Avascular Necrosis Workup

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

Laboratory Studies

  • No laboratory test findings specifically suggest or confirm the presence of avascular necrosis (AVN).
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Imaging Studies

  • Radiography: Plain radiographic findings are unremarkable in early stages of AVN. In mild-to-moderate AVN, radiographs demonstrate sclerosis and changes in bone density. In advanced disease, bone deformities, such as flattening, subchondral radiolucent lines (crescent sign), and collapse of the femoral head, are evident (see images below). Avascular necrosis in the femoral head resulting fAvascular necrosis in the femoral head resulting from corticosteroid therapy. Avascular necrosis of the shoulder showing subchonAvascular necrosis of the shoulder showing subchondral radiolucent lines (crescent sign).
  • MRI
    • MRI is the most sensitive study and is the imaging procedure of choice in AVN, with an overall sensitivity that exceeds 90%. The specificity of MRI is also very high. The use of gadolinium is particularly useful in early detection.
    • MRI findings of AVN include decreased signal intensity in the subchondral region on both T1- and T2-weighted images, suggesting edema (water signal) in early disease. This relatively nonspecific finding is often localized in the medial aspect of femoral head. This abnormality is observed in 96% of cases.
    • The next stage is characterized by a reparative process (reactive zone) and shows low signal intensity on T1-weighted scans and high signal intensity on T2-weighted scans. This finding is diagnostic for AVN (see images below). Avascular necrosis of both femoral heads. This T1-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 TMRI of the distal femur and proximal tibia. This T2-weighted image shows increased signal intensity in the marrow.
    • Advanced AVN is characterized by deformity of the articular surface and by calcification, which are easily detected with radiography and CT scanning.
  • Radionuclide bone scan
    • In early AVN, osteoblastic activity and blood flow are increased; thus, the sensitivity of radionuclide bone scan is better than that of plain films at this stage.
    • The central area of decreased uptake is surrounded by an area of increased uptake. This phenomenon is known as the doughnut sign and indicates the reactive zone surrounding the necrotic area.
    • Limitations of bone scan include the following:
      • In early AVN, bone scan is less sensitive than MRI.
      • Findings are nonspecific.
      • Results are difficult to interpret if disease is bilateral. In unilateral disease, the healthy side can be used for comparison.
  • CT scanning
    • CT scans show sclerosis in the central part of femoral head as an asterisk sign.
    • Changes in the anterior part of the femoral head are easily observed.
    • CT scanning is a good modality to assess the extent of the disease and calcification, but it is not as sensitive as MRI.
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Procedures

  • Bone biopsy can help establish the diagnosis of AVN but is not routinely performed because of the availability of sensitive noninvasive tests such as MRI.
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Histologic Findings

Histology is the criterion standard for diagnosis of AVN, although it is usually unnecessary. The histologic specimen is usually obtained during surgery, although it is occasionally obtained during diagnostic bone biopsy. Histologic changes are observed in both cortical bone and bone marrow.

Necrosis of cortical bone is followed by a regenerative process in surrounding tissues. Increased osteoclastic activity occurs and removes necrotic bone and increased osteoblastic activity as a reparative process.

Bone marrow lesions are usually large. Edema, hemorrhage, fibrilloreticulosis, and hypocellularity are present. Adipocytes in marrow are replaced by eosinophilic debris.

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Staging

Several different staging systems have been developed and continue to be used. Ficat initially developed an AVN staging system based on radiologic findings. This staging system was revised after the widespread use of MRI in the workup of AVN. The staging system presented in the below table is based on the consensus of the Subcommittee of Nomenclature of the International Association on Bone Circulation and Bone Necrosis (ARCO: Association of Research Circulation Osseous). The most important consideration is collapse of the femoral head cortex. Repair and complete recovery may be possible prior to collapse. Afterward, the collapse is irreversible.

Table. Staging of Avascular Necrosis (Open Table in a new window)

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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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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