Avascular necrosis

Dr Andrew Dixon and A.Prof Frank Gaillard et al.

Avascular necrosis (AVN), or more correctly osteonecrosis, is a generic term referring to the ischemic death of the constituents of bone. AVN has a wide variety of causes and can affect nearly any bone in the body. Most sites of involvement have an eponym associated with avascular necrosis of that area, and these sites are discussed individually as each site has unique clinical, etiologic and prognostic features. 

The terms ischemic and avascular necrosis are typically reserved for subchondral osteonecrosis, whereas bone infarct refers to medullary osteonecrosis.

There is no single affected demographic as the underlying predisposing factors are varied.

Infarction begins when the blood supply to a section of bone is interrupted. Once an infarct has become established, just as in other tissues, there is a central necrotic core, surrounded by an ischemic zone, the inner portion being 'almost dead' and the outer portion being hyperemic. Beyond this is normal viable marrow. Between the normal and the ischemic zone that demarcation occurs with the development of viable granulation separating dead tissue. This leads to the double line sign on MRI.

When the infarct is subchondral, a wedge of tissue is typically affected, the apex of which points towards the center of the bone.

Mnemonics: STARSPLASTIC RAGS

Radiographic changes alter with the stage of AVN - see Ficat staging, Steinberg classification.

In general, there is initial minor osteopenia, followed by variable density. Gradually microfractures of the subchondral bone accumulate in the dead bone, which is unable to repair leading to the collapse of the articular surface and the crescent sign of AVN. Eventually the cortex collapses and fragments, with superimposed secondary degenerative change.

MRI is the most sensitive (~95%) modality and demonstrates changes well before plain films changes are visible.

  • diffuse edema: edema is not an early sign; instead, studies show that edema occurs in advanced stages and is directly correlated with pain
  • reactive interface line is a focal serpentine low signal line with fatty center (most common appearance and first sign on MRI)
  • double line sign: serpiginous peripheral/outer dark (sclerosis) and inner bright (granulation tissue) on T2WI is diagnostic
  • rim sign: osteochondral fragmentation
  • secondary degenerative change

Bone scintigraphy is also quite sensitive (~85%) and is the second option after MRI. It is a choice when multiple sites of involvement must be assessed in patients with risk factors, such as sickle cell disease. The findings are different accordingly to the time of the scan:

  • early disease: often represented by a cold area likely representing the vascular interruption
  • late disease: may show a "doughnut sign": a cold spot with surrounding high uptake ring (surrounding hyperemia and adjacent synovitis)

The goal of treatment is to reduce the load on the affected part and to promote revascularization. Treatment varies by location and includes:

  • conservative: anti-inflammatory, analgesia, and reduced/non-weight bearing
  • core decompression
  • joint replacement for end-stage disease
  • MRI and bone scintigraphy have high sensitivity, with MRI studies being the first line for avascular necrosis assessment 
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Article information

rID: 950
Synonyms or Alternate Spellings:
  • Avascular necrosis (AVN)
  • AVN
  • Osteonecrosis

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Cases and figures

  • Case 1: involving humeral head
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  • Case 2
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  • Case 3
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  • Case 4
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  • A0001

Avascular ...
    Case 5
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  • Case 6: navicular
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  • Case 7: scaphoid fracture with early AVN
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  • Case 8
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  • Case 9: Dietrich disease
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  • Case 10
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  • Case 11: background sickle cell disease
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  • Case 12: knee (STIR)
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  • Fourth metatarsal...
    Case 13: fourth metatarsal - abnormal signal
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  • Case 14: Mueller-Weiss disease
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  • Case 15: Kummel disease
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  • Case 16: scaphoid
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  • Case 17: lunate
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  • Case 18: double line sign of talar AVN
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  • Case 19: van Neck-Odelberg disease
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  • Case 20: humerus head
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  • Case 21
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  • Case 22: bilateral femoral head
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