Hip Avascular Necrosis (Osteonecrosis)
Avascular necrosis of the hip is death of bone tissue in the femoral head caused by interruption of its blood supply. Without treatment the bone weakens and collapses, destroying the joint surface. Mr Shakir Hussain, Consultant Orthopaedic Surgeon at the Royal Orthopaedic Hospital Birmingham, treats hip avascular necrosis with hip replacement, and with hip resurfacing in carefully selected pre-collapse cases.
What is hip avascular necrosis?
Hip avascular necrosis is death of bone tissue in the femoral head caused by interruption of its blood supply. Without restoration of perfusion, the bone weakens and the articular surface eventually collapses. It is a circulatory disorder, not a wear-and-tear disorder, and it tends to affect younger patients than osteoarthritis.
The hip is a ball-and-socket joint formed by the femoral head (the top of the thigh bone) and the acetabulum (the socket in the pelvis). The femoral head depends on a delicate network of small blood vessels for its survival. If those vessels are damaged or blocked, the bone cells die in a process called osteonecrosis.
Once the bone has died, the subchondral plate that supports the cartilage above it loses structural strength. Microfractures accumulate, then the bone collapses inward and the smooth spherical shape of the femoral head is lost. Cartilage on top fails secondarily, producing severe secondary arthritis.
Avascular necrosis is the third most common indication for hip replacement in patients under 50 in the UK. Unlike osteoarthritis, which usually progresses over decades, AVN can advance from no symptoms to femoral head collapse within a year or two of onset.
What does hip avascular necrosis feel like?
Hip avascular necrosis typically causes groin pain that has a more abrupt onset than osteoarthritis, worsens with weight-bearing, and limits internal rotation of the hip. Many patients are in their 30s, 40s, or 50s. Once the femoral head collapses, mechanical symptoms such as catching, locking, or sudden giving-way develop.
Early-stage AVN can be silent. Many patients are diagnosed only when an MRI is ordered for unexplained groin pain or after a high-risk drug exposure such as a long steroid course. As the necrotic bone progresses toward collapse, symptoms become more pronounced.
Groin pain with sudden onset
Deep groin or front-of-thigh ache that often appears over weeks rather than years. Patients can frequently remember roughly when the pain started.
Pain on weight-bearing
Pain rising from a chair, climbing stairs, or pushing off the leg when walking. The femoral head is most stressed in these positions, where weakened bone hurts.
Restricted internal rotation
A classic examination finding. Rolling the affected leg inward at the hip is painful and limited compared with the other side, often the earliest physical sign.
Pain referred to the knee
Like hip arthritis, AVN can refer pain down to the knee or thigh. The true source remains the hip joint and requires hip imaging to identify.
Mechanical symptoms after collapse
Once the femoral head collapses, patients describe catching, locking, or sudden episodes of the leg giving way. These signal that the joint surface has failed.
Rest and night pain
Unlike osteoarthritis where rest pain is a late sign, AVN frequently causes rest and night pain even in earlier stages, because the underlying bone itself is failing.
What causes hip avascular necrosis?
Hip avascular necrosis develops when the small blood vessels supplying the femoral head are damaged or blocked, starving the bone of oxygen. The two leading causes are long-term high-dose corticosteroid therapy and heavy alcohol consumption, which together account for more than 65 per cent of non-traumatic cases. A substantial minority remain idiopathic with no identifiable cause.
Several mechanisms can interrupt the femoral head's blood supply. Trauma such as a femoral neck fracture or hip dislocation can tear the small arteries directly. Other causes work indirectly: corticosteroids and alcohol both increase fat globules in the small vessels, blocking them; sickle cell disease causes red blood cells to sickle in the small vessels; and decompression sickness produces nitrogen bubbles that obstruct circulation. Idiopathic AVN, where no cause is found, is the most common type seen in young adults requiring hip replacement.
The most important risk factors are:
- Long-term high-dose corticosteroid use. Oral or intravenous steroids for transplant, asthma, autoimmune disease, or chemotherapy support. Risk rises with both dose and cumulative duration. Brief, low-dose or single intra-articular injections are not the typical trigger.
- Heavy alcohol consumption. Sustained heavy drinking, not occasional use, raises the risk of AVN through changes in fat metabolism and small-vessel function.
- Sickle cell disease. Sickled red blood cells block the small vessels that feed the femoral head, particularly during sickle crises.
- Prior hip trauma or dislocation. A fracture of the femoral neck or a traumatic hip dislocation can tear the blood vessels that supply the femoral head.
- Systemic lupus erythematosus. Both the disease itself and the steroids used to treat it contribute to AVN risk.
- Organ transplantation. The combination of steroids and immunosuppressants raises risk significantly.
- HIV antiretroviral therapy. Particularly older drug regimens; risk is lower with modern medications.
- Chemotherapy. Several agents and the supportive steroids used with them contribute to AVN risk.
- Decompression sickness. Divers and high-pressure workers exposed to rapid decompression.
How is hip avascular necrosis diagnosed?
MRI is the gold-standard imaging test for hip avascular necrosis, with sensitivity and specificity approaching 99 per cent. X-rays are often normal in early disease and can miss AVN until femoral head collapse has begun, so MRI is essential when AVN is suspected. The disease is staged using the Ficat-Arlet system (I to IV) or the modern ARCO 2019 classification, which guides treatment.
Diagnosis begins with a careful clinical history and examination. Mr Hussain will ask about steroid exposure, alcohol use, family history of AVN, prior hip injury, and any underlying medical conditions. Examination tests the hip's range of motion, particularly internal rotation in flexion, the classic painful and restricted movement of AVN. The FABER and Stinchfield resisted straight-leg raise tests help distinguish hip-origin from spine-origin pain.
Imaging is then used to confirm the diagnosis and stage the disease:
- MRI. The gold-standard imaging for AVN, sensitive and specific even in pre-radiographic disease. The characteristic finding is a serpiginous low-signal demarcation line on T1, and a double-line sign on T2 imaging.
- AP pelvic X-ray. Often normal in early AVN. As disease progresses it shows sclerosis, subchondral cysts, the crescent sign (a thin lucency under the joint surface signalling impending collapse), and eventually femoral head flattening.
- Ficat-Arlet staging. Stage I (normal X-ray, MRI changes only), Stage II (sclerosis and cysts but spherical head), Stage III (subchondral crescent sign, head still spherical), Stage IV (collapse with secondary osteoarthritis).
- ARCO 2019 classification. The modern equivalent, which subdivides stage III by the depth of femoral head depression (IIIA below 2 mm, IIIB at 2 mm or more), helping decide whether joint preservation is still viable.
- CT. Useful to quantify subtle collapse when MRI is contraindicated or to plan complex surgery.
Can hip avascular necrosis be treated without a hip replacement?
Pre-collapse avascular necrosis (Ficat I and II) can sometimes be treated with joint-preserving surgery rather than hip replacement. The most evidence-based option is core decompression, often combined with bone marrow aspirate concentrate or expanded mesenchymal stem cells. Once the femoral head has collapsed (Ficat III or IV), joint preservation is no longer effective and hip replacement becomes the right choice.
The natural history of clinically symptomatic AVN is progression to femoral head collapse in the great majority of cases. Drugs alone rarely halt the disease, but in early stages (before collapse) several interventions can slow progression and delay or avoid hip replacement.
- Core decompression with biological augmentation. The workhorse joint-preserving operation for pre-collapse AVN. A small channel is drilled into the necrotic segment of bone to relieve pressure and stimulate healing. Modern practice combines this with bone marrow aspirate concentrate or expanded mesenchymal stem cells, which a 2024 network meta-analysis showed significantly outperforms core decompression alone in preventing progression to hip replacement.
- Vascularised fibular grafting. A more involved option where a section of fibula with its own blood supply is transplanted into the femoral head to provide structural support and revive the bone. About 75 per cent of these procedures survive 10 years in selected pre-collapse hips.
- Bisphosphonates. Drugs that reduce bone resorption. Useful in small lesions affecting less than 10 to 15 per cent of the femoral head, but not disease-modifying on their own.
- Removing the underlying cause. Where possible, stopping high-dose steroids, reducing alcohol intake, or treating sickle cell disease can slow progression and is part of any management plan.
- Activity modification. Reducing weight-bearing activity in the affected hip can ease pain while a treatment plan is decided.
Joint preservation only works before the femoral head collapses. Once the head has flattened (Ficat III with crescent sign through to Ficat IV), hip replacement is the only durable solution. The timing of the decision is critical, which is why early MRI and accurate staging matter so much.
If you take prescribed medication, particularly blood-thinners, anti-inflammatories, or rheumatology drugs, please review Mr Hussain's patient guide on medications to pause before hip or knee surgery as you approach a surgical decision.
When should I consider hip replacement for AVN?
Hip replacement is the right choice once the femoral head has collapsed (Ficat stage III with crescent sign, or stage IV with established secondary arthritis). Earlier than that, joint-preserving surgery can sometimes delay or avoid replacement. The shift from joint preservation to hip replacement happens at the moment of collapse, which is why MRI staging is so important.
The treatment decision in AVN turns on staging in a way that hip arthritis does not. Pre-collapse AVN can sometimes be preserved; post-collapse AVN cannot. The role of the consultation is to determine which side of that line your hip sits on.
Markers that point toward hip replacement rather than joint preservation:
- MRI or X-ray showing the subchondral crescent sign or actual femoral head collapse
- Ficat stage III with depression of 2 millimetres or more (ARCO stage IIIB)
- Ficat stage IV with established secondary arthritis
- Pain that wakes you at night, more than twice a week
- Mechanical symptoms such as catching, locking, or sudden giving way
- Walking distance reduced to under 100 metres before needing to stop
- Joint-preserving surgery already attempted without benefit
- A necrotic segment so large that joint preservation has no realistic chance of working
Many AVN patients are in their 30s, 40s, or 50s. Delaying hip replacement past the point of collapse achieves nothing, and continued mechanical loading on a collapsed femoral head accelerates damage to the acetabulum, making the eventual replacement more complex.
Private consultations with Mr Hussain are available at the Royal Orthopaedic Hospital, Priory Hospital Edgbaston, and Harborne Hospital. See the private consultation and surgery fees page for self-pay pricing and the list of recognised insurers, or book a consultation directly.
What surgical options are available for hip avascular necrosis?
For advanced avascular necrosis with femoral head collapse (Ficat stages III and IV), total hip replacement is the standard treatment. Hip resurfacing is generally not appropriate for advanced AVN because necrotic bone in the femoral head undermines the resurfacing cap. Resurfacing is occasionally used for very small pre-collapse lesions where less than one-third of the femoral head is affected and bone quality is preserved.
Mr Hussain trained in both hip replacement and hip resurfacing, and he is one of relatively few UK surgeons who can offer either approach. For AVN specifically, the staging and the size of the necrotic lesion drive the surgical choice.
Total Hip Replacement
The dead femoral head and the damaged acetabular surface are both replaced with prosthetic components. The metal or ceramic ball on a stem bypasses the necrotic bone entirely, removing the source of pain and restoring a smooth bearing surface.
- The standard treatment for Ficat stage III and IV AVN
- Works equally well whatever the original cause of AVN
- Modern implants designed for 25 to 30 year lifespan
- 10-year survivorship in AVN patients around 92 per cent, comparable to osteoarthritis
- 15-year survivorship of 94 per cent in patients aged under 30 with osteonecrosis
Hip Resurfacing
Hip resurfacing relies on a healthy femoral head as the seat of the cap. In advanced AVN the necrotic dome of the head undermines fixation, so resurfacing is generally not appropriate. It is occasionally suitable for very small pre-collapse lesions.
- Considered only when less than one-third of the femoral head is affected
- Requires good bone quality and no significant cysts
- Reserved for pre-collapse (Ficat stage I or II) disease
- Not appropriate for stage III or IV AVN with collapse
- Patient selection is more restrictive than for osteoarthritis
For a deeper comparison of the two techniques across recovery, return to sport, and implant choice, read Mr Hussain's patient guide on hip resurfacing versus total hip replacement. Patients with AVN should expect Mr Hussain to recommend hip replacement in almost all cases of established disease.
How successful is hip replacement for avascular necrosis?
Total hip replacement gives excellent results in AVN patients, broadly similar to those seen in osteoarthritis at the same follow-up. Survivorship is around 92 per cent at 10 years in AVN cohorts, and modern UK registry data show implant longevity continuing to improve with each generation of bearings and fixation techniques.
Earlier concerns that AVN patients did worse after hip replacement than osteoarthritis patients have been overtaken by modern technique and implants. Contemporary matched cohort studies show comparable 10-year survival. The main caveat is age: AVN patients are typically younger than osteoarthritis patients, so the cumulative lifetime exposure to revision risk is higher, and decisions about bearing surface (ceramic-on-ceramic, ceramic-on-polyethylene) reflect that.
Expertise in hip avascular necrosis treatment in Birmingham
Consultant at the Royal Orthopaedic Hospital
Mr Hussain practises at the Royal Orthopaedic Hospital Birmingham, one of the largest specialist orthopaedic hospitals in Europe, alongside Priory Hospital Edgbaston and Harborne Hospital.
3,000+ arthroplasty cases
From a total of more than 5,000 procedures performed, giving the operative volume and case complexity required for consistently excellent outcomes. Read more about Mr Hussain's training and background.
British Hip Society Travelling Fellowship
Trained at ENDO-Klinik Hamburg under Professor Thorsten Gehrke and Professor Mustafa Citak, the international reference centre for complex hip surgery.
Both hip replacement and hip resurfacing
Many surgeons offer only one technique. Mr Hussain trained in both, allowing the choice to be tailored to the individual patient rather than to a single technique.
Doctify Outstanding Patient Experience 2024, 2025, and 2026
Awarded in three consecutive years, recognising consistently high patient-reported outcomes and communication.
4.98 out of 5 from verified reviews on Doctify. Outstanding Patient Experience Award 2024, 2025, and 2026.
Frequently asked questions about hip avascular necrosis
For more questions about surgery, recovery, fees, and what to expect, see the full frequently asked questions page or read recent patient testimonials.