as you can see and describe the fracture and any associated injuries, then you are good to go. Figure 3.44a and b show a distal radial fracture that was missed on the initial radiographic assessment. We all make mistakes, and we all miss fractures. But learn from your mistakes and even better learn from the mistakes of others.

Key Point

Often the lateral view of the wrist is key to finding subtle distal radial fracture. Look for slight displacement or cortical irregularity of the distal radius.

Pisiform Fracture Fractures of the pisiform are not common, but you may encounter them and it is good to know about them so you can make the diagnosis when called upon. These are usually the result of the fall. They can be difficult to detect on radiographs.

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Wrist

a

b

Fig. 3.44 (a) A distal radial fracture (arrow) that is more subtle and that was missed. (b) The lateral view showing the slight cortical break and dorsal displacement from the fracture

Fig. 3.45  This distal radial fracture was only visible on the lateral view where there is a very subtle cortical break (arrow). Fortunately an eagle-eyed cadet spotted it

This pisiform fracture (Fig. 3.46) is subtle, but apparent on the PA view. But, this is not always the case. Sometimes oblique views (Fig. 3.47) are helpful in seeing the pisiform better, as it is often overlapping with the adjacent carpal bones making fracture detection difficult.

Fig. 3.46  This pisiform fracture is camouflaged, with the fracture line paralleling the ulnar contour of the bone (arrow). Nonetheless, it is a finding you can see

Hamate Fracture Hamate fractures are very difficult to detect on radiographs and often a CT or MRI is required.

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Fig. 3.47  This oblique view nicely brings the pisiform to fore and shows the fracture (arrow) clearly. This was obscured on the other views

Fig. 3.49  Dislocation at the first carpal metacarpal joint. An uncommon injury, and one that you might not initially notice

Carpal Metacarpal Dislocation

Fig. 3.48  A hamate fracture (arrow) that is subtle and could easily be overlooked, especially with the distractor of the ulna styloid process fracture, which may cause you to shut down further search

But don’t give up the ship. You can still find them. It will help if there is a focal clinical concern and exam from the ordering provider, which can help to guide you to look at a location that you might otherwise neglect. Figure 3.48 shows a subtle but discrete fracture along the ulnar aspect of the hamate.

Dislocations at the carpal metacarpal articulations are hard to do, but there are some very determined individuals out there, so it is something that may cross your radar. They can be difficult to spot, because often the dislocation is subtle (Fig. 3.49). There tends to be an association with fractures, so that is something that might help you with the diagnosis. The oblique or lateral views will be key in making the diagnosis as any step off or mal-alignment might not be clear on the PA view. Dislocations at the bases of the fifth and fourth metacarpals tend to be associated with punching walls or other hard inanimate objects.

Stress Fracture Not all trauma is acute. Most stress fractures and bone stress injuries occur in the lower extremi-

Wrist

ties, but one type of athlete is prone to developing them at the wrist.

Gymnasts Adolescent gymnasts can get overuse injuries, bone stress injuries, and stress fracture in their wrists, which occur at the physis. This injury might not be obvious if you don’t know what you looking for. History is going to be extremely helpful in making this diagnosis. There won’t be a discrete fracture line, but what you need to look for is sclerosis and irregularity across the physis of the distal radius (Fig. 3.50). This is the bone around the physis reacting to the stress. On MRI, the injury will be more apparent with prominent edema in the bone.

Carpal Dislocations Dislocation of the carpal bones requires a substantial amount of kinetic energy. These are not an everyday injury, but they are a very serious

Fig. 3.50  A 13-year-old girl. There is abnormal sclerosis and cystic formation spanning the physis of the distal radius, which is telling you that this gymnast has been going at it a bit too hard

37

injury and are surprisingly often not recognized. This is unfortunate as these injuries require reduction and intervention, usually surgical. The lateral view is a key image in diagnosing these injuries, as it will show the extent of the dislocation, which will not be clear on the PA view. The PA view is still an important view. It is often the view we look at first. On this view, we need to evaluate the carpal arcs. In 1977, Dr. Louis Gilula described a method for detecting carpal injuries by evaluating the three carpal arcs. It is worth quoting the eloquent opening statement from his paper. Use of these three normal arcs, joint parallelism and symmetry, overlapping articular surfaces, and other related principles can enable accurate and complete diagnosis. Inaccurate or incomplete diagnoses may result in unnecessary disability. —Louis A. Gilula Carpal Injuries: Analytic Approach and Case Exercises

We cannot match his brevity and skill in evaluating and describing carpal injuries, for that we suggest you read his paper. Our attempt follows. On a frontal (PA) radiograph, the eight carpal bones create a pleasing row of arcs, which should nicely follow the cortical contours of the carpus. Figure 3.51 shows the three carpal arcs. The most proximal carpal arc parallels the cortices of the triquetral, lunate, and scaphoid bones.

Fig. 3.51  The three carpal arcs from proximal to distal

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The mid carpal arc follows the distal cortices of these bones. The third and most distal arcs trace the proximal cortices of the hamate and capitate bones. When glancing at these arcs, look for any step off, disruption or irregularity that breaks the natural curve of the arc. If there is, there is a problem. Key Point

Evaluate the carpal arcs on every PA wrist radiograph to find carpal mal-alignment.

Carpal injuries usually follow a pattern of injury with one particular injury occurring step by step after the next. In general, we can think of the dislocations in two main categories: perilunate dislocations and lunate dislocations, with a third in-between category of a midcarpal dislocation. Perilunate dislocation in which the lunate retains its normal alignment with the distal

a

radius and the other carpal bones are dislocated in relation to the lunate. This is usually in the dorsal direction. Midcarpal dislocation. In this instance, neither the lunate or capitate are normally aligned with the distal radius. This is an injury pattern the lies between a perilunate and lunate dislocation. Lunate dislocation in which the lunate is dislocated and displaced from its normal alignment with the radius. This usually occurs in the volar direction when the lunate is displaced into the carpal tunnel, although it can less commonly dislocated dorsally. Lunate dislocations are more severe in that they involve the tearing of more carpal ligaments than in a perilunate dislocation. Carpal dislocations are often associated with fractures and when describing the dislocation, make sure to mention and describe any associated fractures. Figure 3.52a is a perilunate dislocation. The lateral view is going to be our go-to view to show us how the bones are dislocated. The dramatic

b

Fig. 3.52 (a) The lateral view which shows the normal articulation between the lunate and radius but dorsal displacement of the capitate and scaphoid bones. (b) The PA

view. Those carpal arcs are about as disrupted as they are ever going to get

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Wrist

disruption on the PA view (Fig. 3.52b) shows us that things have really gone sideways. Although not present in this case, make sure you look for any associated fractures. A trans-scaphoid perilunate dislocation (Fig.  3.53a and b) is where the force vectors travel through the mid scaphoid causing a fracture. The lunate remains articulating with the distal radius while the capitate and the distal scaphoid fragment are displaced dorsally. a

Figure 3.54a and b showing a midcarpal dislocation in which the lunate is subluxed volarly and the capitate subluxed dorsally, but neither bone is completely dislocated. In this case, there is an associated fracture of the triquetrum. A clear lunate dislocation is apparent on Fig. 3.55 with the lunate dislocated and displaced volarly. The lunate is forced into the carpal tunnel, which can cause injury to the median nerve. The capitate is normally aligned with the distal radius.

b

Fig. 3.53 (a) The lateral view showing the trans-­scaphoid fracture and perilunate dislocation. The proximal pole of the scaphoid (PS) remains articulating with the lunate (L), whereas the distal pole of the scaphoid (DS) has dislo-

cated dorsally following the capitate (C). (b) The PA view. The carpal arcs are chaotic. There is a displaced fracture through the mid scaphoid (arrow)

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a

b

Fig. 3.54 (a) A midcarpal dislocation, an injury between a perilunate and lunate dislocation. The lunate is subluxed volarly, and the capitate is subluxed dorsally. (b) The PA view showing the now familiar disruption of the carpal

arcs and a small triquetral fracture (arrow), there is an additional small fracture fragment along the proximal capitate

Hand As a reminder proper evaluation of a bone or joint requires at least two individual orthogonal views. Take a look at Fig. 3.56a. Does anything stand out? Do you see the fracture? If you were to call this view normal, it would be hard to fault you. But as soon as you look at the accompanying lateral view (Fig.  3.56b), the fractures are instantly identifiable. A nice illustration of the importance and necessity of orthogonal views. Some fracture will simply not be visible in one view, but clear and present on the other.

Metacarpal Fractures

Fig. 3.55  The lunate is dislocated and displaced volarly

Punch the wall and the wall wins. The wall always wins. Fractures of the fifth and to a lesser degree fourth metacarpals related to an impact injury are exceedingly common and usually obvious (Fig.  3.57). They are often associated with

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Hand

Fig. 3.56 (a) Very difficult to see where the injuries are. (b) On the lateral view, the fractures at the dorsal bases of the fourth and fifth distal phalangeal bones are now easily visible

a

b

angulation, which should be described. What may not be as obvious are fractures at the ­metacarpal bases. These are often trickier to spot and may elude detection on initial evaluation (Fig.  3.58a and b). And remember, don’t punch the walls. Save it for the enemy!

Key Point

Look at the bases of the fourth and fifth metacarpals which may be concurrent with or independent off a distal metacarpal fracture.

Phalangeal Injuries

Fig. 3.57  A typical distal 5th metacarpal fracture, boxer’s fracture as it is sometimes called

A few of the more common injuries you might see that have a higher percentage of going undetected. Figure 3.59a and b show a fracture at the base of the fifth proximal phalanx, which is a relative common place to break a bone after a fall on your hand. These are easily missed. Trust us on this one.

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a

b

Fig. 3.58 (a) The fracture at the base of the fourth metacarpal is more subtle. Can you see it? Remember to pay particular attention to the metacarpal bases as this is a common miss. (b) In this case, it is more obvious on the oblique view Fig. 3.59 (a) Fracture at the proximal aspect of the fifth proximal phalanx. Subtle on this view, where you can see some slight impaction and a subtle fracture line. (b) The fracture is more obvious on this oblique view. There is impaction and angulation, which makes it easier to spot, but this is not always present

a

Volar plate avulsion fractures are also common and are often overlooked. Sometimes all you get is a tiny fleck of bone at the volar base of the

b

middle phalanx (Fig. 3.60). The bigger the fragment, the easier it is to detect. Make use of any mag or zoom functions that are available.

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Hand

Fig. 3.60  A tiny sliver of bone at the site of the volar plate avulsion injury

Dislocations occur. These are usually not a problem to identify (Fig. 3.61), but the extent of the dislocation can be masked on a single view. Make sure to look for any associated fractures.

 humb Ulnar Collateral Ligament T Injury Often from sports-related trauma, the prototypical injury is associated with skiing. You can simply have a ligamentous injury which will likely not be apparent on the radiograph, the fractures are associated with avulsion at the ulnar base of the proximal phalanx. A Stener lesion is a potential complication in which the torn and displaced ulnar collateral ligament are trapped superficial to the adductor aponeurosis. This is something that needs to be evaluated with MRI or US (Fig. 3.62).

Ultrasound Ultrasound is a superb tool for quick and accurate assessment of musculoskeletal injury. It is quick,

Fig. 3.61  Dorsal dislocation at the PIP joint. There is no associated fracture here, but make sure you look

usually readily available and often the site of injury is very superficial, which allows the probe to be placed directly over the area of concern with excellent image resolution. An entire manual could be devoted to ultrasound evaluation, and the scope is large for us to fully address. We offer two straight forward examples of injuries that might be asked about in an urgent care or emergency room setting.

Foreign Bodies Ultrasound is an excellent tool and often the best modality for detecting and evaluating foreign bodies, especially when they are more superficial as in the extremities. While metallic and other denser bodies will show up on a radiograph, many biological and other material may not be evident on a radiograph. But ultrasound sees all. All foreign bodies look alike on ultrasound, irrespective of their origin. Wood splinters, metal,

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Fig. 3.63  A large glass shard in the thenar aspect of the hand. The body is echogenic with a darker surrounding halo, which in the more acute setting is often hemorrhage, but in the chronic setting reflects surrounding granulation tissue

Fig. 3.62  Avulsion fracture at the ulnar base of the first proximal phalanx

sea urchin spines they will all look like an echogenic structure. Their morphology is obviously dependent on the shape of the body. Figure 3.63 is a large glass shard embedded in the thenar region. Over time a rim of hypoechoic granulation tissue will form around the body.

Tendon Laceration/Tear Injuries to the tendons in the hand are easily detectable on ultrasound. Once you know what a normal tendon looks like all you need to do is look for a defect or gap within the tendon. The tendons are very superficial and the probe is often only a few millimeters from the tendon, allowing extent spatial resolution. Figure 3.64 shows a full-thickness laceration of the flexor tendons caused by a blade injury. Normal tendons are slightly echogenic and have a linear internal architecture on long axis images.

Fig. 3.64  showing the laceration of the flexor tendons (bar) just proximal to the MCP joint. The normal tendons proximal and distal to the injury are outlined by the arrows

A defect or tear is hypoechoic with disruption and discontinuity in the normal tendon fibers.

Pelvis and Hips Injuries to the pelvis and hips are usually serious and often the result of substantial injury. Some types of injuries will necessitate surgical management, and some can be managed without. It is good to know the general management for specific injuries so if necessary you can help guide management and get orthopedic surgical involvement if needed. As a general guideline: –– Fractures of the femoral neck, intertrochanteric and subtrochanteric femur are managed with surgery.

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Pelvis and Hips

–– Smaller fractures of the pelvic ring and obturator rings can be managed conservatively –– Isolated greater trochanteric fractures (without intertrochanteric extension) can be managed conservatively.

Fig. 3.65  This may be called normal

Fig. 3.66 (a) There is marrow edema in the intertrochanteric femur. The fracture line is more discrete on the accompanying T1-weighted image. (b) T1 dark fracture line is clear (arrow) extending throughout the intertrochanteric femur

a

Proximal Femoral Fractures Fractures of the proximal femur rank among the most serious. The morbidity and mortality, ­especially in older patients are high. Often you are evaluating older patients with osteopenia. The osteopenia makes a fracture more likely and can obscure smaller fractures on the radiograph making detecting hip fractures difficult, or not possible. Less conspicuous, but still significant fractures can be undetectable on radiographic evaluation and require MR or CT to diagnose. Look at Fig. 3.65. Do you see a fracture? It is extremely difficult to prospectively say that there is a fracture here, yet there is. When the astute radiologist recommends an MRI, we can now distinctly see the injury. The marrow edema in the intertrochanteric femur is from the injury (Fig.  3.66a). The distinct fracture line is better imaged on the T1-weighted image (Fig.  3.66b). Without MRI, this fracture would have gone undedicated. MR is superior to CT in the detection of fractures, although if all that it is available is CT, then it will be preferable to the radiographs, with the caveat that some fractures will also be occult on the CT. If you don’t see a fracture on the radiograph, yet there is a high or persistent clinical concern for a fracture, then an MRI or at least a CT should be obtained. Warning signs are severe pain and b

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the inability to weight bear and ambulate. This is especially true with older patients, and those with osteopenic bones. Not all fractures are so sneaky, and often they are obvious.

Intertrochanteric fractures are common injuries (Fig. 3.67). These are almost always treated with surgery, although there are exceptions, for example, in patients who are not walking. Femoral neck fractures are also common, and another injury that is usually treated with surgical fixation. The femoral neck fracture on the radiograph in Fig. 3.68a is subtle, but detectable as well see impaction of the femoral neck and cortical irregularity. The fracture line is more conspicuous on the CT (Fig. 3.68b). Isolated greater trochanteric fractures, Key Point

Any high clinical concern for a femur fracture should go to MRI.

Fig. 3.67  A typical intertrochanteric femur with impaction and varus angulation

a

without intertrochanteric extension can be treated non-operatively (Fig.  3.69). These are lower kinetic energy injuries, typically from a fall. The fractures can be subtle. Often a CT or MRI is obtained for determining if there is any intertrochanteric extension not apparent on the radio-

b

Fig. 3.68 (a) A subtle femoral neck fracture on the radiograph. The slight impaction should alert you to the injury. When in doubt, call for reinforcements. (b) The femoral

neck fracture (arrows) is still subtle but more clearly defined on the CT

Pelvis and Hips

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Fig. 3.70  A destructive lytic bone metastasis (arrow) associated with an isolated fracture of the lesser trochanter

Fig. 3.69  An isolated fracture of the greater trochanter (arrow). This is a more subtle version

graphs. This information would change management. Isolated fractures of the lesser trochanter are a completely different beast. When you see an isolated avulsion fracture of the lesser trochanter in an adult, you should immediately be on guard. This is not a normal injury and is a pathological fracture, probably from a bone metastasis, although other lesions are possible. Even if you don’t see a bone lesion associated with the ­avulsion injury, there will be one there if you look hard enough—get a CT or MRI. Kids, however, are allowed to have isolated lesser trochanteric avulsion injuries without an associated bone lesion. But remember in adults you need to raise the alarm. Key Point

Isolated lesser trochanteric avulsion injuries in an adult are pathological fractures.

In Fig. 3.70, we see an isolated avulsion fracture of the lesser trochanter. In this case, the adja-

cent lytic metastatic bone lesion should be obvious, but often you will not see a discrete lesion on the radiographs. Figure 3.71 shows an isolated lesser trochanteric avulsion injury in a 14-year-old soccer player. In children and adolescents, this injury is no cause for alarm, and will heal. Femoral stress fractures are often not perceptible on radiographs, at least in the early or initial stages. These require MRI for accurate diagnosis. History will be of great help in diagnosing these injuries, which are usually found in younger athletes, especially runners. The medial femoral neck is where you need to look. If you are to detect it on radiograph look for subtle sclerosis of the bone, periosteal reaction, and/or conical thickening. In rare instances, you may see a discrete cortical fracture line. On MRI, look for cortical and or medullary edema and periosteal edema. If there is a distinct fracture line, then this should be apparent as a thin black line. In this recruit (Fig. 3.72a), we see the typical marrow edema in the medial femoral neck, with a very early transversely oriented fracture line. On the follow-up radiographs several weeks later (Fig. 3.72b), you can actually see the signs of the bone stress injury, although if you didn’t know to

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look closely in the femoral neck, you would probably miss it.

Atypical Femur Fracture Key Points

Fig. 3.71  An isolated lesser trochanteric avulsion injury, in this 14-year-old girl from soccer, not cancer

a

–– They are often bilateral. If you find one, you must look at the contralateral femur. –– Often they are subtle findings only with some slight cortical thickening or periosteal reaction along the lateral femoral cortex. Stay alert and suspicious. –– They can occur anywhere along the lateral cortex of the subtrochanteric femur, but are more common proximally. –– A subtrochanteric femur fracture which occurs in the setting of minimal trauma should prompt you to think that it was related to bisphosphonate use. In these situations, make sure you check the other femur for an impending fracture. –– These are commonly missed, and when do lead to a later catastrophic fracture. Look carefully along the lateral subtrochanteric femur for the early subtle findings!

b

Fig. 3.72 (a) Femoral neck stress fracture. Typical location in the medial femoral neck with a geographic area of marrow edema centered around a small transverse dark fracture line along the medial cortex (arrow). (b) The follow radiographs weeks later. The stress fracture is now

apparent with healing sclerosis in the medial femoral neck and a linear cortical lucency at the site of the fracture. Subtle but symmetry is your friend—the other side is normal. Knowing where to look for stress fractures is important

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Pelvis and Hips

Atypical femoral fractures rank as one of the more subtle and insidious findings, which are easily overlooked and if not noticed can lead to

Fig. 3.73  Cortical thickening and sclerosis along the lateral margin of the subtrochanteric femur. This is an impending fracture, there is even an early discrete transverse fracture line (arrow). Pick up the phone and call this result in before it gets worse

a

b

Fig. 3.74 (a) Impending fracture manifested by only slight cortical thickening (arrow). Fortunately detected by an astute observer. (b) MRI confirmation of the finding showing edema and cortical thickening along the subtro-

catastrophic femur fractures. These fractures are the result of long-term bisphosphonate use, and usually in older women. Long-term bisphosphonate use can cause weakening of the subtrochanteric femur along the lateral cortex, which causes pain and if not treated can result in a catastrophic subtrochanteric femur fracture. If detected earlier, they are usually treated with prophylactic fixation to prevent a fracture. Figure 3.73 is a typical of an atypical femur fracture. There is focal cortical thickening and periosteal reaction in the key location along the lateral femoral cortex. Contrast this to the stress fractures which occur along the medial femoral cortex. The last example is not particularly subtle and should be observed and interpreted correctly. Figure 3.74a shows a far more insidious example. There is only slight cortical thickening along the lateral subtrochanteric femur. This finding was initially missed and was only detected by a teammate who was more attuned to the finding. The MRI (Fig. 3.74b) confirmed the finding. There is marrow edema at the site of impending fracture, adjacent to which is the cortical thickening visible on the radiograph. Figure  3.74c shows the prophylactic intramedullary nail that was placed to prevent a catastrophic fracture. This radioc

chanteric lateral femur. (c) Three months after treatment with an intramedullary nail. the fracture line (arrow) is more discrete

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graph is 3 months from the initial evaluation, and the cortical thickening is more conspicuous and now has a discrete fracture. Figure 3.75a shows what we want to prevent. A displaced subtrochanteric femur fracture with varus deformity. If you see this injury, especially in the setting of minimal trauma, then immediately think that this is an atypical femur fracture and reflexively evaluate the contralateral femur for an impending injury. In this case, the well-trained reader did exactly that and found the injury in the left femur (Fig. 3.75b). The injury was more distal down the femur than is common—a reminder that these injuries can occur anywhere along the subtrochanteric femur. Evaluating only the proximal aspect of the femur is inadequate. a

Fig. 3.75 (a) Catastrophe! A subtrochanteric femur fracture with varus deformity. Associate this pattern as being an atypical femur fracture caused by chronic bisphosphonate use. (b) The contralateral injury is more distally

Sacral Insufficiency Fractures Another injury seen in older individuals and associated with osteopenia. Often caused by minimal trauma. These injuries are almost undetectable on radiographs and will need a CT or MR for accurate diagnosis. Typically, the fractures involve one or both of the sacral alae. The fractures are vertically oriented fracture through the sacrum and may have an associated transverse component extending across the sacrum. There is usually no interventional treatment. Figure 3.76a and b show a typical sacral insufficiency fracture with fracture lines through both sacral alae. The fractures were not apparent on the radiograph.

b

located than normal and is also more subtle. There is focal cortical thickening, sclerosis, and an early fracture line (arrow). This was treated with a prophylactic intramedullary nail

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Pelvis and Hips

a

b

Fig. 3.76 (a) Bilateral insufficiency fractures in the sacrum (arrows). (b) On the axial plane we see the sacral alae fractures (arrows) and can also appreciate more subtle transfers fractures extending across the sacrum

Pelvic and Obturator Ring Fractures Pelvic and obturator ring fractures can either be the result of a high impact injury or lower kinetic fall type injuries. The large dramatic displaced fractures are usually the result of major trauma and are easily recognizable, although it is important to evaluate the whole pelvis, as there is often more than one injury and make sure you observe any additional fractures or associated diastasis or dislocation. Figure 3.77 shows fractures of the left obturator ring, which are typical of injuries sustained in a fall or lower impact energy, usually in older individuals. The site of these fractures is common and repeatable. We see a fracture at the left pubic root, and an associated fracture of the left inferior obturator ring. Additionally, there is a fracture of the right parasymphseal pubic bone. These fractures are subacute, so the callus makes them easier to see, but as you can imagine more acutely, they may just be subtle cortical breaks. To detect them you need to run your eye along the cortical lines that make up the pelvis. Children and adolescents are prone to pelvic avulsion injuries. The two more common sites are at the anterior superior iliac spine and at the anterior inferior iliac spine. These are often smaller injuries, which can be overlooked.

Fig. 3.77  Fractures of the left pubic root (long arrow), left inferior obturator ring (medium arrow), and right parasymphseal pubic bone (short arrow). Typical pelvic fractures after a fall in an older individual. These fractures are subacute

Key Point

Pelvic fractures are usually not isolated injuries. Look for other fractures or diastasis.

An avulsion fracture at the anterior superior iliac spine occurs at the attachment of the sartorius and tensor fascia lata muscles. This injury is usually found in adolescent athletes and is not a common adult injury. Figure 3.78 shows a typical example with avulsed bone fragment off of the anterior superior iliac spine.

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Avulsion fractures of the anterior inferior iliac spine are also seen in adolescent or young athletes. In this case, the avulsion is at the origin of the rectus femoris muscle. Figure 3.79a is an example. The injury is on the left and may be hard to detect. In these cases, symmetry is your friend and evaluation of the normal right side in comparison to the injured left side will help to make the injury more obvious.

The MRI (Fig.  3.79b) makes the avulsion fracture more obvious and nicely shows that the injury as occurred at the tendinous origin of the rectus femoris.

Fig. 3.78  An avulsion fracture of the anterior superior iliac spine

Fig. 3.80  Prominent diastasis at the pubic symphysis. Be sure to be alert for other associated pelvic injuries

a

Diastasis and Dislocations Diastasis at the pubic symphysis can occur in isolation or associated with other pelvic injures. Diastasis at the sacroiliac joints is usually associated with other pelvic injuries. In both cases, make sure you carefully scrutinize the pelvis for fractures or other areas of diastasis. Figure 3.80 shows diastasis at the pubic symphysis. Most cases are quite obvious as the gap and widening between the pubic bones is clear.

b

Fig. 3.79 (a) Avulsion fracture of the left anterior inferior iliac spine (arrow). Compare to the normal right side, as this is a more subtle injury. (b) The accompanying MRI

showing the edema and injury in the bone at the anterior inferior iliac spine, and edema in the avulsed biceps femoris tendon (arrow)

53

Pelvis and Hips

More subtle cases may so slight offset and widening of the pubic symphysis. If needed, there are reference measurements for normal pubic symphyseal distance. Figure 3.81a and b show diastasis at the right sacroiliac joint, note the associated iliac fracture. Dislocations at the hip will not be difficult to detect. They can occur anteriorly or posteriorly. The posterior dislocation is more common. It is a

important to assess for any associated fracture, especially if there is a fracture fragment that is within the joint space, either before or after the dislocation is reduced. The initial dislocation in Fig.  3.82a was reduced in Fig.  3.82b, but pay attention to the small intra-articular fracture fragments which remain trapped in the joint space. The fracture fragments need to be removed. b

Fig. 3.81 (a) Diastasis at the right sacroiliac joint with an adjacent iliac wing fracture. (b) The coronal image allows a good appreciation of the offset and diastasis at the right sacroiliac joint

a

Fig. 3.82 (a) Dislocation at the left hip. The femoral head was dislocated posteriorly, although it is not visible on this image. It is important to observe the fracture fragment layering in the joint space along the posterior acetabulum. The astute observer will also note there is a

b

lipohemarthrosis with a thin linear layering fat-density at the anterior aspect of the joint. (b) The dislocation has been reduced but there are remnant intra-articular fracture fragments (arrows) which, if left in place will cause later problems

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Key Point

Look for any intra-articular fragments associated with a hip dislocation.

Knee The knee is one of the joints in which it is possible to discern an effusion. Any sizable joint effusion in the setting of trauma should be of concern and often indicates that there is an injury. There may be an obvious fracture, or there may be no apparent injury. In this case, the effusion should still alert you to the probability of an occult fracture or bone injury, or as is more often the case, internal derangement in the form of meniscal or ligament injury. One special type of joint effusion is a lipohemarthrosis. In this case, the three components of the effusion, blood, fluid, and fat are visible as

a

distinct layering levels, although often only a fat fluid level is appreciable on a radiograph. If there is fat intermixed with the joint fluid, then the fat most have come from the marrow of the bone and is indicative of a fracture. The associated fracture/bone injury may not be apparent on the radiograph but will be evident on CT or MR. Look at the lipohemarthrosis is Figs.  3.83a and b. The initial radiograph shows a large joint effusion distending the suprapatellar space. Additionally, we can see a fat fluid level at the more superior aspect of the effusion. The three independent fluid components that make up the effusion are more clearly apparent on the CT where the dark fat layer is the most superior, then comes the serum fluid, and finally the red blood cells at the most dependent aspect of the joint. This is last distinction is caused by the separation of the blood components into serum and red blood cells, known as the hematocrit effect. In this case, there was a lateral tibia plateau fracture which we are not showing you.

b

Fig. 3.83 (a) There is a large dense joint effusion distending the suprapatellar recess. We can tell there is a lipohemarthrosis by the fat fluid level more superiorly (arrow). There must be a bone injury for the fat to get in

the joint space. (b) The three distinct layering components of the joint effusion, the dense fat more anteriorly, the next layer is the less dense serum and finally the layering red cells at the most dependent aspect of the joint

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Knee

be of much value in these cases. Where you have a chance to shine is in the identification of smaller, more subtle injuries, many of which are heralds of more significant ligamentous injury. All of these injuries can and have been overlooked and require dedicated evaluation of these potential injury sites to prevent misses.

Key Point

Lipohemarthrosis=fracture!

Traumatic Arthrotomy Any penetrating or lacerating injury at the knee (or any joint) can extend into the joint. Radiographically there will be intra-articular emphysema. If you see this in the setting of trauma, you must mention it as traumatic arthrotomies are treated by joint irrigation due to the high risk for the development of a septic arthritis. Intra-articular emphysema can be difficult to detect on radiographs, but should be easily apparent on CT. Figure 3.84a and b are an example where the intra-articular emphysema is clear on the radiographs. There is soft tissue injury/laceration along the lateral aspect of the joint associated with a patella fracture. This injury will require surgical irrigation.

Less Obvious Knee Injuries The big, displaced fractures are going to be obvious to all, and your expertise is likely not going to a

Less Obvious Knee Injuries

Sulcus or femoral notch sign. An osteochondral depression of the lateral femoral condyle, which is visible on the lateral radiograph. There is a strong correlation with an anterior cruciate ligament tear (Fig. 3.85). Segond fracture. A small avulsion fracture of the lateral tibia, also with a strong correlation with anterior cruciate ligament tears (Figs. 3.86a and b). Reverse Segond fracture. An avulsion fracture along the medial tibia at the medial collateral ligament attachment. This can be associated with medial meniscal and medial collateral ligament injury, as well as a potential posterior cruciate ligament injury (Fig. 3.87). Anterior cruciate ligament (tibial spine) avulsion fracture. An avulsion

b

Fig. 3.84 (a) The dark focus in the superior joint space is the intra-articular emphysema. We can’t accurately localize it to the joint with this one view, but fortunately we have another view. (b) On the Merchant view, we now

clearly see there is emphysema along the lateral joint line and extending into the joint associated with a large lateral soft tissue injury. There is also a displaced fracture of the lateral patella

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ment attaches. As with the anterior cruciate ligament avulsion fracture, the posterior cruciate ligament is usually not torn (Figs. 3.89a and b). Arcuate sign. An avulsion fracture of the fibula head, which can be associated

injury at the attachment of the anterior cruciate ligament. This is usually in adolescent or younger individuals, and the anterior cruciate ligament remains intact with this injury (Figs. 3.88a and b). Posterior cruciate avulsion fracture. An avulsion fracture at the posterior tibial plateau where the posterior cruciate liga-

Fig. 3.85  The arrow points to the subchondral impaction injury of the lateral femoral condyle. A valgus injury pattern associated with anterior cruciate ligament tear

a

Fig. 3.86 (a) Segond fracture, a small fracture along the lateral tibial plateau. Fairly innocuous looking, but there is a high probability of an anterior cruciate ligament tear. (b)

Fig. 3.87  A reverse Segond fracture, with the avulsed fragment from the medial tibial plateau

b

Another example of a Segond fracture, in this case with more complete lateral displacement of the fragment

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Knee

with internal derangement and anterior cruciate ligament injury (Fig. 3.90). Stieda fracture. An avulsion of the medial collateral ligament along the medial femoral condyle. Over time, heterotopic ossification may develop along the medial

a

Fig. 3.88 (a) Avulsion fracture of the tibial spine at the attachment of the anterior cruciate ligament. (b) The companion MRI which better shows the avulsed fracture frag-

a

Fig. 3.89 (a) Avulsion fracture along the posterior tibial plateau (arrow). The adjacent body is a normal fabella. (b) The MRI showing the posterior cruciate ligament attached

joint line as a more obvious sign of the injury. It is common to see signs of this old injury. This has been referred to as a Pellegrini-Stieda lesion, an antiquated term we hope fades into obscurity (Figs.  3.91a and b).

b

ment (arrow) to which the anterior cruciate ligament is attached. You can see that the ligament is not torn

b

to the avulsed fracture fragment. Just like with an anterior cruciate ligament avulsion, the ligament remains intact

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Tibial Plateau Fractures These fractures are one of the more common knee fractures and can be both subtle and small to large significant comminuted injuries. The fractures are most often along with the lateral tibial plateau. As with just about everything in medicine, there are various classifications systems, which may or may not be used or useful to the physicians you practice with. If needed, these can easily be referenced, and we will not go into great detail about tibial plateau fractures. Figure 3.92a and b show a more subtle example of a lateral tibial plateau fracture. In the subtle injuries, there is often a lipohemarthrosis or at least a joint effusion to help alert you to the presence of the injury.

Fig. 3.90  An avulsion fracture of the fibula head. Doesn’t look like a severe injury, but often there are associated ligamentous or meniscal injuries that probably deserve an MRI to evaluate

a

Fig. 3.91 (a) The initial radiograph showed no injury. This follow-up MRI shows edema and thickening of the medial collateral ligament (arrow) reflecting a low-grade sprain/injury. (b) This radiograph is 4 months after the ini-

Patella Fractures Patella fractures (Fig.  3.93a and b) range from the very obvious and displaced to the subtle and barely visible on a radiograph. b

tial injury and the MRI. Now there is curvilinear heterotopic ossification along the medial joint line at the exact site of the medial collateral ligament injury (arrow). This is a common finding

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Knee

a

b

Fig. 3.92 (a) Lateral tibial plateau fracture with slight articular depression. (b) CT is used to better define the fracture and for surgical planning

a

b

Fig. 3.93 (a) Subtle vertical patella fractures. Can you see them? (b) The fractures are confirmed on the Merchant view

Things that will help you detect them: –– History and exam are always important. –– Pre-patellar soft tissue swelling, which alerts you to a potential fracture. –– A Merchant view is helpful in evaluating these fractures and may be the only view that it is apparent.

Bipartite Patella A normal variant, but one that can and is mistaken for a patella fracture. Usually it is straight

forward to distinguish a bipartite patella from a patella fracture.

Distinguishing a Bipartite Patella from a Patella Fracture

–– Look at the other side. Bipartite patellas are usually bilateral. –– Location. Bipartite patellas are at the superior lateral margin of the patella. –– The margins of the bone. Fractures have sharp margins as opposed to the well corticated margins of a bipartite patella.

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Figure 3.94a and b show a typical bipartite patella.

Key Point

A bipartite patella is usually along the superior and lateral aspect of the patella, and will have rough corticated margins, as opposed to the sharp distinct lines of a fracture.

Of course, a bipartite patella does not confer immunity from fracture (Fig. 3.94c).

a

Patella Dislocation Patella dislocations almost always occur laterally. It is unusual to see the actual dislocation on a radiograph, as they are usually reduced before they are imaged, but it does happen (Fig. 3.95a and b). If you don’t see the dislocation, you can see signs of the recent injury. These include the following: –– Lateral subluxation or tilt to the patella, usually best appreciated on a Merchant view –– Small fracture fragment along the medial patella facet –– Soft tissue swelling and a joint effusion

b

c

Fig. 3.94 (a) Bipartite patella, located at the superior and lateral aspect of the patella. The margins are not those of a sharply defined fracture. (b) The bipartite patella as scle-

rotic and corticated margins. Not a fracture. (c) A vertically oriented patella fracture (arrow) and bipartite patella. This fracture was missed on the initial evaluation

Knee

a

Fig. 3.95 (a) A rare example where the dislocated patella is still maligned on the radiograph. Often the small fracture fragments (arrow) are one of the signs of a dislocation in the more common occurrence where the patella is more

61

b

normally located by the time the image is obtained. (b) The accompanying MRI showing the bone contusions and patella retinaculum and medial patella femoral ligament tears

There are usually associated injuries, often of the medial patella retinaculum and medial patella femoral ligament. There are almost always bone contusions in the medial patella facet and lateral femoral condyle, and often there is displaced osteochondral or chondral fragment in the joint space. These injuries are all better imaged with MRI.

Insufficiency Fractures Subchondral insufficiency fractures usually occur along the weight-bearing medial femoral condyle and are almost always in older individuals often with osteopenia. These can be small and subtle areas of injury, which may initially elude detection. It is important to diagnosis them early, to prevent further collapse and damage of the osteochondral bone. Radiographically they present as focal areas of sclerosis and osteochondral irregularity and flattening (Fig.  3.96). On MRI, they are more obvious with marrow edema and often a distinct fracture line (Fig. 3.97).

Stress Fractures Unlike insufficiency fractures, stress fractures occur in athletes and those engaged in repetitive stress sports or activity—usually running. As

Fig. 3.96  An insufficiency fracture of the medial femoral condyle. There is a focal lucent and irregular area of bone associated with a contour abnormality of the articular surface and surrounding reactive sclerosis. This is one of the more obvious examples—earlier manifestations are subtle

with insufficiency fractures, and stress fractures in other areas, the initial radiographic evaluation is usually unrevealing, especially in the earlier stages. Later there may be focal sclerosis or periosteal reaction (Fig. 3.98a). Rarely will you see a discrete fracture line on a radiograph, but this is easily detected with MRI (Fig. 3.98b).

Dislocation Knee dislocations do not present a diagnostic dilemma (Fig. 3.99), but it is important to know

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Fig. 3.97  MRI of a different individual showing a discrete dark subchondral fracture line in the medial femoral condyle with surrounding marrow edema

a

Fig. 3.99  Yes it is dislocated. Now don’t get cocky, and remember there may be vascular injury and you should consider suggesting an angiogram

b

Fig. 3.98 (a) Stress fracture of the medial tibia with sclerosis in the bone and periosteal reaction. (b) The MRI shows the discrete fracture line (arrow) and surrounding marrow edema

63

Ankle

that there may be associated vascular injury and a CT angiogram or equivalent study may be necessary to evaluate for arterial injury. There will certainly be ligamentous injury, as well as possible nerve injury.

Ankle Ankle injuries rank among the most common musculoskeletal injuries. Fractures, especially of the lateral malleolus are common. Bimalleolar, trimalleolar, and isolated posterior malleolar injuries also occur to a lesser extent. In general, the ER, urgent care, and of course the ortho docs can detect these. But there are injuries that are less common, and which are overlooked by the untrained eye. There are six key places to look on every ankle series. Follow this check list. Look and learn. Checklist for Ankle Evaluation

–– –– –– ––

should always include the fifth metatarsal base, but the fracture may only be visible on the lateral view, often as a corner shot which if you don’t know to look there will be missed. We have seen this fracture missed many times on an ankle radiograph. But now you know where to look and will never miss it (Fig. 3.100). Besides the degree of displacement or distraction of the fragment, it is important to comment on how proximal or distal the fracture is in relation to the metatarsal base. One classification system (Torg) uses the distance from the tubercle to classify them as zone 1, zone 2, or zone 3 injuries. Torg Classification of Proximal Fifth Metatarsal Fractures

Zone 1-Fracture of the most proximal bone and involving the tuberosity Zone 2-Fracture at the metaphyseal-­ diaphyseal junction Zone 3-Fracture more distally, involving the proximal diaphysis

Lateral view Base of the fifth metatarsal Anterior process of the calcaneus Capsular avulsion fractures of the dorsal navicular or talus

Frontal/mortise views –– Lateral talar dome –– Lateral process of the talus –– Lateral calcaneus at the origin of the extensor digitorum brevis

 racture at the Base of the Fifth F Metatarsal Very common injuries, which can be easily detected on a foot radiograph. Often only an ankle radiograph is obtained in the setting of a twisting ankle injury. A proper ankle series

Fig. 3.100  Fracture at the fifth metatarsal base. Start looking here and you will pick up many of these fractures that will have otherwise been overlooked. This is a zone 1 injury

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a

Fig. 3.101 (a) Typical fracture of the anterior process of the calcaneus. There is also an old capsular avulsion fracture along the dorsal talus. (b) This fracture of the anterior

b

process of the calcaneus is subacute and would go on to non-union as the result of a delayed diagnosis

The rationale behind this classification system is that the more common and most proximal zone 1 injuries will likely heal with conservative treatment, while the more distal zone 2-3 fractures may need surgery to prevent delayed healing or non-union of the bone.

 racture of the Anterior Process F of the Calcaneus Not a common fracture, but a commonly missed fracture. These may be isolated injuries that can cause persistent pain if not recognized and treated (Fig. 3.101a and b).

Dorsal Capsular Avulsion Fractures These small avulsion fractures are quite common, but can also easily be overlooked if you are not familiar with them. The dorsal capsular ligaments along the talus and or the navicular bone can rip off, often taking a small piece of cortical bone with them (Fig. 3.102). It is common to see the old remnants of these injuries along the dorsal ankle.

Fig. 3.102  A small capsular avulsion fracture off of the dorsal talus

 raumatic Osteochondral Fracture T of the Lateral Talar Dome Acute osteochondral injury and fractures of the talar dome are usually along the lateral aspect and associated with a twisting inversion injury (Fig. 3.103). Osteochondral injuries of the medial

65

Dorsal Capsular Avulsion Fractures

Fig. 3.103  An acute traumatic osteochondral fracture of the lateral talar dome. The lateral injuries are more often the result of an acute injury, whereas the osteochondral injuries along the medial talar dome are more likely degenerative in etiology

talar dome are more often degenerative in etiology resulting from chronic repetitive injury and wear.

 racture of the Lateral Process F of the Talus Often thought of a snowboarder injury as they are prone to the the dorsiflexion and inversion that causes this injury. They are harder to detect on a radiographic ankle series, which is why it is always important to assess the lateral process of the talus on the AP view (Fig. 3.104).

Fig. 3.104  An avulsion fracture of the lateral process of the talus. Easy to miss, which is why we make a note to look here

detected on a foot or ankle radiograph, where there will be an avulsed fragment off of the lateral calcaneus, sometimes it will be only a fleck of avulsed bone, other times a larger fragment (Fig. 3.105).

Distal Fibular Fractures Fractures of the distal fibula are common injuries. There are different versions and different classifications systems, and the fractures can occur at distal or proximal to the lateral malleolus. Small avulsion injuries of the distal fibula fracture (Fig.  3.106) are very common. These injuries can be less obvious than the other types of fractures. Look for adjacent soft tissue swelling and ankle effusion, which are clues that there is an injury.

 racture at the Origin of the Extensor F Digitorum Brevis Muscle

Trimalleolar Fractures

This muscle originates the dorsal lateral calcaneus. An avulsion fracture at this location is not common, but another one of these more subtle ankle injuries that is repeatedly missed. It can be

This is a more severe injury with fractures of the medial and lateral malleoli and of the posterior tibial plafond—the posterior malleolus (Fig.  3.107a and b). These fractures are almost

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Fig. 3.105  An avulsion fracture along the lateral calcaneus at the origin of the extensor digitorum brevis

Fig. 3.106  A subtler version of distal fibular avulsion fracture

a

b

Fig. 3.107 (a) Trimalleolar fracture, in this case associated with an ankle dislocation. (b) The lateral radiograph, which better shows the dislocation at the ankle and the posterior malleolar fracture

67

Dorsal Capsular Avulsion Fractures

always treated with surgical fixation. Isolated posterior malleolar fractures also occur and can be difficult to detect on radiographs unless there is significant displacement of the fragment (Fig. 3.108).

Maisonneuve Fracture A Maisonneuve fracture or injury is an injury pattern with injury along the medial ankle, with forces then transmitted up they syndesmosis that may cause a proximal fibular fracture (Fig. 3.109a and b). The medial ankle injury may be a fracture of the medial malleolus or may be a deltoid ligament injury, which will be apparent when there is widening of the medial ankle clear space. So if you see an isolated medial malleolus fracture or signs of deltoid ligament injury, make sure to image the proximal fibula.

Key Point

Isolated medial malleolar fractures, or signs of medial deltoid ligament injury with widening of the medial ankle should prompt evaluation for a proximal fibular fracture.

Calcaneal Stress Fracture An injury found in new recruits. Stress fractures occur along the posterior aspect of the calcaneus, and when there is a discrete fracture line, it is oriented more perpendicular to the plantar cortex of the calcaneus. Early on they are not visible on the radiographs, but later on there will be a linear area of reactive and healing sclerosis at the site of injury (Fig. 3.110a). A distinct fracture line is usually only visible on MRI (Fig. 3.110b) or sometimes CT.

Achilles Tendon Injury Achilles tendon injury and tendinopathy can be detected on radiographs. We get fixated on the bones and joints on radiographs, but there are other structures we can see. A normal Achilles tendon shadow is a nice thin slightly dense line. If you see thickening or disruption of this shadow on the radiograph, there there is likely to be a problem with the Achilles tendon (Fig.  3.111a and b). Obviously, an MRI or ultrasound will better characterize any injury or abnormality, but the radiograph can alert us that this bears further investigation.

Fracture Blisters To avoid confusion and embarrassment, you need to know what these look like on a radiograph. Fracture blisters are a rare cutaneous injury associated with fractures, often those caused by a high kinetic energy injury. The blisters are obvious to anyone examining the patient, but can be confusing on a radiograph if you are ignorant of their appearance (Fig. 3.112a and b).

Tendon Entrapment

Fig. 3.108  An isolated fracture of the posterior malleolus. This example is apparent, but sometimes there is only some slight cortical step-off and irregularity to alert you to the injury

CT is used to better characterize a fracture and for pre-operative visualization and planning. It is important to not only look and assess the bone injuries, but also evaluate the tendons. Tendons are clearly imaged on CT, and it is

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a

b

Fig. 3.109 (a) Isolated transverse fracture of the medial malleolus. If you see an isolated medial ankle injury, immediately think that there may be an associated proxi-

a

mal fibula fracture, if there is no imaging, then suggest it. (b) You were right, there is a proximal fibula fracture. We will get to work on that good conduct citation

b

Fig. 3.110 (a) Hey boot, why you limping? Oh, you have a stress fracture. Can you see the subtle sclerotic line from the injury in the posterior calcaneus? (b) MRI makes

everything much clearer. The dark stress fracture line is surrounded my edema. Bright is bad

especially important to look for any tendon entrapment within or adjacent to a fracture fragment (Fig. 3.113a and b). This is something

that may get overlooked by the surgeon, and will be an important factor in how the fracture is treated.

69

Dorsal Capsular Avulsion Fractures Fig. 3.111 (a) The Achilles tendon shadow is abnormal with a focal irregular gap, which is suggestive of a tear. The tear was prospectively called on this image, so it is possible to diagnose tendon pathology on a radiograph. (b) The later MRI showing the Achilles tendon tear

a

Fig. 3.112 (a) Yes, there are fractures, but what are those bumpy things along the medial ankle? (b) This is what those fracture blisters look like on CT, cutaneous blisters, which can vary in size. This will be obvious to anyone who has looked at the ankle, but can be confusing on imaging if you don’t know what they are. We have seen them called neurofibromas and other random guesses

a

b

b

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a

Fig. 3.113 (a) The posterior tibial tendon (the grey ovoid structure) is trapped between the medial malleolus fracture fragment and the main body of the tibia. A critical

b

observation to make on the CT. (b) An image at a different level showing the tendon abutting the medial malleolar fracture fragment

Foot Getting near the end. Finally made it to the foot. There are just a few types of injuries we wish to address here.

 ifth Metatarsal Base Fractures F in Kids Just one potential pitfall here, and all it is, is knowing what a normal apophyseal ossification center looks like at the base of the fifth metatarsal so that you don’t start calling fractures on every kiddie foot you see. The apophysis starts to ossify around the age of 10–12 and fuses a few years later. It is a small linear calcification that parallels the metatarsal. Most fractures that occur at the metatarsal base or transverse or more oblique fractures. It is of course possible to have a fracture with an unfused apophysis (Fig. 3.114).

Key Point

A normal apophysis at the base of the fifth metatarsal is a vertically oriented calcification, as opposed to fractures, which are transverse or oblique in orientation.

Lisfranc Injuries The Lisfranc joint refers to the tarsometatarsal joints. Injuries here can be subtle and easily missed, and the consequences of a delayed or missed diagnosis can be damaging to the long-­ term well-being of an individual. Lisfranc injuries typically involve fractures at the metatarsal bases, which may be associated with offset and dislocation of the tarsometatarsal articulations and associated ligamentous injury. There are numerous variations and patterns of these injuries, but the key things to observe are any offset

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Foot

Figure 3.116 shows a more obvious variant of the injury, with widening and off-set at the second tarsometatarsal articulations. Sometimes the fractures and dislocations are very dramatic, but that will be obvious. Metatarsal Neck Fractures Another site of often missed foot fractures are those in the metatarsal necks, particularly those in older patients with demineralized bones. These can be subtle, and sometimes there is only slight angulation and irregularity of the metatarsal neck from the fracture (Fig. 3.117). They will be more obvious as they begin to heal.

Bone Stress Injuries

Fig. 3.114  This 10 year old has a fracture at the fifth metatarsal base (long arrow). The normal apophysis is oriented parallel to the metatarsal and is partially calcified (shot arrow). Remember not to mistake a normal apophysis for a fracture

or disruption of the Lisfranc articulations, usually centered around the first and second tarsometatarsal articulations and any associated fractures. Sometimes a small fleck of avulsed bone is the only sign of an injury (Fig. 3.115a and b). Weight-­bearing images are useful to exacerbate any offset at the joint. In Fig.  3.115c, there is very subtle off-set and disruption between the second metatarsal base and the medial cuneiform. Figure  3.115d shows a normal alignment.

Key Point

A subtle clue of a Lisfranc injury is very slight off-set and disruption between the medial cortical margins of the second metatarsal and medial cuneiform bones.

We have seen stress fractures in the femur, tibia, and calcaneus. The metatarsals are another common site of stress fractures/bone stress injuries. Those 50 mile rucks start to take a toll. As in all stress fractures and bone stress injuries, the initial radiographic evaluation is often unrevealing or shows only subtle abnormality, which requires a heightened awareness to detect. Over time, the injury will become more apparent. Figures 3.118a, b, and c show the evolution of a metatarsal stress fracture over a 3-month period in a 15-year-old runner.

Toe Fractures One last item and one final area for heightened concern is the toe fracture, a very common injury. Another injury that is easily overlooked, especially when a foot radiograph is obtained and you aren’t alerted as to where to focus your evaluation. However, often a dedicated toe radiograph is ordered. In our experience, in the setting of trauma or injury, the probability of there being a fracture on a dedicated toe radiograph is extremely high and you should stay alert to even small cortical injuries. Figure 3.119a and b show a typical fracture. Notice how it is often only on one of the views that it is clear, which is why a single view is inadequate.

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a

b

d

c

Fig. 3.115 (a) Do you see the injury? Sometimes finding are clear, and sometimes they hard to see and require Holmesian observation skills. (b) Let’s zoom in. Two observations that allow you to make the diagnosis. One is the small fleck of avulsed bone (arrow) indicating a fracture, and the other is the slight offset and widening at the first and second tarsometatarsal joints. (c) The weight-­ bearing view on the same individual shows very subtle

off-set between the medial base of the second metatarsal and the medial cuneiform. Look at the medial cortical margins of these two bones. They should line up. They do not line up here. It is not a dramatic off-set, but it is significant. (d) A weight-bearing view of a different individual, showing a normal alignment of the second metatarsal and medial cuneiform bones

Foot

Fig. 3.116  A more obvious Lisfranc injury with disruption of the joint. The second through fifth metatarsals are subluxed laterally

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Fig. 3.117  Fractures of the third, fourth, and fifth metatarsal necks. Can you spot them? The fifth metatarsal fracture is the most obvious with some off-set and early healing sclerosis. The fracture of the fourth metatarsal neck is only perceptible because of the slight angulation. There is even more subtle irregularity of the third metatarsal neck. Also note the osteopenic bones. These injuries are more common in the older and more osteopenic population

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a

b

c

Fig. 3.118 (a) The initial evaluation showing subtle periosteal reaction along the medial aspect of the second metatarsal. A finding recognized by an astute observer and diagnoses as a stress injury. (b) One month later, and the stress injury is more apparent with more exuberant callus

and periosteal reaction. (c) Another month has passed, with increasing periosteal reaction and cortical thickening. The healing process is not as smooth as would be expected, which reflects non-compliance on the part of the patient

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Live Fire Exercises

Fig. 3.119 (a) There is a fracture of the distal fifth proximal phalanx, just harder to see on this view. (b) The displaced fracture is more obvious here

a

Saved Rounds We have aimed to give you an overview of the more common and often sneakier trauma findings. We have stressed things that are often overlooked or underappreciated, especially on radiographic evaluation. Armed with this knowledge you will survive and thrive. But it is always good to stay humble and curious and know that trauma can come in any form and occur anywhere. There will be injuries that we have neither discussed or even imagined. Stick to basic principles and you will succeed.

Live Fire Exercises You’ve been through basic training. Time to test yourself. Train as you fight.

b

We present you with a series of cases. Treat these as a real-life exercise. The context for all of these cases is trauma. Make the observations and generate a succinct report that clearly communicates the diagnosis and any further recommendations you wish to add. There will be three levels to clear. Each harder than the previous. Ready? Kill!

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1

2

3

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4

6

5

7

78

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8

9

Live Fire Exercises

79

10

11

12

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13

14

15

After Action Review Now rate yourself. How did you do? An honest self-assessment will help you get stronger. 1. There is a dorsal triquetral fracture. Hopefully you saw the small fragment. 2. There are minimally displaced fractures of the base of the second and third metatarsals, and likely at the fourth metatarsal base. There is slight lateral displacement of the metatarsals, and as this is a Lisfranc injury pattern you should be questioning if there is an associated tear of the Lisfranc ligament. 3. Two views here for proper evaluation. There are radial styloid, and mid scaphoid fractures associated with a midcarpal perilunate dislocation. The fractures are better appreciated

After Action Review

on the AP view and the perilunate dislocation, with the dorsally displaced capitate is evaluated on the lateral view. The lunate articulation is not normal either, and it is rotated volarly, although not actually dislocated. 4. There is a large joint effusion on the lateral view. In the setting of trauma we hope you thought there there is a fracture, even though you don’t see one. We didn’t provide you with the frontal view, but even if you didn’t see it on that view you should still be suspicious. 5. A trickier challenged. There are two findings to note. One there is not only a large joint effusion, but it is actually a lipohemarthrosis. You can see the fat fluid level along the superior joint space. Second is the subchondral impaction injury of the lateral femoral condyle, which as we have learned is an injury associated with a tear of the anterior cruciate ligament.

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6. A cervical spine injury with a traumatic pars interarticularis fracture at C2 and associated anterior subluxation, as well as a fracture off of the superior endplate of C3. CT and MRI should be performed for better evaluation. 7. An impacted femoral neck fracture. This is a surgical injury. 8. A subtle fracture of the inferior obturator ring. Where you able to spot it? This is a common injury that you will encounter, keep sharp, and look at those rings.

9. A mid scaphoid fracture. 10. Hopefully you’ve kept your ultrasound skills sharp and found the small splinter in the subcutaneous tissues of the foot. 11. A subacute stress fracture of the second metatarsal. 12. There are two findings on this image. A fracture of the fibular neck, and a small Segond fracture along the lateral tibial plateau. Both of these injuries suggest internal derangement.

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fracture line through the fifth distal phalanx (a congenitally fused phalanx in this case, as there is no distinct middle phalanx). But you remember to always look hard at the toes for the small fractures.

13. A small avulsion fracture at the origin of the extensor digitorum brevis tendon. Yes, this is a subtle injury, but that is the point. These injuries are subtle and require knowing where to look to pick them up. Always look here on the ankle radiographs.

14. Only a toe fracture, but one that can easily be missed. It is just a subtle dark transverse

15. An avulsion fracture of the posterior tibial plateau at the attachment of the posterior cruciate ligament. Clearer on the MRI, but a finding your eagle-eyes can appreciate on the radiograph.

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3 Trauma 122. Earhart C, Patel DB, White EA, Gottsegen CJ, Forrester DM, Matcuk GR.  Transient lateral patellar dislocation: review of imaging findings, patellofemoral anatomy, and treatment options. Emerg Radiol. 2013;20:11–23. 123. Ochi J, Nozaki T, Nimura A, Yamaguchi T, Kitamura N.  Subchondral insufficiency fracture of the knee: review of current concepts and radiological differential diagnoses. Jpn J Radiol. 2022;40(5):443–57. 124. Drabicki RR, Greer WJ, DeMeo PJ. Stress fractures around the knee. Clin Sports Med. 2006;25(1):105– 15. 125. Medina O, Arom GA, Yeranosian MG, Petrigliano FA, McAllister DR. Vascular and nerve injury after knee dislocation: a systematic review. Clin Orthop Relat Res. 2014;472:2621–9. 126. Perron AD, Brady WJ, Sing RF. Orthopedic pitfalls in the ED: vascular injury associated with knee dislocation. Am J Emerg Med. 2001;19(7):583–8. 127. Sillanpää PJ, Kannus P, Niemi ST, Rolf C, Felländer-­ Tsai L, Mattila VM.  Incidence of knee dislocation and concomitant vascular injury requiring surgery: a nationwide study. J Trauma Acute Care Surg. 2014;76(3):715–9. 128. Zwitser EW, Breederveld RS.  Fractures of the fifth metatarsal; diagnosis and treatment. Injury. 2010;41(6):555–62. 129. Den Hartog BD. Fracture of the proximal fifth metatarsal. J Am Acad Orthop Surg. 2009;17(7):458–64. 130. Petrover D, Schweitzer ME, Laredo JD.  Anterior process calcaneal fractures: a systematic evaluation of associated conditions. Skelet Radiol. 2007;36:627–32. 131. Renfrew DL, El-Khoury GY. Anterior process fractures of the calcaneus. Skelet Radiol. 1985;14:121– 5. 132. Hirschmann A, Walter WR, Alaia EF, Garwood E, Amsler F, Rosenberg ZS.  Acute fracture of the anterior process of calcaneus: does it herald a more advanced injury to Chopart joint? Am J Roentgenol. 2018;210(5):1123–30. 133. Massen FK, Baumbach SF, Herterich V, Böcker W, Waizy H, Polzer H. Fractures to the anterior process of the calcaneus–clinical results following functional treatment. Injury. 2019;50(10):1781–6. 134. Tehranzadeh J.  The spectrum of avulsion and avulsion-­like injuries of the musculoskeletal system. Radiographics. 1987;7(5):945–74. 135. Stevens MA, El-Khoury GY, Kathol MH, Brandser EA, Chow S. Imaging features of avulsion injuries. Radiographics. 1999;19(3):655–72. 136. Yu JS, Cody ME.  A template approach for detecting fractures in adults sustaining low-energy ankle trauma. Emerg Radiol. 2009;16:309–18. 137. Anderson IF, Crichton KJ, Grattan-Smith T, Cooper RA, Brazier D. Osteochondral fractures of the dome of the talus. JBJS. 1989;71(8):1143–52. 138. Bohndorf K. Imaging of acute injuries of the articular surfaces (chondral, osteochondral and subchondral fractures). Skelet Radiol. 1999;28(10):545–60.

Bibliography 139. Dunlap BJ, Ferkel RD, Applegate GR. The “LIFT” lesion: lateral inverted osteochondral fracture of the talus. Arthroscopy. 2013;29(11):1826–33. 140. Boon AJ, Smith J, Zobitz ME, Amrami KM. Snowboarder’s talus fracture: mechanism of injury. Am J Sports Med. 2001;29(3):333–8. 141. Perera A, Baker JF, Lui DF, Stephens MM. The management and outcome of lateral process fracture of the talus. Foot Ankle Surg. 2010;16(1):15–20. 142. Fadl SA, Ramzan MM, Sandstrom CK.  Core curriculum illustration: anterior process fracture of the calcaneus. Emerg Radiol. 2018;25:205–7. 143. Walter WR, Hirschmann A, Alaia EF, Tafur M, Rosenberg ZS.  Normal anatomy and traumatic injury of the midtarsal (Chopart) joint complex: an imaging primer. Radiographics. 2019;39(1):136–52. 144. Yu SM, Yu JS.  Calcaneal avulsion fractures: an often forgotten diagnosis. Am J Roentgenol. 2015;205(5):1061–7. 145. Ferries JS, DeCoster TA, Firoozbakhsh KK, Garcia JF, Miller RA.  Plain radiographic interpretation in trimalleolar ankle fractures poorly assesses posterior fragment size. J Orthop Trauma. 1994;8(4):328–31. 146. Rammelt S, Boszczyk A.  Computed tomography in the diagnosis and treatment of ankle fractures: a critical analysis review. JBJS Rev. 2018;6(12):e7. 147. Duchesneau S, Fallat LM.  The maisonneuve fracture. J Foot Ankle Surg. 1995;34(5):422–8. 148. He JQ, Ma XL, Xin JY, Cao HB, Li N, Sun ZH, Wang GX, Fu X, Zhao B, Hu FK. Pathoanatomy and injury mechanism of typical Maisonneuve fracture. Orthop Surg. 2020;12(6):1644–51. 149. Dodson NB, Dodson EE, Shromoff PJ.  Imaging strategies for diagnosing calcaneal and cuboid stress fractures. Clin Podiatr Med Surg. 2008;25(2):183– 201. 150. Jacobs JM, Cameron KL, Bojescul JA.  Lower extremity stress fractures in the military. Clin Sports Med. 2014;33(4):591–613.

87 151. Harris CA, Peduto AJ.  Achilles tendon imaging. Australas Radiol. 2006;50(6):513–25. 152. Giordano CP, Koval KJ, Zuckerman JD, Desai P.  Fracture blisters. Clin Orthop Relat Res. 1994;307:214–21. 153. Golshani A, Zhu L, Cai C, Beckmann NM. Incidence and association of CT findings of ankle tendon injuries in patients presenting with ankle and hindfoot fractures. Am J Roentgenol. 2017;208(2):373–9. 154. Tosounidis TH, Daskalakis II, Giannoudis PV. Fracture blisters: pathophysiology and management. Injury. 2020;51(12):2786–92. 155. Herrera-Soto JA, Scherb M, Duffy MF, Albright JC. Fractures of the fifth metatarsal in children and adolescents. J Pediatr Orthop. 2007;27(4):427–31. 156. Gillespie H. Osteochondroses and apophyseal injuries of the foot in the young athlete. Curr Sports Med Rep. 2010;9(5):265–8. 157. Sands AK, Grose A.  Lisfranc injuries. Injury. 2004;35:SB71–6. 158. Desmond EA, Chou LB.  Current concepts review: lisfranc injuries. Foot Ankle Int. 2006;27(8):653–60. 159. Gupta RT, Wadhwa RP, Learch TJ, Herwick SM. Lisfranc injury: imaging findings for this important but often-missed diagnosis. Curr Probl Diagn Radiol. 2008;37(3):115–26. 160. Buddecke DE, Polk MA, Barp EA. Metatarsal fractures. Clin Podiatr Med Surg. 2010;27(4):601–24. 161. Boden BP, Osbahr DC, Jimenez C. Low-risk stress fractures. Am J Sports Med. 2001;29(1):100–11. 162. Chowchuen P, Resnick D.  Stress fractures of the metatarsal heads. Skelet Radiol. 1998;27:22–5. 163. Lin JT, Lee ST.  Metatarsal stress fractures and osteopenia in older women: a high index of suspicion helps in the proper diagnosis and treatment. J Musculoskelet Med. 2004;21(2):83–9. 164. Van Vliet-Koppert ST, Cakir H, Van Lieshout EM, De Vries MR, Van Der Elst M, Schepers T. Demographics and functional outcome of toe fractures. J Foot Ankle Surg. 2011;50(3):307–10.

4

Infection

Foundations Musculoskeletal infections can be thought of as three basic groups: (1) infection of the bone, (2) infection of the soft tissues, and (3) intra-articular infections. Similarly, the sources of a musculoskeletal infection scan also be divided into three groups: (1) direct spread from adjacent infection, (2) contamination from an injury or foreign body, and (3) hematogenous spread. Each of these locations and mechanisms can have characteristic imaging appearances in the acute phase and, in general, have different clinical courses.

Imaging Modalities Plain Radiography As with most of musculoskeletal imaging, the initial approach to infection should be with plain radiography. This is occasionally  diagnostic in the case of osteomyelitis, and further imaging is unnecessary to establish the diagnosis. For soft tissue infection and infectious arthropathy, the plain film is less frequently diagnostic, but, as with osteomyelitis, it serves as the foundational baseline for future comparison. In primary soft tissue infection, comparison to this baseline plain film is used to detect further development of osteomyelitis. For septic arthropathy, the rapid

progression of destructive changes is best seen in-total by plain film, especially when baseline films are available (Fig. 4.1a and b).

Computed Tomography CT imaging is especially advantageous for infections involving the extra-articular soft tissues, and, in general, should always be undertaken with iodinated contrast. The addition of contrast highlights soft tissue abscesses and further differentiates muscle for the adjacent fascial planes and neurovascular bundles (Fig. 4.2). CT will demonstrate joint effusions far better than plain films. Destructive changes are also well seen, but due to the slice-by-slice nature of CT, it is more difficult to reach an overall evaluation of the joint, which can be rapidly done with a single plain film image. CT is also marginally helpful in the setting of osteomyelitis, but more so with the chronic form where it is superior to both plain film and MRI for identifying sequestrum or involucrum. Early cortical destruction can be seen by CT though it can be difficult to distinguish subacute and chronic changes. Subtle associated fractures, frequent in lower extremity neuropathic arthropathy, are often occult on plain film, are seen to advantage by CT, though the impact of these findings on clinical management is limited. The low overall sensitivity and specificity of CT, even

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 B. Plotkin, B. L. Davis, Musculoskeletal Imaging, https://doi.org/10.1007/978-3-031-49021-7_4

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a

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Fig. 4.1 (a and b) Radiographs of the right hip taken approximately 8 weeks apart demonstrate the rapid bony destruction characteristic of septic arthropathy

Fig. 4.2  Axial unenhanced CT of the pelvis demonstrates a large right hip effusion that was occult on the plain films (not shown) in this case of septic arthropathy. Note the marked bony destruction of the right femoral head and the early destructive change along the articular surface of the right acetabulum

for chronic osteomyelitis, reported as 67% and 50% respectively in one study, limits its clinical utility in most patients.

Ultrasound Ultrasound can be especially useful for the detection of soft tissue abscess and joint effusions.

Fig. 4.3  Longitudinal/sagittal ultrasound image of the posterior left elbow quickly documents the presence of a joint effusion. Unlike other imaging modalities, ultrasound-­ guided arthrocentesis can be performed concurrently

Further, ultrasound-guided arthrocentesis can be performed concurrently with diagnostic imaging if clinical capabilities allow (Fig. 4.3). Of the modalities used in the setting of musculoskeletal infection, ultrasound has the most limitations. First, sensitivity and specificity are

Imaging Modalities

entirely operator dependent. In most institutions, the imaging is performed remotely from the radiologist, and the ultrasound technologists ­ rarely have dedicated training in musculoskeletal imaging. Optimum results are predicated upon a thorough understanding of the anatomy in question so that a comprehensive evaluation can be performed and documented. Secondly, given that follow-up ultrasound imaging is unlikely to be performed by the same technologist, serial imaging becomes less reliable as a marker of true change. Similarly, repeat imaging may not be undertaken on the same overall quality of ultrasound device. The small form factor, portability, and lower cost of ­ultrasound machines typically found the emergency department, outpatient medical clinics, and the clinical wards are achieved by sacrifices to overall imaging quality. The larger high-end machines found in the diagnostic radiology department will invariably show more anatomic detail and make direct comparison to the lower quality units difficult. Further, images of ultrasound exams performed in the emergency department, outpatient clinics, and wards are rarely saved to PACS. Ultimately, ultrasound  serves little use in acute or chronic osteomyelitis.

Nuclear Medicine As the cost, availability, and imaging time of MRI have all improved, the variety of nuclear medicine imaging studies available to evaluate infectious and inflammatory conditions of the musculoskeletal system, once a mainstay in clinical practice, have now assumed a supporting role. Additionally, there is a significant logistics component to several of the key radioisotopes, and imaging may be delayed several days while the desired radiopharmaceutical is procured. This is especially true over weekends and holidays and at smaller and remote facilities. Rather than reflexively ordering a study, it always contact the department of radiology to confirm availability

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and coordinating timing for the imaging exam. Nuclear medicine exams can, in general, be thought of as problem-solving techniques. The most common agents encountered include: • Technecium-99m-methylene diphosphonate (99mTc-MDP) • Fluorine-18 Fluoro-2-deoxyglucose (18F-FDG) • Indium-111 (111In)

Magnetic Resonance Imaging Magnetic Resonance Imaging has become the central imaging technique in most cases of musculoskeletal infection. The soft tissues, articular components, and bone marrow are seen to advantage. With the addition of intravenous gadolinium-­ based contrast, further delineation of soft tissue abscesses is achieved. Sensitivity and specificity are reportedly as high as 100% and 99%, respectively. There are two primary drawbacks to MRI. First is the large number of artifacts that can be encountered. Of the artifacts, patient motion is the most likely to be encountered in the imaging osteomyelitis and substantially degrades imaging quality. Frequently motion artifact is to such a degree that the exam becomes nondiagnostic. Incomplete fat saturation can also complicates interpretation of osteomyelitis studies, but that is more easily dealt with by judicious sequence selection as detailed below. Metallic artifact is universally seen around orthopedic prostheses as essentially a complete void of signal with distortion of the adjacent  soft tissues. The degree of artifact depends largely on the physical composition of the prosthesis and the field strength of the scanner with higher scanners producing more artifact. Expense is the second detractor to MRI. A contrast-enhanced MRI exam is orders of magnitude more costly than plain radiography and often not necessary to confirm a suspected diagnosis of osteomyelitis. Ordering in this setting should be

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carefully contemplated weighting the ultimate cost to the patient with the ultimate effect on medical management. In the case of septic arthropathy, ultrasound, which is far faster to be acquired and costs substantially less, should be considered to confirm the presence of a joint effusion. If absent, septic arthropathy can safely be excluded, and, if present, the patient can undergo image-guided arthrocentesis concurrently.

Osteomyelitis

case of osteomyelitis in the adult patient, direct extension from a soft tissue abscess or skin wound must be completely excluded before entertaining hematogenous spread. Often the wound is clinically obvious, and reviewing the electronic medical record for medical photographs of the presenting wound is time well spent.

Acute vs. Chronic

The evaluation of acute osteomyelitis is a daily Pyogenic vs. Nonpyogenic occurrence for most musculoskeletal radiologists reading studies from the emergency department The overwhelming majority of acute and chronic or inpatient wards. In this setting, osteomyelitis osteomyelitis cases are pyogenic. Nonpyogenic of the foot and ankle, especially in diabetics with osteomyelitis tends to be a corner case where the peripheral neuropathy, is the most commonly microbiology results are often surprising to both encountered scenario. Less frequently, bedridden the clinicians and patients alike. Essentially all patients are evaluated for osteomyelitis underlycases of nonpyogenic osteomyelitis are caused ing high-grade pressure ulcers, usually of the by tuberculosis, fungal agents, and syphilis, and ischial tuberosities and sacrum. In daily practice, virtually all cases are indolent and chronic at the all acute osteomyelitis cases are pyogenic, and time of diagnosis. Staphylococcus aureus is the offending organism of exclusion. Chronic osteomyelitis is far less frequent, and Pediatric vs. Adult it is an area where the radiologists can add substantial value. Frequently, the patient presents Bone infection behaves similarly across age-­ with protean symptoms, and, with attention to groups, but it presents differently between the detail, the diagnosis of chronic osteomyelitis can pediatric and adult patient. Of the general causes be first suggested at imaging. Much more unusual of osteomyelitis, the relative infrequency of adja- agents are occasionally involved in chronic cent soft tissue infection and penetrating trauma in osteomyelitis, though their general presentation the pediatric population makes hematogenous tends to be similar from a musculoskeletal imagspread by far the most common etiology. The ing point of view. Multisystem imaging and/or abrupt and acute turn of the metaphyseal blood review of the available prior imaging studies, vessels near the physis of an immature bone results clinical history, and social background is necesin sluggish vascular flow and a predilection for sary to have a hope at suggesting a particular metaphyseal involvement in pediatric osteomyeli- organism (Figs. 4.4a and b). tis. Epiphyseal involvement is a less common presentation and typically seen in infants. In the mature bone, no such vascular anoma- Imaging of Acute Osteomyelitis lies are present, and hematogenous spread affects the bone without concern of anatomic location. In general, the imaging approach to acute osteoHowever, taken in total, hematogenous spread of myelitis is simple. As mentioned earlier, plain infection is far less common than direct extension radiography is foundational, and it is the initial from  adjacent soft tissues or from penetrating study. Recognizing that the plain films are both trauma (to include surgery). When faced with a insensitive and nonspecific, if the diagnosis is

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Fig. 4.4 (a and b) Chronic osteomyelitis with Brodie abscess formation in an 11-year-old female. The metaphyseal location is classic in a pediatric patient due to the sluggish blood flow in the metaphysis

unable to be made by plain film, then MRI (preferably with contrast) follows. Remember, the plain film is the most important sequence on a musculoskeletal MRI. At plain radiography, the earliest sign of bony infection is blurring of the cortex, followed by clear cortical bone loss. This progresses, often rapidly, to frank destruction of the bone. A permeative pattern of mineralization is first ­encountered, followed by frank obliteration of the bone (Fig. 4.5a and b). At MRI, the diagnosis of osteomyelitis rests upon matching diminished T1 bone marrow signal with concomitant increased T2 signal (bone marrow edema). When this is seen at imaging ordered in the context of infection, you can be very confident about osteomyelitis (Fig.  4.6a and b). Intravenous contrast is not required to demonstrate bone marrow edema, and, for the specific diagnosis of acute osteomyelitis, it is unnecessary. Post-contrast sequences are included in musculoskeletal infection MRI protocols to delineate associated soft tissue abscesses and to better depict sinus tracts in chronic osteomyelitis. Intraosseous abscesses, subperiosteal abscess, and any bony defect draining an intraosseous

abscess to the adjacent soft tissues (a cloaca) are also better seen at post-contrast imaging. Accurately matching T1 and T2 signal abnormalities are where the difficulty lies. In the distal lower extremity, the curving surfaces of the toes frequently lead to incompletely (or completely absent) chemical fat saturation. The answer is to essentially demand STIR sequences, where fat saturation is inherent, be performed. T1- and T2-weighted images should be performed in identical planes. Mixing and matching of tissue weighting and imaging planes are useful in other areas of musculoskeletal imaging but substantially complicates the evaluation of osteomyelitis. In the foot and ankle, the sagittal plane should be the primary focus of imaging. In the rest of the skeleton, the axial plane is usually best. Seen to some degree in nearly all foot and ankle osteomyelitis imaging, motion can degrade imaging to such an extent that the study is no longer diagnostic. Only a few things can be done to overcome this limitation. First optimizing the order in which sequences are acquired is extremely useful. In the foot and ankle, the sagittal STIR sequence followed by sagittal T1 sequence should be the first two obtained. In

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a

b

Fig. 4.5 (a and b) Clear cortical bone less is seen about the index finger proximal and middle phalanges adjacent to the interphalangeal joint consistent with acute osteomy-

elitis. Presenting slightly later, there is frank destruction of the fifth metatarsal head in a separate case of acute osteomyelitis

other locations, obtain the axial STIR and axial T1 sequences first. The second approach to limiting motion is to ask the MRI technologists to tape the feet together. Most technologists know to do this, but upon seeing the appearance of the potentially infected foot, a number fail to follow through. If they balk, simply request that hospital-­ provided socks be placed over the feet, and then proceed to secure the feet with tape. Finally radial k-space filling techniques can be employed. The underlying mechanism of motion artifact reduction is beyond the scope of this text; however, these sequences are available on all modern MRI scanners. The penalty paid is combination of longer imaging time and a few additional artifacts specific to these modes.

Occasionally, increased T2 signal is clearly demonstrated, but concomitant loss of T1 signal is not confidently seen. In these cases, it is best to describe the findings as “osteitis” and to clearly communicate that the imaging findings, while suspicious, are not diagnostic for osteomyelitis.  Although, if there is an adjacent soft tissue ulcer or sinus track, it is likely to be early osteomyelitis. In patients who cannot tolerate MRI, nuclear medicine imaging can be undertaken. The triple phase 99mTc-MDP bone scan (arterial blood flow, blood pool, and delayed phases) is the study of choice, preferably with SPECT/CT technique. Acute osteomyelitis will demonstrate generalize increased radiotracer activity on the blood flow

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b

Fig. 4.6 (a and b) Sagittal T1 and axial proton density fat saturated MRI images of the elbow show matched loss of T1 signal and concomitant increased fluid signal within the distal humerus. Ultimately this is a nonspecific finding of

bone marrow edema, however in the setting of the large joint effusion and high clinical concern for infection, these findings are of osteomyelitis. Also note the destruction and erosion of the joint space from the septic arthritis

phase to the infected area, more focal blood pool activity in the soft tissue surrounding the infected bone, and further focal increased in the infected bone on the delayed phase. Both the sensitivity and specificity of 99mTc-MDP bone scans are increased with SPECT/CT imaging.

In chronic osteomyelitis without Brodie’s abscess formation, mild cortical irregularity and subcortical sclerosis are seen at plain radiography. When an abscess is present, it is seen as a lucency. If it contains a sequestrum, then a lucency with an internal radiodensity will be visualized, often with the lucency demonstrating a sclerotic rim representing the involucrum. At MRI, expect to see bone marrow edema with a focal fluid-filled cavity if abscess is present. The periphery of an intraosseous abscess in lined by granulation tissue and will enhance. For the same reason, any sinus tract draining the abscess will also show peripheral enhancement. A sequestrum, formed by dead and necrotic bone fragments will not, however, enhance (Fig. 4.7). CT will usually show the bony details of an intraosseous abscess and any associated sequestrum or involucrum, but the diagnosis is often known by the time CT is considered. If it is undertaken, the use of contrast should be considered to help delineate any associated soft tissue abscess and the details of any draining sinus.

Imaging of Chronic Osteomyelitis While the same approach to imaging acute osteomyelitis holds for chronic osteomyelitis, the expected imaging findings differ. To better understand the expected findings, a review of terminology specific to chronic osteomyelitis is useful: • Brodie’s abscess—a chronic intraosseous abscess • Sequestrum—a dead bone fragment within a Brodie’s abscess • Involucrum—a reactive rind of new bone forming around a Brodie’s abscess

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Fig. 4.7  Axial T2 fat saturated MRI image of the knee at the level of the tibial tuberosity showing a sharply defined fluid-filled space in the medial aspect of the tibial with significant surrounding bone marrow edema in this case of a Brodie’s abscess

Nuclear medicine studies can be helpful in the diagnosis of chronic osteomyelitis but require significant lead time to acquire the isotopes and prepare the radiopharmaceutical. In general, 111 In-tagged white blood cell SPECT/CT is best course of action if other modalities cannot establish the diagnosis and the patient cannot undergo bone biopsy. If you are at this point in the ­imaging evaluation of the patient, enlist the help of your Nuclear Medicine colleagues.

ciitis which is ultimately a surgical diagnosis where “dishwater” fluid is seen tracking along the fascia. Mortality rates approach 25% (higher than the Charge of the Light Brigade in the Battle of Balaclava). The hallmark of necrotizing fasciitis at imaging is the presence of subcutaneous gas, which, unfortunately, is seen in slightly less than 50% of cases. Plain radiography can be entirely normal until late in the clinical course. As such, CT is the most frequently used imaging modality and has a sensitivity of around 80%. Perifascial fluid admixed with soft tissue gas, if present, is the most specific CT finding. Less specific findings include thickening of the deep fascia with or without associated fat stranding. Fascial enhancement is variable. Inflamed, but viable, fascia enhances, however necrotic fascia will not (Fig. 4.8a and b). Given the lengthy time required for imaging, MRI has little role in the work up of suspected necrotizing fasciitis.

Other Soft Tissue Infections

Far more common than necrotizing fasciitis, “routine” infection of the soft tissues is either confined to the skin (cellulitis) or not. Cellulitis is a clinical diagnosis; however, imaging is routinely performed to exclude involvement of the deeper soft tissues. Plain radiography serves little purpose. Ultrasound is the modality of choice and Soft Tissues Infection demonstrates thickening of the skin and subcutaneous edema, which appears as marbling of the From a practical perspective, infection of the soft subcutaneous fat. CT is frequently employed, tissues can be divided into two groups: 1) necro- and, similar to ultrasound, it shows skin thickentizing fasciitis and 2) everything else. ing and edema in the subcutaneous fat. Hopefully MRI is not ordered, but findings would be the expected; skin thickening and nonfocal increased Necrotizing Fasciitis T2 signal within the subcutaneous fat. Assuming an intact immune system, soft tisNecrotizing fasciitis, also referred to as necrotiz- sue infections involving anything deep to the skin ing soft tissue infection (NSTI) is rapidly-­ surface will ultimately organize and form progressing, life-threatening, surgical emergency. abscess(es). These collections of inflammatory If imaging is requested, it should bone after the tissue surrounding infected pockets of fluid have surgery team has at least been notified about the expected imaging findings. At ultrasound, the patient. While more sensitive than physical exam, abscess will have a thick irregular wall surroundno imaging modality can exclude necrotizing fas- ing heterogeneously hypoechoic “dirty” fluid.

Intra-Articular Infection

a

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b

Fig. 4.8 (a and b) Axial CT of the left thigh with IV contrast highlights the salient findings of necrotizing fasciitis, soft tissue gas, and fluid tracking along the superficial and deep fascial planes

Soft tissue edema will surround the abscess, and, as there is hyperemia, increased color Doppler flow is also present. The wall of an abscess is an “organized” mixture of inflammatory cells, fibroblasts, and ingrowing capillaries. The neovascularity of abscesses accounts for the increased color Doppler signal at sonography, but also explains the hallmark CT and MRI finding and rim enhancement. Rim enhancing fluid collections should always be considered highly suspicious for infection, but remember that the sterility of fluid cannot ascertained by imaging. There is an exception  to this rule, the presence of internal gas. If even a single gas bubble is present, infection is essentially guaranteed. The major benefit of cross-sectional imaging, either CT or MRI, in the setting of complicated soft tissue infections lies in the ability to rapidly form a more complete assessment (the coup d'œil of a Clausewitzian clinician). Are there additional abscesses? What is the anatomic relationship to easily identifiable landmarks  to help guide the surgeon? Are there findings of associated osteomyelitis? Intravenous contrast is essentially mandatory. If the patient cannot receive either CT or MRI contrast, pick the other modality. If they can receive neither, a rare situation indeed, it is probably best to get an MRI since small fluid collections will be easily discernable from the adjacent soft tissues.

Intra-Articular Infection Acute onset of joint pain (monoarticular), hyperemia, and diminished range of motion raise the possibility of septic arthropathy. Unfortunately, these are the same presenting features in crystal deposition arthropathy and neuropathic arthropathy. Rapid diagnosis allows implementation of appropriate antibiotic therapy or surgical management, limiting morbidity. Imaging plays an important, but ultimately supporting role, in the diagnosis. As the clinical findings are nonspecific, plain radiography is the first step in the imaging chain. As with osteomyelitis, this establishes a baseline reference for the appearance of the joint. Regardless of imaging modality, the salient imaging feature of septic arthritis is a joint effusion. Effusions are well demonstrated on plain films of the elbow, knee, and tibiotalar joint; however, they are not reliable in the detection of hip effusion, shoulder/glenohumeral joint effusion, or effusions of small joints. CT, MRI, and ultrasound are substantially better at documenting a joint effusion, especially in smaller joints and in the hip and shoulder. For CT and MRI, contrast is not necessary, but is frequently given to exclude infection in the adjacent soft tissues. The added benefit of ultrasound is the ability to perform concurrent image-guided arthrocentesis. With the wide overlap in clinical presentation of infectious and noninfectious acute monoarticu-

98

lar arthropathy as well as the vastly different clinical management of the two, laboratory analysis of the joint fluid is critical. The standard arthrocentesis order set of cell count, crystal evaluation, and aspirate culture may occasionally fall on your shoulders, and you should be familiar. Most joint infections are caused by Staphylococcus, with cultures confirming the diagnosis and sensitivities directing targeted antibiotic therapy. The general approach to the prosthetic joint is the same. Clinical suspicion for infection should be high for new onset of joint pain any time after the immediate perioperative period. Metallic artifact limits the utility of CT and MRI, though the use of dual energy CT and metal artifact reduction sequences does help. Ultrasound is usually your best imaging option, even of the shoulder.

Infection of the Spine As with osteomyelitis in the appendicular skeleton, the sources of infectious agents of the spine are introduced by either (1) hematogenous spread, (2) direct implantation, or (3) spread from adjacent infection. In general, the frequency follows that same order with hematogenous spread the most common. Regardless of source, the osteomyelitis focus can extend to involve the adjacent intervertebral disc (discitis). Of note, direct infection of the disc can be seen in children via a hematogenous route because the disc is still vascularized.

4 Infection

The progression of spine infection from hematogenous origin follows a predictable pattern. The infectious agent organizes in the vertebral body, typically anteriorly and subjacent an endplate (the sites of slowest blood flow in the bone). The endplate is then violated, and the disc space becomes involved. Infection progresses rapidly through the intervertebral disc, and the opposing endplate in the adjacent vertebral body endplate is then involved. As the infection ravages the disc, there is rapidly progressive loss of disc height. This expected progression of changes accounts for the classic imaging findings of osteomyelitis-­ discitis. The opposing endplates are sclerotic and irregular, and there is high-grade loss of the intervening disc space. These findings are typically easily seen on the standard AP and lateral views of the spine, though overlying bony structures of the upper thorax limit utility in the lower cervical and upper thoracic spine, though that is an unusual location. CT shows similar findings, though the addition of contrast can highlight involvement of the adjacent soft tissues. MRI, however, is the modality of choice when approaching spinal infections. In addition to the destruction of the intervertebral disc, endplate irregularity and vertebral body bone marrow edema are seen to advantage. Paraspinal soft tissue edema is frequently encountered, and paraspinal fluid collections, usually anteriorly, ­ are  also delineated. Uncommonly, epidural abscesses can be encountered (Fig. 4.9a–c).

Infection of the Spine

a

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b

c

Fig. 4.9  (a–c) Early irregularity of the L4 inferior end plate seen on the index plain film is a highly suspicious finding in the postoperative spine. By MRI, there is fluid-­ bright signal within the L4-L5 disc space, a nonspecific finding in the perioperative period following partial dis-

cectomy. The second plain films, taken approximately 4 months later, show rapid destruction of the L4-L5 disc space and adjacent vertebral bodies. Anterolisthesis and reactive sclerosis have developed

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4 Infection

Atypical Infections In regard to musculoskeletal infections, atypical agents are generally tuberculosis or fungal. With a few exceptions, infections from atypical entities appear identical to their pyogenic comrades. First, you are more likely to encounter an unusual organism with chronic infections. They are, after all, not affected by “typical” antibiotics. These agents also tend to be more indolent than pyogenic infections leading to a vaguer set of presenting symptoms, and occasionally resulting in significant delay of a correct diagnosis. Because of the slowly progressive clinical course, atypical infections are often “cold” on radionuclide studies. Classic plain film findings of osteomyelitis with little-to-no associated radiopharmaceutical activity (regardless of agent) should clue you into an atypical infection. This is an impression-worthy finding as specimen handling at time of collection is affected. Spinal tuberculosis deserves special mention. Also known as Pott’s disease, spinal tuberculosis accounts for about 15% of extrapulmonary tuberculosis and a full 50% of all skeletal tuberculosis infections. The lower thoracic and lumbar vertebrae are most commonly involved. Universally of hematologic origin, Pott’s disease can have the same imaging features of pyogenic osteomyelitis-­ discitis, but occasionally demonstrates a few unique features. Skip lesions, where noncontiguous vertebral bodies are involved, are almost never seen in nontuberculous infections. Additionally, the infection may remain confined to the vertebral body. Over time, this leads to initial expansion of the vertebral body followed by rapid collapse and progression to vertebra plana. Destruction of multiple contiguous and noncontiguous vertebral bodies, with and without associated disc destruction, ultimately leads to characteristic gibbus formation (from the Latin word for “humpbacked” and forming the same shape as a waxing or waning crescent or gibbous moon) (Figs. 4.10 and 4.11). The neurologic sequela of Pott’s disease can be devastating, with paraplegia being the  most feared. In the setting of active tuberculosis infection, the paraplegia, caused by neuroaxis com-

Fig. 4.10  Sagittal STIR MRI image of the cervical spine shows isolated expansion of the C7 vertebral body with associated bone marrow edema, a unique feature of tuberculous infections of the spine

Fig. 4.11  A classic gibbous deformity is demonstrated on the sagittal CT reconstruction of the thoracolumbar spine. Complete or partial destruction of multiple vertebral levels causes severe exaggeration of the thoracic kyphosis and creates a “humpback” appearance

Bibliography

pression, results from epidural abscess or debris from the destroyed vertebral body and disc. Alternatively, destruction of the anterior vertebral column leads to spinal instability with spinal subluxation or dislocation.

Saved Rounds Given the relative low frequency of tuberculous osteomyelitis in the developed world, practicing (and training) radiologists have little exposure. Now seen almost exclusively at case conferences, Phemister’s triad, composed of (1) joint space narrowing, (2) peri-articular osteopenia, and peripheral erosions, was at one time an instantly recognizable plain film pattern to all radiologists. It still shows up on board exams, so you might as well have seen it at least once (Fig. 4.12). One final note on infection—never, under any circumstance, exclude infection of any kind in the immunocompromised patient.

Fig. 4.12  Phemister’s triad in a case of culture-proven tuberculous septic arthritis of the right knee: Joint space narrowing, periarticular osteopenia, and peripheral erosions

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Bibliography 1. Alaia EF, Chhabra A, Simpfendorfer CS, et al. MRI nomenclature for musculoskeletal infection. Skelet Radiol. 2021;50(12):2319–47. 2. Altmayer S, Verma N, Dicks EA, Oliveira A. Imaging musculoskeletal soft tissue infections. Semin Ultrasound CT MR. 2020;41(1):85–98. 3. Brodie BC.  An account of some cases of chronic abscess of the tibia. Trans Med Chir Soc. 1832;17:238–9. 4. Crim JR, Seeger LL. Imaging evaluation of osteomyelitis. Crit Rev Diagn Imaging. 1994;35(3):201–56. 5. Demirev A, Weijers R, Geurts J, Mottaghy F, Walenkamp G, Brans B.  Comparison of [18 F]FDG PET/CT and MRI in the diagnosis of active osteomyelitis. Skelet Radiol. 2014;43(5):665–72. 6. Erdman WA, Tamburro F, Jayson HT, Weatherall PT, Ferry KB, Peshock RM.  Osteomyelitis: characteristics and pitfalls of diagnosis with MR imaging. Radiology. 1991;180(2):533–9. 7. Fayad LM, Carrino JA, Fishman EK. Musculoskeletal infection: role of CT in the emergency department. Radiographics. 2007;27(6):1723–36. 8. Fernando SM, Tran A, Cheng W, et  al. Necrotizing soft tissue infection: diagnostic accuracy of physical examination, imaging, and LRINEC score: a systematic review and meta-analysis. Ann Surg. 2019;269(1):58–65. 9. Gold RH, Hawkins RA, Katz RD.  Bacterial osteomyelitis: findings on plain radiography, CT, MR, and scintigraphy. Am J Roentgenol. 1991;157(2):365–70. 10. Karchevsky M, Schweitzer ME, Morrison WB, Parellada JA.  MRI findings of septic arthritis and associated osteomyelitis in adults. Am J Roentgenol. 2004;182(1):119–22. 11. Kim KT, Kim YJ, Won Lee J, et al. Can necrotizing infectious fasciitis be differentiated from nonnecrotizing infectious fasciitis with MR imaging? Radiology. 2011;259(3):816–24. 12. King AD, Peters AM, Stuttle AW, Lavender JP.  Imaging of bone infection with labelled white blood cells: role of contemporaneous bone marrow imaging. Eur J Nucl Med. 1990;17(3-4):148–51. 13. Kwee TC, Kwee RM, Alavi A.  FDG-PET for diagnosing prosthetic joint infection: systematic review and metaanalysis. Eur J Nucl Med Mol Imaging. 2008;35(11):2122–32. 14. Love C, Marwin SE, Palestro CJ.  Nuclear medicine and the infected joint replacement. Semin Nucl Med. 2009;39(1):66–78.

102 15. Modic MT, Feiglin DH, Piraino DW, et al. Vertebral osteomyelitis: assessment using MR.  Radiology. 1985;157(1):157–66. 16. Modic MT, Pflanze W, Feiglin DH, Belhobek G.  Magnetic resonance imaging of musculoskeletal infections. Radiol Clin N Am. 1986;24(2):247–58. 17. Morrison WB, Schweitzer ME, Bock GW, et  al. Diagnosis of osteomyelitis: utility of fat-­suppressed contrast-enhanced MR imaging. Radiology. 1993;189(1):251–7. 18. Phemister DB, Hatcher CM.  Correlation of pathological and roentgenological findings in the diagnosis of tuberculosis arthritis. Am J Roentgenol. 1933;29:736–52. 19. Rahmouni A, Chosidow O.  Differentiation of necrotizing infectious fasciitis from nonnecrotizing infectious fasciitis with MR imaging. Radiology. 2012;262(2):732–3. author reply 733

4 Infection 20. Resnick D. Diagnosis of bone and joint disorders. 4th ed. Philadelphia: WB Saunders; 2002. 21. Simpfendorfer CS.  Radiologic approach to musculoskeletal infections. Infect Dis Clin N Am. 2017;31(2):299–324. 22. Tang JS, Gold RH, Bassett LW, Seeger LL.  Musculoskeletal infection of the extremities: evaluation with MR imaging. Radiology. 1988;166(1 Pt 1):205–9. 23. Tigges S, Stiles RG, Roberson JR.  Appearance of septic hip prostheses on plain radiographs. Am J Roentgenol. 1994;163(2):377–80. 24. Toledano TR, Fatone EA, Weis A, Cotten A, Beltran J. MRI evaluation of bone marrow changes in the diabetic foot: a practical approach. Semin Musculoskelet Radiol. 2011;15(3):257–68. 25. Turecki MB, Taljanovic MS, Stubbs AY, et  al. Imaging of musculoskeletal soft tissue infections. Skelet Radiol. 2010;39(10):957–71.

5

Bone Tumors

The good. The bad. The ugly. Almost of all you need to know about bone tumors comes down to one essential question. Is it good, or is it bad? This is the single most important question in day-to-day practice. Is the tumor I’m looking at something to worry about or not? The rest is extra. Yes, it is nice to give a brilliant differential and sound smart and educated, and these are excellent skills to possess and to cultivate. But the primary objective is to be able to recognize something that may kill that individual, and something that will have little to no impact on their existence. We will spend some time learning to evaluate how to distinguish the good from the bad. Only after we have become proficient in this skill, we move to diagnose specific tumor types. Now, it is not always possible to know for sure, or with a reasonable degree of certainty what you are looking at. There will be times where it will be necessary to biopsy the lesion in question, but even in the setting of a busy academic tumor service, this is often not necessary and we can avoid unnecessary interventions utilizing our skill and training. What tools do we have? A simple radiograph will often provide the answer for most bone tumors. MRI is useful for

characterizing the true extent of a bone tumor. It can tell us if it involves other structures and other information that is useful for treatment purposes, but the diagnosis is going to be made on the humble utilitarian radiograph. What are the factors that allow us to judge if a tumor is good or bad? • • • •

reaction Border/zone of transition Age Alone or in battalions.

Let’s go through each of these. In the following discussion, we cover the more common bone tumors (bone tumors in general are relatively rare). This discussion is not a complete or thorough treatise, and in the interests of brevity and focus, we have elected not to discuss some tumors that are rarer, and unlikely to be encountered. Even in our practice at a busy academic center which acts as a referral center for bone and soft tissue tumors, there are some tumors, which are so rarely encountered that the discussion of them is left to those who truly wish to specialize in diagnosing and evaluating these tumors. We have opted to focus on the more high-­yield lesions that you may encounter. As always, be aware that the rare, bizarre, and unexpected may occur. But if you stick to the general principles, seek to identify the good from

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 B. Plotkin, B. L. Davis, Musculoskeletal Imaging, https://doi.org/10.1007/978-3-031-49021-7_5

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the bad and learn to identify these more common bone tumors you will then be trained to a rarefied degree.

Periosteal Reaction The Good Periosteal reaction is the bone’s response to insult or injury. We see this most commonly in the setting of a fracture. Bone will attempt to heal itself. The periosteal reaction is part of the healing process, and smooth new bone will be laid down around the fracture as the bone heals. This is the periosteal reaction we are most familiar with. It is benign, it is smooth, and it is uninterrupted. This is good periosteal reaction (Figs. 5.1 and 5.2).

The Bad When the bone’s healing is interrupted, we get periosteal reaction that is random and more disruptive. The bone tries to keep healing by laying down new bone, but the insult or injury of the bone, be it tumor, trauma, or infection, outpaces the bone’s ability to heal. Thus we see a disruptive pattern of periosteal reaction. In these cases, the periosteal reaction is wilder, in appearance. There are many names that have been assigned to the various types of disruptive periosteal reaction, and while these may be of academic interest, the terms themselves have no meaning or relevance in and of themselves, and what is important is to recognize that the periosteal reaction is disruptive and that this is reflective of a destructive bone force that is outstripping the bone’s ability to heal itself. It’s the setting of tumors, this is a sign of an aggressive tumor and should be recognized as bad (Figs. 5.3 and 5.4).

Fig. 5.1  Smooth benign periosteal reaction. Nothing to worry about here, move along

Fig. 5.2  Benign-appearing periosteal reaction

Periosteal Reaction

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Fig. 5.3 Aggressive periosteal reaction related to an osteosarcoma in the tibia. The periosteal reaction is uneven and irregular, not smooth and clean

The Ugly Sometimes the periosteal reaction is very wild and wooly and extremely disrupted as the area of bone insult or tumor is growing so quickly that it’s destructive forces easily outnumber and outstrip the overwhelmed healing osteoblasts, and the periosteal reaction is quite dramatic and ugly (Figs. 5.5 and 5.6). As you would expect, this is reflective of a very aggressive process, and in the

Fig. 5.4  Lamellated layered lines of new bone formation (periosteal reaction) as the bone responds to the Ewing’s sarcoma in the femur. The square-like cortical defect along the lateral cortical margin is related to an open biopsy

setting of a bone tumor is concerning. Although it should be noted, that some non-malignant bone tumors can grow at a rapid rate causing destructive periosteal reaction. But in these cases, it will still need so intervention to curtail the local destructive effect of the tumor.

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5  Bone Tumors

Fig. 5.6  A different osteosarcoma causing aggressive periosteal reaction. Bad

Border and Zone of Transition

Fig. 5.5  Crazy, ugly, and bad periosteal reaction with interrupted and irregular new bone being laid down, destroyed, and disrupted by an osteosarcoma

We define a lesion as being geographic if it clearly focally located in one specific region of the bone. Once we determine it is geographic, we then assess its border and zone of transition.

Border and Zone of Transition

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Fig. 5.7  Geographic lytic lesion with a narrow zone of transition and a sclerotic border. Looks benign, is benign—in this case, simple unicameral cyst

This refers to the transition between tumor (or tumor-like process) and normal bone. This can be a narrow or abrupt transition between tumor or bone—a narrow zone of transition, or a wider more blurred and less-defined transition, which we will call a wide zone of transition.

Fig. 5.8  Geographic lytic lesion with a narrow zone of transition and a non-sclerotic border. In this case maybe we should be more circumspect with this giant cell tumor

The Good A narrow zone of transition is a sharp clearly demarcated border between tumor and bone. What this reflects is that the tumor is either not growing (a good sign) or so slow growing that the bone has easily surrounded and walled of the lesion and created a nice sclerotic barrier of normal bone around it. In this situation, we will see a sclerotic or at least partially sclerotic border around the lesion. We will call this a narrow zone of transition with a sclerotic border (Fig.  5.7). Almost all tumors with a narrow zone of transition and a sclerotic border are benign. The zone of transition can still be narrow, but the wall around it may not be a nice sclerotic rim. We will call this a narrow zone of transition with a non-sclerotic border (Figs. 5.8 and 5.9). This still likely reflects a slow growing or more benign process, but because it lacks the nice sclerotic rim, we remain alert to the possibility that the lesion may be more aggressive, especially in older individuals where we are always going to be more alert.

Fig. 5.9  Another geographic lytic lesion with a narrow zone of transition and a non-sclerotic border. Looks relatively innocuous, but given this individual was older and had a history of leukemia it was biopsied out of an abundance of caution. The diagnosis was fibrous dysplasia

The Bad When there is no nice sharp margin between tumor and bone, when the border is blurred, irregular, and messy, then this is a wide zone of

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Fig. 5.10  Still a geographic lytic lesion, but with a wide zone of transition, which is more aggressive in appearance. This is not something you want to leave alone. This was a case of giant cell tumor, which was locally aggressive and destructive

transition (Fig.  5.10). This indicates that the tumor is growing and destroying bone faster than the bone can wall off the tumor and is reflective of an aggressive lesion. Again, it may not be a malignant lesion, but it is an aggressive lesion and thus bad.

The Ugly

Fig. 5.11  This cannot be good. A diffusely infiltrating and destructive lytic lesion throughout the humerus. There is a pathologic fracture in the mid humerus. This was lymphoma

tumors don’t occur in kids, they do. But these occurrences are rare and we will work on recognizing them. What we should take away from the age of the individual we are evaluating is that the older they are the most suspicious we should be of a bone tumor, even if it is fairly innocuous looking.

Sometimes the zone of transition is so wide and ill-defined that the lesion is no longer a focal geographic lesion but is infiltrating throughout the bone with amorphous tendrils extending in an ill-­ defined pattern. The lesion cannot be clearly encircled. These tumors are non-geographic and A  lone or in Battalions termed permeative or infiltrative (Fig.  5.11). Universally something you don’t want. Once you see multiple bone lesions, your first thought (at least in an older adult) should be, is this metastasis or is it multiple myeloma? There Age are certainly conditions in which there are multiple benign bone lesions, and we will look at these This is a short and simple factor to keep in mind. In later. But as a good general rule in if there are general, tumors in younger individuals are less multiple bone lesions you should first think of likely to be dangerous. That is not to say that bad metastasis or myeloma (Fig. 5.12).

Good or Bad?

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 hat to Look for in Making this W Judgment? –– Is there periosteal reaction, and if so is it benign or aggressive? –– Is it a geographic lesion, and if so what is the zone of transition like? –– Is it solitary or multiple? While there are benign polyostotic tumors, in general the presence of more than one should make you think of metastasis or myeloma. –– Is this an older or younger individual? We are going to me more suspicious and concerned about a lesion in an older adult than a child. Fig. 5.12 Multiple sclerotic lesions. This cannot be good. This is metastatic prostate cancer

Case 1 (Fig. 5.13)

Key Point

If you see multiple bone lesions, you should reflexively think of metastasis and multiple myeloma.

Good or Bad? Now for some practice. The cases below are presented not for determining a distinct diagnosis, although that is great if you can, but merely for a binary decision. Good or bad. Should this be biopsied or should it be left alone?

Fig. 5.13  CASE 1 Good or bad?

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Case 2 (Fig. 5.14) Case 3 (Fig. 5.15)

Case 4 (Fig. 5.16) Case 5 (Fig. 5.17)

Fig. 5.16  CASE 4 Good or bad? Fig. 5.14  CASE 2 Good or bad?

Fig. 5.17  CASE 5 Good or bad?

Fig. 5.15  CASE 3 Good or bad?

Location

After Action Review Let’s see how you did? Case 1 A geographic lytic lesion with a narrow zone of transition and sclerotic border. There is no aggressive periosteal reaction. There is faint chondroid matrix (something we will address later). There are no concerning imaging findings, and this is a typical benign enchondroma. Good to go. Case 2 A geographic lesion with a wide zone of transition and crazy aggressive periosteal reaction. There is some osteoid matrix, and the growth plates are open so we know they are a kid. This looks bad. It is bad and is typical appearance for an osteosarcoma. Case 3 A geographic lytic lesion with a narrow zone of transition and a sclerotic border. That appearance alone is almost a guarantee of something benign. It is also a child, so we are less worried. This is a benign, and although was not biopsied was likely a cyst or fibroxanthoma. Case 4 A geographic lytic lesion with a wide zone of transition. There is cortical destruction and aggressive periosteal reaction along the medial border. Hopefully you thought this looked scary and was bad. In this case, it was from a metastasis. Case 5 There are multiple lytic lesions just about everywhere you look. They are small and geographic with a narrow zone of transition. But since they are multiple, and this is an older patient (We know we didn’t give you the age) you should be worried. This is bad, and a typical appearance for myeloma.

Refinement Again, to emphasize the most important skill is being able to identify a tumor as good or bad. The rest is hone and polish, spit and shine. Makes you look sharp and professional.

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Now, we will not always get it right, usually this results in us identifying something as bad, when in fact it was not. This is a reasonable price to pay for ensuring that no malignant lesion is left alone. The simple factors we have discussed: periosteal reaction, zone of transition, age, and number are enough to do most of the heavy lifting. With these we can identify bad or concerning tumors. What follows is a further refinement of actually identifying specific histologic types of tumor. This is a secondary, but still a useful skill and we should take the time to familiarize ourselves with the basic principles. There are many factors we can use to help us identify the actual type of tumor. Again, almost all of this can be done with the humble utilitarian radiograph. Advanced fancy imaging is not required and may in fact be a distraction. We should be aware that trying to identify a specific type of tumor based solely on an MRI may lead us into a later ambush, when the radiograph reveals simple and basic information that we didn’t have at the time we evaluated the MRI.  Never try to diagnosis a bone tumor without looking at a radiograph (or CT) of the lesion. Now there are a few exceptions to this dictum, most notably enchondromas, but as a general principle it is important to remember. This is not to minimize the importance of CT and MRI, which are important for staging and evaluating the extent of a tumor.

Key Point

Never try to diagnosis a bone tumor on MRI alone, almost always a radiograph should be also evaluated.

Location Location is of paramount importance, when evaluating bone tumors. It is one of the key factors that will immediately narrow down the possible entities. Once you identify the location you can use other factors to help further refine your diagnosis.

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Fig. 5.18  This chondroblastoma is a good example of an epiphyseal lesion

We will break down location in long bones into two groups. Flat bones (such as the scapula and pelvic bones) do not fit into this characterization although many of the tumors we discuss can also be found in flat bones. The first localization is based on its location based upon its relationship to the physis or in a longitudinal plane.

Fig. 5.19  An osteosarcoma arising in the metaphysis

–– Epiphyseal (Fig. 5.18) –– Metaphyseal (Fig. 5.19) –– Diaphyseal (Fig. 5.20) The second localization is based upon its relationship to the bone in the transverse plane. –– –– –– ––

Centrally located (Fig. 5.21) Eccentrically located (Fig. 5.22) Cortically based (Fig.  5.23) Juxtacortical (Figs. 5.24 and 5.25)

Again, with emphasis—the location of a lesion is of critical importance. Pay attention to where in the bone the tumor is located.

Fig. 5.20  An involuting and sclerosing fibroxanthoma in the diaphysis of the tibia

We will discuss a few short salient characteristics of the more common bone tumors as we review them by their expected locations.

Location

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Epiphyseal (and Apophyseal) Lesions

–– –– –– –– ––

Giant cell tumor Chondroblastoma Aneurysmal bone cyst Clear cell chondrosarcoma Infection

Fig. 5.22  An eccentrically located fibroxanthoma

Fig. 5.21 A centrally located unicameral bone cyst. There is a pathological fracture

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Fig. 5.25  A surface based parosteal osteosarcoma, arising in a juxtacortical location

Fig. 5.23  A cortically based adamantinoma, a lesion almost exclusively located in the cortex of the tibia

Fig. 5.24  A periosteal or juxtacortical chondroma arising along the cortical surface

Giant Cell Tumor –– Even though these originate at the physis and extend toward the articular surface. They are usually considered epiphyseal lesions, although they can also occur at an apophysis. –– Found almost exclusively in skeletally mature individuals. Not a pediatric tumor. –– They are locally aggressive and can look bad and cause significant bone destruction, but they are not generally considered malignant, although in rare cases they can have lung metastasis. –– They have a relatively high rate of reoccurrence after surgical excision. –– Solitary lesions. –– Geographic lytic lesions, which may be expansile and usually lack a sclerotic border. They may have a wide zone of transition and appear very aggressive. –– Commonly seen in the long bones around the knee and of the wrist. Figs. 5.26 and 5.27.

Chondroblastoma

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Key Point

Giant cell tumors almost always occur in skeletally mature individuals. If the physis is still open, it shouldn’t be a giant cell tumor.

Chondroblastoma

Fig. 5.26  A classic appearance of a giant cell tumor. Geographic lytic lesion with a narrow zone of transition and a non-sclerotic border, which is eccentrically located in epiphysis-metaphysis of the proximal tibia. Giant cell tumors arise along the physis and usually extend to the articular surface of the bone

–– These are epiphyseal lesions, and just like giant cell tumors, they can occur at an apophysis. –– A tumor of later childhood or adolescence, not typically an adult tumor, although at the tail end of the the spectrum, they can be found in individuals in their early to mid-20s. Make sure you know the age of the individual before considering the diagnosis of chondroblastoma. –– Geographic lytic lesions with a narrow zone of transition, and usually a sclerotic border. –– On MRI, they may have significant surrounding reactive marrow edema and can be associated with an adjacent joint effusion. –– Most commonly occurring about the knee and in the proximal humerus. Figs. 5.28 and 5.29.

Fig. 5.27  Another giant cell tumor, this one is more aggressive in appearance with a wider zone of transition and cortical thinning and destruction along the medial tibia

Fig. 5.28  A chondroblastoma, eccentrically located in the epiphysis of the proximal femur. There is a narrow zone of transition and a sclerotic border. Make sure you check the age before you commit to the diagnosis of a chondroblastoma. If this were found in a 50 year old, then you should not consider a chondroblastoma

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Fig. 5.29  Another chondroblastoma, this one arising in the posterior calcaneal apophysis. A geographic lytic lesion with a narrow zone of transition and a non-sclerotic border. While not the most common location for a chondroblastoma to occur, it is a site where they will often be found

Aneurysmal Bone Cyst –– Usually found in kids or younger adults. –– Can be found as a secondary component associated with a giant cell tumor or chondroblastoma. –– May be associated with an injury. –– Geographic lytic lesions, expansile (just like its name implies) and often with internal separations and reticulated architecture. They may have a narrow or wide zone of transition and can also appear very locally aggressive. –– Most commonly arising about the knee, although they can also occur in the spine and pelvic bones. Fig. 5.30.

Fig. 5.30 An aneurysmal bone cyst. Expansile geographic lytic lesion with a narrow zone of transition and a non-sclerotic border in the epiphyseal of the proximal fibula with extension into the metaphysis

Clear Cell Chondrosarcoma –– A rare chondrosarcoma variant that occurs in the epiphysis. –– Geographic lytic lesion with a narrow zone of transition, which may or may not have a sclerotic rim, and thus may look unassuming and non-aggressive on the radiograph. A degree of suspicion is required to think of this diagnosis. –– Age will be helpful here as this is typically found in individuals between 30 and 50 years of age. If you seem something that looks like it could be a chondroblastoma, but the age of the individual is 40, then your internal klaxons should ring, and you should worry. –– The majority occur within the proximal femur or proximal humerus. Figs. 5.31 and 5.32.

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Infection –– A focal subacute or chronic infection, sometimes called a Brodie’B abscess. –– This can look like a geographic lytic lesion, with or without a sclerotic border. –– It is less common in the epiphysis, but it can be around the physis tracking into the ­epiphysis, and is worth bearing in mind as a consideration. Fig. 5.33. Metaphyseal Lesions

Fig. 5.31  A clear cell chondrosarcoma. This lesion looks relatively benign. It is geographic with a narrow zone of transition and a non-sclerotic border centered in the epiphysis of the proximal tibia. In a younger patient we could easily call this a chondroblastoma, but in a patient in their 40s, we should be worried and think of clear cell chondrosarcoma. Age is a critical factor in evaluating bone tumors

–– –– –– –– –– –– ––

Unicameral (simple) bone cyst Aneurysmal bone cyst Enchondroma Chondrosarcoma Osteochondroma Osteosarcoma Infection

Fig. 5.32  This tumor looks very similar to the prior, but in this teenager, was a chondroblastoma Fig. 5.33  A geographic lytic lesion with a narrow zone of transition and a non-sclerotic border, which is eccentrically located around the physis of the distal femur and extends into the epiphysis. This was a focal area of infection—Brodie’s abscess

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Unicameral or Simple Bone Cyst

Enchondroma

–– A benign simple fluid-filled cystic lesion almost always found in individuals less than 20 year of age. –– Usually centrally located in the metaphysis, which can extend into the diaphysis. –– Geographic lytic lesion with a narrow zone of transition, usually with a sclerotic border, although it can have a non-sclerotic border. –– When there is a pathologic fracture, a broken fragment floats within the lesion creating the pathognomonic “fallen fragment sign.” (Fig. 5.34)

–– A benign cartilaginous lesion usually easily identifiable by its chondroid matrix although often the more distal extremity (phalangeal bones) enchondromas lack clear identifiable matrix on radiographs. The chondroid matrix of the lesion is usually recognizable with MRI. One of the few lesions where MRI can safely diagnosis the lesion without radiographic correlate. –– The most common phalangeal tumor. –– Centrally located within the metaphysis or the diaphysis when occurring in a long bone. –– Geographic lytic lesion with a narrow zone of transition, which have either a sclerotic or a non-sclerotic border –– There are syndromes with multiple enchondromas, in these cases the individual risk of malignant degeneration is significantly higher than the very low chance of malignant ­degeneration in a solitary enchondroma. Figs. 5.35 and 5.36.

Fig. 5.34  The classic appearance of a unicameral bone cyst with a pathological fracture. The cortical fracture fragment is floating in the middle of the cyst giving the “fallen-fragment” sign

Fig. 5.35  Typical appearance of an enchondroma, here in the distal femur. This is the classic appearance of chondroid matrix. These are common incidental findings

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Fig. 5.37  Chondrosarcoma arising from the iliac bone. There is a large soft tissue component with chondroid matrix, which clearly looks aggressive

Fig. 5.36  Another enchondroma, this one in the proximal phalanx. Enchondromas are the most common phalangeal tumor. This one does have a clear chondroid matrix, but the matrix in the phalangeal enchondromas is not always clear on radiograph. Yes, there is also a fracture

Chondrosarcoma –– When enchondromas go bad. This is a malignant tumor. Just like enchondromas, there will usually be identifiable chondroid matrix. –– A geographic lytic lesion, which may have a narrow or wide zone of transition. –– Concerning imaging findings include growth, size, and endosteal scalloping and cortical breakthrough. –– Most common in the pelvis, femur, and proximal humerus. Figs. 5.37 and 5.38.

Fig. 5.38  Another chondrosarcoma. A geographic lytic lesion with a wide zone of transition centered in the proximal femoral metadiaphysis. There is a focal area of chondroid matrix. Contrast this appearance with the benign enchondroma in Fig. 5.35

Osteochondroma –– A benign exophytic lesion with both an osseous component and an overlying cartilage component, known as a cartilaginous cap. There is a pedunculated and a sessile version. –– In long bones, it originates in the metaphyseal regions and grows away from the

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Fig. 5.39  A sessile osteochondroma arising from the proximal tibia. Note the continuity with the cortical line of the tibia as well as the medullary component. Solitary osteochondromas are a common incidental finding

Fig. 5.40  A different osteochondroma arising from the proximal femur. This one is pedunculated, but still with cortical and medullary continuity

Osteosarcoma epiphysis. –– Identification of continuity between both the cortex and medullary component of the bone is critical in making the correct diagnosis. –– The polyostotic condition, hereditary multiple exostosis (or multiple hereditary exostosis) is an autosomal dominant condition characterized by the growth of multiple osteochondromas. In these individuals, the risk of malignant degeneration of a tumor is significantly higher than the extremely low risk with a solitary osteochondroma. –– Concerning factors for malignant generation include growth, a large cartilaginous cap, and new onset pain Figs. 5.39 and 5.40.

–– A malignant osteoid lesion, the most common intramedullary version of which is seen between the ages of 15 and 25. –– There are other osteosarcoma variants, including surface osteosarcomas, which may occur in different locations. –– Characterized by osteoid matrix, which on radiographic looks fluffy and white in appearance. –– Geographic lesion with a narrow or wide zone of transition, often associated with aggressive periosteal reaction. –– The telangiectatic osteosarcoma variant often has no visible matrix and may look like an aneurysmal bone cyst. –– A scary looking sclerotic lesion about the knee in a teenager should immediately make you think of osteosarcoma. Figs. 5.41, 5.42, and 5.43.

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Key Point

Telangiectatic osteosarcomas can mimic the appearance of an aneurysm bone cyst, and can be difficult to diagnosis. One clue is that they may be aggressively expansile in appearance with a wide zone of transition.

Fig. 5.42  Osteosarcoma in the proximal humerus with extensive periosteal reaction and osteoid matrix, which is very aggressive in appearance

Fig. 5.41  Osteosarcoma in the proximal fibula with abundant fluffy appearing osteoid matrix

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Infection –– A focal Brodie’s abscess is discussed under the epiphyseal lesions. Sometimes there is a sinus track extending through the bone to the cortical surface or to the physis in kids (Fig.  5.44a, b).

Diaphyseal Lesions

Fig. 5.43  A telangiectatic osteosarcoma with no osteoid matrix. This is a geographic expansile lesion, which is eccentrically located in the metadiaphysis of the distal femur. It has a wide zone of transition and cortical breakthrough and destruction along the medial femur. This could be mistaken for an aggressive aneurysmal bone cyst, a potential pitfall, and something like this will require a biopsy to ensure accurate diagnosis

a

–– –– –– –– –– –– –– –– –– ––

Fibrous dysplasia Unicameral bone cyst Aneurysmal bone cyst Fibroxanthoma Enchondroma Chondrosarcoma Infection Metastasis Myeloma Round blue cell tumors: • Lymphoma • Lekemia –– Ewing’s sarcoma

b

Fig. 5.44 (a) The geographic lytic area in the distal femur is an abscess. There is rim of surrounding reactive sclerosis. (b) MRI of the the same individual, which shows the cortically based abscess in the distal femur with

adjacent edema in the marrow and surrounding soft tissue edema. There is focal defect along the posterior aspect of the abscess, which is a track communicating between the medullary aspect of the bone and the adjacent soft tissues

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Fibrous Dysplasia –– A developmental anomaly, in which normal bone does not form. Instead, fibro-osseous tissue develops within the medullary space. –– A geographic lytic lesion with a narrow zone of transition and variable sclerotic borders. It also tends to be a long lesion in a long bone, that is if you ever see a lesion which is still geographic, but extends for a long distance in a long bone, than think fibrous dysplasia. –– Internal fibrous matrix often has a smudgy appearance on radiographs. –– There are two syndromes with polyostotic fibrous dysplasia, which we will discuss later. –– Most commonly found in the pelvis, femur, and tibia. Figs. 5.45 and 5.46.

Fig. 5.46  A typical location for fibrous dysplasia in the proximal femur. A geographic lytic lesion with a narrow zone of transition and sclerotic border. There is some expansion of the bone and internal fibrous matrix

 ibroxanthoma (also Called a Non-­ F Ossifying Fibroma)

Fig. 5.45  Fibrous dysplasia—a long geographic lytic lesion with a narrow zone of transition and a non-sclerotic border. The fibrous matrix is visible as a smudgy or hazy internal density within the lesion

–– A common benign and incidental lesion found in children and young adults, which will usually resolve or involute with age, leaving a ghost-like remnant of residual sclerosis to mark its passing. –– They may continue to grow slightly in younger patients, but their appearance is very typical and are usually easily diagnosed. In the case of large size, pain or pathological fracture they may end up being curettage and grafted. –– Geographic lytic lesion with a narrow zone of transition and a sclerotic border. They are eccentrically located or corticated based. –– Located in the metadiaphyseal regions, and most commonly found in the femur and tibia (Fig. 5.47a, b).

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a

Fig. 5.47 (a) Typical fibroxanthoma. A geographic lytic lesion with a narrow zone of transition and sclerotic border, which is eccentrically located along the diaphysis of

b

the distal tibia. (b) The same individual, showing the fibroxanthoma is slowing involuting overtime with increasing internal sclerosis

Metastasis and Myeloma –– The two most common bone lesions likely to be encountered, especially in older individuals. –– Geographic lytic lesions with a narrow or wide zone of transition, but they should never have a sclerotic border. They may also appear as permeative infiltrating lesions. Figs. 5.48 and 5.49.

Fig. 5.48  A non-geographic infiltrating or permeative lesion in the diaphysis of the femur from breast cancer metastasis

Round Blue Cell Tumors

Fig. 5.49  Lung cancer metastasis. A geographic lytic lesion with a wide zone of transition in the diaphysis of the distal radius. The lesion is expansile with cortical destruction, and there is a permeative component to the lesion along the more proximal radial diaphysis

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Fig. 5.50  Ewing’s sarcoma in the proximal fibula diaphysis, in which all we really see is aggressive periosteal reaction

Centrally Located

Round Blue Cell Tumors –– Lymphoma, leukemia, and Ewing’s sarcoma, which all look similar radiographically. –– Often non-geographic permeative or infiltrative lytic lesions, which may be associated with aggressive periosteal reaction (Fig. 5.50).

–– –– –– –– ––

Fibrous dysplasia Unicameral bone cyst Enchondroma Chondrosarcoma Round blue cell tumors: • lymphoma • leukemia • Ewing’s sarcoma –– Metastasis –– Myeloma

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Eccentrically Located Fibroxanthoma Aneurysmal bone cyst Osteosarcoma Giant cell tumor GES Cortically Based or Juxtacortical Osteofibrous dysplasia Adamantinoma Fibroxanthoma Osteoid osteoma Osteochondroma

Osteofibrous Dysplasia –– A benign lesion that nearly mostly occurs in the tibia, but can be found in the fibula. –– Geographic expansive lytic lesion with a narrow zone of transition and usually a sclerotic border. –– Shares imaging characteristics with an adamantinoma, which is discussed below, and as such biopsy is often required to ensure that it is benign. Fig. 5.51.

Fig. 5.52  Adamantinoma in the anterior cortex of the mid tibia. Similar in appearance to the osteofibrous dysplasia, but longer and more complex in appearance

Adamantinoma –– In contrast to osteofibrous dysplasia, this is a low-grade malignant tumor and requires treatment. –– Almost exclusively in the tibia, but can also occur in the fibula. –– Geographic expansile lytic lesion with a narrow zone of transition and a variable sclerotic border. In contradistinction to osteofibrous dysplasia, adamantinomas tend to be longer, bigger and with more internal complexity. Biopsy is usually necessary for confirmation (Fig. 5.52).

Osteoid Osteoma –– Small benign osteoid tumor, usually found in younger individuals. –– Cortically based, but can also occur within the medullary cavity. Most commonly found in the long bones of the lower extremities. –– Often there is a visible central sclerotic nidus with a lucent rim and surrounding reactive sclerosis. May mimic a Brodie’s abscess. –– Clinically can be painful and symptomatic and is usually treated with ablation, although it may resolve on its own. Fig. 5.53.

Fig. 5.51  Osteofibrous dysplasia in the anterior cortex of the tibia

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The Distal Phalanx One special location to mention is the distal phalangeal bones in the hands. There are two lesions that occur almost universally in this location, but which do not fit well into other groupings. These are glomus tumors and epidermoid inclusion cysts.

Glomus Tumor A benign vascular lesion that occurs beneath the fingernail. They are a soft tissue neuromuscular growth, arising from the glomus body, but can cause erosion and remodeling of the adjacent distal phalangeal bone, in which case on radiographs it will appear as geographic lytic lesion with a narrow zone of transition (Fig. 5.54).

Fig. 5.53  Osteoid osteoma arising from the cortex of the mid femoral diaphysis. We see a sclerotic central nidus with a lucent halo and adjacent smooth and benign appearing periosteal reaction

Fig. 5.54  Glomus tumor involving the fifth distal phalanx. The tumor is causing erosion and remodeling of the phalanx

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Epidermoid Inclusion Cyst There are both soft tissue and bone variants of this entity. It is not a true tumor, but rather the slow growth of an epithelial lined cyst that produces keratin. It is the result of trauma, which displaces keratin producing cells into adjacent soft tissue or bone. Radiographically, its appearance is similar to a glomus tumor—a geographic lytic lesion with a narrow zone of transition (Fig. 5.55).

Key Point

If you see a lytic lesion in a distal phalanx think about glomus tumors and epidermoid inclusion cysts.

Matrix The matrix of the tumor is dependent upon the underlying histology of the tumor. The mineralized matrices are easily recognizable, whereas the non-mineralized forms may be harder to deduce. Correct identification of the matrix material will help you further hone your accurate diagnosis of the tumor.

Types of Tumor Matrix

–– Mineralized • Osteoid • Chondroid –– Non-mineralized • Fluid • Fibrous • Fat

Osteoid –– Osteoid producing tumors will usually produce osteoid matrix. The prototypical example being the osteoid matrix formed by a conventional osteosarcoma. On radiographs, this is a dense soft fluffy appearing matrix (Fig. 5.56).

Chondroid Fig. 5.55  Epidermoid inclusion cyst. Very similar in appearance to the glomus tumor. The distal phalangeal location is key to making the diagnosis

–– Chondroid producing tumors, most classically enchondromas and chondrosarcomas, produce cartilaginous matrix, which radiographically appears finer and more reticulated and stippled than osteoid matrix (Fig. 5.57).

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Fluid –– Cystic lesion contains fluid, which radiographically looks like a simple lytic lesion. The typical appearance would be a unicameral or simple bone cyst, which is a fluid filled cavity in the bone (Fig. 5.58a, b). An aneurysmal bone cyst contains more complex fluid/blood with separate septated cavities.

Fibrous –– As typically seen in fibrous dysplasia where the fibrous bone appears smudgy and a slightly translucent white on radiographs (Fig. 5.59).

Fat

Fig. 5.56  Classic appearance of osteoid matrix, dense fluffy, and cloud-like on the radiograph. Typical of this osteosarcoma

Fig. 5.57  A typical appearance of chondroid matrix in this enchondroma

–– Interosseous lipomas are the prototypical example. These often simply look lucent on radiographs, much like a cyst. It may take MRI or CT to determine the internal components of the lesion are in fact fat (Fig. 5.60).

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a

Fig. 5.58 (a) This is a unicameral or bone cyst. Although an interosseous lipoma could have a similar appearance and also commonly occurs in this portion of the calca-

Fig. 5.59  Fibrous dysplasia in the tibia. Remember a long lesion in long bones (as here) should make you think of fibrous dysplasia. Here we see the typical fibrous matrix

b

neus. (b) The MRI shows us that this is a cyst with fluid, and not fat with the cavity. Both lesions are benign, and it may not be necessary to differentiate between them

Fig. 5.60  This is an interosseous lipoma in the femur, although it is hard to tell that it is a lipoma for sure without an MRI. The location is very good for a lipoma, and the it is non-aggressive in appearance. The calcified internal components are dystrophic calcifications within the fat

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Tumor Mimics There are a few benign conditions that may mimic a tumor and which may lead you astray. Awareness and confident diagnosis of these entities are useful.

Infection –– As we have already seen a focal bone abscess (Brodie’s abscess) can mimic a bone tumor. Infection can present in many ways in the bones and may be a mimic of a bone tumor. It is always worth considering infection as a potential cause (Figs. 5.61 and 5.62).

Fig. 5.62  Geographic lytic lesion in the distal phalanx with cortical destruction. Another case of focal infection. A clue on the image is the irregularity and loss of the soft tissues of the finger

Brown Tumor

Fig. 5.61  There is aggressive periosteal reaction along the distal radius and ulna, along with an infiltrative lytic lesion in the distal radius. Looks scary, in this case, it is the result of osteomyelitis, not tumor. But metastasis could easily look this way

–– Not a tumor, but a focal collection of osteoclastic hyperactivity causing bone resorption and on radiographs, this gives the appearance of a lytic bone lesion. They can be aggressive in appearance. –– These may be solitary or multifocal. Best clue is a history of hyperparathyroidism, often with other imaging findings of hyperparathyroidism. Fig. 5.63. Key Point

If there is a history of hyperparathyroidism, or you see imaging signs of it, then think that the lytic bone lesion you are puzzling over could be a brown tumor.

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Osteonecrosis

Fig. 5.63  Multiple lytic lesions throughout the pelvis and proximal femurs, many are associated with cortical destruction and thinning. This looks scary and your first thought should be of metastasis and multiple myeloma. But, if we look more closely, we see signs of hyperparathyroidism with bone resorption and the sacroiliac joints. These lesions are all brown tumors related to hyperparathyroidism

–– Focal areas of osteonecrosis (bone infarcts) can easily mimic a tumor and are often mistaken for a cartilaginous lesion, as there sclerotic morphology can mimic chondroid matrix. It is usually possible to differentiate between an area of osteonecrosis and a bone tumor, as their appearances and morphology are not identical. –– Osteonecrosis tends to occur in common areas, such as about the knees and is often multifocal. –– Radiographic appearance is often a geographic reticulated sclerotic area (Fig. 5.64).

Fig. 5.64  Multifocal bone infarcts about the knees. The infarcts are focal sclerotic areas of reticulation, and look similar, but recognizably different from chondroid matrix

Tumor Mimics

Giant Bone Island –– Bone islands are common incidental findings and usually recognized as small sclerotic areas in the bone, often with thorn-like margins. Giant bones islands have a similar appearance

a

133

but are much larger (2-4cm). It should not have any associated destructive or disruptive effect on the adjacent bone. –– In general, bone islands (the normal-sized ones) do not grow or change, but rarely they can appear, disappear or grow (Fig. 5.65a, b, c).

b

c

Fig. 5.65 (a) Giant bone island on radiograph. A large focal sclerotic area with thorn-like emanations extending from its periphery. (b) The CT appearance is similar. There is no periosteal reaction, bone destruction, or other

concerning imaging findings. (c) Just a black void on the MRI. No adjacent edema. All good signs and reassuring us that it is just a giant bone island

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Fig. 5.66  Osteopoikilosis. Multiple sclerotic foci, which resemble bone island. Benign

There are three benign sclerosing bone dysplasia, which may mimic tumors and are worth discussing. They are usually quite distinct and easily recognizable.

Fig. 5.67  Osteopathia striata, multiple sclerotic lines in the tibia, here also involving the talus. The long bone appearance is more recognizable

Osteopoikilosis

Melorheostosis

–– An autosomal dominant condition characterized by multiple round focal areas of sclerotic bone, which resemble multiple bone islands. These are benign and asymptomatic (Fig. 5.66).

–– Another benign sclerosing dysplasia, which can affect both the cortical and medullary components of the bone. –– Characteristic appearance of thick irregular shaped linear bone formation, often along a developmental sclerotome. The classic and oft repeated text book description is that of ­“dripping candle wax,” an apt and poetic description that we cannot improve upon. –– While benign, it can be symptomatic and cause bio-mechanical issues, especially if it crosses a joint.

Osteopathia Striata –– A benign sclerosing dysplasia, in which linear bands of sclerotic bone form parallel to the course of a long bone, although also in flat bones. Radiographically it looks like someone took a white sharpie and drew straight lines on the bone. Rare, but easily recognizable (Fig. 5.67).

Fig. 5.68.

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Fig. 5.69  Diffuse metastatic lymphoma. Multiple lytic lesions, rarely a good finding

Fig. 5.68  A classic example of melorheostosis with thick sclerotic bone extending along the distal femur—it really does look like dripping candle wax

Polyostotic Lesions If the bone lesions are multiple, the possibilities are narrowed, and this is an important factor in your diagnosis. Far and away the most common causes of multiple bone tumors are metastasis and myeloma.

Metastasis and Myeloma Remember the “M’s,” although also remember that myeloma does not occur in kids so there will

Fig. 5.70  Multiple small lytic lesions from multiple myeloma

be other considerations. Metastasis in children is also rare. If you see multiple bones lesions, first think metastasis and myeloma, especially in older individuals (Figs. 5.69 and 5.70).

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Polyostotic Fibrous Dysplasia –– Fibrous dysplasia can be polyostotic, and when polyostotic can be associated with two syndromes. –– McCune-Albright syndrome Polyostotic fibrous dysplasia Areas of skin hyperpigmentation Endocrine abnormalities, often associated with precocious puberty –– Mazabraud syndrome Polyostotic fibrous dysplasia associated with intramuscular myxomas. Fig. 5.71.

Multiple Enchondroma Syndromes –– There are two named syndromes associated with multiple enchondromas. –– Ollier disease—Multiple enchondromas. There is a higher risk of malignant degeneration of one of the enchondromas than in a solitary enchondroma.

–– Maffucci syndrome—Multiple enchondromas associated with soft tissue hemangiomas. Also has a higher risk of malignant degeneration of an enchondroma. Fig. 5.72.

Infection –– Infection is a great mimicker and is always worth considering in the setting of multiple bone lesions. Often, the clinical picture will give you the clues you need to make the diagnosis (Fig. 5.73a, b, c).

Brown Tumors –– As discussed above, they can be multifocal and mimic bone tumors. If there is ­hyperparathyroidism, it is always a good idea to consider brown tumors as a diagnosis (Fig. 5.74).

a

Fig. 5.71 (a) Polyostotic fibrous dysplasia. Multiple lytic lesions throughout both hands. It’s not common for fibrous dysplasia to occur in the hands, but it can. (b) The

b

other hand showing more fibrous dysplasia lesions. The fibrous matrix in the distal radius and first metacarpal lesions is particularly typical of fibrous dysplasia

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Caused by malignant proliferation of Langerhans cells. –– Other organ systems, besides bones, can be affected. –– A disease in children or younger adults. Not to be included in your differential of a 50-year-­ old. Always worth including when you see multiple lytic lesions in a child, especially in the skull, which is pretty pathognomonic for Langerhans cell histiocytosis. Fig. 5.75.

Saved Rounds If you have internalized even a minority of what we have presented here, then you are better trained in the diagnosis and recognition of bone tumors that just about anyone else. Congratulations. A few key points to stress again. Fig. 5.72  A child with multiple enchondromas. There are multiple expansile lytic lesions. Noticing that there is chondroid matrix in the distal radius and ulna is your best bet on making the diagnosis

Langerhans Cell Histiocytosis –– Radiographic appearance is variable, from geographic lytic lesions to a more permeative and infiltrative appearance. Usually there are multiple bone lesions, but can be solitary.

• Multiple lytic lesions in adults should instantly make you think of metastasis or myeloma. • It is less important to arrive at a correct histological diagnosis than it is to recognize a lesion that is benign from one that is malignant. Use key findings like the zone of transition, periosteal reaction, age, and number to help make this decision. If there is doubt, than biopsy or at least monitor the lesion.

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a

b

c

Fig. 5.73 (a–c) Multiple lytic bone lesions from disseminated coccidioidomycosis infection, the L2 lesion has

caused ca pathological fracture and collapse of the vertebral body

Live Fire Exercises

Fig. 5.74  These lytic lesions could easily be metastasis or myeloma, but in this case these are brown tumors associated with hyperparathyroidism

139

Fig. 5.75  Multiple lytic lesions in the calvarium. The fontanelle is still open, so we know this is a young person. This is a classic appearance of Langerhans cell histiocytosis

• Beware that even a benign appearing tumor in an older adult should prompt you to consider something more menacing.

Live Fire Exercises Ready to test yourself? Lock and load. Let’s roll.

1 –– Describe the finding. –– Benign or malignant? –– There is only one correct diagnosis in this case. What is it?

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2 –– Describe the finding in this child. –– Benign or malignant? –– Best diagnosis?

4 –– Describe the finding in this middle-aged woman. –– Benign or malignant? –– Best diagnosis? 3 –– Describe the finding in this child. –– Benign or malignant? –– Best diagnosis?

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5 –– Describe the finding in this young adult. –– Benign or malignant? –– Only possible diagnosis?

6 –– Describe the findings in this teenager. –– Benign or malignant? –– Best diagnosis?

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7 –– Describe the findings in this older adult. –– Benign or malignant? –– Best diagnosis?

Live Fire Exercises

8 –– Describe the finding in this teenager. –– Benign or malignant? –– Best diagnosis?

9 –– Describe the findings. –– Benign or malignant? –– Best diagnosis?

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After Action Review Assess yourself, mistakes and misses are normal, but make sure you learn from them. 1 –– Describe the finding. There is a geographic lytic lesion with a narrow zone of transition and a non-sclerotic border in the anterior calcaneus. There is a central sclerotic focus. –– Benign or malignant? Everything we just described sounds benign. –– There is only one correct diagnosis in this case. What is it? This is an interosseous lipoma. There is no other possibility. We can be sure of this diagnosis once we see the dystrophic fat calcification centered within the lesion. If we don’t see this central calcification, then a unicameral bone cyst is also a possibility. Both lesions occur in this location in the calcaneus. 2 –– Describe the finding in this child. There is a small geographic lytic lesion with a narrow zone of transition and a sclerotic border which is in the cortex of the femur. There is faint central sclerosis. There is prominent adjacent smooth and benign-appearing periosteal reaction. –– Benign or malignant? Looks benign. –– Best diagnosis? This is a typical appearance of an osteoid osteoma. These are small benign lesions usually seen in children or young adults. The often elicit abundant, but benign periosteal reaction. They can be painful, but have no malignant potential. 3 –– Describe the finding in this child. There is a geographic lytic lesion with a narrow zone of transition and a non-sclerotic bor-

der centered in the metaphysis of the proximal humerus. There is a pathological fracture through the lesion with a fracture fragment floating in its center. –– Benign or malignant? A benign description for a benign lesion, although there is the complication of the fracture, which will require treatment. –– Best diagnosis? This is a unicameral bone cyst, with the pathognomonic “fallen fragment” sign. 4 –– Describe the finding in this middle-aged woman. There is a geographic lytic lesion with a wide zone of transition centered in the meta-­ diaphysis of the proximal humerus. There is cortical destruction and faint aggressive periosteal reaction. –– Benign or malignant? You should not be calling this benign. Especially in an adult. Looks bad. –– Best diagnosis? When you see an aggressive lytic lesion in an older adult, the first two things you should think of are metastasis and multiple myeloma. This appearance could be either of those, but in this case was a plasmacytoma from myeloma. 5 –– Describe the finding in this young adult. –– There is an exophytic lesion arising from the proximal fibular diaphysis, which has cortical and medullary continuity. –– Benign or malignant? Not scary looking. –– Only possible diagnosis? This is an osteochondroma. There is no other diagnosis to consider. This one is pedunculated, and while rarely a solitary one can undergo malignant degeneration, there are no concerning findings here.

Bibliography

6 –– Describe the findings in this teenager. There is a geographic lytic lesion with a narrow zone of transition and a partially sclerotic border which is centrally located in the diaphysis of the proximal femur. There is internal smudgy matrix, which looks fibrous. There is a pathological fracture through the distal aspect of the lesion. –– Benign or malignant? Looks benign, although it will need treatment as it has weakened the bone and there is now a pathological fracture. –– Best diagnosis? If you see a long lesion in a long bone, think fibrous dysplasia. This is a classic example of fibrous dysplasia.

145

–– Best diagnosis? This is an aneurysmal bone cyst. An expansile lytic lesion. 9 –– -Describe the findings There are multiple geographic lytic lesions. Many are expansile. There are also soft tissue calcifications. –– Benign or malignant? Despite the multitude of lesions, they look benign. –– Best diagnosis? Since we have multiple lesions, we can think of polyostotic conditions. In this case, these are multiple enchondromas. The soft tissue calcifications are phleboliths from hemangiomas. This is Maffucci syndrome.

7 –– Describe the findings in this older adult. There is a geographic expansile and destructive lytic lesion in the scapula, which involves the acromion, and its medial aspect. There is cortical destruction and thinning. –– Benign or malignant? Scary! –– Best diagnosis? Again, aggressive lesions in older adults should prompt the reflexive: metastasis and myeloma. This was a metastatic melanoma lesion. 8 –– Describe the finding in this teenager. There is an expansile geographic lytic lesion with a narrow zone of transition and a non-­ sclerotic border in the distal clavicle. –– Benign or malignant? Here age is crucial in helping us decide. If this were a 60-year-old, we should be worried. In a teenager, we are not as concerned for a malignant process, although the lesion is still locally destructive.

Bibliography 1. Wenaden AE, Szyszko TA, Saifuddin A. Imaging of periosteal reactions associated with focal lesions of bone. Clin Radiol. 2005;60(4):439–56. 2. Miller TT.  Bone tumors and tumorlike conditions: analysis with conventional radiography. Radiology. 2008;246(3):662–74. 3. Chen EM, Masih S, Chow K, Matcuk G, Patel D.  Periosteal reaction: review of various patterns associated with specific pathology. Contemp Diagn Radiol. 2012;35(17):1–5. 4. Gemescu IN, Cheerleader KM, Rehnitz C, Weber MA. Imaging features of bone tumors: conventional radiographs and MR imaging correlation. Magn Reson Imaging Clin. 2019;27(4):753–67. 5. Simon MA, Finn HA.  Diagnostic strategy for bone and soft-tissue tumors. JBJS. 1993;75(4):622–31. 6. Campanacci M, Mercuri M, Gasbarrini A, Campanacci L.  The value of imaging in the diagnosis and treatment of bone tumors. Eur J Radiol. 1998;1(27):S116–22. 7. Giudici MA, Moser RP Jr, Kransdorf MJ. Cartilaginous bone tumors. Radiol Clin N Am. 1993;31(2):237–59. 8. Adler CP, Kozlowski K.  Primary bone tumors and tumorous conditions in children: pathologic and radiologic diagnosis. Springer Science & Business Media; 2012. 9. Motamedi K, Seeger LL. Benign bone tumors. Radiol Clin. 2011;49(6):1115–34.

146 10. Shah JN, Cohen HL, Choudhri AF, Gupta S, Miller SF.  Pediatric benign bone tumors: what does the radiologist need to know?: pediatric imaging. Radiographics. 2017;37(3):1001–2. 11. Hwang S, Hameed M, Kransdorf M.  The 2020 World Health Organization classification of bone tumors: what radiologists should know. Skelet Radiol. 2023;52(3):329–48. 12. Errani C, Tsukamoto S, Mavrogenis AF.  Imaging analyses of bone tumors. JBJS Rev. 2020;8(3):e0077. 13. Mehta K, McBee MP, Mihal DC, England EB. Radiographic analysis of bone tumors: a systematic approach. In Seminars in roentgenology 2017 (52, 4, pp. 194-208). WB Saunders 14. Nomikos GC, Murphey MD, Kransdorf MJ, Bancroft LW, Peterson JJ.  Primary bone tumors of the lower extremities. Radiol Clin. 2002;40(5):971–90. 15. Murphey MD, Choi JJ, Kransdorf MJ, Flemming DJ, Gannon FH.  Imaging of osteochondroma: variants and complications with radiologic-pathologic correlation. Radiographics. 2000;20(5):1407–34. 16. Murphey MD, Robbin MR, McRae GA, Flemming DJ, Temple HT, Kransdorf MJ.  The many faces of osteosarcoma. Radiographics. 1997;17(5):1205–31. 17. Kransdorf MJ, Murphey MD.  Osseous tumors. In: Imaging of bone tumors and tumor-like lesions: techniques and applications. Springer; 2009. p. 251–306. 18. Kransdorf MJ, Murphey MD.  Giant cell tumor. In: Imaging of bone tumors and tumor-like lesions: techniques and applications. Springer; 2009. p. 321–36. 19. Islinger RB, Kuklo TR, Owens BD, Horan PJ, Choma TJ, Murphey MD, Temple HT. Langerhans’ cell histiocytosis in patients older than 21 years. Clin Orthop Relat Res. 2000;379:231–5. 20. Flemming DJ, Murphey MD.  Enchondroma and chondrosarcoma. Seminars in musculoskeletal radiology 2000 (4, 01, 0059-0072). Thieme Medical Publishers, New York, NY 21. Murphey MD, Carroll JF, Flemming DJ, Pope TL, Gannon FH, Kransdorf MJ. From the archives of the AFIP: benign musculoskeletal lipomatous lesions. Radiographics. 2004;24(5):1433–66. 22. Robbin MR, Murphey MD.  Benign chondroid neoplasms of bone. Seminars in musculoskeletal radiology 2000 (4, 01, 0045-0058). Thieme Medical Publishers, New York, NY 23. Murphey MD, Andrews CL, Flemming DJ, Temple HT, Smith WS, Smirniotopoulos JG.  From the archives of the AFIP.  Primary tumors of the spine: radiologic pathologic correlation. Radiographics. 1996;16(5):1131–58. 24. Murphey MD, wan Jaovisidha S, Temple HT, Gannon FH, Jelinek JS, Malawer MM. Telangiectatic osteosarcoma: radiologic-pathologic comparison. Radiology. 2003;229(2):545–53. 25. Murphey MD, Kransdorf MJ. Soft tissue tumors. In: Radiologic-pathologic correlations from head to toe: understanding the manifestations of disease. Springer; 2005. p. 743–54.

5  Bone Tumors 26. Serfaty A, Samim M. Bone tumors: imaging features of the most common primary osseous malignancies. Radiol Clin. 2022;60(2):221–38. 27. Parman LM, Murphey MD.  Alphabet soup: cystic lesions of bone. Seminars in musculoskeletal radiology 2000(4, 01, 0089-0102). Thieme Medical Publishers, New York, NY 28. Murphey MD, Sartoris DJ, Quale JL, Pathria MN, Martin NL.  Musculoskeletal manifestations of chronic renal insufficiency. Radiographics. 1993;13(2):357–79. 29. Sobti A, Agrawal P, Agarwala S, Agarwal M.  Giant cell tumor of bone-an overview. Arch Bone Jt Surg. 2016;4(1):2. 30. Chakarun CJ, Forrester DM, Gottsegen CJ, Patel DB, White EA, Matcuk GR Jr. Giant cell tumor of bone: review, mimics, and new developments in treatment. Radiographics. 2013;33(1):197–211. 31. Chen W, DiFrancesco LM.  Chondroblastoma: an update. Arch Pathol Lab Med. 2017;141(6):867–71. 32. Kransdorf MJ, Stull MA, Gilkey FW, Moser RP Jr. Osteoid osteoma. Radiographics. 1991;11(4):671–96. 33. Chai JW, Hong SH, Choi JY, Koh YH, Lee JW, Choi JA, Kang HS.  Radiologic diagnosis of osteoid osteoma: from simple to challenging findings. Radiographics. 2010;30(3):737–49. 34. Angtuaco EJ, Fassas AB, Walker R, Sethi R, Barlogie B. Multiple myeloma: clinical review and diagnostic imaging. Radiology. 2004;231(1):11–23. 35. Collins MS, Koyama T, Swee RG, Inwards CY. Clear cell chondrosarcoma: radiographic, computed tomographic, and magnetic resonance findings in 34 patients with pathologic correlation. Skelet Radiol. 2003;32:687–94. 36. Cottalorda J, Bourelle S. Modern concepts of primary aneurysmal bone cyst. Arch Orthop Trauma Surg. 2007;127:105–14. 37. Van der Naald N, Smeeing DP, Houwert RM, Hietbrink F, Govaert GA, der DV. Brodie's abscess: a systematic review of reported cases. J Bone Jt Infect. 2019;4(1):33–9. 38. Kransdorf MJ, Moser RP Jr, Gilkey FW. Fibrous dysplasia. Radiographics. 1990;10(3):519–37. 39. O’Donnell RJ, Springfield DS, Motwani HK, Ready JE, Gebhardt MC, Mankin HJ. Recurrence of giant-­ cell tumors of the long bones after curettage and packing with cement. JBJS. 1994;76(12):1827–33. 40. Mravic M, LaChaud G, Nguyen A, Scott MA, Dry SM, James AW. Clinical and histopathological diagnosis of glomus tumor: an institutional experience of 138 cases. Int J Surg Pathol. 2015;23(3):181–8. 41. Lincoski CJ, Bush DC, Millon SJ. Epidermoid cysts in the hand. J Hand Surg (Eur Vol). 2009;34(6):792–6. 42. Gould CF, Ly JQ, Lattin GE Jr, Beall DP, Sutcliffe JB III. Bone tumor mimics: avoiding misdiagnosis. Curr Probl Diagn Radiol. 2007;36(3):124–41. 43. Mhuircheartaigh JN, Lin YC, Wu JS.  Bone tumor mimickers: a pictorial essay. Indian J Radiol Imaging. 2014;24(03):225–36.

Bibliography 44. Greenspan A.  Bone island (enostosis): current concept—a review. Skelet Radiol. 1995;24:111–5. 45. Smith J.  Giant bone islands. Radiology. 1973;107(1):35–6. 46. Brien EW, Mirra JM, Latanza L, Fedenko A, Luck J Jr. Giant bone island of femur. Case report, literature review, and its distinction from low grade osteosarcoma. Skelet Radiol. 1995;24(7):546–50. 47. Ihde LL, Forrester DM, Gottsegen CJ, Masih S, Patel DB, Vachon LA, White EA, Matcuk GR Jr. Sclerosing bone dysplasias: review and differentiation from other causes of osteosclerosis. Radiographics. 2011;31(7):1865–82.

147 48. Mainzer F, Minagi H, Steinbach HL.  The variable manifestations of multiple enchondromatosis. Radiology. 1971;99(2):377–88. 49. Azouz EM, Saigal G, Rodriguez MM, Podda A. Langerhans’ cell histiocytosis: pathology, imaging and treatment of skeletal involvement. Pediatr Radiol. 2005;35:103–15. 50. Stull MA, Kransdorf MJ, Devaney KO.  Langerhans cell histiocytosis of bone. Radiographics. 1992;12(4):801–23.

6

Orthopedic Hardware

Foundations

Hardware Imaging

Orthopedic hardware can be generally divided into three categories: (1) stabilizing hardware, (2) arthroplasty hardware, (3) anchoring hardware. Stabilizing hardware is founded in situations where either a single bone needs to be stabilized to allow biologic fracture healing or when motion between two bones is not desired (arthrodesis). A variety of hardware devices exist to achieve these ends, and the selection of hardware varies greatly between application, fracture geometry, and any additional clinical considerations, such as substantial injury to the surrounding soft tissue envelope. Arthroplasty hardware partially or completely replaces a joint. The basic mechanical configuration of the hardware has remained relatively stable over time with advances made in the underlying material science. Large joint arthroplasties are by far the most common, though there are options for virtually every arthrodial joint. Anchoring hardware provides a way to attach soft tissue structures to bone. A simple suture anchor is the prototypical example. Anchoring hardware is encountered in labral repair and ligamentous reconstructions.

Plain Radiography Plain films are fundamental in the evaluation of hardware. Portable plain films are acquired in the PACU in virtually every operative case where hardware was placed. These films document adequate hardware positioning and exclude any immediate complications such as fracture, dislocation, or component failure. In cases of open reduction internal fixation (ORIF) hardware, alignment across the fracture is also assessed. Subsequent plain films are used to document the progressive bony changes about the implant such as fracture healing.

CT CT can be invaluable when working up hardware complications, but CT is not routinely used in asymptomatic patients. Painful orthopedic hardware and suspected nonunion of a hardware-­ stabilized fracture are two of the more common indications for CT.  The bone–hardware interface can be seen to better advantage than with plain radiography, and thus early perihardware lucencies are more readily detectable. Subtle periprosthetic fracture planes are also much more evident by CT.

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The primary disadvantage of CT is the significant streak artifact caused by the hardware. Due to a combination of beam hardening and photon starvation, the artifacts can be substantial and occasionally make the studies nondiagnostic. Metal artifact reduction techniques provide modest improvement, but the limitations are still significant. Dual energy CT can significantly reduce metal artifacts, but it is not yet widely available. Additionally, our orthopedic surgery, internal medicine, and emergency medicine colleagues are generally unfamiliar with this technology, and, as of now, they usually do not know if their institution has a dual-energy scanner or to specifically request this technique.

MRI Similar to CT, MRI has distinct advantages over plain radiology, but is largely limited by metal artifacts. Detection of abnormalities in soft tissues adjacent to orthopedic hardware is the primary utility of MRI in this setting. Contrast is occasionally needed, depending on the indication.

Nuclear Medicine Nuclear medicine techniques are generally limited to the evaluation of hardware loosening and hardware-related infection. MDP bone scans are not terribly useful in the first year after hardware placement due to bone healing and remodeling.

Hardware Complications Hardware Failure In the most basic terms, the hardware has failed when it no longer functions as intended. Fracture of plate and screw constructs, avulsion of suture anchors, and prosthetic dislocations are just a few of myriad complications. Detection of hardware failure fundamentally affects clinical management. While straightforward when the hardware has grossly failed, picking up early imaging findings can be very difficult indeed. Former Secretary of State Collin Powell’s eighth leadership rule, “Check small things” aptly applies.

Displaced Hardware A fairly uncommon complication, displacement of small hardware components is usually detected by plain radiography and is indicative of a failure, or impending failure, of the orthopedic repair. Displaced anchoring hardware, especially suture anchors, seems to be the most frequently encountered displaced hardware. Knowledge of the original repair and, if you are lucky, accesses to the index post-operative plain film, is invaluable. If you see newly displaced hardware, it’s best to search the electronic medical record for an operative note so that you can piece the story together. When the imaging study is being ordered from a non-­o rthopedic provider, you almost certainly have more experience in this realm, and your recommendations will drive management.

Perihardware Fracture Less commonly encountered than hardware failure, perihardware fractures are usually seen in the setting of trauma, often with an arthroplasty. That being said, the placement of any orthopedic hardware fundamentally alters the biomechanics of the underlying bone  ­creating an opportunity for frank bone failure.

Hardware Infection Following an orthopedic trauma, infection of the traumatic or surgical wound and the underlying hardware is the most common complication. The diagnosis is based on clinical and laboratory grounds, and it would be rare for a patient to present with imaging findings of osteomyelitis prior to any clinical suspicion for infection. Treatment is typically a combination of antibiotic therapy and debridement. The hardware is usually removed. Infection following arthroplasty (prosthetic joint infection) can be devastating and is the most common cause for revision arthroplasty. It is treated separately below (Fig. 6.1a–d).

Hardware Complications

151

a

b

c

d

Fig. 6.1 (a–d) Infected hardware: (a and b) Diffuse thickening and irregularity of the proximal and mid tibial diaphysis are unusual for fracture healing following intramedullary nail stabilization, raising suspicion for infection. (c, d) There

is progression of the bony abnormalities with developing areas of cortical destruction. There is perihardware lucency around both the intramedullary nail and fracture of the screw from increased hardware failure related to infection

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Specific Complications of Arthroplasty Hardware Unlike the other classes of orthopedic hardware, arthroplasty hardware must provide both stability and mobility across the joint. Inherently complicated, revision arthroplasty is necessary for a variety of underlying causes. Of these, the most common are (1) periprosthetic fracture, (2) hardware dislocation, (3) hardware subsidence/ motion, and (4) hardware infection. Periprosthetic fracture can occur in the setting of both major and minor trauma or may be the result of chronic bone stress. Any fracture marginating the prosthesis falls into the category. One particular type of periprosthetic fracture occurs in combination with hardware motion. The far distal aspect of a hardware stem is the location of the most concentrated moment or torque and is the point of high mechanical stress. To help overcome this, all modern hardware is gradually tapered to allow a smooth transition of the articular forces from hardware to native bone. Motion at the tip of the stem may be occult by plain film imaging or appear as a very subtle lucency at and near the tip. At 99Tc-MDP scintigraphy, a “hot spot” will be seen. Pathologic periprosthetic fractures can occur in orthopedic oncology setting, and unfortunately usually denote disease progression. Hardware dislocations are also often seen in the traumatic setting, but can certainly develop in a more indolent fashion. Figure 6.2 This failure mode is obvious on plain films. Periprosthetic fracture and hardware dislocation are the two main complications to look for on the immediate post-arthroplasty images. Subsidence of the arthroplasty hardware is uncommon and most frequently seen in hip arthroplasty. In bipolar hip arthroplasties, either component can be involved, but the femoral component is the usual culprit. Other known trouble spots for subsidence are ankle, shoulder, and intervertebral spinal hardware, but they are far less common. Component loosening is closely related, more frequently encountered, and can be

Fig. 6.2  Hardware dislocation: Complete dislocation of the femoral component of the right hip arthroplasty on this immediate post-operative film

thought of as a precursor to subsidence. The sentinel plain film finding is a developing lucency along the bone–hardware interface, what we describe as a perihardware lucency (Figs. 6.3 and 6.4a, b). Increased radiopharmaceutical uptake on bone scan is the second classic finding in component loosening, and it can be seen before perihardware lucency development. Focal uptake at the tip of a prosthetic component’s stem indicates toggling and abnormal component motion. Of all hardware-related complications, prosthetic joint infection can be the most serious and the most confounding. Imaging plays a supporting role to laboratory analysis in the work up of hardware-related infections. Metallic artifact

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153

can be seen. Often plain film is enough in the appropriate clinical setting to drive further management, typically image-guided arthrocentesis. Nuclear medicine studies are employed less frequently than in the past. Indium-111 labeled white blood cell imaging is very sensitive for prosthetic joint infection. However, since indium labeled leukocytes also accumulate in normal bone marrow, it is not, but itself, very specific. To overcome this challenge, the technetium labeled sulfur colloid study is performed to provide a map of the bone marrow. An area demonstrates radiopharmaceutical uptake on both scans is considered normal/congruent, whereas an area that is active on the 111In-leukocyte scan but does not concentrate 99mTc-sulfur colloid is highly suspiFig. 6.3  Hardware subsidence: There is axial migration cious for infection. Finally, the articulating surfaces of all arthroof the left acetabular cup with thinning of the overlying bone from loosening and subsidence of the acetabular plasty devices experience wear over time. component. Additionally, there are signs of polyethylene Depending on the type of implanted hardware, wear, this is established by observing the asymmetrical location of the femoral head component within the acetab- complications from component wear can be preular component. This is obviously a more advanced and dicted. Wear from polyethylene liners generates obvious finding, early manifestations are more subtle small particles that induce synovitis. The polyethylene wear may cause malalignment of the limits the sensitivity of both CT and MRI. This components, and in the more common setting of leaves plain radiography and, in challenging a hip arthroplasty, we will see that the femoral cases, nuclear medicine, as the primary imaging component shifts from being centered in the modalities. acetabular cup to being located asymmetrically The Centers for Disease Control and Infection (Fig. 6.5a, b). (CDC) distinguishes infections as either acute or MRI is by far the most sensitive imaging chronic with the demarcation at the 90th post-­ modality where expansion of the pseudocapsule operative day. From an imaging standpoint, this with low-to-intermediate T1 and T2 signal intenmakes little difference, but it does predict likely sity. Given the intermediate signal which is often pathogens and treatment course. The defining isointense to muscle, these collections can be difclinical symptom of a prosthetic joint infection is ficult to detect; keep an eye out, check small persistent pain at the arthroplasty site, often lim- things! When large, the collections can extend iting range of motion. Imaging features are all into the iliopsoas bursa or even decompress into nonspecific, however general themes exist. the adjacent soft tissues. Plain radiography findings of hardware-­ Similarly, metal-on-metal arthroplasty related infections largely mimic those of osteo- devices can result in wear-related complications. myelitis and hardware loosening. There is Metal particles can set off inflammatory reacdemineralization of the cancellous and trabecular tions of various types, the scope of which is bone resulting in blurring of the cortex and focal beyond the scope of this text. Inflammatory osteopenia. Perihardware lucencies appear and changes can also be triggered by component corare indistinguishable from that seen with hard- rosion and metal ions. The overall term encomware loosening. In more chronic cases, periostitis passing these complications is adverse local

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a

Fig. 6.4 (a) Failure of the knee arthroplasty. Multiple issues are here. There is disassociation of the proximal tibial stem and prominent osteolysis and loosening of the tibial stem. There is subsidence of the proximal tibial components, and asymmetrical narrowing along the lateral aspect of the arthroplasty. If you note the position of

b

the tibial articular surface to the proximal fibula, you will get a good idea of how much this has subsided and collapsed. (b) The lateral view showing the prominent displacement and loosening of the tibial stem, which extends through the posterior tibial cortex

Hardware Complications

a

155

b

Fig. 6.5 (a, b) Periacetabular osteolysis of the right total hip arthroplasty reflects expansion of the pseudocapsule by fluid and synovitis, ultimately secondary to polyethyl-

ene liner wear in this particular case, as we see by the asymmetric location of the femoral component within the acetabular component

tissue reaction. Some authors use this term to specifically mean one type of complications or another, so beware if you decide to use it in your report; it can be ambiguous. Regardless of names, the high rate of complications to metalon-metal devices, namely hip arthroplasty devices, has resulted in the FDA issuing alerts on these arthroplasty systems. The inflammatory response causes expansion of the joint pseudocapsule with T2 hyperintense fluid. Dehiscence of the pseudocapsule is com-

mon and allows the inflammatory fluid to affect local structures (Fig. 6.6a–c). Decompression into the greater trochanteric bursa and iliopsoas bursa is common. Once there, the inflammation can affect adjacent tendon attachments or the neurovascular bundles. Because of the complications, grading systems have been developed. As discussed in the chapter on reports, use grading systems if that is common practice at your institution. If not, simply describe the findings.

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156

a

b

c

Fig. 6.6 (a–c) Adverse local tissue reaction: (a) Axial T1, (b) Axial T2, and (c) Coronal T1 MR images of the right hip documenting a T1 and T2 hyperintense periar-

ticular fluid collection in this 65-year-old with worsening right hip pain after remote right total hip arthroplasty

Saved Rounds

ter a new device. Chances are that it will be used again at your institution. If you see a subtle hardware complication, contact the surgeon. Often the plain films are ordered by the office staff prior to the appointment which could be several weeks in the future.

It would be quite a challenge to know the specific manufacturer’s names for every type of orthopedic hardware, and fortunately it isn’t necessary. The surgeon knows what was used. That being said, read the operative report when you encoun-

Bibliography

157

Bibliography

Fig. 6.7  All of the major hardware complications except infection are demonstrated in this view of the pelvis. Related to the hardware, there is displacement of the right acetabular cup with a dropped screw, loosening of the right femoral component, a perihardware fracture along the right intertrochanteric plane, and superolateral subsidence of the acetabular cup. Surrounding soft tissue irregularity and punctate soft tissue calcifications reflect the underlying adverse local tissue reaction

Adverse local tissue reactions are classically associated with metal-on-metal hip arthroplasty devices, but know that corrosion is a major source of free metallic ions which are one of the major initiators of the inflammatory process that underlies this class of complications. Corrosion can occur along any metallic surface, regardless of the composition of the weightbearing components (Fig. 6.7).

1. Bottlang M, Fitzpatrick DC, Lutz C, Anderson DD. Biomechanics of fractures and fracture fixation. In: Tornetta P, Ricci WM, Ostrum RF, et al., editors. Rockwood and Green’s fractures in adults. 9th ed. Philadelphia: Wolters Klewer; 2020. 2. Burge AJ.  Total hip arthroplasty: MR imaging of complications unrelated to metal wear. Semin Musculoskelet Radiol. 2015;19(1):31–9. 3. Davis DL, Morrison JJ.  Hip arthroplasty pseudotumors: pathogenesis, imaging, and clinical decision making. J Clin Imaging Sci. 2016;6:17. 4. Fritz J, Lurie B, Miller TT, Potter HG.  MR imaging of hip arthroplasty implants. Radiographics. 2014;34(4):E106–32. 5. https://www.state.gov/dipnote-u-s-departmentof-state-official-blog/colin-l-powells-thirteenrules-of-leadership/. 6. Love C, Tomas MB, Marwin SE, Pugliese PV, Palestro CJ.  Role of nuclear medicine in diagnosis of the infected joint replacement. Radiographics. 2001;21(5):1229–38. 7. Palestro CJ.  Nuclear medicine and the failed joint replacement: past, present, and future. World J Radiol. 2014;6(7):446–58. 8. Pinski JM, Chen AF, Estok DM, Kavolus JJ. Nuclear medicine scans in total joint replacement. J Bone Joint Surg Am. 2021;103(4):359–72. 9. Roemer FW, Crema MD, Trattnig S, Guermazi A.  Advances in imaging of osteoarthritis and cartilage. Radiology. 2011;260(2):332–54. 10. Thippeswamy PB, Nedunchelian M, Rajasekaran RB, Riley D, Khatkar H, Rajasekaran S.  Updates in postoperative imaging modalities following musculoskeletal surgery. J Clin Orthop Trauma. 2021;22:101616. 11. Yanny S, Cahir JG, Barker T, et  al. MRI of aseptic lymphocytic vasculitis-associated lesions in metal-­ on-­metal hip replacements. AJR Am J Roentgenol. 2012;198(6):1394–402.

7

Arthritis

How do we approach and evaluate arthritis or a disease process centered within a joint? Step one in evaluating arthritis, understand the abnormality is within the joint. From there, we will proceed. We will tell you how to identify if the process is joint centered. All understanding of arthritis derives from the realization that there is something wrong within the joint. This can be both the easiest and the hardest part in evaluating arthritis. Step two know that there are a limited number of entities that can cause problems in the joint. We will address them one by one. Step three—Evaluate the findings and compare them to the known causes of arthritis-­ articular centered processes and see which is the best fit. Articular Centered Processes

– – – – – – – –

Osteoarthritis Inflammatory arthritis Septic arthritis Neuropathic arthritis Deposition diseases Hemophilia arthropathy Benign proliferative processes Vascular malformations

Let’s break it down. • We identify that there is something wrong with the joint. • We run through our list of joint centered diseases. • We use our observations, knowledge, and clinical information to narrow the diagnosis down to one or perhaps two most likely possibilities. This process becomes innate after a while, and many processes, such as osteoarthritis are so common and clearly recognizable we run through these steps instantly and seamlessly. It is for the tricker situations that this process becomes more useful. How do we know there is an arthritis or problem with the joint? On initial radiographic evaluation, we look for signs of joint damage. These included: joint space narrowing or destruction, erosions, osteophytes or adjacent reactive sclerosis or cyst formation. Any and/or all of these can be used to isolate a process within the joint. Sometimes all you may see are some small erosions or remodeling from the articular process. At times there will be extensive joint destruction and irregularity, which is easily recognizable. There may be

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times when the articular centered disease is not apparent on the radiographs and cross-sectional imaging may be required. CT, MRI, and ­ultrasound all have a role in evaluating arthritis, and each has its strengths and weakness. For the purposes of this manual, we shall primarily confine ourself with radiographic manifestations and diagnosis.

Radiographic Signs of Arthritis

–– –– –– ––

Joint space narrowing or destruction Erosions Osteophytes Subchondral sclerosis

Let’s start with the biggest and most common of them all.

Fig. 7.1  Severe degenerative osteoarthritis at the shoulder. The joint space is nearly completely narrowed, there is reactive subchondral sclerosis and a large osteophyte off of the medial humeral head

Osteoarthritis Although this is by far and away the most common form of arthritis that you will encounter, we are not going to spend much time discussing it. Osteoarthritis is degenerative wear of the joint. Cartilage is worn, lost, and destroyed, and as this happens the joint spaces narrow, and reactive osteophytes form at the joint margins. This is very common and can occur at any joint. The first carpometacarpal joints, knees, shoulders, and hips are all common places for degenerative arthritis to occur. It can develop as the result of an injury, or simply develop because of the wear and tear of life. The imaging manifestations are usually pretty straight forward. We look for joint space narrowing, marginal osteophytes, and often associated subchondral reactive sclerosis and cyst formation. A few typical examples: Figs.  7.1, 7.2, and 7.3. There are subtle radiographic manifestations of osteoarthritis. Although MRI is the way to go to get a good understanding of any cartilage dam-

Fig. 7.2  A milder form of osteoarthritis at the knee, here just in the medial compartment where there is mild joint space narrowing and small osteophytes

age, we can still get a sense on radiographs, this is most notable at the knee where patella chondral damage is often clearly visible. This is visi-

Osteoarthritis

ble as lucency and irregularity of the subchondral bone, which we can see in the patella and also the trochlea. Since patella chondral damage is a common manifestation of degenerative arthritis in the knee, it is something that can be commonly seen,

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but is often ignored or disregarded as we are not use to thinking that we can evaluate cartilage on radiographs, without associated joint space narrowing. Shift your mindset and know that in some settings, radiographs can evaluate cartilage as well, even in the absence of joint space narrowing or other manifestations of arthritis (Figs. 7.4a and b). Key Point

Patella femoral cartilage damage is often visible on radiographs and can be seen in the absence of joint space narrowing. Look for lucency and cystic irregularity of the subchondral surface.

Erosive Osteoarthritis

Fig. 7.3  Severe osteoarthritis at the hip, another common location

a

A variant worth knowing is erosive osteoarthritis. This is a severe form of osteoarthritis, which, in addition to the typical destruction of the joint space, and osteophytes, there are associated ero-

b

Fig. 7.4 (a) Patella cartilage damage, which is visible on the radiograph. (b) The chondral damage is often more apparent on the Merchant and sunrise views

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Fig. 7.5  Erosive osteoarthritis with joint space narrowing, marginal osteophytes, and central erosions. Here the proximal interphalangeal joints are most severely affected

sions. Erosions are usually not associated with osteoarthritis, but are found in erosive osteoarthritis. This is almost always confined to the interphalangeal joints of the hands, but rarely and less commonly affects the interphalangeal joints in the feet. The classic manifestation of this form of arthritis is characterized by three things: • Joint space narrowing • Marginal osteophytes • Central erosion(s) These three key imaging components are useful for differentiating erosive osteoarthritis from psoriatic arthritis, which also has a predilection for the interphalangeal joints (Fig. 7.5). Now in reality, the erosions are not always confined to the central aspect of the bone and continue in a saw-toothed type jagged pattern along the joint, but they should have a central erosive component. Erosive osteoarthritis can

cause ankylosis of a joint, a rare finding reserved usually for inflammatory arthropathies.

Inflammatory Arthropathies Inflammatory arthropathies are auto-immune diseases characterized by inflammation, which cause erosion and destruction of joints. It can also often affect the spine where there can be erosion and ankylosis. While there is often overlap and indistinct boundaries between the different inflammatory arthropathies, here we will consider them in their more pure and classic forms. Just be aware that in reality disease processes are not so neatly clear cut and don’t always confine themselves to the nice distinct boxes that we have created to name and categorize them. These inflammatory arthropathies can be subdivided into the classically named rheumatoid arthritis and the seronegative versions (not-­

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Inflammatory Arthropathies

positive for rheumatoid factor). The seronegative arthropathies are ankylosing spondylitis, enteropathic-­ related arthritis, and psoriatic arthritis. Inflammatory Arthropathies

Rheumatoid arthritis Juvenile Idiopathic arthritis (JIA) Sero-negative arthropathies –– Ankylosing spondylitis –– Psoriatic arthritis –– Reactive arthropathy –– Enteropathic related

Often each of these have distinct and preferentially joints that are affected, which is the primary way we use to make a judgment about what type of inflammatory arthritis is involved. While it is often possible to differentiate inflammatory arthritis from degenerative arthritis, it is not always possible to definitively say which inflammatory arthropathy is involved. However using the distribution of joints involved, we have a good chance of arriving at a correct diagnosis. What follows are typical manifestations of these disease on radiographs. Many of these examples are of advanced and poorly controlled disease. Hopefully with early treatments, these appearances will be less common, but in our daily practice we still see many examples of advanced destructive disease. A word about one finding, which is often mentioned when talking about the diagnosis of inflammatory arthritis—periarticular osteopenia. This refers to the relative demineralization of the bones about the joints. This finding can be present and associated with inflammatory arthritis. We are making a conscious choice not to discuss this finding further. We have chosen to address it only briefly here, because the finding in and of itself is non-specific and not a marker of inflammatory arthritis per se and in our experience is over used, or over relied upon to arrive at a diagnosis. It is true that this finding can be seen in the setting of inflammatory arthritis, but usually with the other overt signs of the disease. In the absence

of other findings such as joint space narrowing, and erosions, it should not be relied upon. Early and more subtle findings in inflammatory arthritis are detectable on MRI and ultrasound, but this is not within the scope of this manual. Key Point

While osteoarthritis is by far and away the most common form of arthritis, it is easy to fall into the trap of calling everything degenerative arthritis. The lack of osteophytes in the setting of an arthritis should make you consider other possibilities.

Is there any point to which you would wish to draw my attention?' 'To the curious incident of the dog in the night-time.' 'The dog did nothing in the night-time.''That was the curious incident,' remarked Sherlock Holmes. —Arthur Conan Doyle from The Silver Blaze This quote is worth bearing in mind, for when evaluating arthritis one thing to note is the absence of osteophytes, which are typical manifestations of degenerative osteoarthritis. It is not always the case that the absence of osteophytes is a sign of inflammatory arthropathy, but it should make you think and consider that the arthritis you are evaluating is not something common.

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Rheumatoid Arthritis Profile Polyarticular Classic target joints: –Wrist and MCP joints – The interphalangeal joints are typically spared –Mid foot, ankle, and MTP joints –Hips –Knees –Elbows Other joints can of course be involved, these are the more typical and classic. The best way to identify them is to see multiple examples.

Target Recognition Hands/Wrists Bilateral and symmetric involvement. Look for joint space narrowing and erosions.

Fig. 7.6  Severe rheumatoid arthritis, which is centered at the wrist and MCP joints. There are multiple erosions and associated joint space narrowing. On the right, there are

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Often there are subluxations at the MCP joints. Interphalangeal joints are usually spared (Figs. 7.6, 7.7, 7.8, and 7.9).

Feet/Ankles Bilateral and symmetric involvement. Look for joint space narrowing and erosions. MTP joints are favorite sites for involvement, but the ankle and mid foot joints can also be affected. Interphalangeal joints are usually spared (Figs. 7.9, 7.10, and 7.11). Shoulders Bilateral and symmetric. Joint space narrowing with erosions and joint destruction. Erosion of the distal clavicle is possible (Fig. 7.12).

subluxations at the MCP joints. A typical appearance of advanced disease

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Inflammatory Arthropathies

Fig. 7.7  Another example. Bilateral. Symmetric. Advanced rheumatoid arthritis

Fig. 7.9  A small erosion of the distal fifth metatarsal. A typical appearance of rheumatoid arthropathy in the foot. Often the erosions are present without significant joint space narrowing at the MTP joints

Fig. 7.8  Severe destructive erosive rheumatoid arthritis with significant destruction and erosion of the carpal bones and joints

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Fig. 7.10  Severe arthritis at the ankles with near complete loss of the joint spaces. What we don’t see is osteophytes from degenerative arthritis. This is typical of

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inflammatory arthropathy, in this case a typical example of rheumatoid arthritis

Fig. 7.11  Retrocalcaneal erosion. A less common site site for rheumatoid arthritis to target. This is a more common target site for psoriatic or reactive arthritis

Fig. 7.12 Severe erosive rheumatoid arthritis with destruction of the glenohumeral joint

Inflammatory Arthropathies

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Fig. 7.13  Bilateral and symmetric rheumatoid arthritis. The marginal erosions (arrows) are subtle. There is prominent joint space narrowing, and importantly, what we don’t see, are osteophytes to suggest osteoarthritis

Knees Bilateral and symmetric. Erosions tend to be marginal and associated with joint space narrowing (Fig. 7.13). Hips Bilateral and symmetric. Joint space narrowing, usually without associated osteophytes, although there can be secondary or co-existing osteoarthritis. There can be a protrusio deformity (Fig. 7.14).  lbow E Bilateral and symmetric. As elsewhere, there is joint space narrowing, erosion, and destruction without associated osteophytes (Fig. 7.15).

Fig. 7.14  Severe rheumatoid arthritis at the hips. The left is more severely affected and associated with a protrusio deformity. Note the lack of osteophytes. There is severe joint space narrowing

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a

b

Fig. 7.15 (a) Severe joint space narrowing and erosions in rheumatoid arthritis. (b) The lateral view with a different view of the joint space narrowing and erosions, addi-

tionally there is a small joint effusion (hopefully you remember how to spot this)

Sacroiliac Joints Not affected.

tion can be severe and result in the complete destruction of the carpal bones (Figs. 7.16, 7.17, and 7.18).

Juvenile Idiopathic Arthritis

Hips and Knees Can be bilateral or unilateral, as in all inflammatory arthropathies, there is marked joint space narrowing, and erosions without associated osteophytes (Figs. 7.19, 7.20, and 7.21).

Profile A heterogenous mix of inflammatory arthritis with onset before the arbitrary age of 16. Similar to rheumatoid arthritis with the exception that the sacroiliac joints can be affected. Often can be asymmetric, as opposed to rheumatoid arthritis which is bilateral and symmetrical. Since the inflammation often begins before skeletal maturity the cartilage damage that occurs can produce severe and bizarre appearing chronic deformities. Hands/Wrists Bilateral, but often asymmetric. Just as in rheumatoid arthritis, the wrists and MCP joints are preferentially affected, and the interphalangeal joints are spared. When the inflammation starts before the bones are mature, the resultant cartilage destruc-

Ankylosing Spondylitis Profile Typically targets the spine and sacroiliac joints, but can also involve the hips and knees. The smaller more distal joints are usually spared. Fusion of the spine and sacroiliitis are the characteristic findings of the disease, which can be near complete ankylosis or fusion of the spine, or only partial fusion, often seen along the anterior spinal ligament. Late manifestations of the disease are usually quite apparent with ankylosing of the spine, which can involve both the anterior and posterior aspects (Figs. 7.22 and 7.23).

Inflammatory Arthropathies

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Sometimes the ankylosis can be quite dramatic and involve the hips (Fig. 7.24). Ankylosis of the sacroiliac joints should also be obvious, but can be overlooked if not explicitly evaluated (Figs. 7.25 and 7.26). Early findings of sacroiliitis are widening, irregularity, and sclerosis at the joints. In ankylosing spondylitis, this is typically bilateral and symmetric (Fig. 7.27) Earlier manifestations in the spine can be subtle. One finding is known as the ‘shiny corner sign,’ in which there is subtle sclerosis of the anterior endplates, often associated with squaring and flattening of the anterior vertebral body (Fig. 7.28)

Psoriatic and Reactive Arthritis Fig. 7.16  Severe deforming juvenile idiopathic arthritis. There is erosion and near complete loss of the bones of the proximal carpal row, with partial ankylosis between the distal radius and remnant carpal bones. There is also deformity and erosion and the 2nd and 3rd MCP joints and deformities of the fourth and fifth fingers

Profile Both psoriatic and reactive arthropathy have a similar appearance and are often not distinguishable based on imaging. Clinically, the picture may be different and allows a determination. Reactive arthritis is usually associated with a pre-

Fig. 7.17  A less severe case of juvenile idiopathic arthritis. The joint space narrowing at the wrists is not as prominent, but present. These findings are bilateral and symmetric

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Fig. 7.18  The effects of untreated juvenile idiopathic arthritis that has ravaged this unfortunate 24-year-old since childhood. The carpal bones are complete eroded and absent. There are erosions and deformities at the MCP joints

Fig. 7.19  Severe erosive and destructive arthritis at the hips from juvenile inflammatory arthritis. The lytic erosions spanning the hip joints are particularly prominent. Important to not the lack of any significant osteophyte formation

Fig. 7.20  Unilateral, or at least very asymmetric inflammatory juvenile arthritis at the right hip. Here what stands out most is the near complete and uniform loss of the joint space, the erosions are there, just not as prominent as the last case. There is subtle narrowing at the left hip. F

Inflammatory Arthropathies

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Fig. 7.21  Juvenile inflammatory arthritis at the knees. Severe symmetric joint space narrowing with small marginal erosions. This appearance is not specific for JIA, and other inflammatory arthropathies could look like this. No osteophytes—not osteoarthritis

Fig. 7.23  Ankylosing spondylitis with partial ankylosis along the anterior spine. The severe kyphotic deformity is the result of an old injury

Fig. 7.22  Ankylosing spondylitis with partial fusion of both the anterior and posterior aspects of the spine. A classic manifestation of the disease

ceding infection, and later by a non-infectious inflammatory arthritis. Psoriatic arthritis has more of a predilection for the hands, than does reactive arthritis, which is more common in the feet. Typically, the small joints of the hands and feet are involved, with the interphalangeal joints being preferentially affected.

Key findings that help in the diagnosis of psoriatic/reactive arthritis: 1. The disease is often asymmetric, it may be bilateral or unilateral, but tends to lack the mirror-like symmetry of rheumatoid arthritis. 2. In hands, the PIP and DIP joints are preferentially affected, while the carpal and MCP joints may be spared. This is in contradistinction to rheumatoid arthritis, which preferentially affects the proximal joints (wrist and MCP joints) and spares the interphalangeal joints.

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Fig. 7.24  Complete ankylosis across the hip from ankylosing spondylitis

Fig. 7.26  Complete fusion of the sacroiliac joints from long standing ankylosing spondylitis. There is also ankylosis of the spine, although harder to see on the AP view

Fig. 7.25  There is complete ankylosis of the sacroiliac joints, which could be overlooked. The arthritis at the hips is also the result of the inflammatory arthritis. There are some marginal osteophytes reflecting a component of secondary osteoarthritis

3. Erosions tend to me marginal, which is useful in distinguishing from erosive osteoarthritis, which has central erosions. There are central erosions in psoriatic, but these are usually associated with marginal erosion as well, and you shouldn’t see isolated central erosions.

Fig. 7.27  Bilateral and symmetric sacroiliitis from ankylosing spondylitis. there is widening, sclerosis and irregularity of the sacroiliac joints. Left to progress, this will end with complete ankylosis of the joints

4. New bone proliferation/periostitis is another manifestation of psoriatic arthritis, which is absent in rheumatoid arthritis.

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Inflammatory Arthropathies

Fig. 7.28  Early signs of ankylosing spondylitis with sclerosis of the anterior vertebral body endplates (arrows). There is also flattening of the anterior aspect of the vertebral bodies at L3, L4, and L5. This is a subtle finding

5. Advanced disease is associated with deformities, subluxations, and fusion across joints. 6. When causing a sacroiliitis, it tends to be bilateral but asymmetric or unilateral.

Target Recognition Figure 7.29: An advanced case of psoriatic arthritis. Important factors to note are the distribution of the arthritis, which is most severely affecting the interphalangeal joints. While there is some symmetry to the disease, there is asymmetrical involvement of the right second and third MCP joints.

The interphalangeal joints show typical signs of inflammatory arthritis with joint space ­narrowing and erosions. Additionally, there are multiple subluxations. There is severe osteoarthritis at the first CMC joints, which is not related to the inflammatory disease. Figure 7.30a and b: Another case of severe psoriatic arthritis. In this cases, the more proximal joints of the wrist are also badly affected. This is a less common appearance for psoriatic arthritis. Erosions and joint space narrowing affect the interphalangeal joints and the carpal joints. As is typical, the findings are bilateral, but slightly asymmetric. Figure  7.30b is a close-up view of the right finger showing that there is ankylosis across the DIP joint. Figures 7.31 and 7.32: A hallmark of psoriatic arthritis is joint space narrowing and marginal erosions at the interphalangeal joints, often associated with proliferative new bone formation. Figure 7.33: The feet can also be affected. Reactive arthropathy is more common in the feet, and both psoriatic and reactive arthritis can look like rheumatoid arthritis. In this example, the MTP joints are affected with erosion, joint space narrowing, and subluxation—all findings also in rheumatoid arthritis. In this example, the proliferative new bone formation about the MTP joints should help you to distinguish this psoriatic arthritis from rheumatoid. Figure 7.34: Retrocalcaneal erosions are more commonly seen in reactive than psoriatic ­arthritis, and although possible (see earlier example) are less likely in rheumatoid arthritis.

Enteropathic-Related Arthritis Profile This is an inflammatory arthritis associated with inflammatory bowel disease (Crohn’s and ulcerative colitis). In contrast to the other inflammatory arthropathies, there is no clear distinct image defining characteristic of this arthritis. Enteropathic arthritis can affect the spine and look like ankylosing spondylitis.

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Fig. 7.29  Severe deforming psoriatic arthritis

It can cause a sacroiliitis, which tends to be bilateral and symmetric. Small distal digits of the hand and feet can be affected and less commonly the larger joints like knees, hips, and shoulders are involved. All of

these findings are non-specific on their own, and while they may indicate that there is an inflammatory arthritis, further correlation with any history of inflammatory bowel disease is usually needed to associate the arthritis.

Inflammatory Arthropathies

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a

b

Fig. 7.30 (a) Severe erosive psoriatic arthritis, bilateral but asymmetric. (b) A closer view of the right second and third fingers. There is complete fusion across the 2nd DIP

joint. At the 3rd DIP joint, there is severe joint space narrowing and small marginal erosions, findings also present at the PIP joints

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Fig. 7.32  Severe DIP joint space narrowing with small marginal erosions at the 2nd and 3rd DIP joints. There is proliferative bone formation at the 3rd DIP joint (arrows)

Fig. 7.31  Note the severe joint space narrowing at the PIP and DIP joints, without associated osteophytes. There are erosions, more prominent at the DIP joint. These erosions are both marginal and central. There are small marginal erosions at the PIP joint. The proliferative new bone formation (arrow) is a hallmark of psoriatic arthropathy

Fig. 7.33  Psoriatic arthritis at the MTP joints (sparing the first MTP joint). Pay special attention to the new bone formation at the bases of the 3rd, 4th, and 5th proximal phalangeal bones. A distinguishing finding, that helps to separate this from rheumatoid arthritis

Septic Arthritis

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a

b

Fig. 7.34  A retrocalcaneal erosion in psoriatic arthritis

Septic Arthritis It is always important to consider septic arthritis, especially in the setting of a monoarticular arthritis. While a septic arthritis can affect multiple sites, this is less common. A septic arthritis can look like the destructive and erosive arthritis seen in inflammatory arthritis. The joint space will narrow, with erosions. There will often be a joint effusion, which may be detected on the radiographs. Adjacent soft tissue swelling may also provide a clue to the infectious etiology of the arthritis (Fig. 7.35a–b, 7.36, and 7.37). More indolent infections such as fungal and mycobacterial infections will have similar findings, but the the course of the disease is much slower. A pyogenic bacterial infection from staph or strep will rapidly destroy a joint. A more indolent infection will take a much longer time and often is harder to diagnosis as the arthritis can persist for months, or even years without dramatic or rapid destruction. Phemister’s triad is a set of findings that is associated with more indolent infections. It was originally used to describe a septic arthritis/ osteomyelitis from tuberculosis, but is also useful for identifying fungal infections. The trio of radiographic findings are as follows: 1. Marginal erosions. 2. Gradual narrowing and loss of the joint space. 3. Periarticular osteopenia (Fig. 7.38).

Fig. 7.35 (a) Symmetry is your friend. The right sacroiliac joint does not look like the normal one on the left. There is widening, erosion, and irregularity. Remember, with a mono-articular arthritis think of infection. Although it is reasonable to consider an asymmetric sacroiliitis from inflammatory arthropathy. (b) The CT shows the findings clearer. There is destruction, erosion, and irregularity of the right sacroiliac joint. If you’re truly Holmesian in your observation, you will see asymmetric inflammatory stranding along the posterior aspect of the psoas muscle, which is another indication that this was an infectious sacroiliitis

Fig. 7.36  Severe joint space narrowing, with near complete loss of the joint space. No osteophytes, not osteoarthritis. This was destructive septic arthritis

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Key Point

In the setting of a monoarticular arthritis always consider infection.

Fig. 7.38  Phemister’s triad of marginal erosions, preservation of the joint space, and periarticular osteopenia in this individual with long standing septic arthritis caused by the fungal coccidioidomycosis

Fig. 7.37  A more subtle septic arthritis at the PIP joint. There is marked joint space narrowing and small marginal erosions (arrows)

These findings reflect the gradual destruction of the joint, versus the more dramatic and rapid

destruction in the setting of a more common pyogenic staph or strep infections. Fungal or mycobacterial infections can manifest with extensive synovitis and effusion without associated joint damage (Fig. 7.39a and b). A joint aspiration is required for a definitive treatment-oriented diagnosis. For a mycobacterial or fungal infection, a synovial biopsy may be required for a definite diagnosis.

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Neuropathic Arthropathy

a

b

Fig. 7.39 (a) The most prominent finding is the large effusion or distention of the suprapatellar space. (b) The MRI shows extensive, diffuse, and thick synovitis. This was a case of chronic coccidioidomycosis infection in a

resident of Bakersfield California, which seems to be ground zero for this infection. There is no significant cartilage loss or joint destruction despite this infection being present for a few years

Neuropathic Arthropathy

One of the more common clinical scenarios is being asked to identify septic a­ rthritis/osteomyelitis in the setting of destructive neuropathic arthropathy. This can be a difficult task, for the MRI which we rely upon will show abnormalities in both diseases. While there has been much ink spilt on this subject and a far more comprehensive discussion can be found in the literature, we will leave you with a tips, which we find help to separate the two. Always worth remembering that both can be present. The primary finding we use to diagnosis osteomyelitis on MRI is marrow abnormality: edema on fluid sensitive fat-saturated sequences and dark or intermediate marrow signal on T1 sequences. These findings can be present in both osteomyelitis and neuropathic arthropathy, in which the marrow can be very abnormal. The trick is to look for an adjacent ulceration or sinus track. If the abnormal bone (or joint) is adjacent to an ulceration or sinus track, it is likely infected.

Also known as Charcot arthritis, after Jean-Marie Charcot, an eminent French neurologist. Given our current plague of uncontrolled diabetes and its associated peripheral neuropathy, this is an all too common finding. Most common in the feet and ankles, although it can occur at any joint, perhaps most notable at the shoulders, where bilateral destructive neuropathic arthropathy is associated with a central cord lesion or syrinx in the cervical spine. Chronic syphilis infection is a rarer and more historical causes of this arthritis. Radiographically, the disease is characterized by dramatic fragmentation and destruction of the joint, or as in the case of the feet and ankles, involving multiple joints. There may be associated hypertrophic new bone formation. This destruction is dramatic and tragic, although since it is a neuropathic disease, it tends to be painless (Figs. 7.40 and 7.41).

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Fig. 7.40 Severe destructive neuropathic arthropathy centered in the mid foot. A sadly common finding associated with uncontrolled diabetes and its associated periph-

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eral neuropathy. The vascular calcifications are a secondary observation to make and are from the long-­ standing diabetes

Gout Calcium pyrophosphate dihydrate crystal deposition disease (CPPD) Amyloid

Gout

Fig. 7.41 Destructive neuropathic arthropathy at the shoulder. This was also present on the contralateral side and was caused by a central syrinx in the cervical spinal cord. In this case, there is hypertrophic new bone formation in addition to the joint erosion and destruction

Deposition Arthropathy There are three main deposition processes, which can be centered in or around joints and can cause an arthritis.

Key Points –– A common deposition disease, which can occur just about anywhere including weird and unexpected spaces that you may not associate with gout. It is always good to keep gout in mind as it can present in an unusual or atypical manner. When in doubt, think of gout! –– Gout can cause erosions, which are classically described as juxta-articular, the purpose of which is to help distinguish them from the marginal erosions of an inflammatory arthropathy. Sometimes this is not so easy. The idea is marginal erosions are at the edge, but within the joint. In distinction, juxta-articular erosions are at the edge of the joint, but outside the joint space, more along the lateral aspects of joint. Often this is described as leaving an

Deposition Arthropathy

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 alcium Pyrophosphate Dihydrate C Crystal Deposition Disease (CPPD)

Fig. 7.42  The classic gout picture. Three key observations: 1.There are juxta-articular erosions about the first MTP joint. The erosions are just a bit more lateral than a marginal erosion, and these erosions undermine, but preserve the overlying osteochondral surface. 2. The joint space is preserved (an important finding to help eliminate an infectious or inflammatory arthritis). 3. There is soft tissue density-fullness about the joint from the tophus

overhanging articular bone surface above the erosion. –– Another feature to help separate gout from inflammatory or septic arthritis is that the joint space is usually maintained, although in long standing, advanced disease, there will be joint space destruction. –– Often radiographically, dense soft tissue masses are apparent from the tophi. –– Common target sites are the first MTP joints, the first CMC joints, about the knee and involving the olecranon bursa at the elbow. But as we said, gout CAN GO ANYWHERE! (Figs. 7.42, 7.43, 7.44, 7.45, and 7.46).

Key Point

When in doubt think of gout!

Key Points –– A common finding, which can cause a symptomatic arthritis, although it can also be symptomatic. –– It may be present with or without associated degenerative osteoarthritis. In the knee, there is a strong association with patella cartilage damage, often out of proportion to any other degenerative arthritis. –– Radiographically evident by seeing chondrocalcinosis, which are the dense crystals commonly deposited in articular cartilage. It can also deposit in ligaments, tendons, fibrocartilage. It is common to see it in the triangular fibrocartilage complex (TFCC), menisci, bursae, and synovial spaces. It is also commonly deposited in the intervertebral discs. –– May be associated with erosions, although this is rare. –– Often associated with metabolic or endocrine abnormalities (Figs. 7.47 and 7.48).

Amyloid Deposition Arthropathy Key Points –– The rarest of the deposition diseases and is result of proliferation and deposition of amyloid protein in and around joints. This is most commonly associated with real failure and chronic dialysis. –– Radiographically can present with periarticular cysts/erosions often associated with a synovitis or bursitis. –– Shoulders, hips, knees, and wrists are most commonly affected, and it tends to be bilateral. –– Joint spaces are usually preserved (Fig. 7.49).

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Fig. 7.43  Advanced bilateral gout with multiple dense tophi, most notable about the first MTP joints. There are multiple erosions about the first MTP joints, the distal

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fifth metatarsals and throughout the mid foot regions. The first MTP joints are one of the most commonly affected sites

Fig. 7.45  Gout at the olecranon bursa with cloud-like densities typical of gout tophi, and a classic location for gout to affect. There is no erosion or joint space narrowing Fig. 7.44  Gout at the knee with multiple large dense tophi. Harder to see is the lucent erosion near the tibial tuberosity. Joint spaces are maintained

Deposition Arthropathy

Fig. 7.46  Gout can go anywhere. Here is an atypical location, with a gout tophus and erosion in the posterior elements of L5. Looks weird and you mind not think of gout, but if you picture that this soft tissue density at the first MTP joint, it will help you to recognize it as a gout tophus

Fig. 7.47  CPPD with linear calcifications (chondrocalcinosis) in the menisci. In this case, there is no clear joint space narrowing or other findings of arthritis

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Fig. 7.48  Severe arthritis at the shoulder, with both degenerative findings, and surrounding chondrocalcinosis from CPPD

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Hemophilia Arthropathy

Fig. 7.49  Typical findings of amyloid arthropathy with prominent cysts and erosions in the humeral head. The glenohumeral joint space is normal. Although not well imaged on these bone windows, there is extensive subacromial/subdeltoid bursitis

A high proportion of individuals with hemophilia end up with the debilitating effects of hemophilic arthropathy. The chronic intra-articular bleeding causing the deposition of iron within the joint, which mediates a destructive inflammatory cascade, similar to that of rheumatoid arthritis. Radiographically, the appearance is similar to rheumatoid arthritis or juvenile inflammatory arthropathy with erosions, and joint space destruction, which is often present early on in life. Typically, large joints, such as the knee, elbow, and ankle are affected and the small joints of the hand and feet are usually not involved, which is one differentiating factor from rheumatoid or juvenile idiopathic arthritis. Another helpful diagnostic clue is that because of the X-linked genetics of the disease, it is almost entirely a male affliction (Fig. 7.50).

Fig. 7.50  Severe erosive destructive arthritis from hemophilia. It looks very similar to rheumatoid arthritis. Other factors: patient demographics and history will be useful in making the diagnosis

Benign Proliferative Processes

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Key Point

Severe inflammatory appearing large joint arthritis in a young man should prompt you to consider hemophilia arthropathy.

Benign Proliferative Processes Proliferative or neoplastic conditions within a joint are rare. Of the ones you may encounter, almost all are benign. All we will say about intra-­articular malignancies is that they are so rare you might not ever encounter one. Intraarticular metastasis is possible, but again exceedingly rare. The following are four benign proliferative/ neoplastic conditions which are less rare and are worth knowing about. All four of these benign proliferative conditions are mono-articular (baring rare case reports) and if you see multiple joints similarly affected, then these diagnoses can be almost always excluded.

Fig. 7.51 Multiple similarly sized calcified intra-­ articular bodies. A clear diagnosis of synovial osteochondromatosis on the radiograph

Synovial Chondromatosis/ Osteochondromatosis A benign intra-articular proliferative process, which results in the growth of multiple small similarly sized osteochondral bodies. These may be calcified (osteochondromatosis) or remain cartilaginous (chondromatosis). If calcified, they are usually easy recognizable on radiographs. Over time, these bodies can cause arthritis and erosions/remodeling of the periarticular bones. If the bodies are not calcified, these later stage findings may be the only radiographic clue. The MRI appearance is usually clear, with multiple small osteochondral bodies. The knee is the most commonly affected joint, but it can also occur in the hip, elbow, and shoulder. Smaller joints are rarely involved (Figs. 7.51 and 7.52).

Fig. 7.52  The MRI of the same individual showing the multiple dark osteochondral bodies distending the joint space and causing erosions along the anterior and posterior aspects of the humeral head (arrows) These erosions were hard to see on the radiographs

Tenosynovial Giant Cell Tumor A benign synovial proliferative process, which has a diffuse form and a more localized form. Previously, this entity was referred to as pigmented villonodular synovitis.

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Fig. 7.53  Tenosynovial giant cell tumor at the ankle. Radiographically, we see fullness along the anterior and posterior aspects of the tibia talar joint and a small erosion along the dorsal talar neck

Fig. 7.54  The MRI showing the synovial proliferation. This is the diffuse form of tenosynovial giant cell tumor. Along the dorsum of the talus, the mass is causing an erosion

The lesions may bleed and cause hemosiderin deposition within the joint. As with synovial osteochondromatosis, there may be erosion of the adjacent bones, and over time the development of arthritis. Radiographically, there may only fullness or effusion of the joint, although if present, the bone erosions may be visible. MRI is needed to better diagnosis and characterize tenosynovial giant cell tumor. MRI signal characteristics are variable, the ill-defined mass like morphology of the process is what is usually used for diagnosis, more diffuse and infiltrative in the diffuse form, and nodular and focal in the localized form. If resected, there is a high rate or reoccurrence (Figs. 7.53 and 7.54).

Radiographically, you are likely only to see fullness and possibly effusion within the joint. It may co-exist with, or even be related to, a co-­ existent degenerative or inflammatory arthritis. This is usually a clear diagnosis on MRI for two reasons:

Lipoma Arborescens

Vascular Malformations

Another rare proliferative process, in which there is fatty deposition and growth within the synovium.

Hemangiomas and arterial venous malformations can involve the joint. They may occur purely within the joint or can have extension in and

1. It has a typical morphology, often described as a branching frond-like morphology. 2. Since it is fat, the MRI signal will follow fat on all sequences, and there will be no enhancement. The knee, hip, and shoulder are the most common locations, and like the other proliferative processes, are rare in smaller joints (Fig. 7.55).

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Sundries

around the joint with intra- and extra-articular involvement. Radiographically, these may only be apparent by soft tissue fullness, and possibly a calcified phlebolith. The MRI appearance is vari-

able but similar to vascular malformations elsewhere. A focal or infiltrative heterogeneous soft tissue mass, with variable signal characteristics, is often associated with a component of fat. Flow voids from the vessels may also be apparent (Fig. 7.56a and b).

Sundries These are four entities that don’t classically fit into the arthritis or joint-centered category, but are share similarities with arthropathies and are necessary to be familiar with.

 alcific Periarthritis (Calcific C Tendinopathy) In its acute inflammatory phase, calcific periarthritis can mimic a septic joint or a flare up of deposition arthropathy. There is deposition of calcium hydroxyapatite and other calcific elements around a joint. The deposits may be within a tendon, bursa, or other Fig. 7.55  There is a large joint effusion, and the frond-­ like proliferative fatty lesion in the superior joint space is connective elements surrounding a joint. a text book example of this benign proliferative process

a

Fig. 7.56 (a) An intra-articular hemangioma in Hoffa’s fat pad. On this T1 sequence, the lesion has high signal reflecting the fat within the lesion. (b) Fluid sensitive, fat

b

saturated sequence showing areas of high signal from fluid and blood within the hemangioma

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Fig. 7.57  Calcific tendinopathy/periarthritis with amorphous calcific deposits in the supraspinatus tendon. A very common finding about the shoulder

Often this finding is common and quiescent finding. The acute phase is painful, and tends to be associated with resorption of the calcium, which triggers a symptomatic inflammatory response. This is usually a clear diagnosis on radiographs with foci of amorphous dense calcifications around a joint (Figs. 7.57 and 7.58).

Key Point

Calcific periarthritis can mimic a joint infection or gout flare during its acute stage.

 ystemic Lupus Erythematosus (SLE) S and Rhupus The most common radiographic manifestation of the arthritis associated with SLE is a deforming arthropathy, most notable for prominent subluxations at the MCP joints. This is bilateral and symmetric, and in contradistinction to the sub-

Fig. 7.58  Calcific periarthritis along the volar aspect of the DIP joint, This presented with symptoms mimicking an infection with a red, painful and swollen joint

luxations in rheumatoid arthritis is reducible. An older term for this is Jaccoud's arthropathy. The joint spaces are usually relatively preserved, although they can be narrowed from arthritis. Erosions are not typically manifestations of SLE, but can be seen in the rare entity Rhupus, which is syndrome with manifestations and overlap of both rheumatoid arthritis and SLE (Fig. 7.59).

Sundries

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Fig. 7.59  The classic deformities associated with SLE arthropathy. These are reducible deformities. Also note that the joint spaces are maintained, and there are no erosions

 cleroderma and Mixed Connective S Tissue Diseases The most prominent radiographic manifestations of musculoskeletal scleroderma are soft tissue calcifications and erosion or resorption of the distal phalangeal tufts (acro-osteolysis). Erosions and joint space narrowing at the small joints in the hands and feet are possible, but are a less common manifestation, and when present look similar to erosive psoriatic arthritis. Contractures and deformities at the fingers can also be present (Fig. 7.60). Dermatomyositis is another mixed connective tissue inflammatory disease, which although is not commonly associated with arthritis, has some overlapping features with scleroderma. Most notably there can be dramatic soft tissue calcifications related to the myositis. These follow the longitudinal length of the muscle bellies and tend

Fig. 7.60  A classic example of scleroderma. They key observations are the distal soft tissue calcifications, and the bone loss off the second distal phalanx. There is no joint space loss, erosion, or arthritis

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Fig. 7.62  Less dramatic linear calcifications in dermatomyositis. There is no significant arthritis, which is common

Saved Rounds Fig. 7.61  Extensive linear calcifications in dermatomyositis. The calcifications are the result of myositis

to be long sheet-like soft tissue calcifications, versus the smaller more localized soft tissue calcifications in scleroderma (Figs. 7.61 and 7.62).

Sarcoid Sarcoidosis is a granulomatous disease which can have multi-organ involvement. Skeletal manifestations of sarcoid are rare, but do occur. Often they are clearly and instantly recognizable. So although rare, it is worth knowing. Radiographically, sarcoid presents as small lytic lesions in the hands and feet (it can occur in other bones, but the presentation is not as clearly recognizable in the same manner as in the hands and feet). These lesions are often slightly complex and reticulated and may extend to and destroy or disrupt the joint spaces as well as cause bone loss and resorption of the distal phalangeal bones (acro-osteolysis). The pattern is distinct, and nothing else should have this appearance (Fig. 7.63).

Arthritis is very common. The most common form of arthritis is degenerative osteoarthritis, but it is important not to be lulled into complacency and call everything osteoarthritis just because you see an arthritis. Remember to look for signs of inflammatory arthritis, in which osteophytes and other degenerative findings will not predominate. In these cases, there will be joint space narrowing and destruction in the absence of significant ­osteophyte formation, and if you see erosions, there is an inflammatory component. Remember that a mono-articular arthritis should always make you consider the possibility of a septic joint. This is crucial as rapid diagnosis and treatment are important to prevent long-term sequelae and pain. Once you have localized an abnormality within a joint, there is a limited possibility. Run through the list that we have elaborated in this chapter. The diagnosis is there. A special word about gout, which is common, sneaky and can go anywhere. If you see something odd in or around a joint, then think of gout. When in doubt, think of gout!

Live Fire Exercises

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Fig. 7.63  Clearly recognizable as sarcoid. Multiple reticulated lytic lesions. In this case, there is narrowing and deformity of the joint spaces related to the disease as well as acro-osteolysis of the left distal 4th and 5th phalanges

Live Fire Exercises You know the drill. Take these cases as if they were presented to you during a normal workday. Describe the findings, and formulate a clear diagnosis, or if not possible a limited differential. Three levels. Each gets harder. Kill!

1

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What are the findings? What is the diagnosis? 2

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Live Fire Exercises

What are the findings? What is the diagnosis? 3

193

What are the findings? What is the diagnosis?

4

194

What are the findings? What is the diagnosis? 5

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Live Fire Exercises

What are the findings? What is the diagnosis? 6

7

What are the findings? What is the diagnosis?

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What are the findings? What is the diagnosis? 8

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After Action Review

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After Action Review Only through rigorous self-assessment of our flaws can we hope to improve. Where did you go wrong? Where did you succeed? Did you make mistakes? Good. A chance to learn. 1

What are the findings? What is the diagnosis? 9

A few key observations. First there is arthritis, we see this as there is joint space narrowing and erosions. Where is it centered? Well almost all the joints are involved, but it looks most severe in the wrist and, although the interphalangeal joints are narrowed with a few small erosions, we should assess that the primary center of the arthritis is in the proximal wrists. Another important observation is that process is bilateral and symmetrical. It is a polyarticular inflammatory arthritis. Given the symmetry and more proximal involvement, the best diagnosis is…rheumatoid arthritis. 2 This diagnosis should be clear cut and instantly recognizable. We see multiple small calcific bodies in the joint. On this one view, it is difficult to assess the joint space, but it looks preserved. This is a clear example of synovial osteochondromatosis, in which multiple small osteochondral bodies are proliferating within the joint. If they were not calcified, the diagnosis would not be clear on the radiograph, but nothing else will have this appearance. 3

What are the findings? What is the diagnosis?

Three important findings in this case. 1. There are soft tissue calcifications around the distal radial ulna joint and along the radial carpal joints. 2. There is associated arthritis with joint space narrowing.

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3. There are lytic areas in the adjacent bones, which may be erosions. The soft tissue calcification is typical of chondrocalcinosis. Thus we know this is a CPPD-­ related arthritis. 4 Another case of severe bilateral and symmetric arthritis. The mid foot regions are most severely affected where there is erosion and destruction of the joint spaces. There are also prominent subluxations at the MTP joints. A more subtle observation is that the bones are gracile and hypoplastic, which suggests that their development was not normal and that this arthritis has been around for a long time, before he was skeletally mature. In this case, this is an example of juvenile inflammatory arthropathy, although it is reasonable to consider rheumatoid arthritis as well. 5 The ankle is fragmentated with destruction of the tibial talar joint. This level of destruction is beyond that usually capable from an infectious or inflammatory arthritis and this is a typical appearance of destructive neuropathic arthropathy, which favors the feet and ankles. 6 One key finding: There is a juxta-articular erosion along the medial aspect of the distal first metatarsal. One important observation. The first MTP joint is preserved. One subtle pickup. Faint soft tissue prominence along the medial aspect of the joint. These three factors should tell you that this is gout. Remember that gout tends to preserve the joint spaces. 7 There is erosive inflammatory arthropathy as we see from the multiple joints spaces with nar-

rowing and erosions. The interphalangeal joints are most severely affected, and the wrist and MCP joints are not as significantly involved. The distribution is bilateral, but asymmetric. This is typical for psoriatic arthritis. 8 There is dense lobulated soft tissue calcification around the 3rd MCP joint. Although an atypical location, if we imaging this calcification about the shoulder, we can diagnosis this as calcific periarthritis. 9 Just like in the previous case, this soft tissue calcification in the pre-patellar bursa is from calcific periarthritis. An uncommon location, but the morphology and density are typical.

Bibliography 1. Roemer FW, Demehri S, Omoumi P, Link TM, Kijowski R, Saarakkala S, Crema MD, Guermazi A.  State of the art: imaging of osteoarthritis— Revisited 2020. Radiology. 2020;296(1):5–21. 2. Roemer FW, Crema MD, Trattnig S, Guermazi A.  Advances in imaging of osteoarthritis and cartilage. Radiology. 2011;260(2):332–54. Elias DA, White LM. Imaging of patellofemoral disorders. Clin Radiol 2004 Jul 1;59(7):543-57. 3. Greenspan A Erosive osteoarthritis. Seminars in musculoskeletal radiology 2003 (7, 02, 155-160), Thieme Medical Publishers, New York. 4. Marshall M, Nicholls E, Kwok WY, Peat G, Kloppenburg M, van der Windt D, Myers H, Dziedzic K.  Erosive osteoarthritis: a more severe form of radiographic hand osteoarthritis rather than a distinct entity? Ann Rheum Dis. 2015;74(1):136–41. 5. Kidd KL, Peter JB. Erosive osteoarthritis. Radiology. 1966;86(4):640–7. 6. Martel W, Stuck KJ, Dworin AM, Hylland RG.  Erosive osteoarthritis and psoriatic arthritis: a radiologic comparison in the hand, wrist, and foot. Am J Roentgenol. 1980;134(1):125–35. 7. Majithia V, Geraci SA. Rheumatoid arthritis: diagnosis and management. Am J Med. 2007;120(11):936–9. 8. Kellgren JH, Lawrence JS.  Radiological assessment of rheumatoid arthritis. Ann Rheum Dis. 1957;16(4):485. 9. Joaquim AF, Ghizoni E, Tedeschi H, Appenzeller S, Riew KD.  Radiological evaluation of cervical spine

Bibliography involvement in rheumatoid arthritis. Neurosurg Focus. 2015;38(4):E4. 10. Llopis E, Kroon HM, Acosta J, Bloem JL.  Conventional radiology in rheumatoid arthritis. Radiol Clin North Am. 2017;55(5):917–41. 11. Jacobson JA, Girish G, Jiang Y, Resnick D. Radiographic evaluation of arthritis: inflammatory conditions. Radiology. 2008;248(2):378–89. 12. Forrester DM, Brown JC. The radiology of joint disease. Philadelphia: Saunders. 13. Prakken B, Albani S, Martini A.  Juvenile idiopathic arthritis. Lancet. 2011;377(9783):2138–49. 14. Engin G, Acunas B, Acunas G, Tunaci M.  Imaging of extrapulmonary tuberculosis. Radiographics. 2000;20(2):471–88. 15. Chattopadhyay A, Sharma A, Gupta K, Jain S.  The Phemister triad. Lancet. 2018;391(10135):e20. 16. Macnair R, Rajakulasingam R, Singh S, Khoo M, Upadhyay B, Hargunani R, Pressney I. Image-guided synovial biopsy with a focus on infection. Skelet Radiol. 2023;52(5):831–41. 17. Bariteau JT, Waryasz GR, McDonnell M, Fischer SA, Hayda CR, Born CT.  Fungal osteomyelitis and septic arthritis. J Am Acad Orthop Surg. 2014;22(6):390–401. 18. Hatzis N, Kaar TK, Wirth MA, Toro F, Rockwood CA.  Neuropathic arthropathy of the shoulder. JBJS. 1998;80(9):1314–9. 19. Alpert SW, Koval KJ, Zuckerman JD.  Neuropathic arthropathy: review of current knowledge. J Am Acad Orthop Surg. 1996;4(2):100–8. 20. Martín Noguerol T, Luna Alcalá A, Beltrán LS, Gómez Cabrera M, Broncano Cabrero J, Vilanova JC. Advanced MR imaging techniques for differentiation of neuropathic arthropathy and osteomyelitis in the diabetic foot. Radiographics. 2017;37(4):1161–80. 21. Chan RL, Chan CH, Chan HF, Pan NY.  The many facets of neuropathic arthropathy. BJR| Open. 2019;1(1):20180039. 22. Bloch C, Hermann G, Yu TF. A radiologic reevaluation of gout: a study of 2,000 patients. Am J Roentgenol. 1980;134(4):781–7. 23. Monu JU, Pope TL.  Gout: a clinical and radiologic review. Radiol Clin North Am. 2004;42(1):169–84. 24. Resnick D, Niwayama G, Goergen TG, Utsinger PD, Shapiro RF, Haselwood DH, Wiesner KB.  Clinical, radiographic and pathologic abnormalities in calcium pyrophosphate dihydrate deposition disease (CPPD): pseudogout. Radiology. 1977;122(1):1–5. 25. Steinbach LS. Calcium pyrophosphate dihydrate and calcium hydroxyapatite crystal deposition d­ iseases: imaging perspectives. Radiol Clin North Am. 2004;42(1):185–205.

199 26. Sheldon PJ, Forrester DM.  Imaging of amyloid arthropathy. In Seminars in musculoskeletal radiology 2003 (7, 03, 195-204). 2002 . Thieme Medical Publishers, New York, NY. 27. Freire V, Moser TP, Lepage-Saucier M. Radiological identification and analysis of soft tissue musculoskeletal calcifications. Insights Imaging. 2018;9:477–92. 28. Luck JV Jr, Silva M, Rodriguez-Merchan CE, Ghalambor N, Zahiri CA, Finn RS.  Hemophilic arthropathy. J Am Acad Orthop Surg. 2004;12(4):234–45. 29. Melchiorre D, Manetti M, Matucci-Cerinic M. Pathophysiology of hemophilic arthropathy. J Clin Med. 2017;6(7):63. 30. Hughes TH, Sartoris DJ, Schweitzer ME, Resnick DL.  Pigmented villonodular synovitis: MRI characteristics. Skelet Radiol. 1995;24:7–12. 31. Sharma V, Cheng EY.  Outcomes after excision of pigmented villonodular synovitis of the knee. Clin Orthop Relat Res. 2009;467:2852–8. 32. Gouin F, Noailles T.  Localized and diffuse forms of tenosynovial giant cell tumor (formerly giant cell tumor of the tendon sheath and pigmented villonodular synovitis). Orthop Traumato Surg Res. 2017;103(1):S91–7. 33. Ryu KN, Jaovisidha S, Schweitzer M, Motta AO, Resnick D.  MR imaging of lipoma arborescens of the knee joint. AJR Am J Roentgenol. 1996;167(5):1229–32. 34. Doumas C, Vazirani RM, Clifford PD, Owens P.  Acute calcific periarthritis of the hand and wrist: a series and review of the literature. Emerg Radiol. 2007;14:199–203. 35. Li J, Wu H, Huang X, Xu D, Zheng W, Zhao Y, Liu W, Zeng X. Clinical analysis of 56 patients with Rhupus syndrome: manifestations and comparisons with systemic lupus erythematosus: a retrospective case–control study. Medicine. 2014;93(10):e49. 36. Pipili C, Sfritzeri A, Cholongitas E.  Deforming arthropathy in systemic lupus erythematosus. Eur J Intern Med. 2008;19(7):482–7. 37. Sewell JR, Liyanage B, Ansell BM. Calcinosis in juvenile dermatomyositis. Skelet Radiol. 1978;3:137–43. 38. Bassett LW, Blocka KL, Furst DE, Clements PJ, Gold RH.  Skeletal findings in progressive systemic sclerosis (scleroderma). Am J Roentgenol. 1981;136(6):1121–6. 39. Koyama T, Ueda H, Togashi K, Umeoka S, Kataoka M, Nagai S. Radiologic manifestations of sarcoidosis in various organs. Radiographics. 2004;24(1):87–104.

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Metabolic Disorders

Imaging of Metabolic Disorders Physiology of Bone A review of foundational bone physiology is helpful in understanding and predicting the imaging findings in the various metabolic derangements that are encountered. Bone is a living tissue comprised of two basic elements: 1) a living cellular component of osteoblasts, osteoclasts, and osteocytes and 2) an extracellular component made up of an organic matrix and an inorganic matrix. Older bone is continuously replaced by newer bone in a distribution predicted by Wolff’s Law. In the mature adult skeleton, the turnover of bone is usually in balance, and the overall bone mass is relatively constant. Normal bone density increases until around age 40 and then gradually decreases around 3% per decade for men and 8% per decade for women. Osteoblasts produce new bone while osteoclasts resorb and remodel bone. Osteocytes are osteoblasts that have become entrapped in extracellular matrix which induces both functional and morphologic cellular changes. After their differentiation, osteocytes serve as key regulators of osteoblast and osteoclast function. When osteoblastic activity outstrips osteoclastic resorption, a state of “too much bone” exists. Conversely, when the osteoclastic activity exceeds the osteoblasts, there is “too little bone.”

All metabolic bone disorders stem from one of three physiological abnormalities: (1) too much osteoblastic activity, (2) too much osteoclastic activity, or (3) normal amount osteoblastic/osteoclastic activity, but disruption in the organized procession of bone formation and turnover.

Imaging Modalities Plain Radiography As with most things in musculoskeletal imaging, conventional radiography is foundational to the evaluation of metabolic and endocrine disorders of bone. Plain films are more sensitive than most other imaging modalities at detecting increases in bone mineralization but appear essentially normal until around 30% of bone mineralization is lost. Technical factors can, however, alter the apparent density of bone. Overexposed and underexposed images create a false impression of too little or too much bone mineralization, respectively. To counter this, we need to turn our attention to the cortical thickness of a bone which can easily be measured and compared to prior films. For an overall qualitative estimation of bone mineralization, the sum of the cortical thicknesses at the mid-diaphysis of the second or third metacarpal should be about half the diameter of the entire bone.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 B. Plotkin, B. L. Davis, Musculoskeletal Imaging, https://doi.org/10.1007/978-3-031-49021-7_8

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Diminished bone mineralization is correctly termed osteopenia. The term osteoporosis should not be used in this setting as it has a specific meaning discussed in detail below. Any cause of bone resorption outpacing bone formation results in osteopenia, and it is therefore a nonspecific finding seen in both normal physiologic responses (fracture healing and disuse osteopenia) and in metabolic disorders (osteoporosis, osteomalacia, and hyperparathyroidism).

Computed Tomography (CT) CT serves a secondary role in the evaluation of metabolic disorders. It is uncommon for a diagnosis to be made on a CT finding with the appropriate plain film (and laboratory analysis) has already been performed. Vendor-neutral ­third-­party systems are available where lumbar spine CT scans are performed with the patient laying on a calibrated phantom (quantitative CT or QCT). Post-processing of the data allows for estimation of bone mineral density. The overall cost is  far lower than purchasing a dedicated DEXA machine (described below) and with no extra physical space required. CT scanners with these aftermarket packages are usually found at smaller hospitals and outpatient clinics where space and cost considerations are paramount. The emergence of photon-counting CT promises more accurate bone mineral density evaluation; however, a calibrated phantom and proprietary third-­party software are still required, and any facility that can afford a photon-counting scanner already has multiple DEXA machines available.  agnetic Resonance Imaging (MRI) M MRI is occasionally helpful in the setting of metabolic and endocrine disorders of bone. Applications are more limited to evaluation of an underlying bone marrow disorders and in the sarcomatous transformation of Paget disease.  ual Energy X-ray Absorptiometry D (DEXA or DXA) DEXA, now the gold-standard modality for evaluation of bone mineral density, is a maturation of several older techniques (some of which used exotic radioisotopes) that are no longer in clinical practice.

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As the name implies, two different energy X-rays are employed and allow discrimination between bones and surrounding soft tissues. Measurements of X-ray attenuation between the bone and soft tissues can be calculated and compared to reference standards thus enabling patients to be categorized as normal, osteopenic, or osteoporotic. DEXA is the most useful and cost-effective modality in diagnosis osteoporosis. A standard scan of both hips and of the lumbar spine takes about 15 minutes  to complete, and, like many screening exams, the cost is covered by nearly all insurance plans for appropriate patients. The distal forearm can be used as an alternative site should either the hips or the lumbar spine not be usable  or there is clinical concern for primary hyperparathyroidism. A complete review of DEXA interpretation is beyond the scope of this text; however, a few practical points follow. First, results are provided as quantitative bone mineral density, as T-scores, and as Z-scores. The quantitative numbers serve for comparison to prior studies, but in isolation, they are meaningless to clinicians. T-scores compare the patient’s measured bone density to that of a young adult and are the basis for stratification as normal, osteopenic, or osteoporotic. T-scores are the real gold of the DEXA scan. Z-scores compare the patient’s bone density to an age-matched data set and are not terribly useful in day-to-day practice. There is no need to routinely report them, however Z-scores are used in premenopausal females and men under 50 years of age. T-Score of −1.0 or above ➔ Normal T-score between −1.0 and −2.5 ➔ Osteopenia T-score of −2.5 or lower ➔ Osteoporosis Degenerative changes of the lumber spine frequently confound bone mineral density determination. If there is greater than a 1.0 T-score difference between two consecutive vertebral bodies, the outlier is not considered valid for inclusion in either the calculated average bone mineral density for the lumbar spine or the lumbar spine T-score. Furthermore, at least two consecutive levels are necessary for any lumbar spine measurements to be valid. When making comparisons to prior DEXA studies, the exams need to be performed on the

Osteoporosis

exact same machine. Internal variations from unit to unit preclude statistically meaningful comparison between exams, and this is why the model and serial numbers are included on the images. Also note that for any measured anatomic site, the total bone mineral density serves as the basis of comparison to a prior study. The Fracture Risk Assessment Tool (FRAX) estimates risk for hip fracture and major osteoporotic fracture, is usually automatically calculated by the DEXA scanner, and is included as a summary report in the clinical images. An online calculator is also available. There are a number of exclusions that negate the estimated risks, and a simple Yes/No questionnaire that validates FRAX should already be included in the intake paperwork. FRAX is valid for the following patients: • An untreated postmenopausal woman or a man aged 50 or older • With osteopenia by DEXA imaging • With no prior hip or vertebral fracture • And with an evaluable hip for DEXA imaging

Osteoporosis Osteoporotic bone is normally organized, but there is just too little of it. Put a different way, the bone is quantitatively deficient, but the bone is qualitatively normal. Osteoporosis has a variety of different causes, but manifests in essentially two basic variations: (1) generalize or diffuse osteoporosis involving all of the bones and (2) focal or regional distribution where a single bone or region is affected.

Generalized Osteoporosis The most commonly encountered variation is generalized age-related osteoporosis. The spine is particularly affected, and compression deformities are commonly seen. These first affect the endplates resulting in a “codfish vertebrae” or “fish mouth” configuration. Given time and fur-

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ther bone loss, this progresses to frank collapse of the vertebral bodies. Iatrogenic causes of generalized osteoporosis are infrequently seen, and likely less frequently reported as provided clinical indications become more and more sparse. High-dose frequent/daily heparin, longstanding phenytoin (Dilantin) use, and chronic corticosteroid use (or Cushing syndrome!) are the bad actors.

Regional Osteoporosis Unlike generalized osteoporosis, regional osteoporosis is a group of disorders characterized by rapid development and its self-limiting nature. The etiologies of these disorders remain elusive. Though any joint can be affected, the hip and knee are the prototypical examples. Transient osteoporosis of the hip classically affects pregnant women and young men (Fig. 8.1a-d). Regional migratory osteoporosis tends to affect slightly older men and is universally limited to the lower extremity. Flares have a rapid onset and resolve over a period of 6–9 months, but they may recur in either the same joint or involve a separate location, hence the term “migratory.” Localized osteoporosis related to complex regional pain syndrome is a slightly different entity. The osteoporosis is favored to be secondary to increased blood flow, though a concomitant neurologic component could also contribute. The osteoporosis will not only persist, but will worsen, as long as the altered neurovascular state exists.

Imaging Findings in Osteoporosis Imaging findings of osteoporosis reflect the overall loss of bone mass. At plain radiography, there is thinning of the cortices and a vague hazy appearance of the medullary bone. Compression deformities are common in the lumbar spine as discussed above. CT reflects similar findings, but little more.

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a

b

c

d

Fig. 8.1 Transient Osteoporosis: Subtle findings of diminished mineralization of the right femoral head on the AP view of the pelvis (a) is seen to much better advantage on the dedicated AP view of the right hip (b). Coronal T1

MRI image of the pelvis (c) and axial T2 fat saturated MRI image of the right hip (d) confirm edema localized to the right femoral head

At MRI, there is occasionally a stippled appearance of the cortex on T2-weighted sequences in patient with generalized osteoporosis. This is nonspecific, but suggestive in the appropriate setting and may prompt you to recommend formal DEXA screening. In the case of localized osteoporosis, there is uniform bone marrow edema about the affected bone (e.g., throughout the femoral head as above). Joint effusions are usually absent. Two specific entities deserve closer attention. Osteoporosis patients who have been treated with bisphosphonate therapy are at increased risk of

developing atypical femoral fractures. First described in 2005, formal criteria for what constitutes an atypical femoral fracture were codified in 2013 by the American Society for Bone and Mineral Research (ASBMR). The fracture must be: • Distal to the lesser trochanter and proximal to the supracondylar flare And have at least four of the following five features:

Osteomalacia

• Associated with minimal or no trauma • Fracture line originates at the lateral cortical surface and has a substantially transverse orientation • Complete fractures extend through both cortices and may be associated with a medial spike; incomplete fractures only involve the lateral cortex • Fractures are simple or minimally comminuted • Localized periosteal or endosteal thickening of the lateral cortex at the fracture site While atypical femoral fractures are not pathognomonic for bisphosphonate therapy, the use of that medication class substantially increases the risk for developing them. The risk varies by patient age and length of bisphosphonate therapy, but odds ratios exceeding 115 are reported in patients on long-term therapy. As with all statistics, this can be misleading. Just know that while the risk of atypical femoral fractures increases with bisphosphonate use, the overall number of these fractures is quite low. Secondly sacral insufficiency fractures are a cause of significant morbidity, are challenging to diagnosis clinically, and are usually occult on the standard initial imaging evaluation of these patients. Suggesting the presence of an occult sacral insufficiency fracture adds substantial value to the management of the patient, but it requires you to think. As you are reading those lumbar spine or hip radiographs for the ubiquitous indication of “pain,” did you notice that the patient also has contralateral hip trochanteric nail fixation reflecting prior hip fracture or that there are numerous wrist X-rays from 2 years ago from when the patient fell down and fractured their distal radius (both of which should be considered suspicious for osteoporosis in addition to vertebral body and proximal humeral fractures)? A five second review of PACS to see if there is a DEXA can save months of time and frustration for otherwise occult lumbopelvic pain. The chances of identifying sacral insufficiency fractures on plain radiographs are very low. Generally, vertically oriented sclerosis in the sacral ala, sometimes unilaterally, is the only finding. Displaced sacral insufficiency fractures do

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not present as insidious pain to an outpatient provider, so these will come through the ER work list in a more traumatic setting, but can still be difficult to detect by plain film (you did say that the sacrum was obscured by bowel gas in your report didn’t you?). These fractures can also be occult even by CT. Subtle wrinkles in the cortices of the sacral ala may be the only clue. In current practice, MRI is the study of choice where bone marrow edema and, occasionally, associated T1 hypointense lines representing the true fracture planes can be seen. Multiplanar evaluation, both at MRI and CT, is mandatory to have a chance at catching or accurately finding these fractures. If you are reading a lumbar spine MRI, ensure that you look at the sacrum as far laterally as you can on the sagittal STIR sequence as sacral bone marrow edema on the very first or last image is often the only clue. For boards purposes, but rarely seen in routine clinical practice at this time, 99Tc-MDP bone scan will show increased radiopharmaceutical uptake in the sacrum, classically in the shape of an “H” forming the so-called Honda sign.

Osteomalacia Foundations Osteomalacia is a disturbance in the cellular organization and mineralization of the bone. While there is normal bone quantity, there is deficient bone quality. In children, we call this rickets (derived from wrick, an Old English work translating “to twist”). Regardless of patient age, the deficient bone quality is secondary to ineffective calcification of the osteoid matrix, and that is secondary to inadequate amounts of calcium.

Causes Previously, low intake of vitamin D was the most common cause of rickets and osteomalacia. With the advent of widespread availability of fortified foods, that is rarely seen in the developed world. The most common causes now are renal disfunctions and malabsorption. Hyperparathyroidism is

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a less common cause, but the secondary form shows up in renal osteodystrophy, so we will briefly cover it here.

 ow Dietary Vitamin D L While uncommon, low dietary intake of vitamin D is useful since it is easy to understand and, like hyperparathyroidism, also shows up in renal osteodystrophy. Low vitamin D causes poor calcium resorption in the small intestine, resulting in hypocalcemia. Without sufficient calcium, the bone matrix cannot mineralize normally. It is that simple. Malabsorption Intestinal malabsorption causes the loss of both calcium and phosphorous and can be seen in patients with gastric, enteric, and biliary abnormalities (to include patients with bariatric surgeon-­ induced abnormalities). As with any other cause of hypocalcemia, the bone matrix cannot appropriately mineralize. Hyperparathyroidism Hypocalcemia from any cause (primary, secondary, tertiary) stimulates release of parathormone (PTH). PTH has multiple metabolic effects, but just remember that a persistently elevated PTH level results in osteoclast activation to mobilize calcium from the bone in an attempt to normalize the serum calcium levels. Renal Causes The proximal and distal forms of renal tubular acidosis, to include Fanconi syndrome, ultimately result in urinary wasting of calcium. The exact mechanisms are fascinating to the nephrologist, but, for our purposes, they all lead down the pathway of hypocalcemia-induced osteomalacia. Renal osteodystrophy is more complex. The underpinnings are discussed because they reflect the imaging findings. There are two major mechanisms concurrently at play: (1) altered vitamin D metabolism and (2) secondary hyperparathyroidism. The deficient vitamin D metabolism is caused by inability of the diseased kidney to produce sufficient 1-alpha-hydroxylase, the enzyme

necessary to convert inactive vitamin D into the metabolically active form. The secondary hyperparathyroidism stems from the dysfunctional kidney excreting too little phosphate. The hyperphosphatemia drives down serum calcium (the mechanisms are complex; don’t worry about them) which invokes PTH release.

Findings The general radiographic finding in osteomalacia is diffuse osteopenia. Superimposed on this, one occasional sees multiple, often symmetric, cortical lucencies oriented perpendicular to the long axis of the bone. These are the classic Looser zones or pseudofractures of osteomalacia. Looser zones are essentially stress fractures which can never fully or properly heal, and they are most frequently seen along the lateral margins of the scapular bodies (Fig.  8.2), the medial femoral necks (opposite of atypical stress fractures in bisphosphonate-treated osteoporosis!), the pubic rami, and the ribs. The radiographic findings in renal osteodystrophy reflect a combination of the underlying low vitamin D levels and the superimposed

Fig. 8.2  Looser Zone: Irregular sclerotic appearance of the lateral scapular body, just inferior to the neck of the glenoid in an 89-year-old male with osteomalacia is a looser zone or “pseudofracture.”

Hyperparathyroidism

hyperparathyroidism which act in varying degrees from patient to patient. As with any other cause of low vitamin D availability, there is downstream hypocalcemia and poor mineralization of the osteoid matrix. This is further complicated by PTH-driven activation of osteoclasts. We’re now in a setting of increased bone turnover and impaired new bone formation, but there is one more component. The now-rising serum calcium concentration (from calcium mobilized by the osteoclasts) is in the setting of hyperphosphatemia (the kidneys are not excreting phosphate correctly), and that is a set up for creating insoluble calcium-phosphate moieties. The chemical formula for hydroxyapatite for example is Ca10(PO4)6(OH)2, the primary component in these soft tissue calcifications. All of these factors explain the mixed bag of imaging findings of renal osteodystrophy. Subchondral and subperiosteal thinning is common, but looser zones are not. Most patients have a degree of generalized osteopenia, and we encounter one of the most distinctive findings of hyperparathyroidism, brown tumors. These are bone cysts of varying sizes that can contain blood products which appear brown at gross inspection. Brown tumors are usually seen in the mandible, pelvis, and femora, but can be seen anywhere.

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Imaging Findings Most commonly seen are generalized osteopenia and brown tumors. Cortical thinning in the form of subchondral and subperiosteal bone resorption is classic. The subperiosteal resorption is classically seen at the radial aspects of the middle phalanges of the index and long fingers. The calvarium can assume a characteristic mottled appearance termed, “salt-and-pepper.” Distal clavicular osteolysis (a manifestation of subchondral resorption) and acro-osteolysis can also be present (Figs. 8.3, 8.4, and 8.5a–d).

Fig. 8.3  Renal osteodystrophy (hyperparathyroidism): Tumoral calcinosis about the right shoulder and a sharply defined lytic lesion within the distal right clavicle reflecting a brown tumor are seen in this 43-year-old male with end-stage renal disease.

Foundations As above, any cause of hypocalcemia stimulates PTH release. Persistently elevated levels of PTH actives osteoclasts and mobilization of calcium stored in the bone in an effort to restore normal serum calcium levels. Of the various types of hyperparathyroidism, which are usually detected and corrected on clinical and laboratory grounds long before we see significant imaging findings, the primary and secondary forms are the ones you are most likely to see.

Fig. 8.4  Subperiosteal bone resorption of the phalanges, and band-like bone resorption of the most distal phalangeal bones, are classic findings in hyperparathyroidism.

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a

b

c

d

Fig. 8.5 (a–d) Brown Tumors: (a) Sharply defined intramedullary and cortically based lytic lesions in the proximal right femur. (b) A lytic lesion in the proximal left humerus with an associated pathologic fracture. (c) An

expansile and destructive lesion in the mandible. (d) Lytic lesions involving the distal femur and a significant portion of the patella are all brown tumors in various individuals with hyperparathyroidism.

Hyperparathyroidism

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A distinction between the primary and secondary hyperparathyroidism is only important for our purposes since it explains imaging findings. In primary hyperparathyroidism, the parathyroid gland (usually a parathyroid adenoma) has escaped normal regulation and produces excess PTH.  This creates a state of hypercalcemia, and we are more likely to see nephrolithiasis and nephrocalcinosis, the imaging findings of the kidneys trying to dump the excess serum calcium. In secondary hyperparathyroidism, a baseline hypocalcemia (from whatever cause) drives a

c

excess PTH secretion. Since secondary hyperparathyroidism is commonly caused by ­ chronic renal disease, there is also a baseline hyperphosphatemia as detailed above. Consequently, soft tissue calcifications are likely to be seen in secondary hyperparathyroidism, but are far less commonly encountered with primary hyperparathyroidism. When the soft tissue calcifications become extensive enough to create a mass effect, the term tumoral calcinosis is often used, but the purists will take issue with that (Fig. 8.6a–d).

b

d

Fig. 8.6 (a–d) Tumoral calcinosis: Plain radiographs demonstrating tumoral calcinosis in various individuals with secondary hyperparathyroidism.

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a

b

Fig. 8.7 (a and b) Rugger jersey spine: Dense vertebral endplate sclerosis in secondary hyperparathyroidism mimics the wide alternating bands on rugby jerseys.

See the saved rounds at the end of this chapter for a few additional thoughts on tumoral calcinosis. There is also a generalized osteosclerosis which creates a characteristic appearance in the spine. Dense bands along the vertebral body endplates result in a rugger jersey spine (Fig.  8.7a and b).

Paget Disease Foundations First a word about eponyms. Paget disease is named after Sir James Paget, and “Paget disease” is correct, while “Paget’s disease” is less so. SoHo in New York City is South of Houston Street, not

“Houston’s Street.” The Willis Tower (not Willis’ Tower) is at the corner of West Jackson Street and South Franklin Street, not “Jackson’s Street and Franklin’s Street.” This pops up in other places in medicine and musculoskeletal imaging; it’s a Baker cyst, named after Dr. William Baker, not a Baker’s cyst. While we are being pedantic, it is most correct to term the disorder Paget disease of bone to distinguish it from Paget disease of the nipple. In reality, everyone already knows to which one you are referring. Paget disease is fairly common progressive disorder of bone metabolism. The prevalence of Paget disease also varies widely, and it is most common in Great Britain, Australia, and New Zealand. It generally affects middle-aged and older adults with an average onset between 45

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and 55 years of age. The disorder is slightly more common in men (about 3:2).

Pathophysiology The underlying cause is unknown with both viral and genetic etiologies postulated. Regardless, the basic pathophysiology is an imbalance between bone resorption and new bone formation with highly active and disorganized bone remodeling. The disease progresses through a series of three phases which are reflected at imaging: (1) the osteolytic phase, (2) the intermediate or mixed phase, and (3) the sclerotic phase. In long bones, Paget disease begins at the one end of the bone and systematically progresses to the other. As such, different parts of a long bone can be in different phases concurrently. Paget disease may manifest in a single bone or be widespread. In order of decreasing frequency, the disorder affects pelvis, femora, skull, tibiae, vertebral bodies, clavicles, humeri, and ribs. As expected, any bone can be involved.

Fig. 8.8  Lytic phase of Paget disease: Osteoporosis circumscripta is a common calvarial finding in the lytic phase of Paget disease. Usually confined to the frontal, and to a lesser extent, the occipital bones.

Imaging Findings The imaging findings reflect the stage of the disease at time of imaging. In the osteolytic phase, active bone resorption outpaces appositional bone formation. This characteristically moves through long bones in a sharply defined front of osteolysis creating an elongated lucency resembling a “blade of grass.” In the flat bones of the pelvis and skull, a sharply defined rounded lytic lesion is characteristic and termed osteoporosis circumscripta (Fig. 8.8). The intermediate phase of Paget disease shows imaging findings of both bone resorption and bone formation. This phase general favors bone formation, and the disorganized remodeling appears as thickened cortices and irregular coarse trabeculations. The spine assumes a characteristic “picture frame” appearance where the thickened cortical frame the margins of the vertebral bodies. This can be confused with the rugger jersey appearance of the vertebral bodies in second-

Fig. 8.9  Intermediate phase of Paget disease: The intermediate phase of Paget disease is affecting the proximal left femur and is characterized by a mixture of bone resorption and bone remodeling. Early bony expansion in the subtrochanteric diaphysis is also present.

ary hyperparathyroidism, and so it shows up on radiology exams. “Paget makes picture frames” (Fig. 8.9). During the sclerotic phase, the disorganized new bone formation dominates. Abnormal corti-

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a

b

Fig. 8.10 (a and b) Chronic phase of Paget disease: Bony expansion, cortical thickening, and irregular trabecula are the hallmarks of the chronic phase of Paget disease.

cal thickening and expansion of the bone occur. On plain films, thickened and irregular trabecular markings are seen, and there is blurring of the margin between the endosteal cortical surface and the medullary canal (Fig. 8.10a and b). CT and MRI are usually not necessary to diagnose Paget disease, but these modalities can be useful in delineating complications of the ­disease. MRI in particular has substantial utility in the surveillance and evaluation of sarcomatous transformation. As the disease is characterized by highly active bone remodeling, nuclear medicine studies are not terribly helpful. 99Tc-MDP bone scans will be hot on all phases, but more so during the osteolytic phase.

Complications of Paget Disease The abnormal remodeling with ultimate bony expansion of Paget disease leads to several expected complications. The remodeled bone, regardless of phase, is weaker than native bone, and so fractures are far more common. The bony hypertrophy alters

Fig. 8.11  Axial CT of the pelvis demonstrating bony destruction and aggressive periosteal reaction in the left iliac bone are indicative of sarcomatous transformation of Paget disease.

the mechanics of joints leading to osteoarthritis. Similarly, bony expansion necessarily narrows the various neuroforamina in the skull base and spine resulting neurologic complications. Neoplastic transformation, however, is the most feared complication, although fortunately it is rare (Fig. 8.11).

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Conventional osteosarcoma is by far the most common malignant tumor to arise from Paget disease. Fibrosarcoma, undifferentiated pleomorphic sarcoma, and chondrosarcoma follow in order of frequency. Non-sarcomatous degeneration can also occur with primary bone lymphoma and giant cell tumors occasionally seen.

are needed to make the diagnosis where a wavy and flowing hyperostosis is seen reminiscent of dripping candle wax. The bones can become focally expansile. Melorheostosis can be isolated to one bone (forme fruste which translates to frustrated form), one limb (monomelic melorheostosis), or rarely be widely disseminated.

Saved Rounds

Osteopoiklosis and Osteopathia Striata

Acromegaly Caused by an oversecretion of growth hormone, acromegaly occurs after physeal closure. The same disorder in a skeletally immature patient results in giantism. This is usually a clinical diagnosis. Characteristic imaging findings follow the outwardly apparent physical changes. There is overgrowth of the frontal sinuses and elongation of the jaw. The calvarium and facial bones become thickened and sclerotic, and there may be complete obliteration of the diploic space.

Tumoral Calcinosis Of unknown etiology, lobulated calcific deposition form in the periarticular soft tissues. Identical appearing calcifications can be seen in a variety of other disorders including secondary hyperparathyroidism, gout, hypervitaminosis D, and myositis ossifications. When all of these entities are excluded, tumoral calcinosis is correctly used to describe this idiopathic condition. That being said, if you report “interval development of tumoral calcinosis about the right shoulder” in a patient with renal osteodystrophy, everyone will know what you mean.

Melorheostosis Melorheostosis is an uncommon disorder of unknown etiology. It’s worth knowing about because the presenting symptom is pain, worsened by activity. Nothing more than plain films

Both of these disorders are probably related and both are probably inherited in an autosomal dominant fashion with mixed penetrance. Osteopoikilosis is nothing more than numerous bone islands. Osteopathia striata shows linear sclerotic  striations, usually in long bones. Both disorders are benign and asymptomatic. No additional imaging is needed.

Bibliography 1. Bringhurst FR, Demay MB, Kronenberg. Bone and mineral metabolism in health and disease. In: Jameson JL, Fauci AS, Kasper DL, et  al., editors. Harrison’s principles of internal medicine. 20th ed. New  York: McGraw-Hill; 2018. 2. Bruno F, Albano D, Agostini A, et al. Imaging of metabolic and overload disorders in tissues and organs. Jpn J Radiol. 2023;41(6):571–95. 3. Chalhoub D, Orwoll ES, Cawthon PM, et al. Areal and volumetric bone mineral density and risk of multiple types of fracture in older men. Bone. 2016;92:100–6. 4. Chan SS, Rosenberg ZS, Chan K, Capeci C.  Subtrochanteric femoral fractures in patients receiving long-term alendronate therapy: imaging features. Am J Roentgenol. 2010;194(6):1581–6. 5. Choi D, Kim DY, Han CS, et  al. Measurements of bone mineral density in the lumbar spine and proximal femur using lunar prodigy and the new pencil-­ beam dual-energy X-ray absorptiometry. Skelet Radiol. 2010;39(11):1109–16. 6. Desai MA, Peterson JJ, Garner HW, Kransdorf MJ. Clinical utility of dual-energy CT for evaluation of tophaceous gout. Radiographics. 2011;31(5):1365– 75; discussion 1376-1377. 7. Guglielmi G, Muscarella S, Bazzocchi A. Integrated imaging approach to osteoporosis: state-of-­ the-art review and update. Radiographics. 2011;31(5):1343–64. 8. Mauch JT, Carr CM, Cloft H, Diehn FE.  Review of the imaging features of benign osteoporotic and

214 malignant vertebral compression fractures. Am J Neuroradiol. 2018;39(9):1584–92. 9. Mckenna RJ, Schwinn CP, Soong KY, Higinbotham NL.  Osteogenic sarcoma arising in Paget’s disease. Cancer. 1964;17:42–66. 10. Milkman LA.  Pseudofractures (hunger osteopathy, late rickets, osteomalacia). Am J Roentgenol. 1930;24:29–37. 11. Naik M, Khan SR, Owusu D, et  al. Contemporary multimodality imaging of primary hyperparathyroidism. Radiographics. 2022;42(3):841–60. 12. Paget J. On a form of chronic inflammation of bones (Steitisdeformans). Med Chir Trans. 1877;60:37–64.

8  Metabolic Disorders 13. Pugh DG. Subperiosteal resorption of bone; a roentgenologic manifestation of primary hyperparathyroidism and renal osteodystrophy. Am J Roentgenol. 1951;66(4):577–86. 14. Resnick D.  The “rugger jersey” vertebral body. Arthritis Rheum. 1981;24:1191–2. 15. Rosenbaum HD, Hanson DJ. Geographic variation in the prevalence of Paget’s disease of bone. Radiology. 1969;92(5):959–63. 16. Usmani S, Ahmed N, Gnanasegaran G, Marafi F, van den Wyngaert T. Update on imaging in chronic kidney disease-mineral and bone disorder: promising role of functional imaging. Skelet Radiol. 2022;51(5):905–22.

Index

A Achilles tendon injury, 67 Acromegaly, 213 Acromioclavicular injury, 23 Acute osteomyelitis, 92–95 Adamantinoma, 126 Adaptation, 4 Adverse local tissue reaction, 153 Age, 108 Amyloid deposition arthropathy, 181 Anchoring hardware, 149 Aneurysmal bone cyst, 116, 129 Ankle injuries, 63 achilles tendon injury, 67 calcaneal stress fracture, 67 distal fibular fractures, 65 dorsal capsular avulsion fractures, 64 fracture at the anterior process of the calcaneus, 64 fracture at the base of the fifth metatarsal, 63, 64 fracture blisters, 67 lateral process of the talus, fracture of, 65 Maisonneuve fracture, 67 origin of the extensor digitorum brevis muscle, fracture at, 65 tendon entrapment, 67 traumatic osteochondral fracture of the lateral talar dome, 64 trimalleolar fractures, 65 Ankylosing spondylitis, 168 Ankylosis, 169 Anterior process of the calcaneus, fracture of, 64 Anterior shoulder dislocation, 21, 22 Anterior spinal line, 12 Anxiety, 4 Art of medicine, 9 Arthritis ankylosing spondylitis, 168 benign proliferative processes, 185 lipoma arborescens, 186 synovial chondromatosis/osteochodnromatosis, 185 tenosynovial giant cell tumor, 185 vascular malformations, 186 deposition arthropathy, 180

amyloid deposition arthropathy, 181 CPPD, 181 gout, 180, 181 enteropathic related arthritis, 173, 174 erosive osteoarthritis, 161, 162 hemophilia arthropathy, 184 inflammatory arthropathies, 162, 163 juvenile idiopathic arthritis, 168 neuropathic arthropathy, 179 osteoarthritis, 160 psoriatic and reactive arthritis, 169, 173 rheumatoid arthritis, 164 target recognition, 164, 167, 168 septic arthritis, 177, 178 sundries, 187 calcific periarthritis, 187 sarcoid, 190 scleroderma and mixed connective tissue diseases, 189 systemic lupus erythematosus (SLE) and rhupus, 188 Arthroplasty hardware, 149, 152 Atlanto-axial interval, 12 Atlanto-axial widening, 12 Atypical femoral fractures, 49, 204 Atypical infection, 100 Avulsion fracture at the anterior superior iliac spine, 51 Avulsion fractures of the anterior inferior iliac spine, 52 B Base of fifth metatarsal, fracture of, 63, 64 Benign proliferative processes, 185 lipoma arborescens, 186 synovial chondromatosis/osteochodnromatosis, 185 tenosynovial giant cell tumor, 185 vascular malformations, 186 Benign sclerosing bone dysplasia, 134 Benign sclerosing dysplasia, 134 Biceps dislocation, 25 Biceps tendon tear, 30 Bipartite patella, 59, 60 Bone infarcts, 132 Bone islands, 133

© The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 B. Plotkin, B. L. Davis, Musculoskeletal Imaging, https://doi.org/10.1007/978-3-031-49021-7

215

Index

216 Bone physiology, 201 Bone stress fractures, 71 Bone tumors adamantinoma, 126 age, 108 alone or in battalions, 108 aneurysmal bone cyst, 116 border and zone of transition, 106, 108 chondroblastoma, 115 chondrosarcoma, 119 clear cell chondrosarcoma, 116 distal phalanx, 127 epidermoid inclusion cysts, 128 glomus tumors, 127 enchondroma, 118 factors, 103 fibrous dysplasia, 123 fibroxanthoma, 123 giant cell tumor, 114 infection, 117, 122 location, 111, 112 matrix, 128 chondroid producing tumors, 128 osteoid producing tumors, 128 metastasis and myeloma, 124 osteochondroma, 119 osteofibrous dysplasia, 126 osteoid osteoma, 126 osteosarcoma, 120 periosteal reaction, 104, 105 polyostotic lesions, 135 brown tumors, 136 infection, 136 Langerhans cell histiocytosis, 137 metastasis and myeloma, 135 multiple enchondroma syndromes, 136 polyostoic fibrous dysplasia, 136 round blue cell tumors, 125 tumor mimics, 131 brown tumor, 131 giant bones islands, 133 infection, 131 melorheostosis, 134 osteonecrosis, 132 osteopathia striata, 134 osteopoikilosis, 134 unicameral or simple bone cyst, 118 Border and zone of transition, 106, 108 Brodie’s abscess, 117, 122, 126, 131 Brown tumor(s), 131, 136 Burst fracture, 19

Capitellum fracture, 29 Carpal dislocations, 37–39 Carpal metacarpals fractures, 36 Cartilaginous cap, 119 Cartilaginous matrix, 128 Centers for Disease Control and Infection (CDC), 153 Cervical spine, 11, 12 atlanto-axial widening, 12 C1 ring fractures, 14 Clay shoveler’s fracture, 16 dens fractures, 14 facet dislocation-disruption, 12 flexion tear drop fracture, 15 hanged man’s fracture, 15 Chance fracture, 20 Charcot arthritis, see Neuropathic arthropathy Chondroblastoma, 115 Chondroid matrix, 128, 132 Chondrosarcoma, 119 Chronic osteomyelitis, 92, 95, 96 Chronic phase of Page disease, 212 Chronic rotator cuff pathology, 25 Clay shoveler’s fracture, 16 Clear cell chondrosarcoma, 116 Clear lunate dislocation, 39 Common extensor/flexor tendon tear, 31 Compression fracture, 18, 19 CT, 89, 149, 202

C C1 ring fractures, 14 Calcaneal stress fracture, 67 Calcific periarthritis, 187 Calcific tendinopathy, 187 Calcium pyrophosphate dihydrate crystal deposition disease (CPPD), 181

E Elbow injury, 27 biceps tendon tear, 30 capitellum fracture, 29 common extensor/flexor tendon tear, 31 olecranon fracture, 28 tendon injuries, 30

D Decompression, 154 Dehiscence of the pseudocapsule, 154 Dens fractures, 14 Deposition arthropathy, 180 amyloid deposition arthropathy, 181 CPPD, 181 gout, 180, 181 Depressed lateral tibial plateau fracture, 9 Dermatomyositis, 189 Diastasis and dislocations, 52, 53 Displaced dorsal fragment, 32 Distal fibular fractures, 65 Distal phalanx, 127 epidermoid inclusion cysts, 128 glomus tumors, 127 Distal radial fracture(s), 32–34 Dorsal capsular avulsion fractures, 64 Down syndrome, 12 Dual energy X-ray absorptiometry (DEXA or DXA), 202–203

Index terrible triad, 27, 28 EMR record, 9 Enchondroma, 111, 118 Enteropathic related arthritis, 173, 174 Epidermoid inclusion cysts, 128 Erosive osteoarthritis, 161, 162 Ewing’s sarcoma, 125 F Facet dislocation-disruption, 12 Fanconi syndrome, 206 Fat, 129 Fear, 2, 4 Femoral neck fractures, 46 Femoral stress fractures, 47 Fibrous dysplasia, 123, 129 Fibroxanthoma, 123 Fifth metatarsal base fractures in kids, 70 Flexion tear drop fracture, 15 Fluid, 129 Foot injuries bone stress fractures, 71 fifth metatarsal base fractures in kids, 70 Lisfranc injuries, 70, 71 metatarsal neck fracture, 71 toe fractures, 71 Forearm injuries, 31 Galeazzi fracture, 32 Monteggia fracture, 31 Foreign bodies, 43 Formatting matters, 9 Fracture blisters, 67 Fracture risk assessment tool (FRAX), 203 G Galeazzi fracture, 32 Generalized age-related osteoporosis, 203 Giant bones islands, 133 Giant cell tumor, 114 Glomus tumors, 127 Gout, 180, 181 Greater tuberosity fracture, 22 Gymnasts, 37 H Hamate fractures, 35 Hand injuries metacarpal fractures, 40 phalangeal injuries, 41, 42 tendon laceration/tear, 44 thumb ulnar collateral ligament injury, 43 ultrasound, 43 Hanged man’s fracture, 15 Hardware dislocations, 152 Hardware subsidence, 153 Hematocrit effect, 54 Hemophilia arthropathy, 184

217 Hyperparathyroidism, 131, 206, 207, 209, 210 Hyperphosphatemia, 209 Hypocalcemia, 206, 207 I Improvise, 2 Incidental findings, 8 Infection, 117, 122, 131, 136 atypical, 100 imaging modalities CT, 89 MRI, 91, 92 nuclear medicine, 91 plain radiography, 89, 90 ultrasound, 90, 91 in spine, 98 intra-articular infection, 97, 98 osteomyelitis acute, 92–95 chronic, 92, 95, 96 pediatric vs. adult, 92 pyogenic vs. nonpyogenic, 92 soft tissues, 96, 97 necrotizing fasciitis, 96 Infectious and noninfectious acute monoarticular arthropathy, 97–98 Inflammatory arthropathies, 162, 163 Insufficiency fractures, 61 Intermediate phase of Paget disease, 211 Interosseous lipomas, 129 Intertrochanteric fractures, 46 Intra-articular emphysema, 55 Intra-articular infection, 97, 98 Isolated avulsion fracture, 47 Isolated fractures of the lesser trochanter, 47 Isolated greater trochanteric fractures, 46 Isolated lesser trochanteric avulsion injury, 47 J Jean-Marie Charcot, see Neuropathic arthropathy Jefferson fracture, 14 Joint aspiration, 178 Joint effusion, 54 Juvenile idiopathic arthritis, 168 K Key findings, 8 Knee dislocations, 61 Knee injury, 54 bipartite patella, 59, 60 dislocations, 61 insufficiency fractures, 61 less obvious knee injuries, 55 patella dislocations, 60 patella fractures, 58 stress fractures, 61 tibial plateau fractures, 58

Index

218 traumatic arthrotomy, 55 L Langerhans cell histiocytosis, 137 Lateral process of the talus, fracture of, 65 Learn basic skills, 3 Less obvious knee injuries, 55 Lipohemarthrosis, 54 Lipoma arborescens, 186 Lisfranc injuries, 70, 71 Lisfranc joint, 70 Localized osteoporosis, 203 Looser zones, 206 Low dietary intake of vitamin D, 206 Lunate dislocation, 38 M Maffucci syndrome, 136 Magnetic resonance imaging (MRI), 8, 91, 92, 150, 153, 202 Maisonneuve fracture, 67 Malabsorption, 206 Mazabraud syndrome, 136 McCune-Albright syndrome, 136 Medical classification systems, 9 Mediocre reports, 7 Melorheostosis, 134, 213 Metabolic disorders acromegaly, 213 bone physiology, 201 hyperparathyroidism, 207, 209, 210 imaging modalities, 201–203 melorheostosis, 213 osteomalacia, 205–207 osteopathia striata, 213 osteopoikilosis, 213 osteoporosis, 203 imaging findings of, 203–205 Paget disease, 210–212 tumoral calcinosis, 213 Metacarpal fractures, 40 Metastasis and myeloma, 124, 135 Metatarsal neck fracture, 71 Midcarpal dislocation, 38 Mixed connective tissue diseases, 189 Monteggia fracture, 31 Multiple enchondroma syndromes, 136 Musculoskeletal infections, 89 Myeloma, 124 N Narrow zone of transition and sclerotic border, 107, 111, 123 Narrow zone of transition with a non-sclerotic border, 107 Necrotizing fasciitis, 96 Neovascularity of abscesses, 97

Neuropathic arthropathy, 179 Non-ossifying fibroma, 123–124 Nonpyogenic osteomyelitis, 92 Nuclear medicine, 91, 150, 153 O Olecranon fracture, 28 Ollier disease, 136 Origin of the extensor digitorum brevis muscle, fracture at, 65 Orthopedic hardware, 149 anchoring hardware, 149 arthroplasty hardware, 149 complications displacement, 150 failure, 150 infection, 150, 153 perihardware fractures, 150 imaging CT, 149 MRI, 150 nuclear medicine, 150 plain radiography, 149 saved rounds, 156 stabilizing hardware, 149 Osteoarthritis, 160 Osteoblasts, 201 Osteochondroma, 119 Osteochondromatosis, 185 Osteodystrophy, 207 Osteofibrous dysplasia, 126 Osteoid matrix, 128 Osteoid osteoma, 126 Osteomalacia, 205–207 Osteomyelitis acute, 92–95 chronic, 92, 95, 96 pediatric vs. adult, 92 pyogenic vs. nonpyogenic, 92 Osteonecrosis, 132 Osteopathia striata, 134, 213 Osteopenia, 202 Osteopoikilosis, 134, 213 Osteoporosis, 203 imaging findings of, 203–205 Osteoporosis circumscripta, 211 Osteosarcoma, 120 P Paget disease, 210–212 Patella dislocations, 60 Patella fractures, 58 Patient management, 3 Pelvic and obturator ring fractures, 51, 52 Pelvic avulsion injuries, 51 Pelvis and hips diastasis and dislocations, 52, 53 pelvic and obturator ring fractures, 51, 52

Index proximal femoral fractures, 45–50 sacral insufficiency fractures, 50 Periacetabular osteolysis, 156 Periarticular osteopenia, 163 Perihardware fractures, 150 Perihardware lucency, 152 Perilunate dislocation, 38 Periosteal reaction, 104, 105 Periprosthetic fracture, 152 Phalangeal injuries, 41, 42 Phemister’s triad, 101, 177 Pisiform fractures, 34 Plain radiography, 89, 90, 93, 149, 153, 201–203 Polyostotic fibrous dysplasia, 136 Polyostotic lesions, 135 brown tumors, 136 infection, 136 Langerhans cell histiocytosis, 137 metastasis and myeloma, 135 multiple enchondroma syndromes, 136 polyostoic fibrous dysplasia, 136 Posterior spinal line, 12 Pott’s disease, 100 Pre-vertebral soft tissues, 12 Primary hyperparathyroidism, 207 Proximal femoral fractures, 45–50 Pseudofractures, 206 Psoriatic arthritis, 169, 173 Pyogenic osteomyelitis, 92 Q Quality metrics, 8 R Radial k-space filling techniques, 94 Reactive arthritis, 169, 173 Reactive arthropathy, 173 Regional osteoporosis, 203 Renal osteodystrophy, 206 Report structure, 7 header information, 7 Retrocalcaneal erosions, 173 Rheumatoid arthritis, 162, 164 target recognition, 164, 167, 168 Rheumatoid arthropathy, 12 Rhupus, 188 Rib fracture, 27 Rotator cuff tendinopathy, 25 Round blue cell tumors, 125 Rugger Jersey Spine, 210 S Sacral insufficiency fractures, 50, 205 Sarcoid, 190 Sarcoidosis, 190 Scaphoid fractures, 33 Scapula fracture, 22

219 Schatzker classification for tibial plateau fractures, 9 Scleroderma, 189 Secondary hyperparathyroidism, 207 Segond fracture fragment, 8 Septic arthritis, 177, 178 Septic arthropathy, 89 Shiny corner sign, 169 Shoulder, 21 acromioclavicular injury, 23 anterior dislocations, 21, 22 biceps dislocation, 25 chronic rotator cuff pathology, 25 greater tuberosity fracture, 22 scapula fracture, 22 stress injuries of distal clavicle, 23 Soft tissues infection, 96, 97 necrotizing fasciitis, 96 Spinal lamina line, 12 Spines cervical spine, 11, 12, 14 (see Cervical spine) infection in, 98 thoracic and lumbar spine, 18 burst fracture, 19 chance fracture, 20 compression fracture, 18, 19 Spinous process line, 12 Stabilizing hardware, 149 Sternum and sternoclavicular joints, 26 Stress, 3 factor for increase, 4 forces, 4 fractures, 36, 61 injuries of distal clavicle, 23 Subchondral insufficiency fractures, 61 Sundries, 187 calcific periarthritis, 187 sarcoid, 190 scleroderma and mixed connective tissue diseases, 189 systemic lupus erythematosus (SLE) and rhupus, 188 Survival actions, 1–3 psychology of, 3, 4 take care of yourself, 4, 5 Synovial chondromatosis, 185 Systemic lupus erythematosus (SLE), 188 T T2 hyperintense pulmonary mass, 8 Tendinopathy, 67 Tendon entrapment, 67 Tendon injuries, 30 Tendon laceration/tear, 44 Tenosynovial giant cell tumor, 185 Terrible triad, 27 Thoracic and lumbar spine burst fracture, 19 chance fracture, 20 compression fracture, 18, 19

Index

220 Thumb ulnar collateral ligament injury, 43 Tibial plateau fractures, 58 Toe fractures, 71 Transient osteoporosis, 203 Trans-scaphoid perilunate dislocation, 39 Traumatic arthrotomy, 55 Traumatic osteochondral fracture of the lateral talar dome, 64 Triangular fibrocartilage complex (TFCC), 181 Trimalleolar fractures, 65 Triquetral fracture, 32 Tumoral calcinosis, 213 U Ultrasound, 43, 90, 91 Unicameral or simple bone cyst, 118

V Vascular malformations, 186 Volar plate avulsion fractures, 42 W Wide zone of transition, 107–108, 111 Wrist injuries carpal dislocations, 37–39 carpal metacarpals fractures, 36 distal radial fractures, 33, 34 hamate fractures, 35 pisiform fractures, 34 scaphoid fractures, 33 stress fractures, 36 triquetral fracture, 32