Avascular necrosis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

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.

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.

Key points

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.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Traumatic vascular interruption

Femoral-neck fracture and hip dislocation can tear or kink retinacular vessels, making displacement, reduction timing and residual perfusion important determinants.

Glucocorticoid exposure

High-dose or cumulative systemic corticosteroids alter lipid metabolism, marrow pressure, osteocyte viability and vascular function, with susceptibility varying markedly between patients.

Alcohol and metabolic risk

Heavy alcohol exposure promotes marrow-fat enlargement and cellular toxicity; dyslipidaemia, pancreatitis and metabolic disease may contribute to microvascular compromise.

Haematological and vascular causes

Sickle-cell disease, antiphospholipid syndrome, lupus, thrombophilia and decompression sickness impair microcirculation through occlusion, thrombosis or gas emboli.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Marrow and osteocyte death
Interrupted perfusion kills haematopoietic cells, fat cells and osteocytes within a defined subchondral segment while the articular cartilage initially survives.
2
Creeping substitution
Repair advances from viable margins through resorption and new bone formation, temporarily weakening the interface between necrotic and living trabeculae.
3
Subchondral stress fracture
Repeated load exceeds the unrepaired anterosuperior segment, producing the crescent fracture that separates cartilage-bearing bone from deeper support.
4
Articular collapse
Loss of spherical contour concentrates contact pressure, damages cartilage and progresses to secondary osteoarthritis with shortening, stiffness and mechanical pain.
5
Lesion-size effect
Large lateral weight-bearing lesions face greater joint force and collapse risk than small medial foci, so location and extent influence preservation decisions.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Painful internal rotation

Deep groin pain reproduced by internal rotation is an early high-yield hip finding, although it is not specific to osteonecrosis.

Steroid or alcohol exposure

A credible systemic risk sharply increases suspicion when progressive load pain occurs despite initially normal radiographs.

Geographic MRI lesion

A serpiginous low-signal rim surrounding necrotic subchondral marrow defines the characteristic extent and weight-bearing location.

Subchondral crescent

A lucent line just beneath the articular surface represents structural fracture and marks transition toward irreversible collapse.

Loss of sphericity

Flattening and step deformity demonstrate mechanical failure, usually shifting treatment from decompression toward arthroplasty.

Multifocal phenotype

Opposite-hip or other large-joint symptoms in systemic disease suggest additional osteonecrotic sites requiring directed examination and imaging.

Red flags requiring action

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.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
First-line AP pelvis and lateral hip radiographsFirst stepFirst line
Why
Assess shape, sclerosis, crescent fracture, collapse, arthritis and an alternative lesion while comparing both hips.
Interpretation and limitations
Normal radiographs do not exclude early osteonecrosis; crescent or flattening establishes structural progression.
02
MRI without intravenous contrast
Why
Confirm radiographically occult disease and define size, lateral location, marrow response, bilaterality and subchondral integrity.
Interpretation and limitations
This is the reference diagnostic study; large anterosuperior involvement and fracture imply higher collapse risk.
03
CT for subchondral architecture
Why
Clarify a subtle fracture, quantify loss of head contour and provide three-dimensional operative anatomy.
Interpretation and limitations
CT adds cortical detail but is not the preferred screening test when early marrow disease is the question.
04
Cause-directed laboratory assessment
Why
Identify sickle-cell disease, inflammatory or thrombotic disorder, lipid abnormality and treatment-safety constraints.
Interpretation and limitations
No blood test diagnoses osteonecrosis; select tests from exposure, ethnicity, systemic symptoms and operative planning.
05
Joint aspiration when infection is plausible
Why
Exclude septic arthritis before preservation or arthroplasty in an acutely inflamed hip.
Interpretation and limitations
Obtain image-guided synovial fluid for cell count, crystals and cultures before antibiotics when the patient is stable enough, without delaying sepsis treatment.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Transient osteoporosis of hip

Diffuse marrow oedema without a geographic necrotic rim, often in pregnancy or middle age, usually resolves without focal collapse.

Subchondral insufficiency fracture

An irregular fracture line and acute load pain in an older adult can mimic osteonecrosis but has different morphology and management implications.

Septic arthritis

Fever, acute severe restriction, inflammatory response and effusion require urgent aspiration because infection can destroy the joint rapidly.

Femoroacetabular or labral disease

Activity-related impingement, catching and preserved head architecture suggests alternative intra-articular mechanical pathology without characteristic necrotic marrow.

Malignancy or marrow infarction

An aggressive mass, systemic features or diffuse marrow abnormality needs oncological or haematological assessment rather than routine hip-preservation surgery.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Traumatic emergencyRestore alignment and perfusion opportunityFirst stepHip dislocation or displaced femoral-neck fracture creates immediate vascular risk.

1Use trauma ABCDE and document distal vascular and sciatic-nerve function before and after intervention.
2Arrange urgent reduction or fracture surgery through the specialist pathway rather than waiting for elective MRI.
3Confirm concentric reduction and associated fracture with post-reduction imaging as indicated.
4Explain later osteonecrosis surveillance even after technically successful acute treatment.

02DiagnosticFind disease before collapseProgressive hip pain and risk factors persist despite normal or non-diagnostic radiographs.

1AlternativeObtain AP pelvis and lateral hip imaging and assess the opposite side and alternative diagnoses.
2Proceed to MRI without contrast when suspicion remains and define lesion size, location and subchondral integrity.
3Use CT only for a specific cortical or collapse question and aspirate urgently if infection remains plausible.
4Refer symptomatic confirmed disease promptly rather than scheduling serial primary-care radiographs alone.

03Pre-collapsePreserve the femoral headSymptoms and MRI confirm osteonecrosis while the articular surface remains structurally intact.

1Reduce impact and protect loading when pain is substantial while maintaining safe strength and range.
2Modify alcohol and corticosteroid exposure through the responsible clinical team without abrupt steroid withdrawal.
3Obtain hip-preservation review for core decompression and lesion-specific graft or augmentation choices.
4EscalationMonitor both hips and escalate immediately for sudden pain suggesting a new subchondral fracture.

04Post-collapseRestore joint mechanicsFlattening, subchondral failure and secondary arthritis cause persistent functional limitation.

1Use aids, analgesia and activity adaptation as a bridge rather than presenting them as structural reversal.
2Plan total hip arthroplasty according to age, bone quality, deformity, previous preservation surgery and goals.
3Optimise sickle-cell, steroid, transplant, infection and thrombosis risks with relevant specialties.
4Rehabilitate the operated hip while assessing contralateral and multifocal disease that could limit loading.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Supports protected transfers and rehabilitation while definitive stage-directed assessment is arranged.

Paracetamol for symptomatic bridge

Take 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.

May reduce peripheral pain with less systemic exposure, although it cannot penetrate deeply enough to modify femoral-head necrosis.

Topical diclofenac for accessible referred pain

Apply 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.

Reduces further avoidable exposure while preventing adrenal crisis or relapse of the condition that required corticosteroid treatment.

Systemic corticosteroid exposure review

Do not prescribe a fixed osteonecrosis taper; the originating team should use the lowest effective disease-controlling dose and a safe individual reduction schedule where possible.

Never stop sustained treatment abruptly; provide steroid sick-day and card advice where indicated and coordinate infection, glucose, bone and perioperative management.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Femoral-head collapse

Subchondral failure flattens the load-bearing dome and sharply reduces the success of core decompression and other preservation procedures.

Secondary osteoarthritis

Incongruent contact damages acetabular and femoral cartilage, producing progressive stiffness, shortening and pain that commonly requires arthroplasty.

Bilateral and multifocal disease

Systemic causes can affect the opposite hip, shoulders, knees or ankles, leaving unrecognised lesions at risk during rehabilitation.

Procedure failure

Core decompression may not prevent progression, grafts can resorb and osteotomy can complicate later arthroplasty when selection or stage is unfavourable.

Exposure-related systemic harm

Alcohol, glucocorticoid disease and sickle-cell pathology continue affecting infection, wound, thrombosis and contralateral-joint risk beyond the local operation.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Track pain at rest and on loading, walking distance, internal rotation and new night or sudden fracture-like symptoms.
Repeat radiographs or MRI at specialist-defined intervals according to lesion size, symptoms and chosen preservation strategy.
Assess the opposite hip and other symptomatic joints in systemic-risk disease rather than assuming all limitation is unilateral.
After decompression or grafting, follow load restrictions, wound, thrombosis, radiographic collapse and functional progression.
After arthroplasty, monitor infection, dislocation, fixation and rehabilitation with extra planning for sickle-cell or immunosuppression.
Review alcohol and corticosteroid changes with the responsible specialty and document that exposure reduction remains medically safe.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Cartilage initially survives

The joint surface can remain smooth over dead subchondral bone until the supporting trabeculae fracture and collapse.

MRI changes the window

Radiographically silent disease can still be large enough to merit preservation review, making early MRI clinically consequential.

The crescent is a fracture

It is not merely a radiology stage label; it signals loss of subchondral support and sharply worsens preservation prognosis.

Location predicts mechanics

A lateral weight-bearing lesion faces more force and collapse risk than an equally sized medial non-weight-bearing focus.

Risk can be bilateral

Systemic exposures affect both circulations, so a normal opposite radiograph does not always exclude early MRI disease.

No tablet restores contour

Once flattening occurs, medicines and protected loading may ease symptoms but cannot recreate a spherical femoral head.

11Common pitfallsFrequent interpretation and management errors.

01
Reassuring from normal radiographs despite progressive groin pain and strong systemic risk.
02
Waiting for collapse before referring a symptomatic pre-collapse lesion to a hip-preservation service.
03
Using a staging label without documenting lesion size, lateral weight-bearing involvement and subchondral integrity.
04
Attributing an acutely febrile painful hip to osteonecrosis without urgent septic-arthritis assessment.
05
Stopping long-term corticosteroids abruptly in an attempt to reduce further bone risk.
06
Prescribing prolonged non-weight-bearing without strength, VTE and contralateral-joint planning.