Avascular necrosis

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

Avascular necrosis, or osteonecrosis, is bone death caused by lost perfusion. In the hip it usually begins in the anterosuperior femoral head where load is highest. Pain is deep in groin, buttock or thigh and worsens with weight bearing; internal rotation becomes painful or restricted. Ask about fracture or dislocation, dose and timing of oral or intravenous glucocorticoids, heavy alcohol, sickle-cell disease, lupus and antiphospholipid disease, transplantation, HIV treatment, decompression exposure and symptoms in the opposite hip, shoulder or knee.

The diagnostic opportunity is greatest before articular collapse. Plain films may show patchy sclerosis, cysts, a crescent line or flattening but can remain normal for months. MRI detects the geographical necrotic segment and reactive marrow change earlier and identifies occult fracture, transient osteoporosis and malignant marrow disease. Systems such as Ficat or ARCO stage collapse, while lesion size and weight-bearing location add prognosis because a large superior segment is less likely to survive.

Management starts with timely referral, protected activity, mobility support and removal of modifiable causes without destabilising essential treatment. Observation may suit an incidental small low-risk lesion, but symptoms or a substantial weight-bearing lesion need specialist discussion. Core decompression reduces intraosseous pressure and promotes repair in selected pre-collapse disease; grafting and osteotomy are specialised alternatives. Once the joint surface collapses and disability is material, arthroplasty becomes the most predictable reconstruction.

Key points

Suspect femoral-head osteonecrosis in progressive groin or buttock pain with painful internal rotation, especially after glucocorticoids, heavy alcohol, trauma, sickle-cell disease, lupus or transplantation.
Obtain anteroposterior pelvis and lateral hip radiographs first, while recognising that early osteonecrosis can be radiographically invisible.
MRI without contrast is the preferred confirmatory test when suspicion persists and sensitively defines lesion location, size, bilateral disease and early subchondral fracture.
A crescent sign represents subchondral fracture; femoral-head flattening and joint-space change indicate collapse and secondary arthritis.
Refer promptly to hip-preservation or orthopaedic care before collapse; core decompression, sometimes with graft or augmentation, is considered for selected symptomatic early lesions.
After collapse, joint-preserving procedures are less predictable and total hip replacement usually provides the most reliable definitive relief for advanced symptomatic disease.
Reduce modifiable exposure but never stop long-term glucocorticoids abruptly; coordinate the lowest effective dose or steroid-sparing treatment with the responsible team.
No established routine medicine reverses osteonecrosis; analgesia and protected loading control symptoms while stage-specific surgical decisions are made.

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

Traumatic vascular disruption

Femoral-neck fracture, hip dislocation and operative injury can interrupt retinacular supply to the femoral head; displacement and delayed reduction increase risk.

Glucocorticoid and alcohol

High cumulative or intensive systemic glucocorticoids and sustained heavy alcohol exposure are major non-traumatic associations through lipid, marrow-pressure, coagulation and vascular effects.

Systemic vascular risk

Sickle-cell disease, lupus, antiphospholipid syndrome, transplantation, HIV, decompression sickness, Gaucher disease and pancreatitis can impair microvascular flow or increase intraosseous pressure.

Idiopathic and other sites

No cause is found in some adults; femoral head is commonest, but humeral head, knee, talus, scaphoid and lunate can also be affected.

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

1
Interrupted perfusion
Arterial injury, venous congestion, microthrombosis, fat-cell enlargement or sickled cells reduce flow through vulnerable terminal bone circulation.
2
Bone-cell death
Osteocytes and marrow elements die within the ischaemic segment; early articular cartilage remains intact because it receives nutrition from synovial fluid.
3
Repair-interface failure
Revascularisation and resorption occur at the boundary of dead and living bone, but replacement may not withstand repeated subchondral loading.
4
Collapse and arthrosis
Subchondral fracture creates the crescent sign, followed by flattening, incongruity and secondary osteoarthritis; preservation success falls markedly after collapse.

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

Early hip symptoms

Deep groin pain on standing, walking or pivoting may be intermittent initially; examination often first reveals pain at the end of internal rotation.

Established mechanical loss

Antalgic gait, reduced internal rotation and abduction, fixed flexion and rest pain develop as the necrotic segment fractures and flattens.

Steroid-associated pattern

Symptoms may develop months after intensive glucocorticoid exposure and are frequently bilateral, so a remote treatment course remains relevant.

Sickle-cell pattern

Recurrent marrow ischaemia can cause multifocal disease at younger age alongside chronic anaemia, pain crises and previous bone infarcts.

Upper-limb disease

Humeral-head osteonecrosis causes shoulder pain and stiffness; scaphoid or lunate necrosis presents with local wrist pain and collapse.

Collapse clue

A sudden increase in mechanical pain or new loss of motion can mark subchondral fracture even without external injury.

Red flags requiring action

A shortened or rotated limb, major trauma or sudden inability to bear weight requires urgent exclusion of femoral-neck fracture or hip dislocation.
Fever, marked warmth, severe pain with passive movement or immunosuppression requires urgent aspiration and treatment planning for septic arthritis.
Night pain, weight loss, a mass, cytopenias or a destructive lesion suggests malignancy, infection or marrow disease rather than isolated osteonecrosis.
New bilateral hip pain during high-dose glucocorticoids, after transplantation or with sickle-cell disease merits early MRI because symptoms can precede radiographic change.

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 hipFirst stepFirst line
Why
Exclude fracture, advanced osteoarthritis and destruction while identifying sclerosis, cysts, crescent fracture or flattening.
Interpretation and limitations
A normal film does not exclude early disease; collapse and incongruity shift management away from simple decompression toward reconstruction.
02
Preferred confirmatory MRIPreferred
Why
Detect early necrotic bone, define lesion size and weight-bearing location, assess subchondral integrity and examine both hips.
Interpretation and limitations
A serpiginous low-signal rim and inner high-signal line support osteonecrosis; marrow oedema alone is nonspecific and must be separated from fracture or transient osteoporosis.
03
CT for structural staging
Why
Show subtle subchondral fracture and three-dimensional collapse when films or MRI do not resolve surface integrity.
Interpretation and limitations
CT helps operative anatomy but is less sensitive than MRI for earliest marrow disease and should not replace MRI screening.
04
Alternative radionuclide scan
Why
Assess multifocal activity when MRI is contraindicated or cannot cover the clinical question.
Interpretation and limitations
Photopenia with surrounding uptake may occur but is less specific and sensitive than MRI; a negative study cannot confidently exclude early disease.
05
Cause-directed laboratory assessment
Why
Identify systemic disease and establish analgesic or operative safety rather than prove osteonecrosis biochemically.
Interpretation and limitations
Choose FBC, reticulocytes and haemoglobinopathy studies, renal and liver profile, lipids, autoimmune or antiphospholipid tests from the history; no blood test confirms the segment.
06
Urgent joint or fracture testing
Why
Exclude infection or structural injury when presentation is hot, systemic, traumatic or suddenly non-weight-bearing.
Interpretation and limitations
Aspiration with culture is needed for suspected sepsis; CT or MRI follows negative radiographs when occult femoral-neck fracture remains likely.

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

Hip osteoarthritis

Both cause groin pain and restricted internal rotation, but osteoarthritis shows joint-space loss and osteophytes while early osteonecrosis may have a normal film.

Transient osteoporosis or fracture

Transient marrow oedema and occult femoral-neck stress fracture produce acute pain; MRI morphology and clinical context distinguish them.

Septic or inflammatory arthritis

Effusion, synovial inflammation, fever or systemic inflammatory disease can mimic painful restriction; aspiration is urgent when infection remains possible.

Referred periarticular pain

Lumbar radiculopathy, greater-trochanteric pain and iliopsoas disease cause hip-region symptoms, but neurological findings or extra-articular provocation redirect localisation.

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

01First-line recognitionImage risk-associated mechanical painFirst stepFirst lineGroin or joint pain and restricted movement occur after a recognised vascular insult or systemic exposure.

1Exclude fracture, dislocation and septic arthritis from acuity, observations and examination, then document glucocorticoid, alcohol, trauma, haematological and systemic risks.
2Obtain orthogonal radiographs and proceed to MRI of both hips when films are normal or equivocal but clinical probability remains meaningful.
3Stage by collapse, size and load-bearing location, assess other high-risk joints and refer before advising prolonged observation.
4Provide a walking aid, adapt high-impact loading and maintain safe conditioning while diagnosis and surgical strategy are completed.

02Pre-collapse pathwayPreserve the articular surfaceMRI confirms symptomatic necrosis without femoral-head flattening or established secondary osteoarthritis.

1Arrange early specialist hip-preservation assessment because lesion size, position, symptoms and cause determine observation versus intervention.
2Discuss core decompression for selected disease, with grafting or biological augmentation only through experienced services and realistic uncertainty.
3Reduce alcohol and future steroid burden where possible, but taper glucocorticoids only under the prescribing team's plan.
4Use analgesia and protected loading for comfort without claiming that prolonged non-weight-bearing or medicine reliably revascularises bone.

03Collapse escalationReconstruct a failed surfaceEscalationSubchondral fracture, flattening, joint-space loss or persistent disabling pain makes preservation unlikely.

1Confirm symptoms arise from the collapsed joint and optimise anaemia, sickle-cell disease, infection, thrombosis, alcohol, bone health and cardiorespiratory risk.
2DefinitiveDiscuss total hip arthroplasty as the usual definitive reconstruction for advanced femoral-head disease, tailored to age, activity and anatomy.
3Continue mobility, strength and falls support while awaiting surgery and reassess sudden deterioration for complete fracture or progression.

04Systemic-risk modificationPrevent further skeletal injuryDisease is associated with glucocorticoids, alcohol, sickle-cell, lupus, antiphospholipid disease or transplantation.

1Share the diagnosis with the responsible specialist and seek the lowest effective future glucocorticoid exposure or steroid-sparing regimen without abrupt withdrawal.
2Offer alcohol support, optimise smoking and lipids, and ensure sickle-cell or thrombotic disease follows its evidence-based pathway rather than empirical anticoagulation.
3Evaluate contralateral and new joint symptoms promptly because systemic-risk disease may be bilateral or multifocal.

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

Reduces mechanical pain but does not restore perfusion or prevent femoral-head collapse.

Naproxen

Use 250–500 mg orally twice daily with food for the shortest period needed while definitive assessment proceeds; add gastroprotection when indicated and stop without functional benefit.

Avoid active gastrointestinal bleeding, severe kidney impairment and decompensated heart failure; assess anticoagulants and blood pressure. Avoid from 20 weeks of pregnancy unless necessary and from 28 weeks entirely.

Provides non-NSAID relief during imaging, mobility adaptation and surgical planning without altering the necrotic process.

Paracetamol

Take 500–1,000 mg orally when needed at intervals of at least four hours, never exceeding 4,000 mg in 24 hours in a suitable adult; lower the ceiling for low weight, malnutrition, frailty or liver disease.

Check combination products and alcohol or liver risk; regular treatment should be reviewed rather than continued automatically when pain remains severe or function worsens.

Limits further exposure where steroids contributed while preserving control of the original disease.

Glucocorticoid risk modification

No universal taper is safe; the responsible specialist reduces to the lowest disease-controlling dose using an indication-specific schedule, and long-term treatment must never be stopped abruptly.

Rapid reduction can cause adrenal insufficiency or inflammatory relapse; osteonecrosis does not justify withholding life-saving steroids, and pregnancy, infection or surgery requires specialist planning.

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

Subchondral collapse

Structural failure flattens the femoral head and creates incongruity, rapidly reducing feasibility of core decompression or other preservation procedures.

Secondary osteoarthritis

Cartilage breakdown follows loss of smooth joint contour, causing persistent pain, stiffness and disability that often ultimately requires arthroplasty.

Multifocal disease

Systemic exposures can affect both hips and other joints asynchronously, so symptoms elsewhere and the contralateral side require deliberate assessment.

Mobility and treatment harm

Pain-related immobility causes weakness, thrombosis and dependence, while prolonged NSAIDs, opioids or abrupt glucocorticoid withdrawal create secondary harm.

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

Track walking distance, night pain, internal rotation and analgesic requirement; a sudden step-change may indicate subchondral fracture or collapse.
Use follow-up radiographs or MRI at intervals chosen for lesion stage and management intent rather than repeating scans without a decision consequence.
Assess the opposite hip and other symptomatic joints in systemic-risk disease, especially after glucocorticoids or in sickle-cell disease.
Review NSAID toxicity, mobility, thrombosis risk, work and driving limitations while treatment is pending.
After preservation surgery, follow protected loading and rehabilitation instructions and image recurrent pain for progression.
After arthroplasty, monitor infection, dislocation and prosthesis outcomes while continuing management of the systemic cause.

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

Normal radiograph is early

Symptoms can precede radiographic sclerosis or collapse; a normal film in a high-risk patient is a reason for MRI, not dismissal.

Bilateral is often unequal

Both femoral heads may be affected at different stages, so contralateral imaging can reveal a preservation opportunity before severe symptoms.

Crescent means fracture

The subchondral crescent line marks structural failure beneath the articular surface and a poorer prognosis for simple decompression.

Risk can be remote

Osteonecrosis may appear after glucocorticoids have been reduced, so a past intensive course remains important.

Stage drives surgery

Core decompression aims to preserve an uncollapsed surface, whereas arthroplasty replaces a failed one; early referral preserves choice.

11Common pitfallsFrequent interpretation and management errors.

01
Do not exclude osteonecrosis because initial radiographs are normal when risk exposure and deep mechanical pain make it plausible.
02
Do not call all hip-region pain osteonecrosis; septic arthritis, occult fracture, transient osteoporosis, malignancy and spinal referral require distinction.
03
Do not delay orthopaedic referral until collapse is obvious because the preservation window may close during observation.
04
Do not claim protected weight bearing or bisphosphonate is proven to reverse the lesion; evidence for routine disease-modifying medicine is inadequate.
05
Do not abruptly stop systemic glucocorticoids after identifying them as a risk factor.
06
Do not investigate only the symptomatic hip in systemic-risk disease without asking about other joints.