Avascular necrosis – osteonecrosis

Avascular necrosis of the talus. Note the increased subchondral sclerosis of the talar dome. The sagittal T1 MRI clearly defines the extent of the osteonecrosis.
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Avascular necrosis – osteonecrosis

Characteristics

  • ‘Death’ of a (bony) structure secondary to insufficient blood supply.
  • Primary pathology is of unknown aetiology, but secondary AVN is linked with a variety of pathologies – see below.
  • Idiopathic avascular necrosis occurs in childhood in the proximal femoral epiphysis (‘Perthes’ = Legg–Calve–Perthes Disease); See Perthes’ disease. AVN is also seen in childhood hips following SCFE (or SUFE)
  • Associated with steroid use, alcohol abuse, metabolic disease (e.g. Gaucher’s disease), vasculitis (SLE), sickle cell disease, malaria, occupational causes (e.g. deep-sea divers – caisson disease), venous thromboembolism and bone-marrow transplants.
  • Certain bones in adulthood are particularly associated with AVN; the eponyms below are for idiopathic AVN.
  1. Femoral head – see separate section.
  2. Distal femur – usually medial femoral condyle – SONK (spontaneous osteonecrosis of the knee).
  3. Proximal humerus – idiopathic and post-traumatic.
  4. Talus.
  5. Lunate – Kienböck’s disease – see separate section.
  6. Metatarsal head – Freiburg’s disease for second MT head.
  7. Navicular – Köhler’s disease.
  8. Scaphoid – Preiser’s disease.
  9. Capitellum – Panner’s disease – associated with osteochondritis.

Clinical features

  • Classically present with pain of insidious onset.
  • Pain often worse at night.
  • Pain is usually severe and often becomes more bearable after several weeks.
  • Joint locking with loose bodies – separated osteochondral fragments.
  • Reduced function of adjacent joints.

Radiological features

  • The initial radiograph if taken early may be normal.
  • The affected bone becomes sclerotic with later collapse and remodelling.
  • Degenerative change within adjacent joints.
  • MR – 90–100% sensitivity for symptomatic disease.
  • Changes reflect the death of fatty marrow cells.
  • Bone-marrow oedema is manifest as reduced signal on T1 weighted and increased signal on T2 weighted images.
  • Early subchondral collapse is seen as crescentic low signal.
  • In later disease, fibrosis results in low signal on both T1 and T2 weighted images.
Avascular necrosis of the scaphoid: fracture of the waist of scaphoid with increased sclerosis and early collapse of the proximal pole. Coronal T1 MRI demonstrates the loss of normal marrow signal, secondary to AVN, within the proximal pole (asterisk). Idiopathic scaphoid AVN is rare.

Avascular necrosis of the scaphoid: fracture of the waist of scaphoid with increased sclerosis and early collapse of the proximal pole. Coronal T1 MRI demonstrates the loss of normal marrow signal, secondary to AVN, within the proximal pole (asterisk). Idiopathic scaphoid AVN is rare.

Freiberg’s osteonecrosis of the second metatarsal head.

Freiberg’s osteonecrosis of the second metatarsal head.

Management

  • Pain relief with analgesics and immobilisation.
  • Remove any precipitating factors, e.g. drugs, alcohol, occupation.
  • Surgery, if indicated, is generally reparative or reconstructive in nature.
  • Core decompression and vascularised bone graft aims to restore vascularity and prevent further collapse.
  • In severe collapse, reconstructive surgery should be considered.

Reference

James R. D. M., Erskine J. H., Rakesh R. M. (2008). Musculoskeletal Radiology. A-Z Musculoskeletal and Trauma Radiology, 1st edition, Cambridge University Press, Cambridge, 1, 1-176.

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