[Clinical and therapeutic concepts in ischemic femur head necrosis].

Bone ischaemia can result from four mechanisms: (1) interruption of arterial inflow (e.g. after femoral neck fracture), (2) occlusion of venous outflow (possibly due to capsular distension), (3) intravascular arteriolar occlusion (as in sickle cell disease); (4) extravascular sinusoidal tamponade (e.g. in Gaucher's disease). Osteonecrosis following high-dosage corticosteroid administration or alcohol abuse could, theoretically, be due to either intravascular fat embolism or sinusoidal tamponade resulting from the marked fat deposition in the marrow. It is proposed here that, except in traumatic osteonecrosis, vascular insufficiency is part of a cycle of events resembling the familiar soft tissue compartment syndrome of the forearm or leg; no matter whether it started with venous stasis, arteriolar occlusion or capillary tamponade, the result is a diffuse and self-enhancing ischaemia involving all three haemodynamic abnormalities in a vicious circle. The very earliest stage of "idiopathic" osteonecrosis is characterised chiefly by marrow changes; for some (undetermined) period the ischaemic effects are potentially reversible-provided the vicious circle is broken by relieving the high intraosseous pressure. Effective management involves: (a) early diagnosis by MR imaging, measurement of intraosseous pressure and venography: (b) decompression of the bone, and (c) elimination of the etiological factor. Later stages of osteonecrosis cannot be treated by decompression and will need realignment osteotomy, prosthetic replacement or arthrodesis.