Avascular Necrosis Treatment & Management

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

Medical Care

Medical management of avascular necrosis (AVN) primarily depends on the location and severity of disease, as well as the patient's age and general health. Treatment outcomes correlate directly with the stage of the disease. No medical treatment has proven effective in preventing or arresting the disease process. In all patients, establish a firm diagnosis and exclude other conditions such as infections (osteomyelitis) and tumors. Commonly used medical measures for AVN include the following:

  • Conservative measures include limited weight bearing with crutches and pain medications. This may be beneficial and is a reasonable initial course of action if the involved segment is smaller than 15% and far from the weight-bearing region.
  • Immobilization may be helpful in some cases (eg, AVN of the distal femur or tibia).
  • Two uncontrolled studies have shown that bisphosphonates are helpful in delaying collapse of the femoral head and thus delaying the need for surgical intervention. Longer-term data are required before this process can be completely understood and an unqualified recommendation can be made.
  • Statin therapy to prevent corticosteroid-induced AVN may be helpful. Pritchett reported a 1% incidence of AVN in 284 patients who were on statin therapy during the entire period of corticosteroid treatment (average, 7.5 y).[10] The use of high-dose corticosteroids carries a reported 3-20% incidence of AVN.
  • In advanced AVN, the disease course is unaffected by activity and will eventually require surgery.
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Surgical Care

Several surgical procedures have been used in an attempt to treat AVN, with variable success. No surgical procedure is the consensual best among surgeons in the treatment of AVN. In early stages of AVN (precollapse), core decompression with or without bone graft is typically considered the most appropriate treatment. In late stages, characterized by collapse, femoral head deformity, and secondary osteoarthritis, total hip arthroplasty is the most appropriate treatment.

  • Core decompression
    • Researchers postulate that core decompression improves circulation by decreasing intramedullary pressure and preventing further ischemia and progressive joint destruction.
    • The best results vary from 34-95%, which is significantly better than results of conservative treatment. The best results are obtained when treating patients with early AVN (precollapse).
    • Core decompression is also effective for pain control.
  • Bone graft
    • Bone graft options include structural cortical or medullary bone graft and vascularized bone graft with either a muscle-pedicle bone graft or free vascularized fibular graft.
    • Bone grafting is combined with the following:
      • Core decompression, which may interrupt the cycle of ischemia
      • Excision of sequestrum, which may inhibit revascularization of the femoral head
      • Period of limited weight bearing
    • The best results have been reported with free vascularized bone grafts. Success rates of 70% and 91% have been reported in 2 small series.[11, 12]
    • Advantages of free vascularized grafts compared to total hip arthroplasty include the following:
      • Healed femoral head may allow more activity.
      • No foreign body–associated complications occur.
      • If performed during early AVN, lifelong survival of the femoral head is possible.
      • The patient has the option of total hip arthroplasty in the future.
    • Disadvantages of free vascularized grafts include the following:
      • Longer period of recovery
      • Less complete pain relief
      • Variable success rate
      • Lack of effectiveness in advanced disease
  • Osteotomy
    • Several osteotomy procedures have been tried with variable success.
    • Intertrochanteric osteotomies have been performed in patients with posttraumatic AVN.
    • Transtrochanteric rotational osteotomy involves rotation of the femoral head and neck on the longitudinal axis. The necrotic anterosuperior part of the femoral head becomes posterior, and the weight-bearing force is transmitted to what was previously the posterior articular surface, which is not involved in the ischemic process. In 1992, Sugano and colleagues reported excellent results in 56% of patients who underwent this procedure.[13] Transtrochanteric rotational osteotomy is technically demanding.
  • Total hip arthroplasty
    • Most patients with advanced disease (stage III and above) require total hip arthroplasty.
    • Total hip arthroplasty provides excellent pain relief for many years, although most young patients require repeat surgery.
    • With high failure rates (10-50% after 5 y), patients with AVN will probably need a second total hip arthroplasty during their lifetime.
  • Other
    • AVN of the femoral condyles (knees) may respond to more conservative intervention such as arthroscopic lavage and debridement.
    • AVN of the femoral condyles has a better prognosis than hip AVN, although osteoarthritis eventually develops.
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Consultations

Obtain consultation with an orthopedic surgeon. Early intervention can save affected joints and obviate the need for joint replacement.

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Activity

In early AVN, patients should use crutches or other supports to avoid weight bearing. In advanced AVN, the disease course is unaffected by activity; surgery is the only option.

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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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