Avascular necrosis. LCPD - Legg-Calve-Perthes disease
Avascular necrosis
Avascular necrosis can in fact occur in a number of different bones including the Talus and Scaphoid, although the most common, and the focus of this question, is the head of the femur.
AVN is a severe complication of fractures of the head of femur, as well as having a number of additional causes, these include severe periosteal stripping, steroid use, Caisson’s disease, SLE, Radiation and Alcoholism. In fractures of the neck of the femur, damage to the circumflex arteries and their respective radicular arteries can lead to devascularization of the head of the femur (a small amount of blood comes from the teres ligament artery but it is insufficient. The disease is more common in males than females, aged 40s-50s.
AVN is often asymptomatic in the initial stages, however it will develop to pain in the hip, with a limp and a slight reduction of range of movement. Patients will often present with groin pain that worsens with activity, and specifically internal rotation and abduction will be limited. MRI is the most sensitive study, showing early changes in the femoral head, however in practice AP/lateral XR is generally first line.
AVN is classified based on the modified Ficat score:
- 0 - asymptomatic - nothing on XR and MRI
- 1 - symptomatic - nothing on XR but MRI might be positive
- 2 - XR shows sclerosis with no collapse
- 3 - XR shows collapse with crescent sign
- 4 - flat femoral head but no changes in acetabulum
- 5 - joint narrowing and early degenerative joint disease
- 6 - advanced degenerative joint diseases with acetabulum included
Treatment is dependent on the stage:
- 0-1 - treatment is limited with observation
- 2- core decompression
- 3 - consider vascularized fibula or femoral osteotomy
- 4-6 - total hip arthroplasty - appropriate for most patients
Legg-Calve-Perthes disease
LCPD is a self limiting idiopathic osteonecrosis of the femoral head including the necrosis, collapse, repair and remodelling of the head that presents in the first decade of life. It is more commonly found in boys. It is thought the cause is due to a single or multiple vascular events (e.g. vascular hypoplasia) which cause the vascularization followed by revascularization.