Ferri – Avascular Necrosis

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

  1. AVN

  2. Osteonecrosis

  3. 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

  1. 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.

  2. Usually occurs in middle age and is more frequent in males than females

  3. Associated conditions:

    1. Corticosteroid treatment: 35%

    2. Alcohol abuse: 22%

    3. Idiopathic and other: 43%

    4. Hemoglobinopathies, pancreatitis, chronic renal failure, SLE, chemotherapy, decompression sickness

  4. Common sites involved

    1. Femoral head

    2. Femoral condyle

    3. Humeral head

    4. Navicular and lunate wrist bones

    5. Talus

Physical Findings & Clinical Presentation

  1. May be asymptomatic in early stages

  2. Pain in the involved area exacerbated by movement or weight bearing in later stages

  3. Decreased range of motion as the disease progresses

  4. 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.

TABLE1 Proposed Mechanism of Disease of Common Conditions Associated with OsteonecrosisFrom Firestein GS, Budd RC, Gabriel SE, et al.: Kelley’s textbook of rheumatology, ed 9, Philadelphia, 2013, Saunders.
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.

TABLE2 Modified Steinberg Staging System for OsteonecrosisFrom Firestein GS, Budd RC, Gabriel SE, et al: Kelly’s textbook of rheumatology, ed 9, Philadelphia, 2013, Saunders.
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:

  1. Stage 0

    1. Asymptomatic

    2. Normal imaging

    3. Histologic findings only (i.e., silent osteonecrosis)

  2. Stage 1

    1. Asymptomatic or symptomatic

    2. Normal radiographs and CT scan

    3. Abnormal bone scan or MRI

  3. Stage 2

    1. Abnormal radiographs or CT scan, including linear sclerosis, focal bead mineralization, cysts; however, the overall architecture of the involved bone is normal

  4. Stage 3

    1. Early evidence of mechanical bone failure (subchondral fracture), but the overall shape of the bone is still intact

  5. Stage 4

    1. Flattening or collapse of the bone

  6. Stage 5

    1. Joint space narrowing

  7. Stage 6

    1. Extensive joint destruction

Diagnosis

Differential Diagnosis

  1. None in late stages

  2. 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.

FIG.1 

Diagnostic algorithm for osteonecrosis.
MRI, Magnetic resonance image.
From Firestein GS, Budd RC, Gabriel SE, et al.: Kelley’s textbook of rheumatology, ed 9, Philadelphia, 2013, Saunders.

Imaging Studies (Fig. 2)

  1. 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%.

    FIG.2 

    Aseptic necrosis of the hips.
    A, Aseptic necrosis can occur from a number of causes, including trauma and steroid use. In this patient, an anteroposterior view of the pelvis shows a transplanted kidney (K) in the right iliac fossa. Use of steroids has caused this patient to have bilateral aseptic necrosis. The femoral heads are somewhat flattened, irregular, and increased in density. B, Aseptic necrosis in a different patient is demonstrated on an MRI scan as an area of decreased signal (arrows) in the left femoral head. This is the most sensitive method for detection of early aseptic necrosis.
    From Mettler FA, [ed]: Primary care radiology, Philadelphia, 2000, Saunders.
  2. 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.

  3. Bone scan:

    1. Early: “cold” area.

    2. Later: increased radionuclide uptake as a result of remodeling.

    3. Sensitivity in early disease is only 70% and specificity is poor.

  4. CT scan: may reveal central necrosis and area of collapse before those are visible on radiographs.

Treatment

Prevention

  1. Manage etiologic conditions

  2. Minimize corticosteroid use

Nonpharmacologic Therapy

  1. Core decompression: effectiveness 35% to 95% in early phases

  2. Bone grafting

  3. Osteotomies

  4. Joint replacement

Acute General Rx

  1. Decrease weight bearing of affected area.

  2. Pulsing electromagnetic fields applied externally (still experimental).

  3. Peripheral vasodilators (e.g., dihydroergotamine) (unproven).

  4. Late-stage AVN is most often treated by total joint arthroplasty.

  5. A treatment algorithm for osteonecrosis is described in Fig. 3.

    FIG.3 

    Treatment algorithm for osteonecrosis.
    From Firestein GS, Budd RC, Gabriel SE, et al.: Kelley’s textbook of rheumatology, ed 9, Philadelphia, 2013, Saunders.

Prognosis

  1. 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.

  2. Contralateral joint involvement is common (30% to 70%).

Related Content

  1. Avascular Necrosis (Patient Information)