Avascular Necrosis of Femoral Head
Bone death in the ball of the hip joint caused by a lack of blood flow, leading the hip to collapse and develop severe arthritis.
Emergency Management: Not a surgical emergency unless associated with an acute displaced femoral neck fracture or hip dislocation, which require urgent reduction/fixation within 12-24 hours to prevent AVN from starting.
Avascular necrosis (AVN) of the femoral head is a painful, progressive bone disorder characterized by cellular death (necrosis) of bone components due to an interruption of the subchondral blood supply. Without blood, the bone tissue dies and collapses, destroying the overlying articular cartilage and leading to rapid, severe secondary osteoarthritis of the hip joint.
Detailed Overview
The femoral head is uniquely vulnerable to ischemic injury because its blood supply relies almost entirely on terminal branches of the medial circumflex femoral artery; there is very little collateral circulation. Once ischemia occurs, osteocytes and bone marrow cells undergo necrosis. The body attempts to repair this by resorbing the dead bone (osteoclast activity) and laying down new bone (osteoblast activity). However, the resorption process weakens the structural integrity of the subchondral bone plate faster than new bone can be formed. Mechanical stress from weight-bearing eventually causes a subchondral fracture ('crescent sign') and catastrophic collapse of the femoral head.
Epidemiology & Demographics
Usually affects adults between 30 and 50 years of age. Bilateral involvement is seen in up to 70-80% of cases eventually. Men are affected more frequently than women.
Etiological Mechanism
Disruption of blood flow. Can be traumatic (femoral neck fracture, hip dislocation) tearing the vessels, or atraumatic (thrombosis, lipid embolization, intravascular coagulation).
Primary Causes
Trauma is a direct cause. Atraumatic causes are heavily linked to chronic high-dose corticosteroid use, excessive alcohol consumption, and systemic diseases.
Ischemia -> death of hematopoietic cells and osteocytes (within 2-3 hours) -> inflammatory response and creeping substitution (body tries to remove dead bone and put down new bone). Osteoclasts resorb the dead trabeculae, creating a mechanically weak zone just beneath the articular cartilage. Normal weight-bearing puts stress on this weakened area, resulting in microfractures. This progresses to a macro-fracture (subchondral collapse). Once the bone collapses, the cartilage above it dies due to loss of mechanical support, leading to rapid joint degeneration.
Diagnostic Criteria & Guidelines
Diagnosis is confirmed via imaging. MRI is the gold standard and most sensitive modality for early (pre-collapse) diagnosis. Plain radiography is used for staging and identifying structural collapse.
For early, pre-collapse disease (Stage I-II) with small lesions: Conservative management includes protected weight-bearing (crutches), pain management (NSAIDs like Ibuprofen 600mg TID), and strict cessation of alcohol and steroids (if medically possible). However, surgical Core Decompression is the standard first-line intervention to prevent collapse. The surgeon drills a hole into the dead bone to relieve intraosseous pressure and promote new blood vessel ingrowth.
Second-Line & Adjunctive Therapy
For pre-collapse lesions that are larger: Vascularized fibular graft (transplanting a piece of the fibula bone along with its blood vessels into the femoral head). For Stage III (early collapse) in young patients, osteotomies may be attempted to rotate the dead bone away from the primary weight-bearing area.
Surgical & Procedural Management
Total Hip Arthroplasty (THA). The definitive treatment for Stage III (late) and Stage IV (post-collapse) disease. It removes the dead femoral head and replaces it with a metal/ceramic prosthesis, providing immediate pain relief and restoring function. AVN is a leading cause of THA in young adults.
Patient Counseling & Advice
Inform the patient that if the bone has not yet collapsed, drilling the bone (core decompression) might save the hip, but there are no guarantees. If it has already collapsed, a hip replacement is the only definitive fix. Strongly warn about the high risk to the other, currently painless hip.
Follow-Up & Monitoring Schedule
Serial X-rays every 3-6 months to monitor for structural collapse. Immediate evaluation of the contralateral hip if any new symptoms arise.
Preventive Strategies
Judicious use of systemic corticosteroids (use lowest effective dose for shortest duration). Prophylactic statins or bisphosphonates alongside high-dose steroids are under investigation but not yet standard of care.
Without surgical intervention, over 80% of symptomatic hips will collapse within 2 years. Core decompression saves the hip in about 60-70% of early-stage cases. Hip replacement provides excellent long-term outcomes but young patients may outlive the implant, requiring complex revision surgeries later in life.