Avascular Necrosis
- Fred F. Ferri, M.D.
Basic Information
Definition
Avascular necrosis (AVN) is ischemic death of bone due to insufficient blood supply. It is not a specific disease entity but a final common pathway to several disorders that impair blood supply to the femoral head and other locations.
Synonyms
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AVN
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Osteonecrosis
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Aseptic necrosis
ICD-10CM CODES | |
M87 | Idiopathic aseptic necrosis of bone |
M87.1 | Osteonecrosis due to drugs |
M87.2 | Osteonecrosis due to previous trauma |
M87.3 | Other secondary osteonecrosis |
M87.9 | Osteonecrosis, unspecified |
Epidemiology & Demographics
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15,000 new cases per year in the United States. It is most commonly associated with the hip and accounts for 10% of total hip replacements in the United States.
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Usually occurs in middle age and is more frequent in males than females
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Associated conditions:
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Corticosteroid treatment: 35%
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Alcohol abuse: 22%
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Idiopathic and other: 43%
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Hemoglobinopathies, pancreatitis, chronic renal failure, SLE, chemotherapy, decompression sickness
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Common sites involved
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Femoral head
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Femoral condyle
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Humeral head
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Navicular and lunate wrist bones
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Talus
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Physical Findings & Clinical Presentation
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May be asymptomatic in early stages
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Pain in the involved area exacerbated by movement or weight bearing in later stages
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Decreased range of motion as the disease progresses
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Functional limitation
Etiology
Final common pathway of conditions that lead to impairment of the blood supply to the involved bone. Trauma disrupting the blood supply is the most common cause of AVN. Arterial factors are considered the most common cause of AVN. Table 1 describes proposed mechanism of disease of common conditions associated with osteonecrosis.
Mechanism of Osteonecrosis | ||||||||
Associated Condition | Apoptosis | Osteoblast/Osteoclast Homeostasis | Lipid Abnormalities | Coagulation Abnormalities | Oxidative Stress | Parathyroid/Calcium Imbalance | Vascular Plugging | Vasoactive Substances |
Corticosteroids | X | X | X | X | X | X | ||
Bisphosphonates | X | X | X | |||||
Alcohol abuse | X | X | X | X | X | |||
Trauma | X | X | X | |||||
Renal transplantation | X | X | X | X | ||||
Dialysis | X | |||||||
Sickle cell disease | X |
Staging
Table 2 describes the Modified Steinberg Staging System for osteonecrosis.
Stage | Radiographic Appearance | Reversible |
I | Normal radiographs, but abnormal bone scan or magnetic resonance image | Yes |
II | Lucent and sclerotic changes | Yes |
III | Subchondral fracture without flattening | No |
IV | Subchondral fracture with flattening or segmental depression of femoral head | No |
V | Joint space narrowing or acetabular changes | No |
VI | Advanced degenerative changes | No |
Stages:
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Stage 0
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Asymptomatic
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Normal imaging
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Histologic findings only (i.e., silent osteonecrosis)
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Stage 1
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Asymptomatic or symptomatic
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Normal radiographs and CT scan
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Abnormal bone scan or MRI
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Stage 2
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Abnormal radiographs or CT scan, including linear sclerosis, focal bead mineralization, cysts; however, the overall architecture of the involved bone is normal
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Stage 3
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Early evidence of mechanical bone failure (subchondral fracture), but the overall shape of the bone is still intact
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Stage 4
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Flattening or collapse of the bone
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Stage 5
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Joint space narrowing
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Stage 6
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Extensive joint destruction
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Diagnosis
Differential Diagnosis
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None in late stages
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Early: any condition causing focal musculoskeletal pain, including arthritis, bursitis, tendinitis, myopathy, neoplastic bone and joint diseases, traumatic injuries, pathologic fractures
Workup
Fig. 1 describes a diagnostic algorithm for osteonecrosis.
Imaging Studies (Fig. 2)
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MRI: the most sensitive technology to diagnose early aseptic necrosis. The first sign is a margin of low signal. An inner border of high signal associated with a low-signal line is specific for aseptic necrosis (“double line sign”). Sensitivity is 75% to 100%.
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Radiography: insensitive early in the course. The earliest changes include diffuse osteopenia, areas of radiolucency with sclerotic border, and linear sclerosis. Later, a subchondral lucency (crescent sign) indicates subchondral fracture. More advanced cases reveal flattening, collapsed bone, and abnormal bone contour. In late disease, osteoarthritic changes are seen.
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Bone scan:
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Early: “cold” area.
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Later: increased radionuclide uptake as a result of remodeling.
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Sensitivity in early disease is only 70% and specificity is poor.
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CT scan: may reveal central necrosis and area of collapse before those are visible on radiographs.
Treatment
Prevention
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Manage etiologic conditions
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Minimize corticosteroid use
Nonpharmacologic Therapy
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Core decompression: effectiveness 35% to 95% in early phases
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Bone grafting
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Osteotomies
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Joint replacement
Acute General Rx
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Decrease weight bearing of affected area.
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Pulsing electromagnetic fields applied externally (still experimental).
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Peripheral vasodilators (e.g., dihydroergotamine) (unproven).
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Late-stage AVN is most often treated by total joint arthroplasty.
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A treatment algorithm for osteonecrosis is described in Fig. 3.
Prognosis
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When diagnosed at an early stage treatment is appropriate in all cases because 85% to 90% can be expected to progress to a more advanced stage.
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Contralateral joint involvement is common (30% to 70%).
Related Content
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Avascular Necrosis (Patient Information)