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[Clinical and therapeutic concepts in ischemic femur head necrosis]
1Department of Orthopaedic Surgery, University of Bristol, U.K.
Insights
Bone ischemia, a precursor to osteonecrosis, involves a cycle of vascular issues. Early diagnosis and intervention, like bone decompression, can reverse early stages, preventing further bone death.
Area of Science:
- Orthopedics
- Vascular Biology
- Pathophysiology
Context:
- Bone ischemia can arise from arterial inflow interruption, venous outflow occlusion, arteriolar occlusion, or sinusoidal tamponade.
- Conditions like femoral neck fractures, sickle cell disease, Gaucher's disease, corticosteroid use, and alcohol abuse can lead to bone ischemia and osteonecrosis.
- High intraosseous pressure can create a self-enhancing cycle of ischemia, similar to compartment syndrome in soft tissues.
Purpose:
- To propose a unifying theory for the pathophysiology of non-traumatic osteonecrosis.
- To highlight the potential reversibility of early-stage osteonecrosis.
- To outline effective management strategies for bone ischemia and osteonecrosis.
Summary:
- Bone ischemia, a key factor in osteonecrosis, results from various vascular disruptions and can form a self-perpetuating cycle of reduced blood flow.
- Early diagnosis using MR imaging, intraosseous pressure measurement, and venography is crucial.
- Management includes relieving intraosseous pressure through decompression and addressing the underlying cause, with surgical options for advanced stages.
Impact:
- Understanding the cyclical nature of bone ischemia offers new therapeutic targets.
- Early detection and intervention can potentially prevent the progression of osteonecrosis.
- This research provides a framework for managing diverse causes of bone ischemia, from traumatic injuries to systemic diseases.
Abstract:
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.