Avascular Necrosis (AVN) of the Hip: Causes, Symptoms, and Treatment

What Is Avascular Necrosis?

Avascular necrosis (AVN) — also called osteonecrosis or aseptic necrosis — is the death of bone tissue caused by a loss of blood supply. In the hip, it most commonly affects the femoral head (the "ball" at the top of the thighbone). Without adequate blood flow, bone cells die, the bone weakens, and the rounded surface of the femoral head eventually collapses. Once the joint surface loses its smooth contour, the cartilage above it fails and severe arthritis follows.

AVN of the hip frequently strikes younger adults — most commonly between ages 30 and 50 — which makes it particularly significant, since a collapsed femoral head in a young, active person often leads to hip replacement decades earlier than would otherwise be expected. It can affect both hips in 40–80% of cases, so the opposite hip is always evaluated.

Joint Anatomy and Blood Supply

The femoral head depends on a delicate and somewhat fragile blood supply:

Medial femoral circumflex artery: Supplies the majority of blood to the femoral head via the retinacular vessels
Lateral femoral circumflex artery: Contributes a smaller portion
Artery of the ligamentum teres: A small vessel running through the ligament attaching the femoral head to the socket; minor in adults

Because the femoral head receives blood through a limited number of end-arteries with little collateral backup, any interruption — from trauma, clots, fat globules, or vessel inflammation — can starve the bone. The dead bone (the "necrotic segment") cannot repair itself normally, and under the repetitive load of walking it eventually fractures beneath the cartilage and collapses.

Causes and Risk Factors

AVN is broadly divided into traumatic and non-traumatic causes.

Traumatic causes:

Femoral neck fracture: Disrupts the retinacular vessels directly
Hip dislocation: Stretches or tears the blood supply

Non-traumatic causes and risk factors:

Corticosteroids: High-dose or prolonged steroid use is one of the most common causes; thought to alter fat metabolism and cause fat emboli
Alcohol: Heavy, chronic alcohol use is a leading non-traumatic cause
Sickle cell disease: Sickled cells obstruct the small vessels of the femoral head
Caisson disease (the "bends"): Nitrogen bubbles block blood flow in divers
Systemic lupus and other autoimmune disease: Often combined with steroid treatment
Gaucher disease: Lipid-laden cells crowd out the marrow
Radiation and chemotherapy
Clotting disorders (thrombophilia)
Organ transplantation: Linked to high-dose immunosuppression
Idiopathic: In many patients no cause is ever identified

Symptoms

Groin pain: The most common early symptom; deep groin pain (rather than lateral hip or buttock pain) points to true joint pathology
Pain with weight-bearing: Worse with standing and walking, often relieved by rest in early stages
Pain at rest and at night: As the disease advances, pain becomes constant
Limited range of motion: Particularly internal rotation and abduction
Limping (antalgic gait): To offload the painful hip
Pain radiating to the thigh, buttock, or knee

Crucially, AVN is often painless in its earliest stage — it may be detected only incidentally on imaging done for another reason or when the opposite hip becomes symptomatic.

Staging

AVN is staged to guide treatment. The widely used Ficat and Arlet classification describes the progression:

Stage I: Normal X-ray; changes visible only on MRI. Bone is dying but structurally intact.
Stage II: X-ray shows bone density changes (sclerosis and cysts) but the femoral head remains round.
Stage III: The "crescent sign" appears — a subchondral fracture — and the femoral head begins to collapse and flatten.
Stage IV: The head is collapsed, the joint space narrows, and secondary arthritis develops in the socket.

The distinction between pre-collapse (Stages I–II) and post-collapse (Stages III–IV) is the single most important factor in choosing treatment, because joint-preserving surgery is far more effective before the femoral head collapses.

Diagnosis

Physical examination:

Pain and guarding with hip motion, especially internal rotation
Reduced range of motion
Antalgic gait

X-ray: Standing AP pelvis and lateral hip X-rays. Early AVN is often invisible on X-ray; later findings include sclerosis, cysts, the crescent sign, and collapse.

MRI: The gold standard for diagnosis. MRI detects AVN before any X-ray changes appear, identifies the size and location of the necrotic segment, and screens the opposite hip. The size of the necrotic lesion strongly predicts the risk of collapse.

Additional studies: Bone scan may show changes when MRI is unavailable; CT can better define a subchondral fracture.

Treatment

Treatment depends heavily on the stage of disease and the size of the necrotic lesion.

Conservative Management

Non-surgical treatment alone rarely halts the disease but may be used for very small lesions or patients who are not surgical candidates:

Protected weight-bearing: Crutches or a cane to offload the hip
NSAIDs: Ibuprofen, naproxen, or celecoxib for pain control
Bisphosphonates: May slow collapse in some patients (evidence is mixed)
Activity modification: Avoiding impact and heavy loading
Treating the underlying cause: Reducing steroid dose where possible, addressing alcohol use, managing clotting disorders

Because most lesions progress to collapse without intervention, conservative care is generally a temporizing measure rather than a cure.

Surgical Treatment — Joint-Preserving (Pre-Collapse)

When AVN is caught before the femoral head collapses (Stages I–II), joint-preserving surgery aims to save the patient's own hip:

Core decompression: The most common joint-preserving procedure — drilling into the necrotic segment to relieve pressure and stimulate healing, often combined with bone grafting or biologic augmentation
Bone grafting: Vascularized (e.g., free fibula graft) or non-vascularized grafts to support the subchondral bone
Osteotomy: Repositioning the femoral head to shift load away from the necrotic segment (used selectively)

Surgical Treatment — Joint-Replacing (Post-Collapse)

Once the femoral head has collapsed (Stages III–IV) and arthritis has set in, total hip replacement is the definitive treatment and reliably relieves pain and restores function. Because AVN patients are often young, implant longevity and the possibility of future revision are important considerations.