Avascular Necrosis of the Femoral Head

Avascular necrosis is bone death caused by disruption of the local blood supply. The femoral head is most commonly affected because its collateral blood supply is limited and vulnerable. Early recognition is the essential clinical priority, as stage at diagnosis determines treatment options and prognosis.

Other skeletal sites can be affected, including the humeral head, talus and scaphoid. Causes include:

• Trauma, particularly femoral neck fracture and hip dislocation, which directly disrupt the vessels supplying the femoral head.
• Corticosteroid therapy, one of the commonest identifiable non-traumatic causes. Risk relates to cumulative dose and to the pattern of administration, including high-dose pulsed regimens.
• Excess alcohol use.
• Sickle cell disease, through vaso-occlusive microvascular disease within the bone.
• Idiopathic disease, where no cause is identified in a proportion of cases.

Pathophysiology and risk factors

• Loss of blood supply to a region of bone causes localised bone cell death. The mechanism may be direct traumatic vascular injury or vascular occlusion, as in sickle cell disease through microvascular sickling.
• The mechanism in corticosteroid and alcohol-related disease is less clear. Proposed mechanisms are fat embolism, raised intraosseous pressure and direct vascular endothelial toxicity.
• The dead bone is structurally weakened. The overlying articular surface can collapse progressively if the condition is not identified and, where appropriate, treated before collapse occurs.
• The femoral head is the commonest and clinically most significant site, because of its limited and vulnerable blood supply.
• Bilateral involvement is common, particularly with a systemic cause such as corticosteroid therapy, alcohol use or sickle cell disease. Assess the contralateral hip proactively in any confirmed unilateral presentation.
• Corticosteroid-related avascular necrosis is clinically important because this drug class is widely used. Risk relates to cumulative dose, and no threshold is established as completely safe.
• High-dose pulsed corticosteroid administration has a recognised but incompletely understood association with the condition.

• Pain is the characteristic presentation. Onset is progressive and often insidious, most commonly at the hip as groin, thigh or buttock pain. It occurs initially with weight-bearing or activity and may become present at rest as the condition progresses.
• Symptoms are often present for a considerable period before diagnosis. Early presentation is subtle and non-specific, and standard plain radiography is frequently normal in the earliest stages.
• Range of motion of the affected joint is reduced as the condition progresses, particularly in hip involvement. A limp develops where the lower limb is affected.
• Severity and functional impact depend on the site and extent of involvement and on the degree of any structural collapse.
• Explore risk factors specifically and systematically. These include significant trauma, corticosteroid use, significant alcohol use, and conditions associated with avascular necrosis such as sickle cell disease.
• For corticosteroids, ask about cumulative dose, duration and any history of high-dose pulsed administration. The history directs diagnostic suspicion and, in some cases, allows modification of an ongoing contributing exposure.
• Once the articular surface has collapsed, pain and functional limitation become progressively more significant.
• Secondary osteoarthritic change develops over time within the affected joint, reflecting the altered, irregular joint surface contour.

• Magnetic resonance imaging is the most sensitive investigation. It detects early avascular necrosis before any change appears on plain radiography, so it is the investigation of choice when the diagnosis is suspected.
• Early diagnosis, before structural collapse, preserves the range of joint-preserving treatment options.
• Plain radiography is less sensitive for early disease. In established disease it may show the "crescent sign", which reflects subchondral fracture.
• In more advanced disease, radiography shows frank femoral head collapse and secondary osteoarthritic change.
• Staging systems that incorporate both magnetic resonance imaging and plain radiographic findings guide treatment according to disease severity and stage.
• Look for any specific underlying cause or risk factor. Order laboratory investigation where an underlying systemic condition is a consideration, including sickle cell disease where not already known.
• Identifying a modifiable contributing factor, such as ongoing corticosteroid or alcohol exposure, informs overall management. It also reduces the risk of further progression or contralateral involvement.

• Stage at diagnosis determines management. Early-stage disease, identified before structural collapse, offers the widest range of joint-preserving options. Early diagnosis is therefore central to treatment and prognosis.
• Core decompression is an established option for early-stage disease before collapse. A core of necrotic bone is removed from the affected femoral head (or other site) to reduce intraosseous pressure and promote revascularisation.
• Evidence for the degree of benefit of core decompression is variable. It is generally a reasonable joint-preserving option in appropriately selected early-stage presentations.
• Bone grafting is a further joint-preserving option for selected early-stage disease, sometimes combined with core decompression. It aims to give structural support to the affected region while revascularisation and healing occur.
• Total joint replacement, most commonly total hip arthroplasty, is the standard definitive treatment for advanced disease with established collapse and significant pain and functional limitation. It offers reliable symptomatic and functional benefit.
• Avascular necrosis frequently affects younger individuals than those having joint replacement for primary osteoarthritis. This bears on long-term implant durability and the potential eventual need for revision surgery over the patient's remaining lifetime.
• Modify any ongoing contributing risk factor to reduce the risk of progression or contralateral joint involvement. Minimise corticosteroid dose where clinically feasible given the underlying indication, and offer alcohol cessation support where relevant.
• Arrange structured follow up with serial imaging to monitor for progression and to guide the timing of treatment escalation.
• Educate the patient about the specific underlying cause, where identified, and its relevance to ongoing risk.
• Early diagnosis and appropriately timed, staged treatment are the central principle of optimal long-term outcome.