Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Recognise osteonecrosis before articular collapse, stage mechanical integrity with appropriate imaging and refer early enough for joint-preserving treatment while managing causative exposures safely.
Localise pain and reconstruct its evolution. Early disease usually causes deep groin or buttock ache on loading and internal rotation, sometimes referred to the knee. Ask about glucocorticoid formulation, peak dose and cumulative exposure; alcohol; trauma or dislocation; sickle-cell disease; lupus; antiphospholipid syndrome; transplantation; HIV treatment; decompression work and previous radiotherapy. Establish walking distance, aids, occupation and activity goals. Bilateral risk means symptoms in the opposite hip matter.
Observe gait for antalgia and Trendelenburg compensation, compare leg length and inspect scars. Test hip flexion and rotation gently; internal rotation is often the earliest painful restriction. Examine lumbar spine, sacroiliac joint, knee and abdomen for referred pain and record distal neurovascular status. Fever, severe pain through every movement or systemic illness mandates an infection pathway. Avoid forceful impingement testing when subchondral fracture is suspected.
Start with AP pelvis and lateral hip radiographs. Early films can be normal; later findings include patchy sclerosis and lucency, a subchondral crescent and head flattening. The pelvis view also compares the opposite hip. MRI without contrast is the reference study for suspected radiographically occult disease and maps the geographic necrotic segment and surrounding oedema. CT shows a subtle subchondral break and collapse geometry when radiography or MRI leaves a structural question.
Femoral-neck fracture and hip dislocation can tear or kink retinacular vessels, making displacement, reduction timing and residual perfusion important determinants.
High-dose or cumulative systemic corticosteroids alter lipid metabolism, marrow pressure, osteocyte viability and vascular function, with susceptibility varying markedly between patients.
Heavy alcohol exposure promotes marrow-fat enlargement and cellular toxicity; dyslipidaemia, pancreatitis and metabolic disease may contribute to microvascular compromise.
Sickle-cell disease, antiphospholipid syndrome, lupus, thrombophilia and decompression sickness impair microcirculation through occlusion, thrombosis or gas emboli.
Interrupted perfusion kills haematopoietic cells, fat cells and osteocytes within a defined subchondral segment while the articular cartilage initially survives.
Repair advances from viable margins through resorption and new bone formation, temporarily weakening the interface between necrotic and living trabeculae.
Repeated load exceeds the unrepaired anterosuperior segment, producing the crescent fracture that separates cartilage-bearing bone from deeper support.
Loss of spherical contour concentrates contact pressure, damages cartilage and progresses to secondary osteoarthritis with shortening, stiffness and mechanical pain.
Large lateral weight-bearing lesions face greater joint force and collapse risk than small medial foci, so location and extent influence preservation decisions.
Deep groin pain reproduced by internal rotation is an early high-yield hip finding, although it is not specific to osteonecrosis.
A credible systemic risk sharply increases suspicion when progressive load pain occurs despite initially normal radiographs.
A serpiginous low-signal rim surrounding necrotic subchondral marrow defines the characteristic extent and weight-bearing location.
A lucent line just beneath the articular surface represents structural fracture and marks transition toward irreversible collapse.
Flattening and step deformity demonstrate mechanical failure, usually shifting treatment from decompression toward arthroplasty.
Opposite-hip or other large-joint symptoms in systemic disease suggest additional osteonecrotic sites requiring directed examination and imaging.
Diffuse marrow oedema without a geographic necrotic rim, often in pregnancy or middle age, usually resolves without focal collapse.
An irregular fracture line and acute load pain in an older adult can mimic osteonecrosis but has different morphology and management implications.
Fever, acute severe restriction, inflammatory response and effusion require urgent aspiration because infection can destroy the joint rapidly.
Activity-related impingement, catching and preserved head architecture suggests alternative intra-articular mechanical pathology without characteristic necrotic marrow.
An aggressive mass, systemic features or diffuse marrow abnormality needs oncological or haematological assessment rather than routine hip-preservation surgery.
Subchondral failure flattens the load-bearing dome and sharply reduces the success of core decompression and other preservation procedures.
Incongruent contact damages acetabular and femoral cartilage, producing progressive stiffness, shortening and pain that commonly requires arthroplasty.
Systemic causes can affect the opposite hip, shoulders, knees or ankles, leaving unrecognised lesions at risk during rehabilitation.
Core decompression may not prevent progression, grafts can resorb and osteotomy can complicate later arthroplasty when selection or stage is unfavourable.
Alcohol, glucocorticoid disease and sickle-cell pathology continue affecting infection, wound, thrombosis and contralateral-joint risk beyond the local operation.
The joint surface can remain smooth over dead subchondral bone until the supporting trabeculae fracture and collapse.
Radiographically silent disease can still be large enough to merit preservation review, making early MRI clinically consequential.
It is not merely a radiology stage label; it signals loss of subchondral support and sharply worsens preservation prognosis.
A lateral weight-bearing lesion faces more force and collapse risk than an equally sized medial non-weight-bearing focus.
Systemic exposures affect both circulations, so a normal opposite radiograph does not always exclude early MRI disease.
Once flattening occurs, medicines and protected loading may ease symptoms but cannot recreate a spherical femoral head.
Reassuring from normal radiographs despite progressive groin pain and strong systemic risk.
Waiting for collapse before referring a symptomatic pre-collapse lesion to a hip-preservation service.
Using a staging label without documenting lesion size, lateral weight-bearing involvement and subchondral integrity.
Attributing an acutely febrile painful hip to osteonecrosis without urgent septic-arthritis assessment.
Stopping long-term corticosteroids abruptly in an attempt to reduce further bone risk.
Prescribing prolonged non-weight-bearing without strength, VTE and contralateral-joint planning.
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A transplant recipient previously exposed to high-dose corticosteroids has progressive groin pain and painful internal rotation. AP pelvis and lateral hip radiographs are normal. What is the next best test?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Stage by whether the head remains spherical, whether subchondral fracture exists and how much of the lateral weight-bearing surface is involved. Formal systems such as Ficat-Arlet or ARCO provide shared language but should not replace review of actual lesion size and position. Small medial asymptomatic lesions behave differently from large symptomatic anterosuperior lesions. MRI of the opposite hip is appropriate when systemic risk or planned surgery makes occult bilateral disease clinically relevant.
Immediately reduce load when symptoms escalate or a fracture line threatens collapse. Use crutches or a frame and provide analgesia while the preservation team reviews imaging. Protected loading alone may control symptoms in a small early lesion but does not reliably prevent progression. Physiotherapy maintains safe range, abductor strength and cardiovascular conditioning without repetitive impact. Assess VTE risk when mobility becomes substantially restricted.
Core decompression reduces intraosseous pressure and creates channels for vascular ingrowth; it is considered for selected symptomatic pre-collapse lesions. Surgeons may add autologous marrow concentrate, non-vascularised graft, vascularised fibular graft or other augmentation according to lesion and expertise, but evidence and indications differ. Osteotomy moves the necrotic segment away from the principal load zone in uncommon selected patients. Referral before the crescent stage preserves these choices.
Once the head has flattened and cartilage degeneration is symptomatic, preservation is unpredictable. Total hip arthroplasty restores geometry and generally provides reliable pain relief, with bearing and fixation chosen for age, bone, disease and activity. Previous osteotomy or graft surgery can complicate exposure. Sickle-cell disease needs coordinated transfusion, infection, hydration and thrombosis planning; chronic steroid exposure increases infection and adrenal risks; transplantation adds renal and immunosuppression constraints.
Reduce avoidable causal exposure without destabilising the underlying illness. Do not abruptly stop long-term corticosteroids; agree the lowest effective dose or steroid-sparing strategy with the responsible specialty. Support alcohol reduction and manage lipids or thrombophilia only for established indications. Bisphosphonates, statins, anticoagulants and vasodilators have been studied, but none is a universally accepted disease-reversing treatment. Follow symptoms and serial structure rather than using a blood marker as proof of viability.
Check combination products, alcohol, frailty and liver disease; analgesia must not encourage impact through a subchondral fracture.
Avoid broken skin and NSAID hypersensitivity, account for oral NSAIDs, renal and cardiovascular risk and follow pregnancy restrictions.
Never stop sustained treatment abruptly; provide steroid sick-day and card advice where indicated and coordinate infection, glucose, bone and perioperative management.