Orthopaedic Surgery - Hip Avascular Necrosis

Basics

Hip avascular necrosis, also called osteonecrosis of the femoral head, is a condition in which the bone and marrow of the femoral head die because of compromised blood supply.

As the necrotic subchondral bone loses structural strength, the femoral head may collapse. Once collapse occurs, the articular surface becomes incongruent and secondary degenerative arthritis commonly develops.

Classification

Several staging systems are used to describe the extent and progression of femoral-head osteonecrosis.

Ficat and Arlet Classification

Stage I

Plain radiographs are normal, but MRI or other advanced imaging demonstrates osteonecrosis.

There is no collapse of the femoral head.

Stage II

Radiographs show sclerotic or cystic changes within the femoral head, but the articular surface remains intact without subchondral collapse.

Stage III

A subchondral fracture develops beneath the articular surface.

This may appear radiographically as the characteristic crescent sign.

Femoral-head collapse is beginning.

Stage IV

The femoral head has collapsed sufficiently to produce secondary degenerative changes of the hip joint, including joint-space narrowing and acetabular involvement.

Steinberg Classification

The Steinberg system expands on the Ficat and Arlet classification by incorporating lesion size and more detailed stages.

Stage 0

Plain radiographs and bone scintigraphy are normal.

Stage I

Plain radiographs remain normal, but bone scintigraphy or MRI demonstrates osteonecrosis.

Stage II

Radiographs demonstrate sclerosis or cyst formation without subchondral collapse.

Severity can be estimated according to the percentage of the femoral head involved:

A: mild, less than approximately 20%.

B: moderate, approximately 20–40%.

C: severe, greater than approximately 40%.

Stage III

A subchondral fracture or crescent sign is present without substantial flattening of the femoral head.

Extent may be described as:

A: mild, less than approximately 15%.

B: moderate, approximately 15–30%.

C: severe, greater than approximately 30%.

Stage IV

Flattening of the femoral head has occurred, but there is not yet major joint-space narrowing or acetabular involvement.

Severity is based on the amount of surface involvement and depression.

Stage V

Femoral-head flattening is accompanied by joint-space narrowing or acetabular involvement, indicating secondary degenerative arthritis.

Lesion Size

One of the most important prognostic findings on MRI or radiographs is the size and location of the necrotic segment.

Small lesions located away from the primary weight-bearing surface are less likely to collapse than large lesions involving the superior weight-bearing portion of the femoral head.

Prevention

When possible, modifiable risk factors should be addressed.

Corticosteroids

Systemic corticosteroids should be used only when the anticipated benefit for the underlying medical condition outweighs the risk of treatment-related complications.

When long-term corticosteroid therapy is necessary, the lowest effective dose should be used under the direction of the treating medical team.

Alcohol

Heavy alcohol consumption is an important risk factor and should be avoided.

Tobacco

Smoking may adversely affect bone and vascular health and should be discontinued.

Epidemiology

Osteonecrosis of the femoral head occurs more commonly in younger and middle-aged adults than typical primary hip osteoarthritis.

Males are affected more frequently in many series.

Arthroplasty Burden

Osteonecrosis accounts for a meaningful proportion of hip arthroplasties, historically estimated at approximately 5–10% in some series.

Risk Factors

Important risk factors include:

Systemic corticosteroid use, heavy alcohol consumption, hip dislocation, displaced femoral neck fracture, previous surgical disruption of the hip blood supply, decompression sickness, thrombophilic disorders, antiphospholipid syndrome, systemic lupus erythematosus, sickle cell disease, HIV infection, and certain abnormalities of coagulation.

Trauma

Traumatic interruption of the blood supply to the femoral head is a major cause.

Important mechanisms include:

Hip dislocation, displaced femoral neck fracture, and surgical injury to femoral-head vascularity.

Hypercoagulable States

Abnormalities that promote thrombosis may compromise the femoral-head microcirculation.

Examples include:

Protein C or protein S deficiency, activated protein C resistance, antiphospholipid syndrome, and other thrombophilic disorders.

Hematologic Disease

Sickle cell disease is an important cause because repeated vascular occlusion can impair femoral-head perfusion.

Decompression Sickness

Caisson disease or decompression sickness in divers can lead to intravascular gas formation and compromise of osseous blood flow.

Genetics

There is no single inherited pattern for most cases of femoral-head osteonecrosis.

However, inherited thrombophilic disorders may predispose certain patients.

Etiology

The final common mechanism is interruption or compromise of blood flow to the femoral head, followed by ischemia and death of bone and marrow elements.

Corticosteroid-Associated Osteonecrosis

High cumulative exposure to systemic corticosteroids is a well-recognized nontraumatic cause.

The exact mechanism is multifactorial and may involve lipid metabolism, marrow pressure, vascular compromise, and altered bone-cell function.

Alcohol-Associated Osteonecrosis

Heavy alcohol consumption may contribute through lipid abnormalities, marrow changes, and impaired microvascular blood flow.

Gaucher Disease

Marrow infiltration and increased intraosseous pressure can impair circulation in disorders such as Gaucher disease.

Systemic Lupus Erythematosus

Patients with lupus have increased risk related to both the disease process and frequent corticosteroid exposure.

Associated Conditions

HIV infection has been associated with an increased risk of osteonecrosis, potentially related to multiple factors including medication exposure, metabolic abnormalities, and thrombophilia.

Diagnosis

Signs and Symptoms

Some patients are initially asymptomatic, especially in the early pre-collapse stages.

When symptoms develop, they usually reflect irritation or structural failure of the femoral head.

Groin Pain

The most common symptom is deep groin pain.

Pain may radiate into the buttock, thigh, or knee.

Limp

A limp is common as pain increases.

Functional Limitation

Patients may have difficulty walking, running, climbing stairs, or participating in sports.

Advanced disease can substantially impair normal ambulation.

History

Before femoral-head collapse, patients may report gradually increasing atraumatic hip pain.

The history should specifically address corticosteroid exposure, alcohol use, trauma, hematologic disease, autoimmune disease, diving history, and thrombophilic conditions.

After Collapse

Once collapse occurs, the symptoms increasingly resemble those of hip osteoarthritis, including persistent groin pain, stiffness, reduced walking tolerance, and progressive loss of motion.

Physical Examination

Gait

An antalgic limp is common.

Advanced disease may produce compensatory gait changes related to pain, weakness, or loss of hip motion.

Range of Motion

Hip range of motion should be compared with the contralateral side.

Internal Rotation

Painful and reduced internal rotation is a common finding, although it is not specific to osteonecrosis and may occur with many intra-articular hip disorders.

Flexion and Abduction

Flexion and abduction may also become limited as the disease progresses.

Laboratory Tests

There is no serum laboratory test that confirms osteonecrosis.

Coagulation Evaluation

In patients with unexplained or idiopathic osteonecrosis, especially when bilateral or multifocal, evaluation for an underlying thrombophilic disorder may be considered.

Imaging

Plain Radiographs

Initial imaging should include AP and lateral views of the affected hip, usually with an AP pelvis.

Radiographs are particularly useful for detecting:

Subchondral sclerosis, cysts, crescent sign, femoral-head flattening, and secondary arthritis.

Early Disease

Radiographs can remain normal in early osteonecrosis.

A normal radiograph does not exclude the diagnosis when clinical suspicion is high.

MRI

MRI is the most sensitive imaging study for detecting early femoral-head osteonecrosis.

It can identify disease before structural changes appear on radiographs.

T1-Weighted Imaging

On T1-weighted sequences, osteonecrosis often appears as a geographic or wedge-shaped area of low signal intensity.

T2-Weighted Imaging

Fluid-sensitive sequences may demonstrate surrounding high signal related to reactive change or bone marrow edema.

Double-Line Sign

A characteristic MRI finding is the double-line sign, in which a low-signal rim is bordered by a relatively high-signal inner line on T2-weighted images.

Bilateral Imaging

Because nontraumatic osteonecrosis can affect both hips, MRI evaluation of the contralateral femoral head may be appropriate when risk factors are substantial.

Pathological Findings

The final pathologic feature is necrosis of both the osseous trabeculae and marrow elements.

As healing attempts occur at the margin of the lesion, structurally weakened necrotic bone may fail under repetitive weight bearing.

This leads to subchondral fracture and eventual collapse.

Differential Diagnosis

Any process that produces hip pain can mimic osteonecrosis.

Important alternatives include:

Septic arthritis, proximal femoral osteomyelitis, soft-tissue abscess, femoral-neck or femoral-shaft stress fracture, early osteoarthritis, femoroacetabular impingement, and chondrolysis.

Treatment

General Principles

Treatment depends on:

Patient age, symptoms, lesion size, location, cause, degree of femoral-head collapse, and presence of secondary arthritis.

The major distinction is between pre-collapse disease, in which hip-preserving treatment may still be possible, and post-collapse disease, in which arthroplasty is often required.

Remove or Modify the Cause

Whenever possible, reversible risk factors should be addressed.

Corticosteroids

Unnecessary corticosteroid exposure should be reduced or discontinued under the supervision of the physician treating the underlying disease.

Alcohol

Heavy alcohol intake should be stopped.

Tobacco

Smoking cessation should be encouraged.

Activity Modification

Reducing repetitive impact loading may decrease symptoms during early disease.

However, activity modification alone generally does not reliably prevent progression of a large necrotic lesion.

Cane or Crutches

A cane held in the opposite hand can reduce load across the affected hip.

Two crutches may be used temporarily for greater unloading.

Physical Therapy

Physical therapy is useful primarily for:

Gait training, maintenance of motion, strengthening of surrounding musculature, and instruction in assistive-device use.

Forceful weight-bearing exercise over a symptomatic necrotic femoral head should be avoided.

Medication

There is no universally effective medication that reliably reverses established osteonecrosis.

Anticoagulation

Anticoagulation may be considered in carefully selected patients with a documented thrombophilic disorder and early-stage disease, under specialist supervision.

It is not routine treatment for all cases.

Surgery

Surgical treatment is tailored to the stage of disease and the patient’s age and functional demands.

In younger patients with pre-collapse disease, preservation of the native femoral head is emphasized whenever feasible.

Once substantial collapse and arthritis are present, total hip arthroplasty becomes the most reliable treatment.

Core Decompression

Core decompression involves drilling one or more channels into the necrotic area of the femoral head.

The procedure is intended to reduce intraosseous pressure, stimulate vascular ingrowth, and promote healing.

Indications

Core decompression is most effective in early pre-collapse disease with relatively small lesions.

Outcomes are less favorable once substantial subchondral collapse has occurred.

Success

Older series reported success rates of roughly 50–60%, although results vary considerably according to lesion size, stage, and patient selection.

Bone-Grafting Procedures

Various procedures have been developed to support the necrotic femoral head and introduce biologically active bone.

Vascularized Fibular Graft

A vascularized fibular graft may be used in selected young patients with pre-collapse or early-collapse disease.

The operation is technically demanding, and indications vary among centers.

Nonvascularized Bone Grafting

Other techniques include bone grafting through a core tract or through a limited opening in the femoral head or neck.

Trapdoor Procedure

The so-called trapdoor procedure provides direct access to the necrotic segment for removal of dead bone and grafting.

It is used selectively and is not a routine treatment.

Total Hip Arthroplasty

Total hip arthroplasty is the standard treatment for advanced femoral-head collapse with secondary arthritis and disabling symptoms.

Components

Modern total hip replacement typically uses a metal or ceramic femoral head articulating against a highly cross-linked polyethylene or ceramic bearing surface.

Metal-on-metal bearings are generally avoided in contemporary practice because of concerns regarding metal wear debris and adverse local tissue reactions.

Hip Resurfacing

Hip resurfacing has been used in selected younger patients, but indications are limited and the procedure is far less commonly performed than conventional total hip arthroplasty.

Follow-Up

Prognosis

The prognosis depends heavily on whether the femoral head has already collapsed.

Pre-Collapse Disease

Small lesions detected early may remain stable or respond to hip-preserving treatment.

Large lesions involving the weight-bearing dome have a substantially greater risk of progression.

Post-Collapse Disease

Once structural collapse is present, progression toward secondary arthritis is common.

Many symptomatic patients eventually require total hip arthroplasty.

Nonoperative Treatment

Nonoperative management alone frequently fails to prevent progression in symptomatic, structurally significant disease.

It may nevertheless be appropriate for small asymptomatic lesions or patients who are poor surgical candidates.

Complications of Hip-Preserving Procedures

Potential complications include:

Failure of the lesion to heal, continued femoral-head collapse, progression to arthritis, fracture, infection, and need for later arthroplasty.

Complications of Hip Surgery

General operative risks include:

Wound-healing problems, infection, blood loss, neurovascular injury, deep venous thrombosis, and pulmonary embolism.

Complications of Total Hip Arthroplasty

Potential complications include:

Dislocation, infection, periprosthetic fracture, nerve injury, venous thromboembolism, implant wear, osteolysis, and aseptic loosening.

Modern complication rates vary substantially according to patient factors, implant type, and length of follow-up.

Patient Monitoring

Patients with early-stage osteonecrosis should be followed clinically and radiographically for evidence of femoral-head collapse.

An initial follow-up interval of approximately 3–4 months during the first year may be appropriate in higher-risk lesions.

Thereafter, annual or symptom-driven follow-up may be used depending on stability.

Monitoring should assess:

Pain, gait, hip range of motion, lesion size, development of the crescent sign, femoral-head contour, and progression to secondary arthritis.