Avascular necrosis — Rapid | Doctor’s Passport

Synopsis

Recognise osteonecrosis before articular collapse, stage mechanical integrity with appropriate imaging and refer early enough for joint-preserving treatment while managing causative exposures safely.

Suspect femoral-head osteonecrosis with progressive groin, buttock or referred knee pain and painful internal rotation, particularly after steroids, alcohol, trauma, sickle-cell disease or transplantation.
First-line imaging is anteroposterior pelvis plus lateral views of the symptomatic hip; normal radiographs do not exclude early disease.
MRI without contrast is the reference confirmatory and staging test when suspicion persists, defining lesion size, location, bilaterality and subchondral integrity.
A crescent sign is a subchondral fracture; flattening, loss of sphericity and joint-space narrowing establish collapse and secondary arthritis.
Protect weight bearing when pain suddenly worsens or imaging shows subchondral fracture while urgent orthopaedic staging is arranged.
Refer symptomatic pre-collapse disease promptly to a hip-preservation service because core decompression and selected graft or biologic procedures are most useful before structural failure.
After collapse, total hip arthroplasty usually gives the most predictable relief; prolonged conservative care cannot restore femoral-head shape.
Modify alcohol and steroid exposure safely, but no routine medicine reliably revascularises dead bone or substitutes for stage-directed surgery.

Key red flags

A native hip dislocation is time-critical: perform trauma assessment, document sciatic and vascular function and arrange urgent reduction under the appropriate specialist pathway.

Fever, raised inflammatory markers, severe rest pain and a joint effusion may indicate septic arthritis, which requires urgent aspiration and washout decisions.

Sudden escalation of groin pain or new inability to bear weight can represent subchondral fracture and femoral-head collapse.

Bilateral symptoms, sickle-cell crisis, decompression exposure, transplantation or high cumulative glucocorticoid use raises risk at more than one skeletal site.

A destructive or expansile lesion, constitutional symptoms or marrow replacement outside the characteristic pattern requires tumour or infection investigation.

Never stop sustained systemic corticosteroids abruptly when reducing risk exposure; coordinate tapering and steroid-sparing treatment with the prescribing team.

Investigation priorities

First-line AP pelvis and lateral hip radiographsFirst stepFirst line

Assess shape, sclerosis, crescent fracture, collapse, arthritis and an alternative lesion while comparing both hips.

Management branches

Traumatic emergencyRestore alignment and perfusion opportunity

Hip dislocation or displaced femoral-neck fracture creates immediate vascular risk.

Use trauma ABCDE and document distal vascular and sciatic-nerve function before and after intervention.
Arrange urgent reduction or fracture surgery through the specialist pathway rather than waiting for elective MRI.
Confirm concentric reduction and associated fracture with post-reduction imaging as indicated.
Explain later osteonecrosis surveillance even after technically successful acute treatment.

Key medicines

Paracetamol for symptomatic bridgeTake 500 to 1,000 mg orally when needed, leaving at least four hours between doses and limiting total intake to 4 g per day, with a lower maximum for low weight or hepatic risk.Check combination products, alcohol, frailty and liver disease; analgesia must not encourage impact through a subchondral fracture.

Topical diclofenac for accessible referred painApply 2 to 4 g of diclofenac 1.16% gel to intact painful lateral hip or knee skin per dose, within the licensed maximum of three or four daily applications for a short trial.Avoid broken skin and NSAID hypersensitivity, account for oral NSAIDs, renal and cardiovascular risk and follow pregnancy restrictions.

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