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Part 1 book “Imaging of bones and joints” has contents: Acute trauma and overuse injuries - essentials, acute trauma and chronic overuse (according to region); infections of the bones, joints, and soft tissues; tumors and tumor like lesions of bone, joints, and the soft tissues,… and other contents.
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Simply visit MediaCenter.thieme.com and, when prompted during the registration process, enter the code below to get started today 444L-XP25-S85K-YMB5 Imaging of Bones and Joints A Concise, Multimodality Approach Klaus Bohndorf, MD Professor of Radiology MR Highfield Center Department of Biomedical Imaging and Image-guided Therapy Medical University of Vienna Vienna, Austria Mark W Anderson, MD Professor of Radiology MSK Imaging Department of Radiology University of Virginia Charlottesville, Virginia, USA Mark Davies, MRCP, FRCR Professor of Radiology Department of Radiology Royal Orthopaedic Hospital Birmingham, UK Herwig Imhof, MD Professor of Radiology Formerly Department of Biomedical Imaging and Image-guided Therapy Medical University of Vienna Vienna, Austria Klaus Woertler, MD Professor of Radiology Department of Radiology Technical University of Munich Munich, Germany 2181 illustrations, including 338 on the Thieme MediaCenter Thieme Stuttgart • New York • Delhi • Rio de Janeiro Library of Congress Cataloging-in-Publication Data is available from the publisher This book is an authorized, adapted, and revised version of the 3rd German edition published and copyrighted 2014 by Georg Thieme Verlag, Stuttgart Title of the German edition: Radiologische Diagnostik der Knochen und Gelenke Translator: Grahame Larkin, Stuttgart, Germany Illustrator: Christiane and Dr Michael von Solodkoff, Neckargemünd, Germany 3rd German edition 2014 1st Italian edition 2003 1st Portuguese edition 2006 © 2016 Georg Thieme Verlag KG Thieme Publishers Stuttgart Rüdigerstrasse 14, 70469 Stuttgart, Germany +49 [0]711 8931 421, customerservice@thieme.de Thieme Publishers New York 333 Seventh Avenue, New York, NY 10001, USA +1-800-782-3488, customerservice@thieme.com Thieme Publishers Delhi A-12, Second Floor, Sector-2, Noida-201301, Uttar Pradesh, India + 91 120 45 566 00, customerservice@thieme.in Thieme Publishers Rio, Thieme Publicaỗừes Ltda Edifớcio Rodolpho de Paoli, 25 andar, Av Nilo Peỗanha, 50 Sala 2508 Rio de Janeiro 20020-906 Brasil + 55 21 3172 2297/+ 55 21 3172 1896 Cover design: Thieme Publishing Group Typesetting by Ziegler + Müller, Kirchentellinsfurt, Germany Printed in Germany by Aprinta GmbH, Wemding ISBN 978-3-13-240647-6 Also available as an e-book: eISBN 978-3-13-240876-0 Important note: Medicine is an ever-changing science undergoing continual development Research and clinical experience are continually expanding our knowledge, in particular our knowledge of proper treatment and drug therapy Insofar as this book mentions any dosage or application, readers may rest assured that the authors, editors, and publishers have made every effort to ensure that such references are in accordance with the state of knowledge at the time of production of the book Nevertheless, this does not involve, imply, or express any guarantee or responsibility on the part of the publishers in respect to any dosage instructions and forms of applications stated in the book Every user is requested to examine carefully the manufacturers’ leaflets accompanying each drug and to check, if necessary in consultation with a physician or specialist, whether the dosage schedules mentioned therein or the contraindications stated by the manufacturers differ from the statements made in the present book Such examination is particularly important with drugs that are either rarely used or have been newly released on the market Every dosage schedule or every form of application used is entirely at the user's own risk and responsibility The authors and publishers request every user to report to the publishers any discrepancies or inaccuracies noticed If errors in this work are found after publication, errata will be posted at www.thieme.com on the product description page Some of the product names, patents, and registered designs referred to in this book are in fact registered trademarks or proprietary names even though specific reference to this fact is not always made in the text Therefore, the appearance of a name without designation as proprietary is not to be construed as a representation by the publisher that it is in the public domain This book, including all parts thereof, is legally protected by copyright Any use, exploitation, or commercialization outside the narrow limits set by copyright legislation, without the publisher's consent, is illegal and liable to prosecution This applies in particular to photostat reproduction, copying, mimeographing, preparation of microfilms, and electronic data processing and storage Cover image source: de.123rf.com/profile_3dclipartsde'>3dclipartsde / 123RF Lizenzfreie Bilder Contents Acute Trauma and Overuse Injuries: Essentials 1.1 Normal Skeletal Development, Variations, and Transitions to Pathologic Conditions (W Michl) 1.1.1 Normal Skeletal Development 1.1.2 Variations and Disturbances of Skeletal Development 1.1.3 Transitions to Pathologic States 1.2 Fractures: Definition, Types, and Classifications (K Bohndorf) 1.2.1 Definition and Classification 1.2.2 Fracture Types 1.2.3 Classifications 1.3 Fractures in Children (W Michl) 1.3.1 Special Features of Fractures in Children 1.3.2 Battered-Child Syndrome 1.4 Fractures of the Articular Surfaces: Subchondral, Chondral, and Osteochondral Fractures (K Bohndorf, S Trattnig) 1.4.1 Subchondral Fracture 1.4.2 Chondral Fracture 1.4.3 Osteochondral Fracture 1.5 Stress and Insufficiency Fractures (K Bohndorf) 1.5.1 Classification 1.5.2 Insufficiency Fractures and Destructive Arthropathy 1.5.3 Pathologic Fractures 1.5.4 Transient Osteoporosis and Transient Bone Marrow Edema 1.6 Fracture Healing 1.6.1 Primary Fracture Healing (Direct Cortical Reconstruction) (K Bohndorf) 1.6.2 Secondary Fracture Healing (Fracture Healing by Callus Formation) (K Bohndorf) 1.6.3 Radiological Assessment after Fracture Fixation of the Peripheral Skeleton (E Knoepfle) 1.6.4 Radiological Assessment after Implantation of a Joint Prosthesis in the Peripheral Skeleton (E Knoepfle) 1.7 Complications after Fractures 1.7.1 Delayed Union, Nonunion, and Posttraumatic Bone Cyst Formation (K Bohndorf) 1.7.2 Posttraumatic Disturbances of Growth in Children and Adolescents (W Michl) 1.7.3 Disuse Osteoporosis (K Bohndorf) 1.7.4 Complex Regional Pain Syndrome (K Bohndorf) 1.7.5 Posttraumatic Osteoarthritis (K Bohndorf) 1.8 Traumatic and Overuse Injuries to Muscles, Tendons, and Tendon Insertions (K Bohndorf, A Seifarth) 1.8.1 Muscles 1.8.2 Tendons 1.8.3 Tendon Insertions (Enthesopathy) 1.9 Practical Advice on Diagnostic Radiography in Traumatology (K Bohndorf) 1.9.1 Report of Findings 1.9.2 Follow-Up Reviews 1.9.3 What to Avoid Acute Trauma and Chronic Overuse (According to Region) 2.1 Cranial Vault, Facial Bones, and Skull Base (H Imhof, N Jorden) 2.1.1 Fractures of the Cranial Vault 2.1.2 Basilar Skull Fractures 2.1.3 Fractures of the Petrous Bone 2.1.4 Facial Bone Fractures 2.2 Spine 2.2.1 Anatomy, Variants, Technique, and Indications (T Grieser) 2.2.2 Mechanisms of Injury and Classifications (T Grieser) 2.2.3 Special Traumatology of the Cervical Spine and the Craniocervical Junction (T Grieser) 2.2.4 Injury Patterns of the “Stiff” Spine (T Grieser) 2.2.5 Stable or Unstable Fracture? (T Grieser) 2.2.6 Fresh or Old Fracture? (T Grieser) 2.2.7 Differential Diagnosis “Osteoporotic Versus Pathologic Fracture” (T Grieser) 2.2.8 Stress Phenomena in the Spine: Stress Reaction and Stress Fracture (Spondylolysis) of the Neural Arches (T Grieser) 2.2.9 Value of MRI in Acute Trauma (T Grieser) 2.2.10 Radiological Assessment after Surgery of the Spine (R Fessl) 2.3 Pelvis 2.3.1 Fractures of the Pelvic Ring (E J Mayr) 2.3.2 Acetabular Fractures (E J Mayr) 2.3.3 Fatigue Fractures of the Pelvis (E J Mayr) 2.3.4 Hip Dislocation/Fracture Dislocations of the Hip (E J Mayr) 2.3.5 Pubalgia (Osteitis Pubis) (K Bohndorf) 2.4 Shoulder Joint (K Woertler) 2.4.1 2.4.2 Anatomy, Variants, and Technique Impingement 2.4.3 Rotator Cuff Pathology and Biceps Tendinopathy 2.4.4 Pathology of the Rotator Interval 2.4.5 Shoulder Instability 2.4.6 Other Labral Pathology 2.4.7 Postoperative Complications 2.5 Shoulder Girdle and Thoracic Wall (N Jorden) 2.5.1 Sternoclavicular Dislocation 2.5.2 Clavicular Fracture 2.5.3 Acromioclavicular Dislocation 2.5.4 Scapular Fracture 2.5.5 Sternal and Rib Fractures 2.5.6 Stress Phenomena of the Acromioclavicular Joint 2.5.7 Posttraumatic Conditions Secondary to Injuries of the Shoulder Girdle 2.6 Upper Arm 2.6.1 Proximal Humeral Fractures (N Jorden) 2.6.2 Humeral Shaft Fractures (N Jorden) 2.6.3 Distal Humeral Fractures (N Jorden) 2.6.4 Radiological Assessment after Surgery of the Upper Arm (E Knoepfle) 2.7 Elbow Joint (E McNally, O Ertl, K Bohndorf) 2.7.1 Medial Compartment 2.7.2 Lateral Compartment 2.7.3 Anterior Compartment 2.7.4 Posterior Compartment 2.7.5 Osteochondral Lesions: Traumatic Lesions, Panner's Disease, and Osteochondritis Dissecans 2.7.6 Neuropathies 2.8 Forearm (A Altenburger) 2.8.1 Proximal Fractures of the Forearm 2.8.2 Radial Head and Neck Fractures 2.8.3 Shaft Fractures of the Forearm 2.8.4 Distal Forearm Fractures 2.8.5 Instability of the Distal Radioulnar Joint 2.8.6 Ulnar Impingement Syndrome 2.8.7 Radiological Assessment after Surgery of the Forearm (E Knoepfle) 2.9 The Wrist (J Zentner) 2.9.1 Anatomy, Variants, Technique, and Indications 2.9.2 Fractures and Dislocations and Their Complications 2.9.3 Carpal Instabilities and Malalignments 2.9.4 Triangular Fibrocartilage Complex 2.9.5 Ulnocarpal Impaction Syndrome 2.9.6 Tendons of the Wrist 2.10 Metacarpals and Fingers (J Zentner) 2.10.1 Anatomy, Technique, and Indications 2.10.2 Fractures 2.10.3 Tendon and Ligament Lesions 2.11 Hip Joint 2.11.1 Anatomy, Variants, and Techniques (C W A Pfirrmann, R Sutter) 2.11.2 Fractures (C W A Pfirrmann, R Sutter) 2.11.3 Femoroacetabular Impingement (C W A Pfirrmann, R Sutter) 2.11.4 Labral Lesions (C W A Pfirrmann, R Sutter) 2.11.5 Chondromalacia and Synovitis (C W A Pfirrmann, R Sutter) 2.11.6 Muscle and Tendon Injuries (C W A Pfirrmann, R Sutter) 2.11.7 Slipped Capital Femoral Epiphysis (C W A Pfirrmann, R Sutter) 2.11.8 Radiological Assessment after Fracture Fixation and Joint Replacement of the Hip (W Michl) 2.12 Femur and Soft Tissues of the Thigh 2.12.1 Anatomy and Technique (O Ertl) 2.12.2 Fractures (O Ertl) 2.12.3 Muscle Injuries of the Thigh (O Ertl) 2.12.4 Radiological Assessment after Surgery of the Thigh (E Knoepfle) 2.13 Knee Joint 2.13.1 Indications and Technique (S Trattnig, K M Friedrich, K Bohndorf) 2.13.2 Cruciate Ligaments (S Trattnig, K M Friedrich, K Bohndorf) 2.13.3 Medial Supporting Structures (S Trattnig, K M Friedrich, K Bohndorf) 2.13.4 Lateral Supporting Structures (S Trattnig, K M Friedrich, K Bohndorf) 2.13.5 Patella, Quadriceps Muscle, and Anterior Ligaments (S Trattnig, K M Friedrich, K Bohndorf) 2.13.6 Menisci (S Trattnig, K M Friedrich, K Bohndorf) 2.13.7 Cartilage (S Trattnig, K M Friedrich, K Bohndorf) 2.13.8 Bursae and Plicae (S Trattnig, K M Friedrich, K Bohndorf) 2.13.9 Findings after Cartilage Replacement Therapy (S Trattnig, K M Friedrich, K Bohndorf) 2.13.10 Radiological Assessment of Knee Replacement Surgery (E Knoepfle) 2.14 Lower Leg 2.14.1 Fractures (E.-M Wagner) 2.14.2 Radiological Assessment of Surgery of the Lower Leg (E Knoepfle) 2.14.3 Soft Tissue Injuries and Stress Reactions of the Lower Leg (K Bohndorf) Fig 5.14 Osteomyelofibrosis (a) Sclerosis of the axial skeleton, here in the hip joint (b) MRI confirms diffuse bone marrow infiltration and splenomegaly Fig 5.13 Osteoporosis in a 47-year-old woman The bone marrow of the spine demonstrates increased fat accumulation for the patient's age (a) Increased bone marrow signal (fatty marrow) on the T1W image (b) Significantly decreased signal intensity on the corresponding fat saturated image Fig 5.16 Systemic mastocytosis (Images courtesy of B Jobke, Heidelberg, Germany.) (a) Significantly increased sclerosis of the vertebrae (b) Patchy sclerosis of the bone marrow Fig 5.15 Mastocytosis Peripheral focal osteosclerosis The image is not specific, but manifestation and location are certainly typical Fig 5.17 Systemic mastocytosis (Images courtesy of B Uffmann, Vienna, Austria.) (a) Hypointensity of the bone marrow on the T1W image in the presence of diffuse infiltration (b) Patchy hyperintensity of the bone marrow on the fat-saturated T2W image 5.5 Malignant Disorders of the Bone Marrow 5.5.1 Multiple Myeloma/Solitary Plasmacytoma Pathology Myeloma arises from an asymptomatic premalignant proliferation of monoclonal plasma cells Multistep genetic and microenvironmental changes lead to the transformation of these cells into a malignant neoplasm Myeloma is thought to evolve most commonly from a monoclonal gammopathy of undetermined clinical significance (usually known as MGUS) that progresses to smoldering myeloma and, finally, to symptomatic multiple myeloma Myelomatous plasma cell proliferation leads to displacement of the hematopoietic stem cells within the bone marrow Multiple myeloma accounts for approximately 1% of neoplastic diseases and 13% of hematologic cancers and usually develops in older age A solitary plasmacytoma is less common (~ 5% of cases) and is distinguished from multiple myeloma Solitary plasmacytoma is characterized by a mass of neoplastic monoclonal plasma cells in either bone or soft tissue without evidence of systemic disease attributed to myeloma (increased calcium, renal insufficiency, anemia, or multiple bone lesions) The most common location of a solitary plasmacytoma in bone is in the axial skeleton The incidence increases exponentially with advancing age Solitary plasmacytoma of bone carries a significant risk of progressing to multiple myeloma The osseous pattern of involvement of multiple myeloma is quite variable Usually there is diffuse involvement of varying degree that is not always evident on imaging, but it may exhibit multifocal micro- and/or macronodular lesions or a mixed picture Depending on location, the lesions may destroy the cortex and invade adjacent soft tissues The axial skeleton and proximal tubular bones (regions with hematopoietic marrow) are primarily affected Extraosseous manifestation is rare Typically, a bone marrow biopsy is taken from the iliac crest, and if this proves to be negative then a biopsy of a focal lesion is performed (best done under CT guidance) Clinical presentation Apart from nonspecific general symptoms (B symptoms), bone pain, and pathologic fractures occur as a result of increased bone absorption Displacement of normal blood-forming cells in the bone marrow results in anemia, a tendency to bleed, and infections Complications • Fractures • Bone infarctions and osteonecrosis • Amyloidosis (in 5–10% of cases of multiple myeloma) (Chapter 8.6) Radiography Purely osteolytic foci (absent intralesional matrix calcifications) without marginal sclerosis are evident and create the impression of being circumscribed, as if “punched out” ( Figs 5.18 and 5.19) An infiltrative, moth-eaten pattern is also possible Cortical bone is commonly destroyed Abnormal soft tissue opacity adjacent to an involved bone is suspicious for soft tissue invasion A periosteal reaction creating the impression of a so-called neocortex is possible Diffuse involvement may express itself in the form of “osteopenia,” together with corresponding subjective symptoms A sclerotic margin may form around the lesion during and after chemotherapy ( Fig 5.20) Note The still commonly used classification of multiple myeloma according to Durie and Salmon includes radiographic evidence of osteolytic lesions as one criterion Standard radiography, however, is not commonly used for detecting osteolytic lesions, and has been replaced by what is known as plasmacytoma CT (see following text) Standard radiography should only be used for clarifying localized pain (circumscribed lytic lesion, fracture?) It is also not suitable for monitoring therapy CT Plain low-dose spiral CT from the vertex to the thigh (plasmacytoma CT) has established itself as a fast and, in comparison with radiography, more sensitive examination for diagnosing and staging myeloma of the axial skeleton Radiation exposure is no greater than it is for screening with conventional radiographs (axial skeleton, head, bilateral proximal humerus, and proximal femur) With the option of generating multiplanar reconstructions, osteolytic lesions of the spine at risk of fracture can be detected and assessed significantly earlier ( Figs W5.5–W5.7) Important findings The findings in Table 5.1 have proven useful for judging whether the osteolytic lesions detected are typical for multiple myeloma MRI The MRI appearance of the lesions is nonspecific (hypointense on T1W, hyperintense on fluid-sensitive sequences, contrast enhancement; Fig 5.21; Figs W5.8 and W5.9; see also Fig W5.7) The bright disk sign (Chapter 5.1) in the spine is helpful in cases of diffuse involvement Caution The marrow changes can be so subtle in some cases of multiple myeloma that in the early stages, the MRI may appear “normal.” A typical, albeit rare, feature is the “salt and pepper” (variegated) pattern caused by minute cell clusters and islands of fat (see Fig 5.5) Follow-up studies after successful treatment show regression of the lesions and replacement with fatty marrow over the longer term Table 5.1 Myeloma CT findings based on the Durie-Salmon radiographic staging system Evaluation Finding Normal No cortical bone destruction, no intratrabecular radiolucencies > 1 cm Unclear finding (“nonspecific”) No cortical bone destruction, circumscribed intratrabecular radiolucencies > 1 cm Pathologic finding (“typical” for plasmacytoma) Evidence of cortical destruction associated with intratrabecular radiolucencies Fracture risk • In tubular bones: cortical bone destruction of > 50% of the circumference • In vertebrae: cortical bone destruction of > 50% of the lateral, anterior or posterior wall Fig 5.18 Multiple myeloma (a) Sharply defined osteolytic lesions of the ischial tuberosity and the lesser trochanter (b) As well as these lesions, whole-body MRI clearly demonstrates a multifocal involvement of the pelvis (arrows) and a diffuse infiltration of the spine Fig 5.19 Plasmacytoma Patchy osteolytic lesions without marginal sclerosis Fig 5.20 Plasmacytoma Osteolytic lesions with thin sclerotic margins after treatment Fig 5.21 Plasmacytoma (a) Multiple chronic vertebral fractures, smaller nodular lesions (arrows) (b) Additional involvement of the pedicle and posterior elements of T10 Note MRI is currently the most sensitive imaging modality for identifying marrow involvement with multiple myeloma and is particularly useful in detecting diffuse involvement Whole-body MRI is also capable of detecting peripheral lesions, which is important because this may alter the stage of the disease (see, for example, Fig W5.9) Dynamic contrast-enhanced and diffusion-weighted MRI are new and promising quantitative methods for classifying the disorder and monitoring therapy, but these are not yet used in routine clinical practice NUC MED FDG-PET CT has the advantage of demonstrating osteolytic lesions by CT, while at the same time providing a scintigraphic quantification of the activity of the lesion The latter is also used for monitoring therapy FDGPET CT is very well suited for detecting extramedullary lesions However, diffuse alterations are less well detected than by MRI In many centers an extended staging system (Durie-Salmon PLUS) is used instead of the classic Durie-Salmon staging system ( Table W5.1) This system relies on MRI and PET-CT as the decisive imaging modalities In these cases routine screening CT is superfluous Note A technetium bone scan is not indicated for multiple myeloma since there is little if any osteoblastic activity with these lesions DD • Diffuse pattern on MRI and PET: Reconversion (Chapter 5.1.2), leukemia, and bone marrow stimulation cannot be distinguished from each other by MRI and PET • Multifocal lesions on MRI: Atypical hemangiomas (coarse longitudinal trabeculae on CT help with differentiation.) Metastases • Osteolytic lesions on the radiograph and CT: Metastases, especially from thyroid and renal cell carcinoma The latter are usually well vascularized and have a peripheral and cortical location Further differential diagnoses Lymphoma, leukemia, primary bone tumors, hyperparathyroidism Related Disorders MGUS (monoclonal gammopathy of unknown significance) This is a common condition in older patients, characterized by monoclonal gammopathy in the blood and a very low tumor load There is only a very low risk of developing full-blown multiple myeloma over time POEMS (polyneuropathy, organomegaly, endocrinopathy, M-proteins, skin changes) This is a rare paraneoplastic syndrome associated with monoclonal gammopathy The radiographs may show numerous, variably sized sclerotic bone lesions Caution Not all components of POEMS syndrome may be present, but there should be a minimum of three to make the diagnosis PEST (papilledema, extravascular volume overload, sclerotic bone lesions, and thrombocytosis/erythrocytosis) Imaging demonstrates sclerotic lesions (known as sclerotic myeloma) Waldenstrom macroglobulinemia This disorder involves the production of immunoglobulin M paraprotein by lymphoplasmacytic cells Skeletal manifestations are nonspecific and resemble those of plasmacytoma, but are less marked 5.5.2 Lymphoma Lymphomas are a heterogeneous group of disorders characterized by the proliferation and accumulation of abnormal lymphocytes, particularly in lymphatic organs (lymph nodes, spleen) and occasionally in other organs By definition, Stage IV includes any involvement of bone marrow Pathology Lymphomas are divided into two main categories: Hodgkin's and non-Hodgkin's lymphomas The prevalence of bone involvement is quite varied It is low in Hodgkin's lymphoma at the time of diagnosis, but is more common with recurrences It is variable with non-Hodgkin's lymphoma, depending on the histological subtype Bone involvement is diffuse and multifocal, or it results from direct invasion by adjacent nodal masses Solitary bone lesions are less common Pure bony involvement of lymphoma is rare (non-Hodgkin's lymphoma) but can develop in any part of the skeleton Lymphomas may develop anywhere in the musculoskeletal system, including the subperiosteal space, epidural space, and muscles Clinical presentation Lymphadenopathy and possible hepatosplenomegaly are the main features General symptoms, such as fever, night sweats, and weight loss (B symptoms) are indicative of a poorer prognosis Radiography Osteolytic and/or osteoblastic lesions are encountered Osteolytic lesions often display a highly aggressive pattern of bone destruction, moth-eaten or permeative, to such an extent that the cortex might even appear preserved on standard radiographs, even though an adjacent soft-tissue shadow is already present Complex or malignant types of periosteal reaction are common CT CT reveals that bone destruction and osteosclerosis often coexist, even in lesions that appear predominantly lytic on the radiograph ( Figs 5.22–5.24) NUC MED The bone scan may identify focal bone involvement, although this would presuppose an osteoblastic reaction of the bone lesion FDG-PET is very well suited for staging, monitoring of therapeutic response, and follow-up of lymphomas FDG-PET CT well demonstrates any therapeutic response to therapy of Hodgkin's disease and diffuse large B-cell lymphoma MRI MRI is the modality of choice for assessing any symptomatic regions in order to establish the diagnosis and for assessing cases in which there is clinical suspicion of spinal cord or nerve root compression Fig 5.22 Lymphoma infiltration of the entire L4 vertebra exhibits a pathologic fracture (a) Lytic and sclerotic alterations (b) Bulging of the posterior margin past the posterior spinal line resulting in severe spinal stenosis, typical for tumor-related vertebral collapse Fig 5.23 Non-Hodgkin's lymphoma (a) Axial CT slice through L2 displays a mixed osteolytic/osteosclerotic lesion (b) Hypointense tumor on a T1W image infiltrating the normally fatty marrow Fig 5.24 Non-Hodgkin's lymphoma (a) Diffuse patchy hypointensity of the bone marrow (note also evidence of prior laminectomy of L3) (b) Irregular contrast enhancement of the bone marrow Large amount of residual tumor posteriorly (c) CT demonstrates only localized sclerosis in S1 The appearance of bone involvement is nonspecific and includes diffuse bone marrow infiltration, a diffuse variegated picture or focal bone marrow displacement ( Fig W5.10; Figs 5.22–5.24) The alterations may resemble those of plasmacytoma Caution Typically, MRI will often demonstrate a large soft-tissue component despite seemingly preserved cortical bone (known as the wrap-around sign, i.e., the soft-tissue component appears to surround the intact cortical bone), when in actual fact there is permeative bone infiltration ( Fig 5.25) 5.5.3 Leukemia Leukemia arises as a result of an uncontrolled proliferation of malignant hematopoietic cell clones The result is the spread of these lymphoid or myeloid cells in the bone marrow, ultimately leading to the infiltration of extramedullary organs and the invasion of the peripheral blood Imaging is not employed for the primary diagnosis of leukemia The use of radiography, CT, and MRI is limited to the diagnostic work-up of localized pain or possible complications of therapy Illness- and therapy-related complications include gout (Chapter 10.9), septic arthritis (Chapter 3.3), avascular necrosis (Chapter 6), bone infarction (Chapter 6) and osteomyelitis (Chapter 3.1) A chloroma (granulocytic sarcoma) is a variant of leukemia with a localized accumulation of blasts in the bone (lytic lesions), periosteum, lymph nodes, or soft tissues MRI displays a mass demonstrating nonspecific signal intensity ( Fig 5.26) 5.6 Therapy-related Bone Marrow Alterations Blood transfusions Multiple blood transfusions may cause bone marrow hemosiderosis (Chapter 5.3.1) Glucocorticoids Imaging plays an important role in demonstrating complications related to steroid use Bone infarction and osteonecrosis are commonly seen during steroid therapy, especially with long-term administration of steroids after bone marrow transplantation (Chapter 6) Osteomyelitis also occurs more frequently in these patients Chemotherapy The reaction of the various bone marrow disorders to chemotherapy is complex, depending on the underlying condition and the substances used ( see References for Chapter 5) Bone marrow–stimulating factors These substances increase the number of hematopoietic cells in the marrow (thus shortening the duration of aplasia after chemotherapy, for example); that is, they lead to marrow reconversion Here too, the pattern may be patchy, with focal islands of red marrow or a nodular appearance Caution The type of cells involved cannot be reliably differentiated on the MRI sequences currently available It is therefore not possible to distinguish between stimulated or regenerative bone marrow from malignant cell infiltration Radiotherapy In the acute phase (1–3 days) bone marrow reacts with the development of edema (known as radiation osteitis: hypointense on T1W images and hyperintense on fluid-sensitive sequences with somewhat increased contrast enhancement) Eventually (the time span is variable, depending on the dose, possibly beginning after only 10–14 days), the number of hematopoietic cells in the marrow is reduced after successful radiotherapy and fat degeneration occurs ( Figs 5.27 and W5.11) The latter is irreversible at over 40 Gy Typically the radiation margins are clearly demarcated within the marrow Caution The probability of an insufficiency fracture occurring as a complication of radiotherapy is increased ( Fig W5.12); this should not be mistaken for tumor recurrence Avascular necrosis may also result from radiation Bone marrow transplantation Focal lesions may persist after preparatory high-dose induction chemotherapy; it is still not certain whether this has any effect on survival An edematous pattern appears within the first week of bone marrow transplantation (autologous or allogenic stem-cell transplantation) Regeneration of blood-forming marrow takes place over the next months, especially in the periphery of the vertebrae, resulting in a typical bandlike (“picture-frame”) pattern The central vertebral marrow is not recruited until later In the long term, conversion back to fatty marrow takes place See Chapter 8.5 for possible toxic complications from various substances during therapy Fig 5.25 Non-Hodgkin's lymphoma (a) Extensive, ill-defined permeative bone destruction The cortex is also infiltrated (b) Bone marrow infiltration is evident on the T1W image (c) On the T2W sequence, tumor has infiltrated into the subperiosteal region and adjacent soft tissues The extent of cortical destruction is not fully recognizable on MRI (wrap around sign) Fig 5.26 Chloroma in chronic lymphocytic leukemia (a) Sclerosis of the proximal tibia (b) Focal infiltration of the bone marrow (c) Nonspecific contrast enhancement Fig 5.27 Non-Hodgkin's lymphoma with manifestation in the lumbar spine (a) MRI prior to radiotherapy (b) Follow-up after radiotherapy The bone marrow within the radiation field has undergone fatty degeneration ... Interventions Involving the Bone, Soft Tissues, and Joints 12 .1 Arthrography (N Jorden) 12 .1. 1 Indications 12 .1. 2 Contraindications 12 .1. 3 Technique 12 .1. 4 Complications 12 .2 Biopsy (K Bohndorf, A Seifarth) 12 .2 .1 Indications... Bohndorf, T Grieser) 11 .5 .1 Soft Tissue Calcifications 11 .5.2 Soft Tissue Ossifications 11 .6 Compartment Syndrome (T Grieser) 11 .7 Rhabdomyolysis (T Grieser) 11 .8 Peripheral Nerve Entrapment and Nerve Compression Syndromes (T... Tendons of the Wrist 2 .10 Metacarpals and Fingers (J Zentner) 2 .10 .1 Anatomy, Technique, and Indications 2 .10 .2 Fractures 2 .10 .3 Tendon and Ligament Lesions 2 .11 Hip Joint 2 .11 .1 Anatomy, Variants, and Techniques (C