Introduction / Definition

Avascular necrosis (AVN), or osteonecrosis, of the femoral head represents a progressive ischaemic disorder characterised by cellular death of trabecular osteocytes and marrow elements. When structural repair mechanisms fail, microfractures accumulate within dead subchondral bone, precipitating articular collapse (crescent sign) and subsequent secondary osteoarthritis. It predominantly affects patients between the third and fifth decades of life, often presenting bilaterally and carrying significant lifetime disability.

Epidemiology & Aetiology

The annual incidence is estimated at 1.5–3.0 per 100,000, with a distinct male predilection in non-traumatic disease (approx. 3:1). Bilateral involvement occurs in over 60–80% of non-traumatic presentations, mandating contralateral screening.

Aetiologies are divided into traumatic and non-traumatic:

• Traumatic: Intracapsular neck of femur fractures (rate directly correlates with initial displacement and delayed reduction; up to 30–50% in Garden III/IV) and traumatic hip dislocations (risk escalates from 2–10% if reduced within 6 hours to >40% if delayed).
• Non-Traumatic: Multifactorial cascades (microvascular thrombosis, fat emboli, marrow hypertension). Key associations include:
  • Corticosteroid exposure (strongest dose-dependent association, particularly cumulative doses >2000 mg prednisolone or high-dose pulse therapy).
  • Chronic excess alcohol intake (>400 mL ethanol/week).
  • Haemoglobinopathies (Sickle Cell Disease / Thalassemia) causing microvascular sludging and vaso-occlusion.
  • Hypercoagulable disorders (Factor V Leiden, Antithrombin III deficiency, Antiphospholipid syndrome).
  • Gaucher disease, systemic lupus erythematosus (SLE), and immunosuppression (post-organ transplantation).
  • Caisson disease (decompression sickness / dysbarism).
  • Idiopathic (Chandler's disease).

Relevant Anatomy

Perfusion to the femoral head relies on a terminal, extraosseous arterial ring situated at the base of the femoral neck, derived predominantly from the medial femoral circumflex artery (MFCA) with minor contributions from the lateral femoral circumflex artery (LFCA):

• Deep branch of the MFCA: Perforates the posterior-superior capsule to form the lateral retinacular vessels, which supply over 80% of the weight-bearing anterosuperior dome of the femoral head.
• Inferior retinacular vessels: Branch from the trochanteric and MFCA systems, supplying the inferior head and epiphysis.
• Ligamentum teres artery (artery of the fovea capitis): Arises from the obturator artery; contributes negligibly in adults (supplying <10% adjacent to the fovea), rendering the femoral head vulnerable to watershed ischaemia.

Classification Systems

Staging is crucial for determining prognosis and selecting joint-preserving versus joint-sacrificing interventions.

Ficat and Arlet Classification

• Stage 0: Pre-clinical, pre-radiographic. Normal radiographs and MRI (histological or intraosseous pressure diagnosis).
• Stage I: Normal radiographs; abnormal MRI (marrow changes) or bone scintigraphy.
• Stage II: Radiographic osteosclerosis, osteopenia, and cystic changes within the femoral head. Contour remains intact.
• Stage III: Crescent sign (subchondral radiolucency / fracture) indicating early mechanical collapse.
• Stage IV: Articular flattening, progressive collapse, acetabular involvement, and advanced secondary osteoarthritis.

Steinberg (University of Pennsylvania) Classification

Expands Ficat by quantifying lesion size into subcategories (A: <15%, B: 15–30%, C: >30% head involvement) and includes Stages 0 through VI (Stage V: joint space narrowing; Stage VI: extensive advanced degenerative changes).

Modified Kerboul Necrotic Angle

Quantifies necrotic volume by summing the necrotic arc angles on mid-sagittal and mid-coronal T1-weighted MRI sequences:

• <200°: Low risk of collapse.
• 200°–250°: Moderate risk.
• >250°: High risk of collapse (>80%).

Clinical Presentation & Examination

Patients typically present with insidious, progressive groin pain, which may radiate to the anteromedial thigh or knee. Symptoms worsen with weight-bearing and impact loading; nocturnal pain indicates active intraosseous hypertension or structural collapse.

• Examination: Antalgic or Trendelenburg gait; restricted internal rotation in 90° flexion is typically the earliest physical finding. Provocative manoeuvres such as the FADIR (Flexion, Adduction, Internal Rotation) test elicit anterior impingement-like pain.

Investigations

• Plain Radiographs: Standard AP pelvis, AP hip, and frog-leg lateral radiographs. Frog-leg lateral views provide the highest sensitivity for detecting the early subchondral crescent sign in the anterosuperior head.
• Magnetic Resonance Imaging (MRI): Gold standard (>99% sensitivity/specificity). Essential sequences include coronal T1 and fluid-sensitive (T2 fat-suppressed or STIR) images.
  • T1-weighted sequence: Low-signal demarcation line separating healthy from necrotic bone (band-like sign).
  • T2-weighted sequence: Double line sign (pathognomonic), representing a hyperintense inner hyperaemic/granulation tissue margin and a hypointense outer sclerotic boundary.
  • Marrow oedema pattern correlates with acute microfracture, severe pain, and imminent collapse.
• Radionuclide Scintigraphy / CT: CT defines structural collapse and subchondral integrity when planning preservation surgery. Bone scan ('cold spot' early, 'doughnut sign' during repair) is reserved for MRI-contraindicated cases.

Management

Treatment strategy hinges on whether the femoral head has structurally collapsed (pre-collapse vs post-collapse).

Non-Operative Management

Conservative modalities carry poor outcomes for halting disease progression but may be used in asymptomatic, non-weight-bearing locations or non-surgical candidates:

• Protected weight-bearing (crutches) to reduce peak shear stress.
• Medical therapy (Bisphosphonates to retard osteoclastic resorption; iloprost or statins) has failed to demonstrate reproducible disease-modifying outcomes in randomised trials, and is not recommended for definitive prevention of collapse.

Joint-Preserving Operative Management (Pre-Collapse: Ficat I–II, Kerboul <200°)

• Core Decompression: Standard of care for early pre-collapse stages (Ficat I/II). Percutaneous drill decompression (e.g. 8–10 mm single reaming or multiple 3.2 mm drillings) reduces intraosseous venous hypertension and stimulates vascular ingrowth. Can be augmented with bone marrow aspirate concentrate (BMAC) or demineralised bone matrix.
• Vascularised Fibular Graft (VFG): Free vascularised fibula transfer with microvascular anastomosis to lateral circumflex femoral vessels provides structural support to the subchondral plate and active biological revascularisation. Highly technically demanding, associated with donor site morbidity (peroneal nerve palsy, flexor hallucis weakness).
• Non-Vascularised Bone Grafting (Phemister technique, lightbulb procedure): Structural allograft or autograft through a trapdoor technique; variable long-term success.
• Rotational Osteotomies (Sugioka transtrochanteric): Designed to rotate the necrotic segment away from the superior weight-bearing area; technically challenging and complicates subsequent arthroplasty.

Joint Arthroplasty (Post-Collapse: Ficat III–IV, Steinberg IV–VI)

• Total Hip Arthroplasty (THA): The definitive standard of care once subchondral collapse or secondary osteoarthritis has occurred. Cementless fixation is standard. Bearing selection (ceramic-on-crosslinked polyethylene or ceramic-on-ceramic) accommodates the high demand and young age of typical AVN cohorts. Modern uncemented components yield long-term survival >95% at 10–15 years, overcoming the historically high failure rates seen in early cemented series.

Complications

• Femoral head collapse and rapid secondary coxarthrosis.
• Acetabular erosion and severe bone loss.
• Donor-site morbidity following vascularised fibular grafting (peroneal neurapraxia, chronic ankle pain).
• Failure of core decompression (conversion rate to THA within 2–5 years exceeds 30–40% in large lesions).

Exam Pearls

• The deep branch of the medial femoral circumflex artery (lateral retinacular system) is the vital vascular leash jeopardised in capital collapse and intracapsular neck fractures.
• Always interrogate the contralateral hip on coronal MRI in non-traumatic disease (up to 80% risk of bilateral involvement).
• A crescent sign confirms subchondral fracture; head-preserving procedures (core decompression) fail reliably once this appears (post-collapse stage).
• In younger patients with Sickle Cell Disease undergoing THA, ensure preoperative haematology optimisation to prevent perioperative sickling crises, avascular bone infarction, and elevated prosthetic joint infection rates.