Avascular Necrosis Clinical Presentation

  • Author: Jeanne K Tofferi, MD, MPH, FACP; Chief Editor: Herbert S Diamond, MD   more...
 
Updated: Jan 19, 2012
 

History

  • Avascular necrosis (AVN) may be asymptomatic and is occasionally discovered incidentally on radiographs. Symptoms depend on the affected joint. Medullary infarcts are usually silent, and infarcts of the small bones of the hands and feet are often symptomatic.
  • Pain in the affected joint is typically the presenting symptom of AVN, regardless of the location. Patients with AVN of the femoral head often report groin pain that is exacerbated by weight bearing. The pain may initially be mild but progressively worsens over time and with use. Eventually, the pain is present at rest and may be present at night.
  • Large infarcts, such as those due to Gaucher disease and hemoglobinopathies, are associated with very severe pain.
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Physical

  • Initially, the physical examination findings of AVN may be unrevealing. Abnormal physical findings depend on the location and severity of disease. With progression of AVN of the hip, joint function deteriorates and the patient may walk with a limp. AVN of smaller, non–weight-bearing joints typically does not cause significant disability.
  • Patients with AVN may have tenderness around the affected bone.
  • Both active and passive joint movements may be restricted and painful.
  • A neurologic deficit may be present if a nerve is affected (compressed) because of necrosis and compression deformity of affected bones.
  • Advanced AVN can cause joint deformity and muscle wasting.
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Causes

AVN is associated with several clinical conditions. The following etiological factors have been identified:

  • Primary or idiopathic
  • Secondary or associated with an underlying condition
    • Trauma
    • Systemic corticosteroid use or Cushing disease[9]
    • Alcohol abuse
    • Systemic lupus erythematosus (with or without antiphospholipid syndrome), as well as other connective-tissue diseases
    • Hematologic (sickle cell disease, hemoglobinopathies)
    • Metabolic (hyperlipidemia, gout, renal failure)
    • Orthopedic disorders (slipped capital femoral epiphysis, congenital dysplasia of the hip, Legg-Calve-Perthes disease)
    • Infection (osteomyelitis, HIV infection [controversial])
    • Renal transplantation
    • Radiation therapy
    • Pancreatitis (uncommon)
    • Gaucher disease
    • Malignancy (marrow infiltration, malignant fibrous histiocytoma)
    • Caisson disease
    • Pregnancy
    • Bisphosphonate use
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Contributor Information and Disclosures
Author

Jeanne K Tofferi, MD, MPH, FACP  Assistant Chief, Department of Rheumatology, Walter Reed Army Medical Center

Jeanne K Tofferi, MD, MPH, FACP is a member of the following medical societies: Alpha Omega Alpha and American College of Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

William Gilliland, MD, MPHE, FACP, FACR  Staff Rheumatologist, Walter Reed Army Medical Center; Professor of Medicine, Assistant Dean of Curriculum, Uniformed Services University of the Health Sciences

Disclosure: Nothing to disclose.

Specialty Editor Board

Bryan L Martin, DO  Associate Dean for Graduate Medical Education, Designated Institutional Official, Associate Medical Director, Director, Allergy Immunology Program, Professor of Medicine and Pediatrics, Ohio State University College of Medicine

Bryan L Martin, DO is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Allergy, Asthma and Immunology, American College of Osteopathic Internists, American College of Physicians, American Medical Association, and American Osteopathic Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Lawrence H Brent, MD  Associate Professor of Medicine, Jefferson Medical College of Thomas Jefferson University; Chair, Program Director, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center

Lawrence H Brent, MD is a member of the following medical societies: American Association for the Advancement of Science, American Association of Immunologists, American College of Physicians, and American College of Rheumatology

Disclosure: Abbott Honoraria Speaking and teaching; Centocor Consulting fee Consulting; Genentech Grant/research funds Other; HGS/GSK Honoraria Speaking and teaching; Omnicare Consulting fee Consulting; Pfizer Honoraria Speaking and teaching; Roche Speaking and teaching; Savient Honoraria Speaking and teaching; UCB Honoraria Speaking and teaching

Alex J Mechaber, MD, FACP  Senior Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine

Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD  Adjunct Professor of Medicine, Division of Rheumatology, University of Pittsburgh School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa

Disclosure: Merck Ownership interest Other; Smith Kline Ownership interest Other; Zimmer Ownership interest Other

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Avascular necrosis in the femoral head resulting from corticosteroid therapy.
Avascular necrosis of the shoulder showing subchondral radiolucent lines (crescent sign).
Avascular necrosis of both femoral heads. This T1-weighted image shows decreased signal intensity in both femoral heads.
MRI of the distal femur and proximal tibia. This T2-weighted image shows increased signal intensity in the marrow.
Table. Staging of Avascular Necrosis
StageClinical and Laboratory Findings
Stage 0
  • Patient is asymptomatic.
  • Radiography findings are normal.
  • Histology findings demonstrate osteonecrosis.
Stage I
  • Patient may or may not be symptomatic.
  • Radiography and CT scan findings are unremarkable.
  • AVN is considered likely based on MRI and bone scan results (may be subclassified by extent of involvement [see below]).
  • Histology findings are abnormal.
Stage II
  • Patient is symptomatic.
  • Plain radiography findings are abnormal and include osteopenia, osteosclerosis, or cysts.
  • Subchondral radiolucency is absent.
  • MRI findings are diagnostic.
Stage III
  • Patient is symptomatic.
  • Radiographic findings include subchondral lucency (crescent sign) and subchondral collapse.
  • Shape of the femoral head is generally preserved on radiographs and CT scans.
  • Subclassification depends on the extent of crescent, as follows:
    • Stage IIIa: Crescent is less than 15% of the articular surface.
    • Stage IIIb: Crescent is 15-30% of the articular surface.
    • Stage IIIc: Crescent is more than 30% of the articular surface.
Stage IV
  • Flattening or collapse of femoral head is present.
  • Joint space may be irregular.
  • CT scanning is more sensitive than radiography.
  • Subclassification depends on the extent of collapsed surface, as follows:
    • Stage IVa: Less than 15% of surface is collapsed.
    • Stage IVb: Approximately 15-30% of surface is collapsed.
    • Stage IVc: More than 30% of surface is collapsed.
Stage V
  • Radiography findings include narrowing of the joint space, osteoarthritis with sclerosis of acetabulum, and marginal osteophytes.
Stage VI
  • Findings include extensive destruction of the femoral head and joint.
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