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Avascular Necrosis Clinical Presentation

  • Author: Jeanne K Tofferi, MD, MPH, FACP; Chief Editor: Herbert S Diamond, MD  more...
Updated: Jun 16, 2016


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.



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. Findings may include the following:

  • 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 result in joint deformity and muscle wasting.


AVN may be primary or idiopathic. For AVN that is secondary or associated with an underlying condition, the following etiologic factors have been identified:

  • Trauma
  • Systemic corticosteroid use or Cushing disease[10]
  • 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)
  • Osteomyelitis
  • HIV infection[11, 12] (controversial)
  • Allogeneic bone marrow transplantation[13, 14]
  • Radiation therapy
  • Pancreatitis (uncommon)
  • Gaucher disease
  • Malignancy (marrow infiltration, malignant fibrous histiocytoma)
  • Caisson disease
  • Pregnancy
  • Bisphosphonate use
  • Denosumab use[15, 4]
Contributor Information and Disclosures

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, American College of Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

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, American College of Rheumatology

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Janssen<br/>Serve(d) as a speaker or a member of a speakers bureau for: Abbvie; Genentech; Pfizer; Questcor.

Chief Editor

Herbert S Diamond, MD Visiting Professor of Medicine, Division of Rheumatology, State University of New York Downstate Medical Center; 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, Phi Beta Kappa

Disclosure: Nothing to disclose.

Additional Contributors

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, American Osteopathic Association

Disclosure: Nothing to disclose.


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.

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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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