Avascular Necrosis

Failure of the blood supply to the end of a bone, resulting in ischaemic necrosis of bone and marrow

Aetiology

  • Greater incidence in males
  • Typical age 35-50 years
  • Most commonly affects the head of the femur, but can affect other bones too e.g. wrist, head of humerus

Pathophysiology

Idiopathic AVN

  1. Coagulation of the intraosseous microcirculation
  1. Venous thrombosis causes retrograde arterial occlusion
  1. Intraosseous hypertension
  1. Decreased blood flow results in necrosis of a segment of bone
  1. There will be patchy sclerosis before subchondral collapse and irregularity of the articular surface occurs
  1. Resultant bone and joint damage can lead to significant structural collapse of the bone → secondary OA
    1. Can also secondarily affect osteoarthritic joints causing collapse of the articular surface and rapid deterioration
Risk factors
  • Irradiation
  • Trauma
  • Increased coagulability - thrombophilia, sickle cell disease, antiphospholipid deficiency in SLE, pregnancy
  • Dysbaric disorders (decompression sickness - Caisson disease)
    • Rare cause which causes AVN from nitrogen gas bubbles forming in the circulation after too rapid a depressurization after deep sea diving
  • Alcoholism and steriod (ab)use
    • Alter fat metabolsim which can result in mobilisation of fat into the circulation
    • Sludges up the capillary system and promotes coagulation within prone areas of bone
    • Increased fat content of the marrow can compress venous outflow from the bone causing stasis and ischaemia
  • Hyperlipidaemia - increased fat in circulation

AVN associated with trauma

  • Secondary to fractures (femoral neck, proximal humerus, waist of scaphoid and talar neck) - the fracture disrupts the blood supply to an entire portion of bone
  • Decreased blood flow → necrosis → collapse

Commonly affected sites

  • Femoral head
  • Femoral condyles
  • Head of the humerus
  • The capitellum
  • The proximal pole of the scaphoid
  • The proximal part of the talus

Clinical presentation

  • Can be asymptomatic
  • Examination is usually normal unless disease has advanced to collapse/OA

Femoral head AVN

  • Insidious onset of groint pain exacerbated by stairs or impact
  • Bilateral disease in 80% of cases

Investigations

  • Early cases may only show changes on MRI, later changes can be visible on x-ray
  • The 'hanging rope sign' is a later sign of femoral head AVN - patchy sclerosis of the weight bearing area of the femoral head with a lytic zone underneath formed by granulation tissue from attempted repair
  • Following collapse of the articular surface, the articular surface will be irregular on imaging and as secondary OA develops the associated signs will be visible (LOSS)

Management

Reversible

  • If the articular surface has not collapsed in an amenable site, AVN can be reversed
  • Bisphosphates
  • Core decompression - drilling performed under fluoroscopy to 'decompress' the bone to prevent further necrosis and help healing
  • Curettage and bone grafting
  • Vascularised fibular bone graft

Irreversible

  • If the articular surface has collapsed, generally joint replacement is usually required in the hip, knee or shoulder to control symptoms
  • Rotational osteotomy can be considered if less than 15% of femoral head damaged (rare)
  • Fusion can be considered in the wrist or foot/ankle