Avascular (Aseptic) Necrosis of the Femoral Head (HIP)

Descriptive text is not available for this imageBASICS

DESCRIPTION

  • Avascular (aseptic) necrosis results from bone blood supply interruption (either traumatic or nontraumatic occlusion).
  • The femoral head is the most common site.
  • A self-limiting idiopathic avascular necrosis of the hip that occurs in children is known as Perthes disease (see “Perthes Disease”).

ETIOLOGY

  • Traumatic
    • Slipped capital femoral epiphysis
    • Hip fracture
    • Hip dislocation
    • Complication of casting, bracing, surgery
  • Nontraumatic
    • Glucocorticoid or chemotherapy
    • Malignancy (leukemia)
    • Idiopathic (older, after physeal closure); similar to adult avascular necrosis
    • Idiopathic (younger, before physeal closure, Perthes disease)
    • Dysbaric osteonecrosis (Caisson disease)
    • Sickle cell disease
    • Septic arthritis
    • Gaucher disease
    • Viral infection (HIV, cytomegalovirus [CMV])
    • Radiation therapy
    • Hypercoagulable states
    • Hypothyroidism
    • Growth hormone deficiency (before and during growth hormone therapy)

RISK FACTORS

Age

  • The age of the child at onset of avascular necrosis is a strong prognostic indicator of outcome.
  • Glucocorticoid-induced avascular necrosis is more common in children ≥8 years of age.

Genetics

  • Variable, depending on cause
  • Glucocorticoid-induced avascular necrosis may have an underlying genetic predisposition.

PATHOPHYSIOLOGY

  • Death and necrosis of bone with gradual blood supply return
  • Necrotic bone gradually resorbed and replaced by new bone, but there is a disconnect between bone resorption and formation leading to net bone loss.
  • During bone resorption, structural integrity of femoral head may be reduced, leading to collapse.

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