AVASCULAR NECROSIS OF THE HIP
Osteonecrosis | Progressive Collapse | Joint-Preserving vs Arthroplasty
FICAT-ARLET STAGING
Critical Must-Knows
- Bilateral in 50-80% - always image contralateral hip, counsel about second hip
- MRI gold standard - detects Stage I (pre-radiographic) disease before collapse
- Core decompression best for Ficat I-II (pre-collapse), controversial for Stage III
- Crescent sign (subchondral fracture) = collapse imminent, poor outcomes with joint preservation
- THA outcomes worse than primary OA: younger age, higher dislocation, more osteolysis
Examiner's Pearls
- "Stage I-II = joint preservation window (core decompression ± grafting)
- "Stage III-IV = arthroplasty preferred in most patients over 40 years
- "Steinberg adds lesion size (under 15%, 15-30%, over 30% of head) to staging
- "ARCO classification most comprehensive: adds location (medial/central/lateral columns)
Critical AVN Exam Points
Pathophysiology Triad
Vascular insult disrupts femoral head blood supply. Three mechanisms: direct vessel injury (trauma, surgery), thrombosis/embolism (coagulopathy, sickle cell), extravascular compression (Gaucher, steroids cause fat hypertrophy). Final common pathway = ischemia, osteocyte death, trabecular collapse.
Staging Determines Treatment
Pre-collapse (Ficat I-II) vs Post-collapse (III-IV). Joint preservation (core decompression, grafting, osteotomy) only works before crescent sign appears. Once collapse starts (Stage III), progression to arthritis is inevitable without arthroplasty.
Bilateral Disease
50-80% bilateral within 2 years. Always MRI contralateral hip even if asymptomatic. Counsel about risk of second hip. Stagger surgeries if bilateral decompression needed (infection, anesthetic risk).
Young Patient Dilemma
Age under 40 = arthroplasty complications. Higher activity, longer life expectancy = revision burden. Consider joint preservation even in Stage III if patient motivated. Inform about THA revision rates (15-20% at 10 years in young AVN).
Quick Decision Guide
| Patient Age | Ficat Stage | Lesion Size | Treatment | Key Pearl |
|---|---|---|---|---|
| Any age | I-II (pre-collapse) | Under 30% head | Core decompression ± NVBG | 80% success in Stage I, 65% in Stage II |
| Under 40 years | III (early collapse) | Any size | Valgus osteotomy or THA | Osteotomy rotates necrotic segment - needs intact lateral column |
| Over 40 years | III (collapse) or IV | Over 30% head | Total hip arthroplasty | Cementless fixation preferred, beware osteolysis in young |
| Sickle cell disease | Any stage | Any size | THA with special considerations | Exchange transfusion pre-op, cemented femoral stem |
ASEPTICRisk Factors for AVN
Memory Hook:ASEPTIC necrosis = sterile bone death from vascular insult, not infection!
MEDALFemoral Head Blood Supply (Why AVN Happens)
Memory Hook:MEDAL = Medial circumflex is the GOLD standard blood supply - lose it, lose the head!
DRILLCore Decompression Principles
Memory Hook:DRILL holes in the femoral head to decompress and revascularize before collapse!
REVISIONComplications of THA in AVN
Memory Hook:AVN THA outcomes need REVISION more than primary OA - counsel young patients!
Overview and Epidemiology
Why AVN Matters in Orthopaedics
AVN is the great imitator - can present like hip OA, but affects young patients (30-50 years) with devastating functional impact. Unlike OA, AVN is often bilateral (50-80%), progressive (2-5 years to collapse), and has modifiable risk factors (steroids, alcohol). Early diagnosis with MRI can identify pre-radiographic disease (Stage I) when joint-preserving surgery (core decompression) has 80% success. Once collapse occurs (crescent sign), arthroplasty is inevitable but outcomes are worse than primary OA due to young age and poor bone quality.
Demographics and Burden
Age: Peak incidence 30-50 years (productive working age)
Gender: Males 4-8 times more common (alcohol, steroid use patterns)
Bilateral: 50-80% develop contralateral hip AVN within 2 years
Progression: 80-90% of untreated hips collapse within 2-5 years
Economic: Young patients = decades of disability, multiple revisions, high healthcare costs
Risk Factor Prevalence
Steroid-induced: 30-40% of AVN cases (most common non-traumatic cause)
Alcohol-related: 20-30% of AVN cases (over 400mL ethanol per week)
Idiopathic: 30-40% no clear cause despite workup
Traumatic: Femoral neck fracture (30% AVN), hip dislocation (10-25% AVN)
Sickle cell: 10-50% of sickle cell patients develop AVN by age 35
Pathophysiology and Vascular Anatomy
The Vulnerable Femoral Head Blood Supply
Tenuous perfusion + extracapsular vessels = AVN susceptibility. The femoral head relies on retinacular vessels ascending the posterior neck (from medial circumflex femoral artery) - these are extracapsular and easily disrupted by: (1) Intracapsular fractures (hemarthrosis, vessel kinking), (2) Hip dislocation (vessel stretch), (3) Intraosseous pressure over 30mmHg (venous outflow obstruction), (4) Thrombosis (hypercoagulable states, sickle cell), (5) Fat emboli (steroids, alcohol, Gaucher). Once vessels are damaged, ischemia leads to osteocyte death within 12-48 hours, followed by trabecular collapse (2-5 years).
Blood Supply Architecture
| Vessel | Contribution | Pathway | Clinical Significance |
|---|---|---|---|
| Medial circumflex femoral artery (MFCA) | 70-80% | From profunda femoris → posterior neck → posterosuperior retinacular vessels | Primary blood supply - injury = AVN |
| Lateral circumflex femoral artery (LFCA) | Under 20% | From profunda femoris → anterior neck, metaphysis | Minor femoral head contribution |
| Artery of ligamentum teres | Variable (0-30%) | From obturator artery → fovea centralis | Minimal in adults, cannot sustain head alone |
Pathophysiological Mechanisms
Direct Vessel Injury
Trauma:
- Femoral neck fracture: Displaces head, stretches/tears retinacular vessels (30% AVN rate)
- Hip dislocation: Posterior dislocations stretch MFCA branches (10-25% AVN, higher if delayed reduction)
- Surgical iatrogenic: Hip pinning, osteotomy, excessive retractor pressure
Radiation: Vessel fibrosis and obliteration in cancer treatment
Understanding these mechanisms helps explain why urgent reduction of hip dislocations and anatomic fracture reduction are critical.
Histopathological Progression
Natural History of Untreated AVN
Vascular insult → cessation of blood flow → osteocyte death within 12-48 hours. Bone matrix remains intact initially. MRI shows marrow edema (dark T1, bright T2) before any structural change.
Dead osteocytes → empty lacunae on histology. No acute inflammation (sterile process). Surrounding viable bone attempts revascularization → interface zone forms. Sclerotic rim appears on XR as new bone is laid down at interface (Stage II).
Granulation tissue invades from periphery → osteoclastic resorption of dead bone → weakens trabeculae. "Creeping substitution" - new bone forms on dead trabeculae scaffolds. Head still spherical but mechanically weakened.
Mechanical failure of weakened trabeculae → subchondral fracture → crescent sign on XR/MRI. Fracture propagates → segmental collapse → head loses sphericity. Cartilage remains viable initially but shear forces develop.
Incongruent joint → cartilage degeneration → joint space narrowing → osteophytes → acetabular changes. Secondary OA develops. Both femoral and acetabular surfaces involved.
Classification Systems
Ficat-Arlet Classification
Original 1985, Modified by Steinberg 1995
| Stage | Symptoms | XR Findings | MRI Findings | Treatment Options | Prognosis |
|---|---|---|---|---|---|
| I | Pain or asymptomatic | Normal | Positive (band sign) | Core decompression ± NVBG | 80% success with surgery |
| II | Pain with activity | Sclerosis, cysts, no collapse | Positive, demarcated lesion | Core decompression ± grafting/osteotomy | 60-70% success, depends on lesion size |
| III | Pain at rest and activity | Crescent sign, collapse | Subchondral fracture, fluid | Osteotomy (young) or THA | Poor with preservation, THA preferred |
| IV | Severe pain, limp | Collapse + acetabular changes | Arthritis, joint effusion | Total hip arthroplasty | THA definitive, revision risk 15-20% at 10 years |
Ficat Staging Key Distinction
Crescent sign (subchondral fracture) = Stage III = poor prognosis for joint preservation. This is the critical inflection point. Before crescent sign (Stages I-II), trabecular architecture is intact and core decompression can relieve pressure and promote revascularization (80% success in Stage I). Once crescent sign appears, subchondral bone has fractured, collapse is underway, and joint preservation fails in 70-80% of cases. In patients over 40 years, THA is preferred at Stage III.
Clinical Assessment
History
Onset: Insidious groin pain over weeks to months (vs acute trauma)
Character: Dull ache progressing to sharp pain with weight-bearing
Radiation: Groin to anterior thigh, knee (L3 referred pain)
Aggravating: Weight-bearing, stairs, rising from chair, internal rotation
Relieving: Rest, non-weight-bearing, analgesia
Functional: Limp, reduced walking distance, difficulty with shoes/socks
Risk Factors: ASEPTIC mnemonic - systematically ask about steroids (dose, duration), alcohol (quantity per week), trauma, clotting disorders, sickle cell, Gaucher, pancreatitis
Examination
Gait: Antalgic (shortened stance phase on affected side), Trendelenburg if chronic
Look: Usually normal (no swelling unless Stage IV OA), leg length discrepancy if chronic collapse
Feel: Groin tenderness, no effusion palpable
Move:
- Active ROM: Painful limitation (especially internal rotation and abduction)
- Passive ROM: Loss of internal rotation earliest sign, flexion-adduction-internal rotation (FADIR) painful
- Specific tests: Log roll test painful, FABER positive
Neurovascular: Intact (unless chronic with nerve compression)
Other joints: Examine shoulders, knees (multifocal AVN common in sickle cell, steroids)
Beware the Occult Contralateral Hip
Always examine both hips and image both sides. AVN is bilateral in 50-80% of cases, often asymptomatic initially. Patients presenting with unilateral symptoms may have MRI-positive AVN in the contralateral hip (Stage I) requiring surveillance or prophylactic treatment. Failure to image the contralateral side is medicolegal risk - patient develops second hip AVN 2 years later asking why it was not detected earlier.
Differential Diagnosis
| Condition | Key Distinguishing Features | Imaging Findings |
|---|---|---|
| Primary hip OA | Older age (over 60), gradual onset, no risk factors, unilateral | Joint space narrowing, osteophytes, subchondral sclerosis |
| Transient osteoporosis of hip | Third trimester pregnancy or middle-aged men, self-limiting (6-12 months) | Diffuse marrow edema on MRI, NO band sign, XR normal or osteopenic |
| Stress fracture femoral neck | Athletes, military recruits, acute pain, no risk factors | MRI shows fracture line (not band), XR may show cortical break |
| Bone tumour (metastasis, myeloma) | Older age, night pain, weight loss, no trauma | MRI shows mass lesion, XR shows lytic/blastic lesion |
| Labral tear | Mechanical symptoms (clicking, catching), younger athletic patients | MRI arthrogram shows labral tear, no bone marrow edema |
Investigations
Imaging Protocol for Suspected AVN
Views: AP pelvis (both hips for comparison), lateral affected hip, frog-leg lateral
Stage I: Normal (pre-radiographic - MRI needed)
Stage II: Sclerosis (increased density at interface), cystic changes, preservation of sphericity
Stage III: Crescent sign (subchondral lucency = fracture), flattening of head
Stage IV: Collapse, secondary OA changes (joint space narrowing, osteophytes, acetabular sclerosis)
Utility: Staging for treatment decisions, monitoring progression, excluding other pathology.
Sensitivity: 99% for early AVN (can detect Stage I before XR changes)
Specificity: 95% when band sign present
Findings:
- Band sign: Low signal line on T1 and T2 (interface between necrotic and viable bone)
- Double line sign: Low signal outer rim + high signal inner rim on T2 (granulation tissue)
- Geographic pattern: Wedge-shaped or band-like lesion in anterosuperior head
Protocol: Coronal and axial T1, T2, STIR sequences of both hips
Value: Detects pre-radiographic disease, determines lesion size (Steinberg substaging), identifies bilateral disease, monitors treatment response.
CT: Detects sclerosis, cysts, crescent sign, but less sensitive than MRI for Stage I. Useful for surgical planning (valgus osteotomy, measuring lesion location).
Bone Scan: Cold in center (no uptake in necrotic bone), hot rim peripherally (reparative response). Less specific than MRI, radiation exposure, no anatomic detail.
Role: Second-line if MRI unavailable or contraindicated (pacemaker, severe claustrophobia).
Baseline: FBC (sickle cell, Gaucher), ESR/CRP (exclude infection), LFTs (alcohol-related liver disease), lipid profile
Coagulation Screen: Protein C, Protein S, Antithrombin III, Factor V Leiden, Lupus anticoagulant, Anticardiolipin antibodies (if young, idiopathic, bilateral)
Specific Tests: Hemoglobin electrophoresis (sickle cell), Gaucher enzyme assay, HIV serology
Rationale: Identify modifiable risk factors (cease steroids if possible, alcohol cessation), screen for systemic disease requiring treatment, counsel about contralateral hip risk.
Management Algorithm
Treatment Decision Framework
Joint Preservation Strategy
Goal: Prevent collapse, promote revascularization, preserve native joint
Non-Operative Management (Observation)
- Small lesions (under 15% of head - Steinberg A)
- Medial location (non-weight-bearing zone)
- Asymptomatic or minimal symptoms
- Patient refuses surgery
Observation alone has 80% progression rate in Stage I-II, so reserved for very small medial lesions.
- Activity modification: Reduce impact loading, crutches if symptomatic
- Medications: NSAIDs for pain, bisphosphonates (alendronate) may slow progression
- Risk factor modification: Cease alcohol, reduce/taper steroids if possible
- Surveillance: MRI every 6 months for 2 years, then annually if stable
Inform patient that 80% progress without surgery - observation is not benign neglect.
Core Decompression (Gold Standard Stage I-II)
- Reduces intraosseous pressure (from over 30mmHg to under 10mmHg)
- Creates drill track for revascularization (granulation tissue)
- Removes necrotic marrow (decompresses venous congestion)
- Stimulates bone remodeling
Success rate: 80% in Stage I (prevents collapse), 60-70% in Stage II (depends on lesion size).
- Positioning: Supine on radiolucent table, hip in neutral or slight flexion
- Entry point: Lateral cortex 2-3cm distal to greater trochanter, just above lesser trochanter
- Trajectory: Fluoroscopy guidance, aim for center-center position on AP and lateral
- Drill: 8-10mm cannulated drill, advance to subchondral bone (leave 5mm intact)
- Grafting: Consider non-vascularized bone graft (from iliac crest) to fill defect
- Closure: Deep fascia, subcutaneous, skin, drain usually not needed
Complications: Femoral neck fracture (under 1% - avoid multiple tracts, lateral cortex violation), infection, neurovascular injury.
- Weight-bearing: Touch weight-bearing (10-20kg) on crutches for 6-8 weeks
- Progression: Gradual increase to full weight-bearing at 8-12 weeks based on pain
- Surveillance: XR at 6 weeks, 3 months, 6 months, then annually for 2 years
- Success criteria: No progression of collapse, pain resolution, MRI shows revascularization
Failure indicators: Crescent sign develops, increasing pain, progression to Stage III = consider arthroplasty.
When to Add Bone Grafting
Non-vascularized bone graft (NVBG) + core decompression improves outcomes in Stage II large lesions. Cortical strut graft from fibula or iliac crest provides structural support to weakened subchondral bone (80-90% success in Stage II B-C vs 60% with core decompression alone). Technique: Insert strut graft through drill tract to contact subchondral plate (tantalum rod is modern alternative - inert, porous, promotes bone ingrowth).
Surgical Technique
Pre-operative Planning
Consent Points
Risks:
- Success rate: 80% Stage I, 60-70% Stage II, under 30% Stage III
- Femoral neck fracture: Under 1% (requires protected weight-bearing 6-8 weeks)
- Infection: Under 1% (prophylactic antibiotics)
- Neurovascular injury: Under 0.5% (sciatic nerve, femoral vessels)
- Progression despite surgery: 20-40% require THA in future
- DVT/PE: Standard surgical risk (LMWH prophylaxis)
Emphasize that this is joint preservation attempt - not guaranteed to prevent collapse.
Equipment Checklist
Required:
- Radiolucent table (fracture table or standard OR table)
- C-arm fluoroscopy (AP and lateral views)
- 8-10mm cannulated drill system with guidewire
- Power drill with variable speed
- Bone graft harvesting set (if adding NVBG)
- Standard hip surgical tray
Optional Adjuncts:
- Tantalum rod (10mm diameter, 100-120mm length)
- Iliac crest bone graft instruments
- Fibular strut graft instruments (if adding structural support)
Patient Positioning
Setup
Supine on radiolucent table (fracture table not essential but helpful for traction control).
- Hip position: Neutral rotation or slight internal rotation (opens lateral cortex access)
- Knee: Flexed 10-20 degrees (relaxes iliopsoas, improves fluoroscopy)
- Contralateral leg: Abducted and externally rotated (allows C-arm access)
- Arms: Across chest or on arm boards (away from operative field)
Ensure full range of C-arm movement for AP and lateral views before draping.
- Skin prep: Chlorhexidine or iodine from umbilicus to knee, lateral to midline
- Draping: Standard hip draping exposing proximal femur to mid-thigh
- C-arm draping: Sterile cover over C-arm intensifier
- Landmarks: Palpate greater trochanter, mark entry point 2-3cm distal to GT on lateral thigh
Confirm adequate fluoroscopy images (AP pelvis showing both hips, perfect lateral of affected hip) before incision.
Surgical Approach and Technique
Step-by-Step Core Decompression
Location: Lateral thigh, 2-3cm distal to tip of greater trochanter, just above lesser trochanter level
Size: 3-4cm longitudinal incision parallel to femoral shaft
Depth: Through skin and subcutaneous tissue to fascia lata
Fluoroscopy confirms position - entry point should be proximal to lesser trochanter to avoid stress riser at narrowest femoral neck.
- Incise fascia lata in line with skin incision
- Split vastus lateralis fibers bluntly (no intermuscular plane - direct muscle split)
- Expose lateral femoral cortex with retractors (Hohmann on anterior and posterior edges)
- Periosteum: Minimal stripping (reduces devascularization)
Avoid Lateral Cortex Violation
Critical: Entry point must be distal to greater trochanter but proximal to lesser trochanter. Too distal = stress riser at narrow femoral neck = fracture risk. Confirm position on AP and lateral fluoroscopy before drilling.
Trajectory Planning:
- AP view: Aim for center of femoral head (bisects head diameter)
- Lateral view: Aim for center of femoral head (anterior-posterior midpoint)
- Target: Subchondral bone 5mm deep to articular cartilage (DO NOT breach cartilage)
Technique:
- Use 2.4-2.8mm guidewire through cannulated system
- Hand-drill guidewire through lateral cortex (careful control)
- Advance under fluoroscopy guidance to center-center position
- Stop 5mm short of subchondral plate on lateral view
- Confirm position on AP and lateral before proceeding
Multiple passes to "find" the correct trajectory waste bone and weaken neck - plan trajectory carefully before drilling.
- Drill size: 8-10mm cannulated drill over guidewire
- Speed: Slow (100-200 RPM) to avoid thermal necrosis
- Irrigation: Copious saline irrigation during drilling (cool bit, clear debris)
- Depth: Advance to 5mm from subchondral plate (measure on fluoroscopy)
- Confirmation: Final AP and lateral images confirm center-center position, 5mm margin
DO NOT:
- Drill multiple tracts (weakens femoral neck = fracture risk)
- Breach lateral cortex widely (stress riser)
- Penetrate subchondral plate (articular cartilage damage, intra-articular communication)
Suction through drill to remove necrotic marrow and blood (decompress intraosseous pressure).
Indications for Adding Bone Graft:
- Large lesion (over 30% of head - Steinberg C)
- Stage II with significant cystic changes
- Structural support needed (tantalum rod or fibular strut)
Non-Vascularized Bone Graft (NVBG):
- Harvest corticocancellous graft from ipsilateral iliac crest (2-3cm incision)
- Morselized cancellous bone OR cortical strut (from fibula or iliac crest)
- Pack through drill tract to contact subchondral plate
- Provides structural support and osteogenic cells
Tantalum Rod:
- 10mm diameter porous tantalum rod (100-120mm length)
- Insert through drill tract to contact subchondral plate
- Promotes bone ingrowth (porous structure), inert, radiopaque (easy follow-up)
- More expensive than NVBG but easier to insert, less donor site morbidity
Confirm graft or rod position on final fluoroscopy images.
- Fascia lata: Absorbable suture (Vicryl 1 or 0) in interrupted or continuous fashion
- Subcutaneous: 2-0 Vicryl to close dead space
- Skin: Subcuticular 3-0 Monocryl or staples
- Dressing: Standard sterile dressing, no drain needed (minimal dead space)
Final check: Ensure no retained swabs, instrument count correct, fluoroscopy images saved.
Intraoperative Pearls and Pitfalls
Do's (Pearls)
- Single drill tract only (multiple tracts weaken neck)
- Center-center position on AP and lateral (maximizes decompression)
- 5mm subchondral margin (prevents articular cartilage damage)
- Slow drilling speed with irrigation (prevents thermal necrosis)
- Measure guidewire depth before drilling (prevents overpenetration)
- Save fluoroscopy images for medicolegal documentation
Don'ts (Pitfalls)
- Do NOT drill multiple tracts (femoral neck fracture risk)
- Do NOT violate lateral cortex widely (stress riser)
- Do NOT breach subchondral plate (articular damage, joint communication)
- Do NOT drill without fluoroscopy confirmation (malposition common)
- Do NOT attempt in Stage III-IV with collapse (failure rate over 70%)
- Do NOT skip postoperative protected weight-bearing (fracture risk)
Understanding these technical details helps anticipate complications and optimize outcomes.
Complications
| Complication | Incidence | Risk Factors | Prevention/Management |
|---|---|---|---|
| Progression to collapse (untreated) | 80-90% at 5 years | Large lesion (over 30%), lateral location, Stage II, no treatment | Early diagnosis (MRI), core decompression in Stage I-II, risk factor modification |
| Bilateral AVN | 50-80% within 2 years | Systemic cause (steroids, alcohol, sickle cell, coagulopathy) | MRI both hips at diagnosis, surveillance imaging, prophylactic treatment if Stage I contralateral |
| Femoral neck fracture (core decompression) | Under 1% | Multiple drill tracts, lateral cortex violation, early weight-bearing | Single central tract, avoid lateral cortex, protected weight-bearing 6-8 weeks |
| Core decompression failure | 20-40% (Stage I-II) | Large lesion (over 30%), Stage III, lateral location, delayed diagnosis | Patient selection (Stage I-II only), add bone grafting if large lesion, realistic expectations |
| THA revision (AVN patients) | 15-20% at 10 years | Age under 40, high activity, poor bone quality, polyethylene wear | Counsel about revision risk, cross-linked poly, large head size, activity modification |
| THA dislocation | 2-5% | Young active patients, posterior approach, component malposition | Optimize component position, repair posterior capsule, large head (36mm+), patient education |
Monitor for Progression Despite Treatment
Core decompression does not guarantee success - 20-40% of Stage I-II patients still progress to collapse. Monitor with clinical review and imaging (XR at 6, 12, 24 months) for signs of failure: (1) Increasing pain despite initial improvement, (2) Crescent sign develops on XR, (3) MRI shows progression of necrosis. If failure detected early (before major collapse), consider salvage with vascularized fibular graft or proceed to arthroplasty. Delaying arthroplasty until severe collapse makes surgery more difficult (bone loss, acetabular involvement).
Postoperative Care and Rehabilitation
Rehabilitation After Core Decompression
- Analgesia: PCA or oral opioids, transition to paracetamol + NSAIDs
- DVT prophylaxis: LMWH (enoxaparin 40mg daily) for 14 days, TED stockings
- Mobilization: Physiotherapy Day 1, non-weight-bearing on crutches
- Wound: Check drain (if used), remove at 24 hours, dry dressing
- Discharge: Usually Day 1-2 once mobile on crutches, safe at home
- Weight-bearing: Touch weight-bearing (10-20kg) on two crutches
- Exercises: Quadriceps isometric, ankle pumps, hip abduction (prevent stiffness)
- Precautions: Avoid pivoting, twisting, impact activities
- Pain: Expect groin discomfort for 2-4 weeks (surgical pain)
- Follow-up: Clinic at 6 weeks with XR (check for fracture, progression)
- Weight-bearing: Increase to 50% at 6 weeks, progress to full weight-bearing by 12 weeks
- Crutches: Wean from two crutches → one crutch → stick → unaided
- Exercises: Progressive resistance (hip abduction, flexion), stationary bike, pool
- Return to work: Sedentary work at 6 weeks, manual work at 12 weeks
- Imaging: XR at 3 months (assess for healing, progression)
- Activity: Gradual return to impact activities (running, sport) at 6 months if pain-free
- Surveillance: XR at 6, 12, 24 months, then annually for 5 years
- Success criteria: No pain, no progression on XR, return to activities
- Failure signs: Increasing pain, crescent sign develops, MRI shows progression → consider arthroplasty
Understanding this timeline helps set patient expectations - core decompression is a slow recovery (3-6 months to full activity) but preserves the native joint.
Outcomes and Prognosis
| Treatment | Success Definition | 5-Year Outcome | 10-Year Outcome | Failure Predictors |
|---|---|---|---|---|
| Core decompression (Stage I) | No collapse, pain relief | 80% | 70% | Large lesion (over 30%), lateral location, delayed diagnosis |
| Core decompression + graft (Stage II) | No progression to THA | 65-70% | 60% | Lesion over 30%, crescent sign present, lateral location |
| Valgus osteotomy (Stage III) | Hip preservation, no THA | 60-70% | 40-50% | Age over 40, collapse over 2mm, inadequate intact arc (under 90 degrees) |
| THA (AVN patients) | Implant survival, no revision | 95% | 85-90% | Age under 40, cementless stem in poor bone, high activity level |
Predictors of Poor Outcome
Large lateral lesions in young patients = highest risk of progression. The combination of (1) lesion over 30% of head (Steinberg C), (2) lateral location (maximal weight-bearing forces), (3) age under 40 (high activity), (4) Stage II or worse at diagnosis predicts 80-90% progression to collapse despite core decompression. Consider free vascularized fibular graft in this group if patient refuses arthroplasty. Conversely, small (under 15%) medial lesions detected early (Stage I) have 80-90% success with core decompression - emphasize importance of early diagnosis.
Quality of Life Considerations
Joint Preservation Impact
Advantages:
- Preserves native anatomy and proprioception
- No implant-related complications (dislocation, wear, loosening)
- No activity restrictions lifelong
- Delays or avoids THA (and future revisions)
Disadvantages:
- 20-40% failure rate requires future THA
- Prolonged recovery (6-12 months to full activity)
- Risk of collapse during healing period
- Not suitable for all patients (age, lesion size, stage)
Arthroplasty Impact
Advantages:
- Predictable pain relief (95% at 2 years)
- Rapid functional recovery (6 weeks to normal activities)
- Durable (85-90% survival at 10 years)
- Definitive solution for failed joint preservation
Disadvantages:
- Activity restrictions lifelong (no high impact sports)
- Revision risk in young patients (15-20% at 10 years)
- Dislocation risk (2-5% in AVN patients)
- Psychological impact of "artificial joint" in young patients
Evidence Base and Key Trials
Core Decompression for Early AVN: Meta-Analysis
- Meta-analysis of 24 studies, 1206 hips with Ficat Stage I-II AVN
- Core decompression prevented progression to collapse in 63.5% overall
- Success rate Stage I: 84%, Stage II: 63%, Stage III: 22%
- Addition of bone grafting (NVBG or tantalum rod) improved outcomes to 75-80% in Stage II
Vascularized Fibular Grafting for Advanced AVN
- Systematic review of free vascularized fibular graft for AVN (22 studies, 1298 hips)
- Overall success rate (survival without THA) 75% at 10 years
- Best results in Stage II ARCO (85% survival), worst in Stage III (60% survival)
- Donor site morbidity: 10% (ankle pain, stress fracture, saphenous nerve injury)
THA for AVN vs Primary OA: Registry Comparison
- Compared 4657 THA for AVN vs 252,391 THA for primary OA (mean age 61 vs 69 years)
- 10-year implant survival: AVN 88% vs OA 94%
- Revision rate higher in AVN: HR 1.53 (dislocation HR 1.8, aseptic loosening HR 1.4)
- Younger age (under 55) strongest predictor of revision in AVN group
Tantalum Rod Implantation for Early AVN
- RCT comparing tantalum rod vs core decompression alone (108 hips, Stage II-IIIA AVN)
- 5-year survival without THA: Tantalum 80% vs Core decompression 59%
- Harris Hip Score improved more with tantalum (76 vs 68 points at 5 years)
- No difference in complications (femoral neck fracture under 1% both groups)
Bisphosphonates for AVN Prevention: RCT
- RCT of alendronate (70mg weekly) vs placebo in 40 patients with Stage I-II AVN
- Reduced progression to collapse at 2 years: Alendronate 25% vs Placebo 60%
- Mechanism: Reduces bone resorption phase (prevents trabecular weakening)
- Safe, no serious adverse events, well-tolerated
Exam Viva Scenarios
Practice these scenarios to excel in your viva examination
Scenario 1: Early AVN Diagnosis and Management (Standard, 2-3 min)
"A 38-year-old man presents with a 4-month history of right groin pain. He is on long-term steroids for Crohn's disease (prednisolone 20mg daily for 18 months). Examination reveals painful internal rotation. Plain XR of the hip is normal. What is your assessment and management?"
Scenario 2: Surgical Technique and Decision-Making (Challenging, 3-4 min)
"A 35-year-old woman with bilateral hip AVN (Ficat Stage IIIA on right, Stage II on left) secondary to SLE and long-term steroids presents with severe right hip pain and collapse on XR. She is desperate to avoid hip replacement. Walk me through your management options and preferred approach."
Scenario 3: Complication Management (Critical, 2-3 min)
"A 42-year-old man underwent core decompression for Stage II AVN 18 months ago. He presents with worsening groin pain over the last 3 months. How do you assess and manage this?"
MCQ Practice Points
Blood Supply Anatomy Question
Q: What is the main blood supply to the adult femoral head? A: Medial circumflex femoral artery (MFCA) provides 70-80% of blood to the femoral head via posterosuperior retinacular vessels. The MFCA arises from the profunda femoris artery, forms an extracapsular ring with the lateral circumflex femoral artery at the femoral neck base, then sends deep branches (retinacular vessels) that ascend the posterior femoral neck under the capsule to reach the femoral head. The artery of ligamentum teres (from obturator artery) contributes minimally in adults (under 20%). This anatomy explains why intracapsular femoral neck fractures and posterior hip dislocations cause AVN (retinacular vessels are disrupted).
Staging Classification Question
Q: What is the significance of the crescent sign in AVN? A: Crescent sign = subchondral fracture = Ficat Stage III = poor prognosis for joint preservation. The crescent sign appears as a radiolucent line beneath the subchondral plate on XR or MRI, representing a fracture through weakened necrotic bone. Once present, the femoral head has begun to collapse, trabecular architecture is irreversibly damaged, and joint preservation surgery (core decompression) fails in 70-80% of cases. The crescent sign is the critical inflection point between pre-collapse disease (Stages I-II where core decompression has 60-80% success) and post-collapse disease (Stages III-IV where arthroplasty is preferred). In patients over 40 years with crescent sign, THA is recommended over attempted joint preservation.
Risk Factors Question
Q: What cumulative steroid dose increases AVN risk? A: Over 2000mg cumulative prednisone equivalent or over 20mg/day for over 3 months. Steroid-induced AVN is the most common non-traumatic cause (30-40% of all AVN cases). The mechanism involves adipocyte hypertrophy causing increased intraosseous pressure (over 30mmHg normal under 10mmHg) and venous outflow obstruction, leading to ischemia. Risk is dose-dependent and time-dependent. Other high-risk factors include chronic alcohol use (over 400mL ethanol per week), sickle cell disease (10-50% develop AVN by age 35), and coagulopathies (Factor V Leiden, Protein C/S deficiency). Idiopathic AVN accounts for 30-40% despite extensive workup.
Treatment Decision Question
Q: What is the success rate of core decompression for Stage I AVN? A: 80% success in preventing collapse at 5-10 years. Core decompression reduces intraosseous pressure (from over 30mmHg to under 10mmHg), creates a drill tract for revascularization, and removes necrotic marrow. Success rates decline with advancing stage: Stage I (pre-radiographic) 80%, Stage II (sclerosis/cysts, no collapse) 60-70%, Stage III (collapse/crescent sign) under 30%. Adding non-vascularized bone graft or tantalum rod improves outcomes in Stage II large lesions (over 30% of head) to 75-80%. The procedure involves a lateral approach, fluoroscopy-guided drilling from above the lesser trochanter to center-center position, leaving 5mm of subchondral bone intact. Postoperative protected weight-bearing (touch weight-bearing for 6-8 weeks) is essential to prevent iatrogenic femoral neck fracture.
THA Outcomes Question
Q: How do THA outcomes in AVN patients compare to primary OA? A: Worse outcomes - 15-20% revision rate at 10 years (vs 5-10% in OA). AVN patients are younger (mean age 50 vs 70 in OA), more active, have poorer bone quality (necrotic sclerotic bone), and higher complication rates. Specific risks: (1) Dislocation 2-5% (vs under 1% in OA) due to younger age and higher activity, (2) Aseptic loosening and osteolysis from polyethylene wear (high activity, long life expectancy), (3) Periprosthetic fracture (osteoporotic or sclerotic bone), (4) Infection (immunosuppression from steroids, SLE, or underlying disease). Registry data shows implant survival at 10 years is 85-90% for AVN vs 94-95% for OA. Counsel extensively about revision burden, activity restrictions, and realistic expectations. Use highly cross-linked polyethylene, large femoral heads (36mm or larger), and optimize component position to minimize complications.
Bilateral Disease Question
Q: What percentage of AVN cases are bilateral? A: 50-80% develop contralateral hip involvement within 2 years. Bilateral disease is the rule, not the exception, in AVN (especially with systemic causes like steroids, alcohol, sickle cell, coagulopathy). This has important management implications: (1) Always MRI both hips at diagnosis even if contralateral hip is asymptomatic (may detect Stage I disease amenable to prophylactic core decompression), (2) Counsel patients about risk of second hip requiring treatment, (3) Consider prophylactic core decompression or close surveillance (MRI every 6 months) for asymptomatic contralateral Stage I AVN, (4) Stage bilateral surgeries if both hips need intervention (infection risk, anesthetic burden, mobilization challenges). Idiopathic AVN has lower bilateral rate (30-40%) compared to steroid-induced (70-80%) or sickle cell disease (over 80%).
Australian Context and Medicolegal Considerations
AOANJRR Data (Australian Orthopaedic Association National Joint Replacement Registry)
AVN THA Outcomes in Australia (2023 Report):
- AVN accounts for 5% of all primary THAs (approximately 2500 cases per year)
- Mean age 58 years (vs 69 years for OA)
- 10-year cumulative revision rate: 12.8% for AVN vs 6.5% for OA
- Younger age (under 55) strongest predictor: 18% revision rate at 10 years
- Cementless femoral stems perform better in AVN patients (under 55 years)
- Metal-on-metal bearings have higher revision rates (avoid in AVN patients)
Registry Recommendations:
- Use cementless fixation in young AVN patients (bone ingrowth potential)
- Large femoral head diameter (36mm or larger) reduces dislocation risk
- Highly cross-linked polyethylene for all AVN patients (reduces wear)
- Mandatory reporting of all primary and revision THAs to registry
Australian Guidelines and Resources
Pharmaceutical Benefits Scheme (PBS):
- Bisphosphonates (alendronate) PBS-listed for osteoporosis, not specifically for AVN
- Steroid-induced osteoporosis prevention: Consider bisphosphonates in patients on over 7.5mg prednisolone daily for over 3 months
eTG (Therapeutic Guidelines) Antibiotic Prophylaxis:
- THA prophylaxis: Cefazolin 2g IV (or vancomycin 15mg/kg if penicillin allergy)
- Extended prophylaxis (48 hours) not recommended (single dose adequate)
Australian Orthopaedic Association Guidelines:
- VTE prophylaxis: LMWH for 28-35 days post-THA (rivaroxaban alternative)
- Antibiotic prophylaxis: Single dose pre-incision (cefazolin 2g)
Medicolegal Considerations in AVN Management
Key Documentation Requirements:
1. Informed Consent for Core Decompression:
- Success rate (80% Stage I, 60-70% Stage II, under 30% Stage III)
- Risk of failure (20-40% require THA in future despite surgery)
- Complications: Femoral neck fracture (under 1%), infection, neurovascular injury, progression despite surgery
- Alternative treatments: Observation (80% progress), arthroplasty, bisphosphonates (limited evidence)
- Postoperative commitment: Protected weight-bearing 6-8 weeks, gradual return to activities 3-6 months
2. Informed Consent for THA in Young AVN Patients:
- Higher revision risk (15-20% at 10 years vs 5-10% in OA)
- Activity restrictions lifelong (no high-impact sports, running, jumping)
- Dislocation risk (2-5% - higher than primary OA)
- Longevity concerns: May require multiple revisions over lifetime (age 40 with THA = possible 2-3 revisions)
- Alternative joint preservation options discussed and declined (document reasoning)
3. Bilateral Disease Discussion:
- Document that both hips were imaged (MRI) at diagnosis
- If contralateral hip has early disease, document discussion of prophylactic treatment vs observation
- Document patient understands 50-80% risk of second hip involvement
4. Steroid Counseling:
- Document discussion with prescribing physician (gastroenterologist, rheumatologist) about steroid minimization
- Document patient understands dose-dependent risk of AVN
- Consider alternative immunosuppression if AVN develops (steroid-sparing agents)
Common Litigation Issues:
- Delayed diagnosis (patient has Stage III/IV at presentation due to failure to MRI earlier)
- Failure to image contralateral hip (misses early bilateral disease)
- Inadequate consent (patient not informed about 20% failure rate of core decompression, later sues when requires THA)
- Premature THA (offering arthroplasty in Stage II without discussing joint preservation options)
- Femoral neck fracture from core decompression (improper technique - multiple drill holes, lateral cortex violation)
Australian Public Hospital Pathways
Presentation to Emergency Department:
- Hip pain, difficulty weight-bearing → XR hip, consider MRI if high suspicion and normal XR
- If AVN suspected, refer to orthopaedic outpatient clinic (Category 3 - non-urgent, 365-day target)
Outpatient Orthopaedic Clinic Assessment:
- Confirm diagnosis with MRI both hips, stage disease (Ficat classification)
- Discuss treatment options (conservative, core decompression, arthroplasty)
- List for surgery if indicated (Category 2 elective for symptomatic Stage II-III - 90-day target, Category 3 for asymptomatic surveillance)
Private Practice Pathway:
- GP referral to orthopaedic surgeon with MRI both hips
- Clinic assessment and treatment planning
- Surgery in private hospital (typical wait 4-12 weeks)
- Medicare rebate for THA approximately 40% of surgeon fee (patient co-payment or private health insurance gap)
Avascular Necrosis of the Hip
High-Yield Exam Summary
Key Anatomy
- •Medial circumflex femoral artery = 70-80% of femoral head blood supply
- •Posterosuperior retinacular vessels ascend posterior neck (at risk in displaced #NOF)
- •Artery of ligamentum teres = minimal contribution in adults (under 20%)
- •Extracapsular vessels vulnerable to trauma, thrombosis, and compression
Classification (Ficat-Arlet)
- •Stage I = Normal XR, MRI positive (band sign), 80% core decompression success
- •Stage II = Sclerosis/cysts, no collapse, 60-70% core decompression success
- •Stage III = Crescent sign (subchondral fracture), collapse started, under 30% core decompression success
- •Stage IV = Secondary OA, acetabular involvement, THA definitive treatment
Treatment Algorithm
- •Stage I-II small lesion (under 30%) = Core decompression ± grafting
- •Stage II large lesion (over 30%) = Core decompression + NVBG or tantalum rod
- •Stage III under 40 years = Valgus osteotomy or vascularized fibular graft (consider THA)
- •Stage III over 40 years or Stage IV any age = Total hip arthroplasty
Surgical Pearls
- •Core decompression: Lateral entry 2-3cm distal to GT, center-center position, leave 5mm subchondral bone
- •Protected weight-bearing (touch WB) for 6-8 weeks post-decompression (prevent femoral neck fracture)
- •THA in AVN: Cementless fixation, large head (36mm+), cross-linked poly, counsel about 15-20% revision at 10 years
- •Valgus osteotomy: Requires intact medial column, rotates lateral necrotic segment out of weight-bearing
Complications
- •Bilateral disease in 50-80% within 2 years (always MRI both hips)
- •Core decompression failure in 20-40% of Stage II (progression to collapse despite surgery)
- •Femoral neck fracture under 1% (avoid multiple tracts, lateral cortex, early weight-bearing)
- •THA revision in 15-20% at 10 years (young age, high activity, poor bone quality)