DOI: 10.1148/rg.244035151
RadioGraphics 2004;24:1029-1049
© RSNA, 2004
Imaging Findings in Musculoskeletal Complications of AIDS1
C. Santiago Restrepo, MD,
Diego F. Lemos, MD,
Hernan Gordillo, MD,
Richard Odero, MD,
Thomas Varghese, MD,
William Tiemann, MD,
Francisco F. Rivas, MD,
Rogelio Moncada, MD and
Carlos R. Gimenez, MD
1 From the Department of Radiology, Louisiana State University Health Sciences Center, 1542 Tulane Ave, Rm 212, New Orleans, LA 70112. Presented as an education exhibit at the 2002 RSNA scientific assembly. Received June 17, 2003; revision requested July 17 and final revision received January 16, 2004; accepted January 16. All authors have no financial relationships to disclose. Address correspondence to C.S.R. (e-mail: crestr@lsuhsc.edu).
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Abstract
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Patients with human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS) are susceptible to a variety of complications that can affect the musculoskeletal system. These complications can be infectious, inflammatory, or neoplastic or can take some other form. Infection (cellulitis, necrotizing fasciitis, soft-tissue abscess, pyomyositis, osteomyelitis, septic arthritis) is the most common complication. Inflammatory processes include various arthritides as well as polymyositis. Non-Hodgkin lymphoma and Kaposi sarcoma are the two most common neoplasms in this patient population. Miscellaneous disorders include osteonecrosis, osteoporosis, rhabdomyolysis, anemia-related abnormal bone marrow, and hypertrophic osteoarthropathy. The underlying mechanisms leading to these diseases are complex and not fully understood but are thought to be multifactorial. Radiology may play an important role in early diagnosis and treatment planning in this population, in whom clinical and laboratory findings are commonly equivocal and nonspecific. Although biopsy is often necessary for the final diagnosis, it is important for the radiologist to be familiar with the different types of musculoskeletal disease in HIV-positive and AIDS patients so that an appropriate differential diagnosis can be established.
© RSNA, 2004
Index Terms: Acquired immunodeficiency syndrome (AIDS), **.20,2 **.241, **.298, **.329 • Bones, diseases, 40.241, 40.298, 40.56, 40.70, 40.832, 40.861 • Bone neoplasms, 40.329 • Muscles, diseases, 40.20, 40.614
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LEARNING OBJECTIVES FOR TEST 3
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After reading this article and taking the test, the reader will be able to:
- List the musculoskeletal complications of HIV infection and AIDS.
- Describe the imaging appearances of these complications.
- Discuss the roles of different imaging modalities in the diagnosis and treatment of these disease entities.
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Introduction
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The acquired immunodeficiency syndrome (AIDS) epidemic claimed more than 3 million lives worldwide in 2002, and an estimated 5 million people became infected with human immunodeficiency virus (HIV) that year, bringing to 42 million the total number of people living with the virus, 980,000 of whom live in North America. The best current projections suggest that an additional 45 million people will become infected between 2002 and 2010 (1). Imaging plays an essential role in the evaluation of these patients. Central nervous system (CNS), pulmonary, and abdominal complications affecting patients with HIV infection and AIDS have been extensively documented and discussed in the literature. However, musculoskeletal complications in this population are less well described. The underlying mechanisms leading to these complications are complex and not completely understood but are thought to be multifactorial, involving not only the immunosuppressed status of the patients, but also the virus itself, as well as complex immunologic, environmental, and genetic interactions. HIV infection diminishes the body’s defense mechanisms by impairing T lymphocyte response, which predisposes the patient to a wide variety of opportunistic infections, immune-related neoplasms, and inflammatory disorders. Although musculoskeletal abnormalities in patients with HIV infection and AIDS are not as common as pulmonary and CNS disorders, a wide variety of osseous, articular, and soft-tissue diseases may be encountered (2).
In this article, we review a wide spectrum of musculoskeletal disorders and their imaging appearances in patients with AIDS. These disorders may be infectious (cellulitis, necrotizing fasciitis, soft-tissue abscesses, pyomyositis, osteomyelitis, septic arthritis), inflammatory (arthritis, polymyositis), or neoplastic (lymphoma, Kaposi sarcoma) or may take a different form (osteonecrosis, osteoporosis, rhabdomyolysis, anemia, hypertrophic osteoarthropathy). Many of these conditions are not specific for HIV infection and AIDS and can be seen in other forms of immunosuppression, but others have been more specifically associated with this particular immunodeficiency.
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Infectious Processes
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Infection is the most common musculoskeletal complication in patients with AIDS. The immunocompromised patient is susceptible to opportunistic and nonopportunistic infections affecting the skin, underlying soft tissues, bones, and joints. Soft-tissue infections include superficial and deep cellulitis, necrotizing and nonnecrotizing fasciitis, soft-tissue abscesses, and pyomyositis. Osteomyelitis and septic arthritis are typical examples of infectious involvement of the bones and joints, respectively. The most frequently cultured bacterial agent is Streptococcus aureus, but multiple other organisms have also been reported.
Making a clinicoradiologic distinction between superficial and deep cellulitis, necrotizing fasciitis, and myositis or pyomyositis is often difficult but is necessary because their treatments differ. The key elements that allow differentiation are (a) the depth of soft-tissue involvement and (b) the presence of necrosis. Cross-sectional imaging techniques make such differentiation possible through analysis of compartmental anatomy and evaluation of radiologic findings in the subcutaneous fat, superficial and deep fascia, and muscles (2–8).
Cellulitis
Cellulitis is an acute inflammatory condition of the skin that is characterized by swelling, erythema, calor, and localized pain in the affected area (2,5–7). Cellulitis is frequently due to bacterial infection or local trauma that compromises the dermis and subcutaneous tissue (2). It may be caused by indigenous flora such as S aureus or S pyogenes colonizing the skin or by exogenous bacteria. Cellulitis caused by S aureus spreads from a central localized infection such as an abscess, an infected foreign body, or folliculitis, whereas cellulitis due to S pyogenes is a more rapidly spreading process associated with lymphangitis and fever.
Although the diagnosis of cellulitis is clinical, accurate differentiation between superficial cellulitis and cellulitis associated with a deep-seated infection is better achieved with computed tomography (CT) or magnetic resonance (MR) imaging (2). In superficial cellulitis, CT and MR imaging demonstrate inflammatory changes that involve the subcutaneous fat but do not extend beyond the superficial fascia (Fig 1). Abnormal imaging findings include thickening of the skin, septation of the subcutaneous fat, and thickening of the underlying superficial fascia, with scattered ill-defined hypointense areas on T1-weighted MR images, a striated pattern of hyperintensity on T2-weighted images, and moderate diffuse enhancement on contrast material–enhanced images (8,9). When such signal intensity abnormalities are found in the deep soft tissues (eg, deep fascia or muscles), a diagnosis of deep cellulitis, fasciitis, or myositis with or without necrosis should be proposed (6). The MR imaging findings in cellulitis and fasciitis are different from those in primary bacterial myositis: Disproportionate involvement of the muscles compared with subcutaneous tissue or muscle compromise without associated subcutaneous tissue involvement suggests the diagnosis of bacterial myositis (10,11).
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Figure 1. Superficial and deep cellulitis and myositis in a 42-year-old man. Axial CT scan obtained at the level of the middle third of the leg shows inflammatory changes in the subcutaneous soft tissues, with fluid collections surrounding the intramuscular compartments in the lateral aspect of the leg adjacent to the tibialis anterior muscle and in the medial compartment adjacent to the soleus muscle (solid arrows). Inflammatory changes consistent with myositis are also seen within the soleus muscle (open arrow).
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Patients with cellulitis do not need surgical intervention; a conservative approach with antibiotics and local supportive measures is sufficient. When necrosis is demonstrated, surgery is the mainstay of treatment (5).
Necrotizing Fasciitis
Both necrotizing and nonnecrotizing fasciitis are commonly preceded by trauma in patients with some degree of immunosuppression but can also be primary findings. Necrotizing fasciitis is a relatively rare but rapidly progressing infection that represents a life-threatening surgical emergency. It is characterized by extensive necrosis of the superficial and deep anatomic planes, usually accompanied by severe systemic toxicity (4,5,12). One of the most important predictors of mortality is delay in the diagnosis of necrosis (4). At clinical examination, necrotizing fasciitis may manifest as unexplained fever and pain in the early stages, with progression to brawny edema and tenderness. In the late stages, there is local coagulopathy and thrombosis of the blood vessels with necrosis of the deep soft tissues.
MR imaging is useful in differentiating necrotizing fasciitis from severe cellulitis with or without secondary abscess formation and pyomyositis (4). Some authors suggest that even though MR imaging findings tend to lead to overestimation of the extent of deep soft-tissue compromise, the presence of deep fascial involvement at MR imaging favors a diagnosis of necrotizing fasciitis (5). Caution should be exercised because a finding of deep fascial edema is not specific for necrotizing fasciitis and nonnecrotizing inflammatory conditions can have a similar imaging appearance (12). The imaging findings in necrotizing fasciitis are similar to those in cellulitis but are more severe with deeper involvement, including thickening of the affected fascia, fluid collections along the deep fascial sheaths, and extension into the intermuscular septa and the muscles (5,8). Muscle necrosis occurs when the fascial envelope is affected (9). Necrotizing fasciitis typically does not enhance after administration of gadolinium-based contrast material (4). MR imaging and, to a lesser extent, CT are useful in assessing the extent and depth of the inflammatory process and the involvement of adjacent osseous structures (Fig 2).
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Figure 2a. Necrotizing fasciitis in a 45-year-old male intravenous drug abuser. Coronal (a) and axial (b) fat-suppressed T2-weighted MR images show high-signal-intensity inflammatory changes involving both the subcutaneous fat in the medial surface (arrow in a) and the gastrocnemius and soleus muscles (arrows in b) of the left leg. This hyperintensity is consistent with deep-seated infection or necrotizing fasciitis.
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Figure 2b. Necrotizing fasciitis in a 45-year-old male intravenous drug abuser. Coronal (a) and axial (b) fat-suppressed T2-weighted MR images show high-signal-intensity inflammatory changes involving both the subcutaneous fat in the medial surface (arrow in a) and the gastrocnemius and soleus muscles (arrows in b) of the left leg. This hyperintensity is consistent with deep-seated infection or necrotizing fasciitis.
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Patients with nonnecrotizing fasciitis must also be followed up clinically and with MR imaging to assess for late development of necrosis. Surgical debridement, early fasciotomy, and aggressive therapy with antibiotics are the recommended therapeutic strategies for these patients (4).
Soft-Tissue Abscesses
Most bacterial infections in the soft tissues remain localized. These infections can extend and develop into an abscess depending on the immunologic status of the patient. In such cases, MR imaging will show a well-demarcated fluid collection that is hypointense on T1-weighted images, is hyperintense on T2-weighted images, is surrounded by a low-signal-intensity pseudocapsule with all sequences, and demonstrates peripheral rim enhancement after intravenous administration of gadolinium-based contrast material (Fig 3). These features are useful in differentiating abscesses from cellulitis or fasciitis (2,8,9).
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Figure 3a. Soft-tissue abscess in a 21-year-old man with a history of intravenous drug abuse. Axial unenhanced (a) and contrast-enhanced (b) fat-suppressed T1-weighted MR images of the hand show extensive inflammatory changes and abscess formation within the muscles and soft tissues of the thenar and palmar region. An abscess is seen within the first dorsal interosseous and adductor pollicis muscles (arrow). This fluid collection has low signal intensity on the unenhanced image and peripheral ring enhancement with central low signal intensity on the contrast-enhanced image. The absence of tendon sheath and bursal involvement helped rule out the presence of horseshoe abscess formation.
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Figure 3b. Soft-tissue abscess in a 21-year-old man with a history of intravenous drug abuse. Axial unenhanced (a) and contrast-enhanced (b) fat-suppressed T1-weighted MR images of the hand show extensive inflammatory changes and abscess formation within the muscles and soft tissues of the thenar and palmar region. An abscess is seen within the first dorsal interosseous and adductor pollicis muscles (arrow). This fluid collection has low signal intensity on the unenhanced image and peripheral ring enhancement with central low signal intensity on the contrast-enhanced image. The absence of tendon sheath and bursal involvement helped rule out the presence of horseshoe abscess formation.
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When an abscess is suspected, needle aspiration is mandatory. Treatment includes antibiotics and percutaneous drainage (8).
Pyomyositis
Pyomyositis, or bacterial myositis, is characterized by pyogenic inflammation of the muscle and, in our experience, is one of the most common musculoskeletal complications of AIDS. S aureus is the most frequently cultured organism, although other pathogens such as S pyogenes, Mycobacterium tuberculosis, M avium-intracellulare, Nocardia asteroides, Cryptococcus neoformans, and Toxoplasma, Salmonella, and Microsporidia species have also been reported (2,7). Pyomyositis is also referred to as tropical pyomyositis because it is endemic to warm, humid environments and has been seen only infrequently in industrialized nations. Although bacterial myositis is rare outside the tropics, the number of cases has been rising in the United States, and this entity is currently not uncommon in the AIDS population (10,13). The increasing prevalence of pyomyositis in HIV-infected patients may be explained by the higher prevalence of intravenous drug abuse, rhabdomyolysis, and repetitive trauma in this population (7). Pyomyositis can be divided into three clinical stages. The first stage is characterized by localized pain in one muscle group with induration of the overlying skin and low-grade fever. Mild elevation of the white blood cell (WBC) count may also be present. The second stage is characterized by escalating pain, fever, and edema of the affected muscle. Aspiration of the muscle reveals pus. In the third stage, a fluctuant abscess may be noted with necrosis of the muscle, and the patient may become septic. Blood cultures are positive in only 5% of cases (7,14).
CT demonstrates areas of muscle enlargement with decreased attenuation of the muscle secondary to edema. Intramuscular fluid collections may also be observed. Intravenous administration of contrast material can help differentiate necrotic from viable musculature because the nonviable tissue will demonstrate lack of enhancement. CT can also demonstrate the presence of abscesses, which typically appear as well-defined fluid collections with enhancing walls (Fig 4). CT is also extremely useful in providing localization for therapeutic aspiration and surgical planning (7).
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Figure 4. Pyomyositis in a 25-year-old woman. Axial contrast-enhanced CT scan of the lower neck demonstrates multiple abscesses in the soft tissues and muscles of the supraclavicular space and neck (arrows). Results of aspiration confirmed M tuberculosis myositis and lymph node involvement.
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MR imaging is more sensitive than CT in the detection of inflammatory changes within the muscles. On T1-weighted images, pyomyositis may appear as a central area of low signal intensity within the muscle, in some cases surrounded by a peripheral rim of high signal intensity that probably represents blood products (13,14). Pus inside the abscess can be either isointense or hyperintense with T1-weighted sequences depending on the proteinaceous content of the fluid collection. On T2-weighted and short inversion time inversion-recovery (STIR) images, the abscessed collection is hyperintense. Areas of abnormal high signal intensity in adjacent muscles represent unorganized phlegmonous collections, edema, or hyperemia (Fig 5). After contrast material injection, necrotic tissue manifests as a low-signal-intensity area surrounded by a hyperintenseenhancing rim (Figs 3, 6) (13,14). Although gas-forming myonecrosis is typically associated with Clostridium infection, in the HIV-infected and AIDS population the most commonly observed myonecrosis is nonclostridial myonecrosis, especially in intravenous drug abusers. Abnormal gas in the necrotic tissue is easily identified at radiography, CT, and MR imaging (Figs 6, 7) (8,15).
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Figure 5a. Pyomyositis in a 35-year-old man. (a) Axial contrast-enhanced fat-suppressed T1-weighted MR image demonstrates extensive inflammatory changes involving the deep muscles of the right midthigh, with enhancement within the vastus intermedius muscle that extends into the adductor muscles (arrows). Note the increased diameter of the right thigh compared with the left thigh. (b) On an axial fat-suppressed T2-weighted MR image, there is extensive cellulitis of the superficial and deep compartments with diffuse myositis of almost all the right-sided muscles, with less diffuse involvement of the left thigh. Note also the bilateral fluid collections superficial to the vastus lateralis muscles (arrows).
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Figure 5b. Pyomyositis in a 35-year-old man. (a) Axial contrast-enhanced fat-suppressed T1-weighted MR image demonstrates extensive inflammatory changes involving the deep muscles of the right midthigh, with enhancement within the vastus intermedius muscle that extends into the adductor muscles (arrows). Note the increased diameter of the right thigh compared with the left thigh. (b) On an axial fat-suppressed T2-weighted MR image, there is extensive cellulitis of the superficial and deep compartments with diffuse myositis of almost all the right-sided muscles, with less diffuse involvement of the left thigh. Note also the bilateral fluid collections superficial to the vastus lateralis muscles (arrows).
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Figure 6a. Pyomyositis with myonecrosis in a 38-year-old man. (a) Coronal T1-weighted MR image shows extensive myonecrosis affecting the medial compartments of the lower extremities, with bilateral hypointense fluid collections (arrows). (b) On a coronal fat-suppressed T2-weighted MR image, the bilateral fluid collections demonstrate high signal intensity. The multiple round, ill-defined low-signal-intensity areas within the necrotic collection on the left side (arrows) represent abnormal gas bubbles. (c) Axial contrast-enhanced fat-suppressed T1-weighted MR image shows intense peripheral rim enhancement surrounding the bilateral fluid collections (arrows) and the gas bubbles within the necrotic tissue on the left side.
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Figure 6b. Pyomyositis with myonecrosis in a 38-year-old man. (a) Coronal T1-weighted MR image shows extensive myonecrosis affecting the medial compartments of the lower extremities, with bilateral hypointense fluid collections (arrows). (b) On a coronal fat-suppressed T2-weighted MR image, the bilateral fluid collections demonstrate high signal intensity. The multiple round, ill-defined low-signal-intensity areas within the necrotic collection on the left side (arrows) represent abnormal gas bubbles. (c) Axial contrast-enhanced fat-suppressed T1-weighted MR image shows intense peripheral rim enhancement surrounding the bilateral fluid collections (arrows) and the gas bubbles within the necrotic tissue on the left side.
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Figure 6c. Pyomyositis with myonecrosis in a 38-year-old man. (a) Coronal T1-weighted MR image shows extensive myonecrosis affecting the medial compartments of the lower extremities, with bilateral hypointense fluid collections (arrows). (b) On a coronal fat-suppressed T2-weighted MR image, the bilateral fluid collections demonstrate high signal intensity. The multiple round, ill-defined low-signal-intensity areas within the necrotic collection on the left side (arrows) represent abnormal gas bubbles. (c) Axial contrast-enhanced fat-suppressed T1-weighted MR image shows intense peripheral rim enhancement surrounding the bilateral fluid collections (arrows) and the gas bubbles within the necrotic tissue on the left side.
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Figure 7. Pyomyositis in a 23-year-old man with AIDS and a history of intravenous drug abuse. Radiograph demonstrates multiple gas collections (arrows) within the soft tissues of the medial and posterior left thigh.
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If antibiotic therapy is initiated before substantial suppuration occurs, surgery can be avoided. Unfortunately, due to delay in the diagnosis, the majority of patients require abscess drainage and surgical debridement (13).
Osteomyelitis
Osteomyelitis is infection of the bone and a common infectious cause of musculoskeletal complications in AIDS patients (16). Bone infection in these patients can result from hematogenous spread, direct extension from a contiguous focus of infection, or direct inoculation. The organism most frequently identified is S aureus, but other common and opportunistic pathogens including Salmonella species, Neisseria gonorrhoeae, C neoformans, Escherichia coli, M tuberculosis, M avium-intracellulare, M hemophilum, M kansasii, and N asteroides have also been reported (2,17). At clinical examination, osteomyelitis can manifest as pain, erythema of the overlying soft tissues, and an elevated erythrocyte sedimentation rate. The most frequently involved bones are the tibia, wrist bones, femoral heads, ribs, and thoracolumbar spine (7). Radiography is not sensitive in the detection of early osteomyelitis because it does not demonstrate changes until 10–14 days after the onset of the infectious process, when lytic lesions or periosteal reaction is evident (Fig 8). Technetium-99m methylene diphosphonate (MDP) bone scintigraphy and gallium-67 and indium-111–labeled WBC scintigraphy are the most sensitive methods for the detection of early osteomyelitis (7). However, these examinations have a low specificity because of their inability to help distinguish between bone remodeling secondary to trauma, degenerative processes, and infection. Typical manifestations of osteomyelitis at bone scintigraphy include increased radiotracer uptake on blood flow, blood pool, and delayed static images of the affected bone obtained approximately 24–48 hours after the onset of infection. The reported sensitivity of bone scintigraphy ranges from 69% to 100% (17,18). Ga-67 and In-111–labeled WBC scintigraphy serve as complements to bone scintigraphy and increase the specificity in establishing the diagnosis of osteomyelitis. Ga-67 scintigraphy is considered positive for osteomyelitis if the uptake in the affected area is greater than the uptake at Tc-99m MDP bone scintigraphy. The reported sensitivity and specificity for Ga-67 scintigraphy combined with bone scintigraphy are 70% and 83%–93%, respectively (17,18). WBC scintigraphy is positive at an earlier stage than is bone scintigraphy and is more useful than MR imaging in postoperative patients. WBC scintigraphic findings can be made more specific for osteomyelitis if compared with findings at Tc-99m sulfur colloid bone marrow scintigraphy. Bone remodeling with aberrant bone marrow uptake can be differentiated from infection by comparing findings obtained with the two imaging methods: Aberrant bone marrow uptake after trauma or surgery is similar at WBC and bone marrow scintigraphy, whereas uptake in infection is different.
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Figure 8a. Chronic osteomyelitis in a 41-year-old man. Anteroposterior (a) and lateral (b) radiographs show extensive soft-tissue ulceration of the distal forearm associated with periosteal reaction of the distal ulna and, to a lesser extent, of the distal radius projecting into the interosseous space. Results of pathologic analysis proved extensive necrotic changes, but no definitive bacteria or infectious agent could be identified.
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Figure 8b. Chronic osteomyelitis in a 41-year-old man. Anteroposterior (a) and lateral (b) radiographs show extensive soft-tissue ulceration of the distal forearm associated with periosteal reaction of the distal ulna and, to a lesser extent, of the distal radius projecting into the interosseous space. Results of pathologic analysis proved extensive necrotic changes, but no definitive bacteria or infectious agent could be identified.
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CT of the affected region may demonstrate soft-tissue swelling and periosteal reaction, medullary changes, and focal cortical erosions or trabecular coarsening. MR imaging is more sensitive than CT in detecting bone marrow edema secondary to osteomyelitis and the associated soft-tissue inflammatory changes. The reported sensitivity and specificity of MR imaging for detection of osteomyelitis are 82%–100% and 53%–94%, respectively (17,18). T1-weighted images demonstrate low signal intensity in the affected bone (Figs 9, 10), whereas on T2-weighted images the corresponding areas have high signal intensity. MR imaging with intravenously administered gadolinium-based contrast material offers comprehensive depiction of the extent of both bone and soft-tissue infection; it also helps identify areas of devitalized tissue (17–19). Imaging findings in osteomyelitis are nonspecific and may also be observed in fractures, neoplasms, and metabolic processes. Correlation with the patient’s history is essential in formulating a differential diagnosis. Definitive diagnosis is best established with bone needle biopsy.
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Figure 9. Osteomyelitis in a 41-year-old woman. Coronal contrast-enhanced fat-suppressed T1-weighted MR image demonstrates osteomyelitis of the right wing of the sacrum and septic arthritis of the right sacroiliac joint. Abscesses with peripheral rim enhancement are seen within the right iliac and gluteal muscles and the sacrum. Aspiration and culture demonstrated M tuberculosis infection.
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Figure 10. Osteomyelitis and septic sacroiliitis in a 46-year-old female intravenous drug abuser with septic endocarditis. Axial T1-weighted MR image demonstrates a hypointense lesion in the right sacroiliac joint (arrow) with extension into the right iliac bone and sacrum. Pathologic analysis demonstrated S pyogenes.
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Early treatment interventions including surgical curettage and intravenous administration of sensitive antibiotics may reduce the risk of severe sequelae.
Tuberculosis infection and bacillary angiomatosis are two specific forms of osteomyelitis that have been observed with increasing frequency in HIV-infected and AIDS patients.
There has been a reappearance of tuberculosis infections in the general population that has been linked to the expanding AIDS epidemic. Up to 3% of tuberculosis infections in HIV-infected patients involve the musculoskeletal system. The thoracolumbar spine is the most frequent site of osseous involvement in tuberculosis. The knee and hip are other common sites (20,21). Clinical symptoms are extremely variable and nonspecific. Pain is the most common complaint. Skeletal involvement is often secondary to hematogenous spread. The infection typically begins in the anterior aspect of the vertebral body and extends into the disk space, subligamentous area, and adjacent soft tissues. In the advanced stages, epidural extension can occur.
Radiography demonstrates erosion of the anterior vertebral bodies with deformity. An adjacent soft-tissue mass may be seen. CT is useful for detecting destructive changes involving the cortical bone of the vertebral bodies. Calcifications in the paravertebral soft tissues with fluid collections are frequently seen, findings that are consistent with abscess formation. MR imaging is the preferred modality for imaging the spine. T1-weighted images demonstrate decreased signal intensity within the vertebral marrow secondary to edema, with corresponding high signal intensity on T2-weighted images. Soft-tissue and epidural extension of the infectious process can easily be identified. Epidural extension manifests as posterior displacement of the thecal sac and deformity of the spinal cord (Fig 11). Arachnoiditis manifests as thickened nerve roots that enhance with contrast material administration (20).
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Figure 11a. Acute spondylodiskitis and vertebral osteomyelitis in a 46-year-old woman. (a) Sagittal T1-weighted MR image shows acute spondylodiskitis and vertebral osteomyelitis with epidural collections (open arrow) and dural enhancement (solid arrows) at the C5-C6 level. These inflammatory findings are nonspecific and can be observed in a variety of granulomatous, fungal, and bacterial infections. One week later, the patient developed extensive wedge deformity and collapse of C5 and C6. (b) Axial contrast-enhanced T1-weighted MR image demonstrates abnormal dural enhancement and cord compression secondary to the epidural fluid collections (arrows).
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Figure 11b. Acute spondylodiskitis and vertebral osteomyelitis in a 46-year-old woman. (a) Sagittal T1-weighted MR image shows acute spondylodiskitis and vertebral osteomyelitis with epidural collections (open arrow) and dural enhancement (solid arrows) at the C5-C6 level. These inflammatory findings are nonspecific and can be observed in a variety of granulomatous, fungal, and bacterial infections. One week later, the patient developed extensive wedge deformity and collapse of C5 and C6. (b) Axial contrast-enhanced T1-weighted MR image demonstrates abnormal dural enhancement and cord compression secondary to the epidural fluid collections (arrows).
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Bacillary angiomatosis is an unusual form of osteomyelitis that specifically affects the HIV-infected population. The causative pathogens implicated in this disease are Bartonella quintana and B henselae (formerly classified as Rochalimaea quintana and R henselae) (7,22–27). In our experience, bacillary angiomatosis is uncommon compared with staphylococcal osteomyelitis. Clinical features of bacillary angiomatosis include hemangioendothelial proliferation in the skin, lymph nodes, bones, and visceral organs. Patients may present with fever, abdominal symptoms, anemia, hepatomegaly, or splenomegaly. Cutaneous and subcutaneous lesions are the most commonly recognized manifestations of bacillary angiomatosis at physical examination (23,25). Osteolytic bone lesions are common and are helpful in distinguishing bacillary angiomatosis from Kaposi sarcoma (22–24). Osteomyelitis due to M hemophilum infection should also be considered as a possible cause of lytic bone lesions in AIDS patients who present with ulcerating skin lesions (28).
Imaging work-up includes radiography, which usually demonstrates osteolytic foci that may range from well-circumscribed lytic lesions involving the cortex to ill-defined lesions with extensive cortical destruction, medullary permeation, and periosteal reaction. Bone scintigraphy reveals increased radiotracer uptake in the affected areas (22,23). CT demonstrates well-defined nonsclerotic lytic lesions. MR imaging shows well-defined lytic lesions with low and high signal intensity on T1- and T2-weighted images, respectively (23–26). Pathologic analysis with Warthin-Starry stain of a biopsy sample of the lesion will demonstrate characteristic pleomorphic bacillary organisms (22). In a recent case report, pyomyositis was shown to be the sole manifestation without osseous or cutaneous findings (27).
Septic Arthritis
Infection of joints can arise from hematogenous spread or contiguous extension from neighboring soft-tissue infection or osteomyelitis. Joint infection is most frequently seen in intravenous drug abusers. At clinical examination, these patients present with fever, pain, erythema, soft-tissue swelling, and decreased range of motion of the affected joint. Radiography may reveal joint effusion, bone erosion, osteoporosis, and indistinct margins of the joint with joint space narrowing. MR imaging is more sensitive in the detection of early changes in septic arthritis, revealing signal intensity abnormalities in the bone marrow and soft tissues, both of which have edema-like signal intensity (ie, are hypointense on T1-weighted images and hyperintense on fat suppressed T2-weighted images or STIR images). Septic bursitis of the olecranon, prepatellar, and subdeltoid bursae has also been described in immunocompromised patients (Fig 12) (14). Extension of infection from the joint space into surrounding bursae is also easily recognized at MR imaging. S aureus, N gonorrhoeae, Candida albicans, and M tuberculosis are some of the most frequently cultured pathogens, but other fungal pathogens and unusual organisms should also be considered in immunocompromised patients (21).
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Figure 12a. Septic arthritis and bursitis in a 42-year-old woman. (a) Coronal fat-suppressed T2-weighted MR image shows extensive fluid collections within the bursae around the shoulder, especially the subacromial (subdeltoid) bursa (arrows). (b) On a sagittal contrast-enhanced fat-suppressed T1-weighted MR image, the fluid collections (arrows) exhibit low signal intensity with no enhancement.
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Figure 12b. Septic arthritis and bursitis in a 42-year-old woman. (a) Coronal fat-suppressed T2-weighted MR image shows extensive fluid collections within the bursae around the shoulder, especially the subacromial (subdeltoid) bursa (arrows). (b) On a sagittal contrast-enhanced fat-suppressed T1-weighted MR image, the fluid collections (arrows) exhibit low signal intensity with no enhancement.
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Management includes aspiration and culture of joint fluid, which is critical in determining the causative organism and its sensitivity to drug therapy with antibiotics.
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Inflammatory Processes
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Musculoskeletal inflammatory processes in HIV-infected and AIDS patients include various arthritides as well as polymyositis. The most common rheumatic manifestation associated with HIV infection is arthralgia (29,30). The clinical course of arthritis in patients with HIV infection and AIDS ranges from short-lived treatable disease to severe, poorly responding arthritis (14). The arthritides most commonly associated with HIV infection are articular pain syndrome, Reiter syndrome, psoriatic arthritis, and the syndromes of oligoarthritis and polyarthritis (2,14,31,32). Classification of arthritis in HIV-infected and AIDS patients can be difficult because these patients often present with incomplete or unusual manifestations of rheumatologic disease (30). Polymyositis is the most common muscular manifestation in HIV-infected patients and must be distinguished from pyomyositis, which is its most important differential diagnosis, because their treatments differ (22).
Arthritis
The mechanisms proposed for the commonly observed arthritides in the HIV-infected and AIDS population are complex and multifactorial and include HIV-related P-24 antigen that has been localized in synovial tissue of HIV-infected patients with arthritis, activation of the immune system, genetic factors, human leukocyte antigen–B27 and environmental factors, infection with arthritogenic micro-organisms, and molecular mimicry (33–39). Some researchers believe that decreased helper T cell depletion allows immune-regulated arthritides to occur (14).
Human leukocyte antigen–B27 appears to play a role in the pathogenesis of Reiter syndrome and is present in 70%–80% of affected patients, whether HIV-positive or HIV-negative. Reiter syndrome has been described in HIV-infected patients following infection with Yersinia, Salmonella, and Shigella species (38,39). Some patients with HIV infection and Reiter syndrome can present with the incomplete form of this disease (urethritis, arthritis, conjunctivitis) (40,41). Classic radiographic features of Reiter syndrome include asymmetric alterations of synovial joints, symphyses, and entheses; bone erosion with adjacent bone proliferation; and paravertebral ossification. Reiter syndrome has a predilection for the lower extremity, particularly the small articulations of the foot. The calcaneus, ankle, knee, and sacroiliac joints are usually involved (42). These features do not appear to be different from those seen in non–HIV-infected individuals.
Psoriatic arthritis has a higher prevalence among HIV-infected and AIDS patients than in the general population. Exacerbation of underlying psoriasis or development of the disease in high-risk individuals requires assessment for HIV infection. Psoriatic rash is characterized dermatologically by the eruption of circumscribed, discrete and confluent reddish silver–scaled maculopapules that occur predominantly on the elbows, knees, scalp, and trunk (2). The rheumatologic characteristics of psoriatic arthritis are similar to those of Reiter syndrome, except there is a greater predilection for the small articulations of the wrist and hand. Psoriatic arthritis tends to be polyarticular and asymmetric, in which case it rapidly progresses to a deforming and incapacitating form of the disease (43). Involvement of the sacroiliac joint and spine is rare.
Patients with symmetric polyarthritis involving the small joints of the hands have been designated as having acute symmetric polyarthritis. This entity behaves clinically like rheumatoid arthritis, but patients are negative for the rheumatoid factor (30). Radiographic findings include osteopenia, soft-tissue swelling, joint effusions, joint space narrowing, marginal erosions, periosteal reaction, and joint deformities such as flexion contractures, ulnar deviations, and swan neck deformities (2). Features that help differentiate symmetric polyarthritis from classic rheumatoid arthritis are proliferative bone formation and periostitis (42). Occasionally, an erosive variety with little or no proliferative features occurs and may be confused with rheumatoid arthritis.
HIV-associated arthritis can also occur. This arthritis is oligoarticular, asymmetric, and peripheral. It primarily affects the knees and ankles (44). Proposed explanations include direct viral infection of the joint. This arthritis has a short duration of 1–6 weeks. Radiography may reveal a joint effusion in some cases.
Arthralgia and painful articular syndrome are the most common rheumatic manifestations of HIV infection (37). Painful articular syndrome is an uncommon arthropathy characterized by acute onset of severe, sharp, self-limited joint or bone pain lasting for up to 48 hours (45). The knee is most commonly affected, but the elbow and shoulder can also be involved. Radiographic features are nonspecific and range from no abnormality to joint effusions with or without periarticular osteopenia (14).
The diagnosis of undifferentiated spondyloarthropathy is made in patients with seronegative arthritis who do not meet the criteria for the diagnosis of Reiter syndrome or psoriatic arthritis (32,43). Radiographic findings include osteoporosis, soft-tissue swelling, bone erosion, and periosteal reaction (2). Arthritis in HIV-infected and AIDS patients tends to be severe and unresponsive to conventional medications. In addition, immunosuppressive agents are usually contraindicated in HIV-positive patients (2,32). Inflammatory musculoskeletal complaints tend to be more frequent during the late stages of HIV infection; however, arthritis may precede the diagnosis of HIV infection (46,47). In addition, there are reports of systemic lupus erythematosus, rheumatoid arthritis, and psoriasis going into remission with HIV infection. The prevailing theory is that this remission is secondary to profound immunosuppression (14).
Polymyositis
Bilateral symmetric proximal muscle weakness and elevated serum creatine kinase levels help distinguish polymyositis from pyomyositis at clinical examination (48). Myositis in patients with HIV infection and AIDS can be a result of host response to the virus, secondary to zidovudine (formerly called azidothymidine [AZT]) therapy, or caused by opportunistic infections such as toxoplasmosis (46,48). HIV-related polymyositis can be difficult to distinguish from AZT myopathy (30,46,48). Some investigators postulate that HIV infection causes an immunologic response that leads to muscle invasion by inflammatory elements (10). In HIV-associated polymyositis, HIV antigens are occasionally observed in endomysial macrophages (49). The mechanism proposed for AZT myopathy involves the interaction between AZT and mitochondrial DNA polymerase (30). Drug-related myositis improves with cessation of therapy and is a dose-related phenomenon (37,38,50,51).
Patients with polymyositis are not routinely evaluated radiologically. However, when an imaging examination is requested, MR imaging is the preferred modality. Polymyositis can be isointense relative to muscle on T1-weighted images; thus, T2-weighted or STIR images are necessary to establish the diagnosis (16). Unlike with pyomyositis, rim enhancement is not present in polymyositis (50). AIDS-related peripheral neuropathy can have MR imaging features similar to those of polymyositis (52). Imaging findings alone will not allow differentiation in some cases, and biopsy of the abnormal tissue may be necessary because biopsy can help differentiate HIV-related polymyositis from AZT myopathy (30,50).
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Other Myopathies
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Besides myopathies with infectious causes (eg, pyomyositis and infectious myositis with opportunistic infections) and those with inflammatory causes (eg, polymyositis, AZT myopathy), there are other myopathies that are observed in the HIV-infected and AIDS population, including necrotizing noninflammatory myopathy, nemaline (rod) myopathy, and myositis ossificans. In addition, subclinical myopathy can also occur in these patients (31).
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Neoplasms
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Non-Hodgkin lymphoma (NHL) and Kaposi sarcoma are the two most common neoplasms observed in HIV-infected and AIDS patients and account for the majority of neoplastic musculoskeletal involvement in this population (7).
Lymphoma
NHL is the second most common type of tumor in patients with HIV infection and AIDS after Kaposi sarcoma (50). NHL is seen 60 times more frequently in AIDS patients than in the general population and is one of the criteria for the diagnosis of AIDS in an HIV-infected person (53). Since the introduction of highly active antiretroviral therapy, there seems to have been an increase in the prevalence of NHL in the AIDS population (54). Hodgkin lymphoma has been described in HIV-infected and AIDS patients in scattered reports and is not considered diagnostic for AIDS. Most NHL occurs in the late stages of HIV infection, with CD4 counts below 200 cells per microliter (55). NHL in HIV-infected and AIDS patients tends to be advanced at presentation and highly aggressive, with a poor prognosis and poor response to treatment. Extranodal and widely disseminated disease, including muscle and bone involvement, is also more frequently found in this population, particularly in children. Extranodal sites of disease at the time of diagnosis have been reported in 60%–95% of patients with AIDS-associated NHL and as the only sites of disease in as many as one-third of cases (56). About 20% of AIDS patients with multisystemic NHL have disease extension to bone and muscle (55,57). The presence of primary bone NHL in the absence of extraskeletal disease has also been reported in AIDS patients, affecting the lower extremities, spine, pelvis, and skull (7). Only 8% of all patients with extranodal NHL have bone marrow involvement, whereas bone marrow lesions are seen in almost one-third of affected AIDS patients (58). Patients with AIDS and NHL osseous extension present with fever, painful unilateral limb swelling, weight loss, and pathologic fracture (7).
According to the literature, lymphomas affecting bone can produce lytic lesions, sclerotic lesions, or "mixed" lesions with an indistinct zone of transition. In our experience and that of others, HIV-associated NHL bone lesions are usually lytic (Figs 13, 14a, 14b, 15a, 15b) (59). Among the lytic changes, the most frequently seen is a permeative pattern with cortical destruction, often associated with a soft-tissue mass (Fig 15a) (57,60). Muscle lesions, some of which are associated with an adjacent bone lesion, are commonly described in the psoas muscle and the lower extremities (52). Periosteal reaction is not commonly associated with NHL (14). The imaging features of musculoskeletal involvement by NHL are similar to those of many bone tumors (2); however, bone lesions in AIDS-related lymphoma tend to be more sharply marginated and to grow more rapidly than those associated with Kaposi sarcoma (58). CT is the primary staging modality for lymphomas because of its generally superior spatial resolution. CT shows the bone changes with better conspicuity and can also suggest the presence of an associated soft-tissue mass (Fig 15a). High-speed CT is particularly beneficial in the chest, where respiratory and cardiac motion tend to degrade MR images. MR imaging has superior contrast resolution in soft tissue, often allowing distinction between a small focus of tumor and surrounding normal soft tissue far better than is possible with CT (Figs 14c, 15c, 15d) (55). MR imaging is the method of choice for evaluating bone marrow changes and characterizing adjacent soft-tissue involvement. Bone marrow changes are seen as areas of hypointensity on T1-weighted images (Fig 14f) and as areas of hyperintensity on STIR images or fat-saturated fast spin-echo T2-weighted images. The associated soft-tissue mass appears hyperintense on T2-weighted images. CT, MR imaging, and scintigraphy (Fig 14g) have a complementary role in evaluating affected patients. Imaging findings are similar to those in osteomyelitis, and clinical correlation is often needed. In general, individual imaging features of Burkitt lymphoma and other NHLs do not differ significantly, so that biopsy is required for differentiation (55). In one small series, noncleaved cell (Burkitt and non-Burkitt) lymphoma was the most common histologic subtype (40% of cases), followed by large cell lymphoma (30%) and large cell immunoblastic lymphoma (30%) (61).
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Figure 13a. NHL in a 40-year-old man. (a) Radiograph of the pelvis shows an ill-defined lytic lesion in the right iliac bone (arrows). (b) Axial contrast-enhanced CT scan helps confirm the lytic lesion, demonstrating cortical disruption of the iliac bone (solid arrows) with an associated enhancing soft-tissue mass involving the right iliacus muscle (open arrow).
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Figure 13b. NHL in a 40-year-old man. (a) Radiograph of the pelvis shows an ill-defined lytic lesion in the right iliac bone (arrows). (b) Axial contrast-enhanced CT scan helps confirm the lytic lesion, demonstrating cortical disruption of the iliac bone (solid arrows) with an associated enhancing soft-tissue mass involving the right iliacus muscle (open arrow).
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Figure 14a. Multicentric B-cell NHL in a 44-year-old man. (a) Anteroposterior chest radiograph shows multiple osteolytic lesions (arrows) involving the right humerus, the right and left scapulae, the medial third of the right clavicle, and multiple left ribs. (b) Follow-up chest radiograph obtained 3 months later demonstrates progression of the disease, with diffuse lymphomatous involvement of both lungs and more prominent multiple osteolytic lesions (arrows). (c) Sagittal T1-weighted brain MR image shows a soft-tissue tumor with both extradural involvement (solid arrow) and subgaleal extension (open arrow) within the medullary cavity of the parietal bone. (d) On an axial T2-weighted MR image, the soft-tissue mass has intermediate signal intensity due to bone involvement and extends to the subgaleal space (solid arrow). Abnormal signal intensity owing to tumor involvement is also seen within the left parietal bone (open arrow). (e) Anteroposterior radiograph of the right knee shows a destructive osteolytic lesion of the proximal lateral tibial metaphysis (arrow). (f) Sagittal T1-weighted MR image shows the infiltrative tumor that is isointense relative to muscle and replaces the bone marrow of the proximal tibia (arrow). Flexion deformity of the knee secondary to pain is also appreciated. (g) Tc-99m bone scintigram (left) with magnified view (right) show extensive abnormal radiotracer uptake at the level of the distal femur and proximal tibia (solid arrows) and in the skull (open arrow). There is also abnormal uptake in the proximal femoral shaft (arrowheads).
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Figure 14b. Multicentric B-cell NHL in a 44-year-old man. (a) Anteroposterior chest radiograph shows multiple osteolytic lesions (arrows) involving the right humerus, the right and left scapulae, the medial third of the right clavicle, and multiple left ribs. (b) Follow-up chest radiograph obtained 3 months later demonstrates progression of the disease, with diffuse lymphomatous involvement of both lungs and more prominent multiple osteolytic lesions (arrows). (c) Sagittal T1-weighted brain MR image shows a soft-tissue tumor with both extradural involvement (solid arrow) and subgaleal extension (open arrow) within the medullary cavity of the parietal bone. (d) On an axial T2-weighted MR image, the soft-tissue mass has intermediate signal intensity due to bone involvement and extends to the subgaleal space (solid arrow). Abnormal signal intensity owing to tumor involvement is also seen within the left parietal bone (open arrow). (e) Anteroposterior radiograph of the right knee shows a destructive osteolytic lesion of the proximal lateral tibial metaphysis (arrow). (f) Sagittal T1-weighted MR image shows the infiltrative tumor that is isointense relative to muscle and replaces the bone marrow of the proximal tibia (arrow). Flexion deformity of the knee secondary to pain is also appreciated. (g) Tc-99m bone scintigram (left) with magnified view (right) show extensive abnormal radiotracer uptake at the level of the distal femur and proximal tibia (solid arrows) and in the skull (open arrow). There is also abnormal uptake in the proximal femoral shaft (arrowheads).
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Figure 14c. Multicentric B-cell NHL in a 44-year-old man. (a) Anteroposterior chest radiograph shows multiple osteolytic lesions (arrows) involving the right humerus, the right and left scapulae, the medial third of the right clavicle, and multiple left ribs. (b) Follow-up chest radiograph obtained 3 months later demonstrates progression of the disease, with diffuse lymphomatous involvement of both lungs and more prominent multiple osteolytic lesions (arrows). (c) Sagittal T1-weighted brain MR image shows a soft-tissue tumor with both extradural involvement (solid arrow) and subgaleal extension (open arrow) within the medullary cavity of the parietal bone. (d) On an axial T2-weighted MR image, the soft-tissue mass has intermediate signal intensity due to bone involvement and extends to the subgaleal space (solid arrow). Abnormal signal intensity owing to tumor involvement is also seen within the left parietal bone (open arrow). (e) Anteroposterior radiograph of the right knee shows a destructive osteolytic lesion of the proximal lateral tibial metaphysis (arrow). (f) Sagittal T1-weighted MR image shows the infiltrative tumor that is isointense relative to muscle and replaces the bone marrow of the proximal tibia (arrow). Flexion deformity of the knee secondary to pain is also appreciated. (g) Tc-99m bone scintigram (left) with magnified view (right) show extensive abnormal radiotracer uptake at the level of the distal femur and proximal tibia (solid arrows) and in the skull (open arrow). There is also abnormal uptake in the proximal femoral shaft (arrowheads).
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Figure 14d. Multicentric B-cell NHL in a 44-year-old man. (a) Anteroposterior chest radiograph shows multiple osteolytic lesions (arrows) involving the right humerus, the right and left scapulae, the medial third of the right clavicle, and multiple left ribs. (b) Follow-up chest radiograph obtained 3 months later demonstrates progression of the disease, with diffuse lymphomatous involvement of both lungs and more prominent multiple osteolytic lesions (arrows). (c) Sagittal T1-weighted brain MR image shows a soft-tissue tumor with both extradural involvement (solid arrow) and subgaleal extension (open arrow) within the medullary cavity of the parietal bone. (d) On an axial T2-weighted MR image, the soft-tissue mass has intermediate signal intensity due to bone involvement and extends to the subgaleal space (solid arrow). Abnormal signal intensity owing to tumor involvement is also seen within the left parietal bone (open arrow). (e) Anteroposterior radiograph of the right knee shows a destructive osteolytic lesion of the proximal lateral tibial metaphysis (arrow). (f) Sagittal T1-weighted MR image shows the infiltrative tumor that is isointense relative to muscle and replaces the bone marrow of the proximal tibia (arrow). Flexion deformity of the knee secondary to pain is also appreciated. (g) Tc-99m bone scintigram (left) with magnified view (right) show extensive abnormal radiotracer uptake at the level of the distal femur and proximal tibia (solid arrows) and in the skull (open arrow). There is also abnormal uptake in the proximal femoral shaft (arrowheads).
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Figure 14e. Multicentric B-cell NHL in a 44-year-old man. (a) Anteroposterior chest radiograph shows multiple osteolytic lesions (arrows) involving the right humerus, the right and left scapulae, the medial third of the right clavicle, and multiple left ribs. (b) Follow-up chest radiograph obtained 3 months later demonstrates progression of the disease, with diffuse lymphomatous involvement of both lungs and more prominent multiple osteolytic lesions (arrows). (c) Sagittal T1-weighted brain MR image shows a soft-tissue tumor with both extradural involvement (solid arrow) and subgaleal extension (open arrow) within the medullary cavity of the parietal bone. (d) On an axial T2-weighted MR image, the soft-tissue mass has i | |
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Abstract
LEARNING OBJECTIVES FOR TEST...
