You are in: eMedicine Specialties > Radiology > MUSCULOSKELETAL Bone InfarctArticle Last Updated: May 7, 2008AUTHOR AND EDITOR INFORMATIONSection 1 of 12
  Author: Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP, Chairman of Medical Imaging, Professor of Radiology, NGHA, King Fahad National Guard Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia Ali Nawaz Khan is a member of the following medical societies: American Institute of Ultrasound in Medicine, Radiological Society of North America, Royal College of Physicians, Royal College of Physicians and Surgeons of the United States, Royal College of Radiologists, and Royal College of Surgeons of England Coauthor(s): Muthusamy Chandramohan, MBBS, DMRD, FRCR, Consultant Radiologist, Bradford Teaching Hospitals, UK; Ian Turnbull, MD, Lecturer, Department of Radiology, University of Manchester; Consulting Neuroradiologist, Hope Hospital, Salford, Manchester and North Manchester Hospital; Sumaira MacDonald, MBChB, PhD, MRCP, FRCR, Lecturer, Sheffield University Medical School; Endovascular Fellow, Sheffield Vascular Institute; Charles Edward Hutchinson, MD, FRCR, Senior Lecturer, Department of Diagnostic Radiology, University of Manchester Editors: Michael A Bruno, MD, Associate Professor, Departments of Radiology and Medicine, Pennsylvania State University College of Medicine; Director, Radiology Quality Management Services, Milton S Hershey Medical Center, Pennsylvania State University College of Medicine; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; Javier Beltran, MD, Chair, Department of Radiology, Maimonides Medical Center; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; Felix S Chew, MD, MBA, EdM, Professor, Department of Radiology, Vice Chairman for Radiology Informatics, Section Head of Musculoskeletal Radiology, University of Washington Author and Editor Disclosure Synonyms and related keywords: osteonecrosis, aseptic necrosis, avascular necrosis, ischemic necrosis, metaphyseal lesion, diaphyseal lesions, bone blood supply, ischemic bone death, bone necrosis, bone death, bone infarction, idiopathic osteonecrosis, secondary osteonecrosis, Legg-Calvé-Perthes disease, slipped femoral capital epiphysis, bone infarction, spontaneous bone infarct, AVN, traumatic osteonecrosis, Gaucher disease, hemophilia, Caisson disease, dysbaric osteonecrosis, pancreatitis, systemic lupus erythematosus, radiation-induced osteonecrosis INTRODUCTIONSection 2 of 12
  BackgroundBone infarct refers to ischemic death of the cellular elements of the bone and marrow. A considerable lack of uniformity exists in the use of terminology for bone infarct. At present, the term osteonecrosis is accepted and used widely. In general, bone infarct refers to lesions occurring in the metaphysis and diaphysis of bone. Lesions in the epiphysis are called avascular necrosis (AVN). Osteonecrosis can be idiopathic or secondary to a number of conditions that reduce blood supply to the bone; such conditions include an intraluminal abnormality, an extrinsic compression, or a combination of both. CT scans, MRIs, and bone scans play a significant role in diagnosing the disease at an early stage and thereby reducing the number and/or severity of complications and morbidity associated with the disease. PathophysiologyIschemic cell death Ischemic cell death and necrosis are the result of a reduced blood supply to the bone, which in turn can result from either an intrinsic abnormality in the blood vessel supplying part of the bone, an extrinsic abnormality, or a combination of both. The rapidity with which cell death occurs depends on the cell type and the degree and duration of the anoxia. Hematopoietic cells are sensitive to anoxia and are the first to die after reduction or removal of the blood supply; they usually die within 12 hours. Experimental evidence suggests that bone cells composed of osteocytes, osteoclasts, and osteoblasts die within 12-48 hours and that marrow fat cells die within 5 days. The death of bone does not alter its radiographic opacity. Living bone becomes osteoporotic as a result of osteoclastic bone resorption secondary to reactive hyperemia. Dead bone cannot undergo resorption; therefore, it appears relatively more opaque. Repair of ischemic bone occurs in 2 phases. First, when dead bone abuts live marrow, capillaries and undifferentiated mesenchymal cells grow into the dead marrow spaces, while macrophages degrade dead cellular and fat debris. Second, mesenchymal cells differentiate into osteoblasts or fibroblasts. Under favorable conditions, layers of new bone form on the surface of dead spongy trabeculae. If sufficiently thickened, these layers may increase the radiopacity of the bone; therefore, the first radiographic evidence of previous necrosis may be patchy sclerosis resulting from repair. Histologic features At histologic examination, medullary necrosis appears yellow with occasional flecks of calcium. A serpiginous capsule of grayish glistening collagen may surround the area of necrosis. Minor differences appear in the patterns of response for juxta-articular bone necrosis, but the pattern and sequence of events are similar to those of medullary necrosis. Beneath the articular cartilage in juxta-articular necrosis, the depth of the yellow necrotic marrow varies, and bone trabeculae are devoid of osteocytes. Vascular granulation tissue or grayish glistening collagen separates this dead tissue from underlying living bone. Within this border zone and some distance deep within it, dead bone trabeculae may be broadened by formation of new living bone on their surfaces. This process corresponds to the radiographic sclerotic line or mottled areas of increased opacity. Trabecular fractures occur in the dead bone immediately beneath the subchondral plate, resulting in a radiographic crescent of subchondral lucency. Later, a wrinkle appears in the articular cartilage at the margin of the dead zone, followed by cracks and fissures leading to structural collapse. Causes of osteonecrosis Causes of osteonecrosis and associated conditions include the following:
Related eMedicine topics: FrequencyUnited StatesThe overall incidence in the United States appears to be the same as that found internationally (see below). InternationalEstimates of the rate of steroid-induced osteonecrosis range from 2-4% to more than 25%. AVN of the femoral head occurs in 60-75% of patients with femoral neck fractures, 25% of patients with hip dislocations, and 15-40% of patients with a slipped capital femoral epiphysis. Osteonecrosis is a complicating factor in 10-15% of patients with a scaphoid fracture. Osteonecrosis associated with SLE occurs in 5-6% of patients; some estimates are as high as 40%. Changes within the shoulder girdle are reported in 1-3% of patients undergoing radiation therapy for breast carcinoma. Hyperlipidemia is demonstrated in 80% of patients with idiopathic osteonecrosis; approximately 60% and 40% of the cases of idiopathic osteonecrosis are associated with alcohol ingestion and hyperuricemia, respectively. The incidence of osteonecrosis after renal transplantation varies from 3-41%; usually, it is less than 20%. In deep-sea divers, the incidence is 5-10%. About 40-50% of patients with AVN of the talus have an associated talar fracture with a subtalar dislocation. Mortality/MorbidityMorbidity and mortality related to a bone infarct depend on the site of involvement, stage of disease, and possible complications.
RaceBone infarct associated with sickle cell disease is common in black people of African origin. Bone infarcts associated with Gaucher disease are predominant in the Jewish population. Sex
Age
AnatomyThe blood supplies to the humeral and femoral heads, talus, and scaphoid bone are critical to the development of AVN at these sites (see Images 1-6). Clinical DetailsClinical features of bone infarct depend on the stage of the disease and the site of involvement. Patients with medullary infarcts are usually asymptomatic.1 If present, symptoms are nonspecific in the early stages of the disease. Patients with juxta-articular lesions may have disability. Before the onset of structural failure and collapse, patients with juxta-articular bone infarcts are usually asymptomatic. Localized pain is the most common presentation for both medullary and juxta-articular infarcts. Patients with juxta-articular infarcts can present with joint pain and limitation of movement. If unrecognized and untreated, the affected bone is liable to disintegrate further, with a consequent increase in pain and disability. In sickle cell disease, the patient may present with severe bone and abdominal pain associated with sickle cell crisis.2 In Legg-Calvé-Perthes syndrome and slipped femoral capital epiphysis, the presenting feature can be groin pain and limping, and the pain may be referred to the thigh and knee.3 In spontaneous osteonecrosis of the tibia, pain may be localized to the knee joint level, particularly over the medial condyle. Spontaneous osteonecrosis is often associated with pain, tenderness, swelling, and restriction of movement. In osteochondritis dissecans, symptoms may vary or be absent; it usually affects the non–weight-bearing surface of the medial femoral condyle. Preferred ExaminationPlain radiography is not sensitive in the detection of bone infarction. However, plain radiography has a role in the differential diagnosis. Radionuclide imaging and MRI are much more sensitive than plain radiography and may show changes caused by altered hemodynamics early in the course of disease. CT scanning is complementary to the other techniques, but it is not as sensitive as radionuclide imaging or MRI. CT scans may demonstrate subtle trabecular irregularity with bone necrosis when plain radiographic findings are normal. Ultrasonography may be useful in differentiating bone infarction from osteomyelitis in patients with sickle cell disease.4, 5, 6, 7, 8, 9, 10 Limitations of TechniquesNo radiologic findings are specific for bone infarction. A variety of pathologies may mimic bone infarction, including stress fractures, infections, inflammations, and metabolic and neoplastic processes. A bone infarct may mimic a bone tumor on imaging. The limitations apply to all imaging modalities, including plain radiography, radionuclide studies, CT, and MRI. However, when the global picture is considered, including the history, clinical findings, and course of events, the diagnosis can be achieved with the help of imaging in most patients.11 DIFFERENTIALSSection 3 of 12
Calcium Pyrophosphate Deposition Disease Legg-Calve-Perthes Disease Neuropathic Arthropathy (Charcot Joint) Osteochondritis Dissecans Stress Fracture Other Problems to Be ConsideredInflammations
RADIOGRAPHSection 4 of 12
FindingsPlain radiographic findings in established osteonecrosis may be characteristic of the disease. In the epiphyseal region, an arclike, subchondral, lucent lesion may be associated with areas of patchy loss of bone opacity intermingled with sclerotic areas and bone collapse. In the diametaphyseal region, a sheetlike lucency of varying size is usually surrounded by shell-like sclerosis and/or calcification and periostitis. In flat or complex bones, patchy lucencies and sclerosis are often associated with bone collapse or fractures (see Images 10-12, 16-24, 26-28). Posttraumatic osteonecrosis Posttraumatic osteonecrosis usually follows a fracture; most cases occur in areas with vulnerable blood supply, such as the femoral head, humeral head, talus, or scaphoid bone. Infarcted bone appears opaque as a result of compression. The femoral head is the most common site of osteonecrosis, which is a well-known complication of femoral head fractures and dislocations. Additionally, subchondral fracture of the femoral head has been associated with osteonecrosis, transient osteoporosis of the hip, and Pastel disease (ie, rapidly progressing osteoarthritis of the hip). Radiographs obtained several months after the onset of symptoms may show a radiolucent crescent parallel to the articular surface secondary to subchondral collapse of the necrotic bone. Often, flattening of the articular surface is demonstrated, but the joint space tends to be preserved. The opacity of the infarcted femoral head is increased. Steinberg has classified the radiologic appearance into 6 stages, as follows12:
Radiographic changes in traumatic osteonecrosis of the talus are delayed (by 1-3 mo) and become apparent with osteoporosis of the surrounding bones, which creates relatively increased opacity in the body of the talus. The increase in radiopacity may be associated with a collapse of the articular surface. Occasionally, a subchondral radiolucent band is demonstrated in the proximal talus; this finding is related to bone resorption. This Hawkins impingement sign usually indicates the presence of viable bone with an intact blood supply. Osteonecrosis of the humeral head is usually a complication of a fracture of the anatomic neck or severe fracture dislocation. Radiographic findings are delayed; they include flattening, sclerosis, and irregularity of part of the articular surface of the humeral head. In the scaphoid bone, 10-15% of the fractures are complicated by osteonecrosis in the proximal pole of the scaphoid bone. Plain radiographic findings include relatively increased opacity in the infarcted pole of the scaphoid bone. This appearance may be delayed for 4-8 weeks, a period possibly associated with delayed union or nonunion of the fracture; collapse of the infarcted part of the bone; and, eventually, changes related to secondary osteoarthrosis. Osteonecrosis of the capitate may occur after accidental or occupational trauma. The proximal part of the capitate is the site of AVN. After trauma or prolonged stress, AVN also may affect the lunate; the other carpal bones; the tarsal navicular bone; the mandibular condyle; the patella; the glenoid region of the scapula; and, occasionally, the metatarsal bones. Osteonecrosis of the vertebral body (ie, Kümmell disease) usually occurs weeks to years after acute trauma. It usually causes vertebral collapse in middle-aged or elderly men or women. Generally, the lower dorsal or upper lumbar vertebrae are involved. Gas may be apparent in the vertebral body and may extend into the psoas muscles. These changes are depicted more elegantly on CT scans than on other images. Spontaneous infarction of the femoral head is uncommon and affects men more often than women, in the group aged 40-70 years. Infarction may be unilateral or bilateral. The radiographic appearance depends on the severity of the disease. A minor form of femoral head infarction is recognized; this form affects a superficial area of the femoral head in a segmental distribution. The disease is nonprogressive. Radiographs may show a lobulated or segmental subcortical lucency, which may be surrounded by a sclerotic margin. The latter is better demonstrated on CT scans. Spontaneous osteonecrosis Spontaneous osteonecrosis around the adult knee (ie, Ahlbäck disease) is a distinct clinical entity that affects women more often than men. It commonly affects the medial femoral condyle and less commonly affects the medial or lateral tibial condyle. Initial radiographic findings are usually normal. Weeks or months later, subtle flattening and sclerosis of the weight-bearing femoral or tibial condyle may be seen. If untreated, further depression, sclerosis, and joint space narrowing occur. If the affected area is small, spontaneous recovery may ensue if weight-bearing is avoided. Conventional tomography may show angular or wedge-shaped areas of patchy sclerotic bones and subtle collapse of the bone surface that is undetected on plain radiographs. The diagnosis of spontaneous osteonecrosis of the knee is being questioned. Current theories suggest that this entity is actually a subchondral stress fracture that most often occurs in the medial femoral condyle. Spontaneous osteonecrosis of the tarsal navicular in adults (ie, Mueller-Weiss syndrome) may occur, especially in women. Plain radiographic features include medial or dorsal protrusion of a portion of the bone or the entire navicular bone. These findings are often associated with a comma-shaped deformity caused by collapse of the lateral part of the bone. The disease may be bilateral or asymmetric and may be associated with pathologic fractures. The disease can be progressive at times, and it is associated with severe pain and disability. This syndrome is distinct from the osteochondrosis of the tarsal navicular bone that occurs in children (ie, Köhler disease). Osteonecrosis secondary to Cushing disease Osteonecrosis secondary to Cushing disease occurs as a result of excess levels of endogenous steroids. Most of the steroids are present in the vertebral bodies. Characteristic features are osteoporosis, osteosclerosis, subchondral radiolucent shadows, wedging and/or collapse, and bone fragmentation associated with a relatively normal articular space. Gaucher disease Osteonecrosis that affects the epiphysis and diaphysis is a known complication of Gaucher disease and is commonly associated with bone pain. In the long bones, bands of sclerosis and radiolucency alternate. These findings are associated with periostitis and a bone-within-bone appearance identical to that seen in sickle cell disease.13 Hemophilia Osteonecrosis may complicate hemophilia and is usually found in the femoral head and talus. Bone infarction results from intraosseous hemorrhage with the subsequent collapse of bone or intracapsular hemorrhage and an elevation in intra-articular pressure that causes vascular compromise and eventual osteonecrosis. Radiographic features are similar to those of traumatic osteonecrosis. Ossification related to bleeding in the periarticular region may be apparent. Caisson disease or dysbaric osteonecrosis Two types of bone lesions that occur in patients with dysbaric osteonecrosis can be identified on plain radiographs: juxta-articular lesions, which are more common and mostly affect the head of the humerus and femur, and diaphyseal and metaphyseal lesions that occur at a distance from the joint. Juxta-articular alterations are frequently encountered in the region of the head of the femur and humerus. They are depicted as radiopaque areas, spherical segmental radiopaque areas that may eventually produce a snow-capped appearance, radiolucent subcortical bands termed the crescent sign, and osseous collapse and fragmentation. Diaphyseal and metaphyseal lesions are demonstrated as ill-defined radiopaque foci; irregular intraosseous areas of shell-like calcification; and, rarely, radiolucent defects. These changes may be unilateral or bilateral. Pancreatitis Osteonecrosis is a known complication of pancreatitis; it is usually associated with chronic or inactive forms of pancreatitis.14 Epiphyseal involvement is characterized by lucencies of mottled appearance or lucencies interspersed with sclerosis, subchondral radiolucent areas, and partial or complete collapse of the involved bone. Diaphyseal and metaphyseal involvement is associated with radiolucency, calcification, and periosteal new bone formation. The distal femur and the proximal tibia are the sites most commonly involved. Pregnancy Osteonecrosis in pregnancy appears to be closely associated with childbirth. The femoral and humeral heads are the sites most commonly involved. Systemic lupus erythematosus The pathogenesis of osteonecrosis in patients with SLE is not clear, and the role of steroids is speculative. The overall radiographic appearances of bone infarcts are similar to those of infarcts in patients without SLE. The most commonly affected sites are the humeral head, femoral condyles, tibial plateaus, and talus. An unusual feature is the involvement of small bones of the wrist, hands, and feet; examples include the carpus, tarsus, and metatarsal and metacarpal heads. Radiation-induced osteonecrosis Exposure to internal or external, accidental, or diagnostic and/or therapeutic radiation may produce diverse osseous changes, including disruption of growth, bone infarction, scoliosis, and benign and malignant neoplasms. Osseous changes are usually related to dose and age. Various parts of the skeleton respond differently upon exposure to radiation. Most osseous changes result from secondary radiation exposure during radiation therapy for soft tissue cancers. Common sites of involvement include the mandible, skull, shoulder, sternum, and shoulder. The threshold for osseous radiation injury is believed to be 3000 cGy, with cell death occurring at 5000 cGy. Radiation osteitis is manifested by a mottled appearance with a mixture of osteoporosis, increased opacity, and coarse trabecular pattern demonstrated on plain radiographs. Different bones develop radiation-induced changes at varying times after the initial insult. Mandibular osteonecrosis commonly appears 1 year after radiation exposure; at other sites, the latent period is longer. Osteonecrosis is considerably more common in the mandible than in other bones owing to its compact bone structure and poor blood supply. In addition, the mandible is exposed to a higher radiation dose because of its superficial location. Bone necrosis is usually mild and may be aseptic or associated with infection. Osteonecrosis appears as an ill-defined area of bone destruction without a sequestrum. An associated soft tissue mass is unusual with osteonecrosis; the presence of a soft tissue component suggests tumor recurrence. Radiation necrosis of the skull usually occurs after a minimum radiation dose of 3500 cGy. The radiographic appearance is that of a mixed lytic and sclerotic area within the calvarium. If the osteonecrosis is associated with soft tissue necrosis, infection and/or osteomyelitis may ensue. Osteonecrosis of the shoulder girdle may follow radiation therapy for breast carcinoma. Osteopenia is common after radiation therapy and is often associated with disorganized bone trabeculae that resemble findings in Paget disease. Pathologic rib fractures are common and often multiple. The edges of rib fractures show resorption, and the tips are often pointed or sclerotic. Clavicular and scapular fractures are often associated with these rib fractures. Radiation necrosis of the humerus may develop as long as 7-10 years after radiation therapy. Changes include patchy bone resorption, fractures, and necrosis of the humeral head with a slipped proximal humeral head epiphysis. Radiation necrosis of the sternum may follow treatment of breast cancer. Osseous changes may be mild and may be demonstrated as osteoporosis, abnormal trabecular patterns, localized lucencies, and sclerosis. More severe changes include abnormalities in alignment with localized pectus excavatum or complete necrosis of one or more segments of the sternum. Unilateral or bilateral femoral neck fractures are reported in 2% of patients who are exposed to pelvic irradiation. These fractures are commonly subcapital. Often, sclerotic changes occur, and trabecular opacity increases in the femoral neck, preceding a fracture. Fractures usually heal normally with abundant callous formation. Protrusio acetabuli is also reported to occur after radiation therapy of the pelvis; this condition may be associated with peritoneal calcification. Changes indistinguishable from osteitis pubis may occur in the symphysis pubis. Radionecrosis of the sacroiliac joints may cause widening and irregularity of the joint space. This condition is often associated with sclerosis, which is commonly symmetric and bilateral. Pathologic fractures of pelvic bones may occur after radiation therapy; these can involve the sacrum and may extend into one or both innominate bones. Complications resulting from osteonecrosis Complications from osteonecrosis usually are well depicted on plain radiographs. Cartilaginous abnormalities, such as fibrillation, erosions, and joint space narrowing, may affect joints. Changes of secondary osteoarthrosis may be apparent in cases involving significant collapse of an articular surface that occurs after an infarction. Loose bodies, either chondral or osteochondral, may be seen in a joint embedded within the depressed part of the bone or within the synovium. Cystic degeneration in areas of bone infarction may occur, particularly in the diaphysis of tubular bones. Appearances are those of a well-marginated expanding osteolytic area eroding the cortex. The well-marginated cyst and the lack of cortical disruption help in differentiating the cyst from a malignant degeneration. Malignant degeneration (eg, sarcoma) is a known complication of bone infarction irrespective of etiology.15 Men are affected more often than women; patients are usually aged 40-70 years. Typically, the distal part of the femur or proximal tibia is involved, although other sites may be affected as well. The radiographic appearance is that of a soft tissue mass associated with bone destruction at a site of previous bone infarction. Degree of ConfidenceRadiographic features of bone infarction do not occur until several months after the onset of symptoms; therefore, plain radiography is not a sensitive technique in the detection of bone infarction. However, plain radiography has a role in the differential diagnosis. False Positives/NegativesEarly radiographic features of a bone infarct, particularly in the metaphyseal region of long bones, lack specificity. Vague areas of radiolucencies may mimic infections and neoplastic processes. Osteochondritis dissecans may mimic spontaneous osteonecrosis around the knee. Radiographic findings in dysbaric osteonecrosis are indistinguishable from those of osteonecrosis resulting from other causes. Virtually identical features may be seen with bone islands. Osteonecrosis of the vertebral body may be difficult to differentiate from an osteoporotic fracture and vertebral collapse secondary to malignancy. Cyst formation that occurs after bone infarction is occasionally difficult to differentiate from a malignant degeneration, particularly in early stages when the cysts are poorly marginated. Mimics of malignant degeneration of bone infarcts include fibrosarcoma, malignant fibrous histiocytoma, chondrosarcoma, and, rarely, osteosarcoma. Radiation-induced mandibular osteonecrosis may be difficult to differentiate from tumor recurrence. Other regions of radiation osteonecrosis may mimic osteomyelitis. Radionecrosis of the shoulder girdle may mimic Paget disease. Changes indistinguishable from osteitis pubis may occur in the symphysis pubis, with radionecrosis. Radionecrosis of the sacroiliac joints may mimic osteitis condensans ilii. CT SCANSection 5 of 12
FindingsCT scans demonstrate central or peripheral areas of reduced attenuation. Reformatted sagittal and coronal images show subchondral fractures and collapse of the articular surface. CT findings may show subtle trabecular irregularity associated with bone necrosis when plain radiographic findings are normal. Collapse or buckling of articular surfaces indicates more advanced disease and influences the choice of treatment. Degree of ConfidenceAs with conventional radiography, CT is not sensitive in the detection of bone infarcts. However, CT scans can help in diagnosing bone infarction earlier than would be the case with plain radiographs. The sensitivity of CT in the diagnosis of bone infarction is lower than that of MRI and bone scintigraphy. False Positives/NegativesAs with plain radiography, early CT features of a bone infarct lack specificity, particularly in the metaphyseal region of the long bones. Vague radiolucencies may mimic infections and neoplastic processes. MRISection 6 of 12
FindingsIschemic bone changes become apparent in hematopoietic tissues on MRIs within 6-12 hours. Ischemia is detectable in osteophytes, osteoblasts, and osteoclasts within approximately 2 days. An inflammatory response surrounding the devascularized bone, resulting from increased vascularity and granulation tissue, is demonstrated well as an interface on MRIs. A risk of subsequent AVN is associated with the early conversion of active marrow to fatty marrow in the proximal femur and with prominent physeal scars that close off the femoral head (see Images 7-9, 13-15, 29). MRI characteristics of bone infarction are variable focal abnormalities and are commonly demonstrated as patchy areas of low signal intensity on T1-weighted spin-echo images. Diffuse abnormal signal intensity may be present in osteonecrosis of the femoral head; these changes are reflected on both T1- and T2-weighted images. The most characteristic appearance is the double-line sign, which consists of a hyperintense inner ring and a hypointense outer ring, on T2-weighted MRIs. This finding reflects the reactive interface between ischemic and nonischemic bone. The absence of a double-line sign does not exclude osteonecrosis. On T1-weighted MRIs, the interface appears as a low-signal-intensity line, which reflects a combination of granulation tissue and, to a lesser extent, sclerotic bone. Gadolinium-enhanced short–inversion recovery images demonstrate diminished enhancement in early infarctions of the femoral head. In sickle cell disease, acute bone infarcts are caused by sequestration of red blood cells in the bone marrow. Thus, non-enhanced T1-weighted fat-saturated sequences appear to be diagnostic of acute bone infarcts.9 Contrast enhancement aids in the diagnosis of acute osteomyelitis.10 Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. No consensus has been reached regarding the best MRI sequences or imaging planes to use, although sagittal images, particularly when combined with the application of surface coils and small fields of view, appear to be more helpful than other images.16 Degree of ConfidenceMRI is considered more sensitive than standard scintigraphy. MRI is sensitive in the detection of spontaneous infarction around the knee. MRI is useful in assessing the response to therapy, particularly the response of the femoral head to core decompression in which ischemic areas may shrink and edema may resolve. However, more often, the MRI characteristics of the infarcted area change little over time. False Positives/NegativesDiffusely distributed abnormal MRI findings of osteonecrosis in the femoral head may mimic transient osteoporosis of the hip, infection, or neoplasia. For instance, diffuse abnormal signal intensity on both T1- and T2-weighted images may mimic findings in infective and neoplastic processes. ULTRASOUNDSection 7 of 12
FindingsA combination of scintigraphy and ultrasonography has been used in the differentiation of osteomyelitis from bone infarction in patients with sickle cell disease.4, 5 Scintigraphic studies are useful in locating all areas of suggested osteomyelitis. Ultrasonography has a role in confirming the presence of a subperiosteal fluid collection and in guiding aspiration, which can be performed to distinguish a hematoma from an abscess. In one series of 23 patients in whom osteomyelitis was associated with sickle disease, 21 patients had a subperiosteal fluid collection that was more than 10 mm at its thickest point. By contrast, patients with sickle cell crises had fluid collections less than 10 mm. Aspiration of fluid under ultrasonographic guidance is useful in differentiating osteomyelitis from infarction. In patients with osteomyelitis, the identification of the organism guides antibiotic administration. Needle decompression can help to relieve pain in patients with osteomyelitis and sickle cell crises. NUCLEAR MEDICINESection 8 of 12
FindingsAfter acute osteonecrosis occurs, technetium-99m diphosphonate uptake can be absent after 72 hours. Subsequently, with revascularization and associated osteoblastic repair, intense activity is seen. The clinical assessment of posttraumatic AVN of the femoral head is difficult, though the preoperative identification of AVN is important. The displacement at the fracture site and the degree of femoral head ischemia are significantly correlated, but plain-film radiology is not reliable in the prediction of ischemia. The appearances on isotopic scans depend on the time elapsed since injury. Initially, the area of infarction has a photon-deficient or doughnut-like appearance, with increased activity surrounding the photopenic area. Subsequently, the photopenic area shrinks; as healing progresses, activity becomes uniform and intense. These changes are reliable, with a predictive value of 92.5%. Further improvement may be achieved by using single-photon emission tomography (SPECT). The major role of SPECT is in demonstrating a persistent photopenic defect resulting from incomplete vascularization. Because myeloid tissue death precedes death of osteophytes, it has been proposed that radiocolloid imaging is superior to imaging with 99mTc diphosphonate in determining the viability of the femoral head, although some success has been achieved by using 99mTc sulfur colloid or 99mTc antimony colloid. However, false-positive scanning results have been reported in inactive marrow, particularly in elderly patients. The scaphoid bone is the most frequently fractured carpal bone. Approximately one quarter to one half of fractures are missed on radiographs. Isotopic bone scans are 100% sensitive in the diagnosis of scaphoid fractures. AVN of the proximal fragment of the scaphoid bone is often a concern. On scintigraphs, a photopenic area may be demonstrated in the proximal fragment. In patients with sickle cell disease, bone infarcts are typically multiple during the course of a sickle cell crisis. Areas of infarction are demonstrated as photopenic foci within 72 hours after the crisis. Splenic infarcts are also known to take up 99mTc diphosphonate and are a useful hint to the presence of sickling (see Image 25).17 Revascularization results from collateral vessels that are predominantly derived from the periosteal blood supply; revascularization can be observed on isotopic bone scans as peripheral stripes of enhanced activity that extend with the healing process. However, a true bone infarct seldom occurs in an epiphysis because the epiphysis usually has an adequate collateral blood supply. Ischemia may stimulate only osteoblastic activity, which results in increased isotope uptake without a photopenic stage. This feature poses problems in differentiating a bone infarct from osteomyelitis in the setting of sickle cell disease. Scanning with gallium-67 citrate may be required because its uptake is decreased or absent in acute infarction and is normal or increased in healing infarcts. 67Ga citrate is useful in differentiating septic infarction from fulminant photon-deficient osteomyelitis. Similar changes occur in patients with Gaucher disease. In these patients, vascular compromise is caused by the accumulation of lipid-filled enlarged histiocytes within the medulla. The radioactivity is reduced, with a subsequent increase in isotopic uptake in the healing phase. 67Ga citrate is invaluable in differentiating photo-deficient osteomyelitis from a bone infarction. Radiation necrosis is dose dependent and most probably is related to alteration in the microvasculature rather than direct bone damage. In most instances, affected bone is incidentally irradiated during the course of therapy in an adjacent organ. The isotopic uptake in radiation necrosis is variable. Changes indistinguishable from radiation necrosis may occur as a result of frostbite. Bone scintigraphy reveals a focal increase in activity in spontaneous osteonecrosis around the knee, which can be identified long before radiographic changes become apparent. Similar findings apply to AVN of the talus that occurs after trauma. Steroid-induced AVN causes a variety of changes, a fact that probably reflects its multifactorial etiology. A large photopenic area may be seen, similar to changes associated with major vascular compromise; however, more often, intense activity is noted at the site of infarction. These changes are less common than findings of patchy areas of increased accumulation of the radionuclide, sometimes with a streaky pattern of increase in the uptake. On occasion, multiple small areas of uptake are seen in the infarcted area. Caisson disease is characterized by large areas of increased activity, which mostly is juxta-articular. The role of radionuclide scans is proposed to lie in predicting the development of necrosis in the lesions and thereby predicting the risk of the later development of osteoarthrosis. Degree of ConfidenceRadionuclide uptake can be absent after 72 hours in viable osteocytes, whereas MRI findings are not altered for as long as 6 weeks. MRI findings in a series of 8 patients were negative, whereas radionuclide studies showed decreased isotope uptake in early osteonecrosis in patients at risk for AVN. This observation is not surprising because MRI depicts osteonecrosis by demonstrating bone marrow edema. However, studies have revealed that fat cells are resistant to ischemia, dying 5 days after the initial insult. Though MRI findings may be negative, findings from isotopic scans may become positive during this period. Many investigators have found that the series of changes in femoral neck fractures are reliable in ascertaining the viability of the femoral head. The accuracy in the prediction of such viability is 92.5%. Bone scanning appears to be more sensitive than MRI in the detection of AVN of the scaphoid bone, but it is less specific. In scaphoid fractures, demonstration of a focal area of hyperemia and increased uptake provide reassurance in indicating revascularization. Scintigraphic changes in steroid-induced osteonecrosis are detectable months before any abnormal findings are discernible on radiographs. Radionuclide scans have a sensitivity of 89% in detecting ischemic necrosis; by contrast, radiologic methods have a sensitivity of 41%. False Positives/NegativesImaging characteristics of a bone infarct per se are nonspecific, and increased activity can be caused by a variety of conditions such as fractures, infections, inflammations, and metabolic and neoplastic processes. Photon-deficient bone lesions may occur with early osteomyelitis, plasmacytoma, histiocytosis X, bone metastases, and sickle cell crises. ANGIOGRAPHYSection 9 of 12
FindingsIntramedullary phlebography has been used in the diagnosis of bone infarction in the femoral head. The technique involves traversing the trochanteric bone with a bone needle, such as the Jamshidi needle, and injecting radiographic iodinated contrast material through it. Normal venographic findings thus obtained are usually characterized by painlessness on injection and by the demonstration of draining veins without diaphyseal reflux or stasis. When necrosis of the femoral head is present, the injection is painful and is usually followed by reflux into the diaphysis and stasis of the contrast agent for as long as 15 minutes. Degree of ConfidenceThe exact sensitivity of intramedullary phlebography is not known. The technique is invasive, and because there are so many other techniques now available, phlebography is seldom indicated. The technique must be performed by a radiologist with expertise in this area. False Positives/NegativesPhlebography may fail to reveal useful findings, and both false-positive and false-negative results may occur. INTERVENTIONSection 10 of 12
Measurements of intramedullary pressure obtained by placing a cannula directly into the marrow space of the trochanteric region can reflect the viability of the bone. The procedure is performed with local anesthesia, and pressures greater than 30 mm Hg are regarded as abnormal. The oxygen saturation can also be studied; a saturation greater than 85% in a sample of blood removed through the cannula is indirect evidence of circulatory failure. In the diagnosis of bone infarct, the use of intramedullary pressure measurements has been eclipsed by MRI. Medical/Legal Pitfalls
Special Concerns
MULTIMEDIASection 11 of 12
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