Osteonecrosis

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Avascular necrosis (AVN), or more correctly "osteonecrosis", is a generic term referring to ischaemic 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 ischaemic and avascular necrosis are typically reserved for subchondral osteonecrosis, whereas bone infarct refers to medullary osteonecrosis.

Epidemiology

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

Pathology

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 ischaemic zone, the inner portion being 'almost dead' and the outer portion being hyperaemic. Beyond this is normal viable marrow. Between the normal and the ischaemic zone that demarcation occurs with 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 centre of the bone.

Aetiology
  1. trauma (fracture or dislocation)
  2. Caissoncaisson disease
  3. haemoglobinopathies, e.g. Sicklesickle cell disease
  4. pregnancy related AVN
  5. radiotherapy
  6. connective tissue disorders
  7. renal transplantaiontransplantation
  8. corticosteroid excess (both endogenous and exogenous)
  9. pancreatitis
  10. gout
  11. Gaucher disease
  12. alcohol

Mnemonics: STARS, PLASTIC RAGS

Eponymous AVNs
Location specific AVN

Radiographic features

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

Plain film

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

MRI

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

  • diffuse oedema
  • focal serpiginous low signal line with fatty center (most common appearance)
  • double line sign sign on T2WI is diagnostic
  • osteochondral fragmentation: rim sign
  • secondary degenerative change
Bone scan

Bone scintigraphy is also quite sensitive (~85%).

Early disease

Often represented by a cold area likely representing vascular interruption.

Late disease

May show a "doughnut sign": cold spot with surrounding high uptake ring.

Treatment and prognosis

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

  • conservative: anti-inflammatory, analgesia and reduced, non weight bearing
  • core decompression
  • joint replacement for end stage disease

See also

  • -<li><a href="/articles/caisson-disease-1">Caisson disease</a></li>
  • -<li>haemoglobinopathies, e.g. <a href="/articles/sickle-cell-disease">Sickle cell disease</a>
  • +<li><a href="/articles/caisson-disease-1">caisson disease</a></li>
  • +<li>haemoglobinopathies, e.g. <a href="/articles/sickle-cell-disease">sickle cell disease</a>
  • -<li><a href="/articles/renal-transplant-related-complications">renal transplantaion</a></li>
  • +<li><a href="/articles/renal-transplant-related-complications">renal transplantation</a></li>

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