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  • Bone infarction

  • Ischemic bone necrosis

  • Osteonecrosis




  • 733.4 Aseptic necrosis of bone

  • 733.42 Aseptic necrosis of femoral head and neck




  • M87 Osteonecrosis

  • M87.1 Osteonecrosis due to drugs

  • M87.2 Osteonecrosis due to previous trauma

  • M87.3 Other secondary osteonecrosis

  • M87.8 Other osteonecrosis

  • M87.9 Osteonecrosis, unspecified




  • 4H: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated with Joint Arthroplasty1

  • 4I: Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated with Bony or Soft Tissue Surgery2



Patient is a 48-year-old male who was hit by a car while riding his bicycle. Patient has a fractured pelvis and subluxed hip. After 6 weeks, patient began walking increased distances and was starting to feel better. Six months later, his hip began to become painful and stiff. Patient noticed an increase limp and difficulty putting weight onto his leg. Physician ordered an X-ray, which showed avascular necrosis (AVN) changes in the hip bone.


  • AVN results from disrupted or lost blood flow to a joint or bone, resulting in damage to or death of bone tissue

  • Femoral head is the most vulnerable site for development of AVN

    • Anterolateral aspect is particularly vulnerable as it is the principal weight-bearing region and site of greatest mechanical stress

FIGURE 179-1

Coronal T1-weighted MR image of the pelvis in a patient with bilateral hip avascular necrosis. Note the serpiginous low signal abnormality in the subchondral regions of the femoral heads (arrowheads). (From Chen MYM, Pope TL, Ott DJ. Basic Radiology. 2nd ed. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.)

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FIGURE 179-2

Avascular necrosis, bilateral hips (Stage 4). (Reproduced with permission from Simon RR, Sherman SC, Koenigsknecht SJ. Emergency Orthopedics, The Extremities. 5th ed. © 2007, McGraw-Hill Inc., New York, NY.)

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Essentials of Diagnosis

  • Known causes can be traumatic or atraumatic, including:

    • Corticosteroid use

    • Alcohol abuse

    • Intravascular coagulation from marrow fat enlargement, vessel wall injury, or thromboembolic event

  • Early imaging with MRI is imperative as success of conservative treatment correlates with earlier stages

General Considerations

  • AVN of the hip in children is known as Legg–Calvé–Perthes syndrome

  • Can be idiopathic

  • Clinical AVN affects the ends of long bones

  • May result from local edema (compartment syndrome), occlusive vessel disease, fat embolism, or hypertrophy of fat cells, which block blood supplies and result in necrosis/death of marrow cells and osteocytes


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