📋 Key Information Summary
- Referred pain is common: hip pathology may present as isolated groin, buttock, or knee pain, and lumbar spine pathology frequently mimics hip disease — always examine both regions.
- Age is the single best discriminator: in children ≤10 years consider Perthes disease and transient synovitis; in adolescents consider SCFE and DDH; in adults ≥50 years osteoarthritis dominates.
- Developmental dysplasia of the hip (DDH) affects 2–3 per 1,000 live births in Australia; universal clinical screening (Ortolani/Barlow) at birth and selective ultrasound at 6 weeks remain standard practice.
- Slipped capital femoral epiphysis (SCFE) is an orthopaedic emergency — weight-bearing restriction and urgent surgical pinning are required to prevent avascular necrosis and premature arthritis.
- Perthes disease (Legg–Calvé–Perthes) peaks at ages 4–8 years; MRI with gadolinium is the gold-standard for assessing femoral head viability and containment.
- Transient synovitis is the most common cause of acute hip pain in children aged 3–10 years but is a diagnosis of exclusion — Kocher criteria help differentiate from septic arthritis.
- Hip osteoarthritis (OA) affects >1.8 million Australians; first-line management includes education, exercise therapy, weight management, and simple analgesia per OARSI/EULAR guidelines.
- Trochanteric bursitis (greater trochanteric pain syndrome) presents with lateral hip pain worse at night and on activity; conservative management with physiotherapy is first-line; corticosteroid injection is second-line.
- Avascular necrosis (AVN) of the femoral head has numerous causes including corticosteroid use, alcohol excess, and trauma; MRI is the most sensitive early investigation; Ficat staging guides treatment.
- Leriche syndrome (aortoiliac occlusive disease) presents with bilateral buttock claudication, absent femoral pulses, and erectile dysfunction in males — it is a vascular emergency requiring urgent CT angiography.
- Red flags requiring urgent referral: acute non-weight-bearing child, fever with hip pain (rule out septic arthritis/osteomyelitis), progressive neurological deficit, suspected fracture, and acute limb ischaemia.
- Aboriginal and Torres Strait Islander Australians have higher rates of hip OA, delayed presentation of paediatric hip conditions, and reduced access to orthopaedic and rheumatology services in remote communities.
Introduction & Australian Epidemiology
Hip, buttock, and groin pain constitutes a significant proportion of musculoskeletal presentations across Australian general practice. The hip joint is a deep, congruent ball-and-socket synovial joint that transmits substantial axial loads during gait, making it susceptible to a wide range of mechanical, inflammatory, infective, neoplastic, and vascular pathologies. Critically, pain arising from the hip may be perceived in the groin, lateral thigh, buttock, or even the knee via shared segmental innervation (L1–S1), and conversely, lumbar spine pathology frequently mimics hip disease.
The aetiology of hip and groin pain is strongly age-dependent. In the paediatric population, developmental dysplasia of the hip (DDH), transient synovitis, Legg–Calvé–Perthes disease, and slipped capital femoral epiphysis (SCFE) represent the key differential diagnoses. In young adults, femoroacetabular impingement (FAI), labral tears, sportsman's groin (athletic pubalgia), and avascular necrosis (AVN) are more prevalent. In the middle-aged and elderly, hip osteoarthritis (OA), greater trochanteric pain syndrome, insufficiency fractures, and malignancy must be considered. Vascular causes, including aortoiliac occlusive disease (Leriche syndrome), are an important and often under-recognised cause of buttock and hip pain, particularly in patients with cardiovascular risk factors.
In Australia, hip OA affects approximately 1.8 million people and is the leading indication for total hip replacement, with over 50,000 procedures performed annually (Australian Orthopaedic Association National Joint Replacement Registry, 2023). DDH occurs in approximately 2–3 per 1,000 live births, with higher rates reported in breech presentations, firstborn females, and Indigenous Australian populations. SCFE has an incidence of approximately 10 per 100,000 children per year, with higher rates in Pacific Islander, Māori, and Indigenous Australian children.
Clinical pearl: The single most important initial question when assessing hip, buttock, or groin pain is the patient's age. Age-based differential diagnosis is the foundation of the diagnostic model described in this article and prevents both missed diagnoses and unnecessary investigations.
Hip Pain Diagnostic Model
A structured, age-based approach to hip, buttock, and groin pain improves diagnostic accuracy and reduces time to appropriate management. The following model integrates history, examination findings, and age-stratified differential diagnosis.
Anatomical Pain Zones
| Pain Location | Likely Source | Common Diagnoses |
|---|---|---|
| Anterior groin | Hip joint (intra-articular) | OA, AVN, FAI, labral tear, SCFE, DDH, septic arthritis |
| Lateral hip | Peri-articular / extra-articular | Greater trochanteric pain syndrome, ITB syndrome, meralgia paraesthetica, referred lumbar |
| Buttock / posterior | Posterior hip, SIJ, lumbar spine | Lumbar radiculopathy, piriformis syndrome, SIJ dysfunction, ischial bursitis, aortoiliac occlusion |
| Medial groin / adductor | Adductor complex / pubic symphysis | Athletic pubalgia, adductor tendinopathy, osteitis pubis, inguinal hernia |
| Referred to knee | Hip joint via obturator nerve | SCFE, Perthes, OA, AVN — always examine the hip in a child with knee pain |
Age-Based Differential Diagnosis
| Age Group | Key Differentials | Red Flags |
|---|---|---|
| Neonate (0–6 months) | DDH, congenital hip dislocation | Positive Ortolani/Barlow, asymmetric skin folds, leg-length discrepancy |
| Child (3–10 years) | Transient synovitis, Perthes disease, septic arthritis, osteomyelitis, leukaemia | Fever >38.5°C, non-weight-bearing, raised CRP/ESR/WCC, refusal to bear weight >48 h |
| Adolescent (10–16 years) | SCFE, Perthes (late), avulsion fracture, FAI | Acute worsening, inability to bear weight, bilateral symptoms (endocrine cause for SCFE) |
| Young adult (18–45 years) | FAI, labral tear, AVN, athletic pubalgia, sacroiliitis | Night pain, systemic symptoms, recent corticosteroid use, alcohol excess |
| Older adult (>50 years) | OA, trochanteric bursitis, insufficiency fracture, metastasis, polymyalgia rheumatica, Leriche syndrome | Unexplained weight loss, night pain, history of malignancy, acute vascular insufficiency |
Systematic History Framework
- Onset: acute (fracture, SCFE, septic arthritis), subacute (Perthes, AVN), insidious (OA, AVN)
- Aggravating factors: weight-bearing (mechanical), rest/night (inflammatory, malignancy, AVN), activity (impingement, tendinopathy)
- Relieving factors: rest (mechanical), movement (inflammatory arthropathies)
- Associated symptoms: fever, weight loss, night sweats (infection, malignancy), claudication (vascular), erectile dysfunction (Leriche)
- Risk factors: corticosteroid use, alcohol, SLE, sickle cell disease (AVN); breech birth, family history (DDH); obesity, endocrine disorders (SCFE)
Essential Physical Examination
1
Gait Assessment
Antalgic gait, Trendelenburg (gluteus medius weakness), short-leg gait, waddling gait (bilateral DDH)
2
Inspection
Leg-length discrepancy (true vs apparent), muscle wasting (gluteal, quadriceps), skin folds symmetry, scoliosis
3
Palpation
Greater trochanter (tenderness = GTPS), ASIS, pubic symphysis, inguinal canal, sacroiliac joint, femoral pulse
4
Range of Motion
Flexion, internal rotation (earliest lost in OA), external rotation, abduction, adduction; FABER/Patrick test
5
Special Tests
FADIR (impingement), FABER (SIJ/hip), Thomas test (fixed flexion deformity), Trendelenburg, log roll (irritability), Ober's test (ITB)
6
Neurovascular
Femoral, popliteal, dorsalis pedis, posterior tibial pulses; peroneal nerve (foot drop); straight leg raise (lumbar)
Hip Pain in Children
Paediatric hip pain demands a high index of suspicion for serious pathology. The differential diagnosis is age-dependent, and several conditions are orthopaedic emergencies. A limping child should always be assessed urgently.
Developmental Dysplasia of the Hip (DDH)
DDH encompasses a spectrum from mild acetabular dysplasia to frank dislocation of the femoral head. It occurs in approximately 2–3 per 1,000 live births in Australia and is more common in females (F:M = 4:1), firstborn children, breech presentation, and positive family history. Aboriginal and Torres Strait Islander infants may have higher rates of late-detected DDH, particularly in remote communities.
Screening & Diagnosis
- Clinical screening: Ortolani manoeuvre (detected dislocation reduced) and Barlow manoeuvre (stable hip dislocated) are performed at birth, then at each well-child visit up to 12 months.
- Ultrasound: hip ultrasound at 4–6 weeks is recommended for all infants with risk factors (breech, family history, clinical instability). Graf method assesses α-angle (>60° normal) and β-angle.
- X-ray: after 4–6 months of age when the femoral head begins to ossify. Hilgenreiner's line, Perkins' line, and the acetabular index are assessed.
- Late presentation: may present with delayed walking, Trendelenburg gait, limb-length discrepancy, or asymmetric skin folds in a child who was not screened.
Management
| Age at Diagnosis | Treatment | Notes |
|---|---|---|
| 0–6 months | Pavlik harness (dynamic splint) | Success >90%; worn full-time for 6–12 weeks, then weaned. Monitored by ultrasound. |
| 6–18 months | Closed reduction under GA + hip spica cast | Adductor tenotomy may be required; arthrogram confirms concentric reduction. |
| >18 months | Open reduction ± pelvic/femoral osteotomy | Higher complication rate; requires paediatric orthopaedic subspecialist. |
Key point: The Pavlik harness is most effective when initiated before 3 months of age. Delayed diagnosis beyond 6 months significantly reduces non-operative success rates and increases the risk of avascular necrosis. All Australian states recommend DDH screening as part of routine neonatal and infant health checks.
Transient Synovitis
Transient synovitis (irritable hip) is the most common cause of acute hip pain in children aged 3–10 years, accounting for up to 85% of acute hip presentations. It typically follows a viral upper respiratory tract infection and presents with acute-onset hip or groin pain, limp, and reduced internal rotation.
Kocher Criteria — Differentiating Transient Synovitis from Septic Arthritis
| Criterion | Points |
|---|---|
| Fever >38.5°C | 1 |
| Inability to bear weight | 1 |
| ESR >40 mm/h | 1 |
| WCC >12.0 × 10⁹/L | 1 |
- 0 criteria: probability of septic arthritis <0.2%
- 1 criterion: 3.0%
- 2 criteria: 40.0%
- 3 criteria: 93.1%
- 4 criteria: 99.6%
Septic arthritis is an orthopaedic emergency. If ≥2 Kocher criteria are present, or if the child is acutely unwell, joint aspiration (ultrasound-guided) under GA is mandatory. Delays beyond 24–48 hours risk permanent cartilage destruction and femoral head necrosis. Blood cultures and IV antibiotics (flucloxacillin 50 mg/kg IV 6-hourly + ceftriaxone 50 mg/kg IV daily for MRSA/Gram-negative cover) should be commenced empirically.
Management of transient synovitis: rest, simple analgesia (paracetamol 15 mg/kg 4–6-hourly, ibuprofen 5–10 mg/kg 8-hourly), and observation. Most cases resolve within 7–10 days. Weight-bearing is allowed as tolerated. Follow-up within 48 hours is essential to confirm improvement — if symptoms worsen, re-evaluate for septic arthritis.
Legg–Calvé–Perthes Disease
Perthes disease is an idiopathic avascular necrosis of the femoral head affecting children aged 4–8 years (peak 5–7 years). It is more common in males (M:F = 4:1), and bilateral involvement occurs in 10–15% of cases. The pathogenesis involves disruption of the blood supply to the femoral epiphysis, leading to necrosis, re-ossification, and potential remodelling over 2–5 years.
Clinical Features
- Insidious onset of limp ± hip or knee pain
- Reduced internal rotation and abduction (early loss of hip internal rotation is characteristic)
- Trendelenburg gait if significant
- May be bilateral (10–15%); distinguish from bilateral AVN or multiple epiphyseal dysplasia
Investigations
- X-ray pelvis AP + frog-leg lateral: initial investigation. May be normal in early disease (first 4–6 weeks). Look for subchondral lucency (crescent sign), femoral head sclerosis, widening of joint space, and later fragmentation.
- MRI with gadolinium: most sensitive early investigation; assesses femoral head viability and extent of necrosis. Useful for staging when X-rays are equivocal.
- Bone scan: less commonly used; shows decreased uptake in the avascular phase.
Staging (Waldenström)
Stage I
Initial / Necrosis
Femoral head sclerosis, subchondral fracture (crescent sign). Joint space widening.
Duration: 6–12 months
Stage II
Fragmentation
Irregular ossification, femoral head fragmentation, resorption of necrotic bone.
Duration: 1–2 years
Stage III–IV
Re-ossification & Remodelling
New bone formation. Femoral head remodelling. Final shape determines long-term outcome.
Duration: 2–5 years total
Prognostic Factors
The Catterall classification (Groups I–IV based on extent of head involvement) and the lateral pillar classification (Herring: A, B, C) are used to predict outcome. Age at onset <6 years, lateral pillar A or B, and containment of the femoral head are favourable prognostic indicators.
Management
- Containment principle: the femoral head must be contained within the acetabulum during the active phase to allow symmetrical remodelling. Options include Petrie casting (abduction broomstick plaster), Scottish Rite orthosis, or surgical containment (femoral or pelvic osteotomy) for high-risk cases.
- Physiotherapy: maintain range of motion; avoid impact loading during the active phase.
- Surgical indications: femoral head at risk (head risk signs on X-ray), age >8 years at onset, lateral pillar C, loss of containment. Varus derotation osteotomy or Salter innominate osteotomy may be performed.
- Long-term follow-up: is essential. Femoral head shape at maturity determines long-term outcome. Some patients develop premature OA requiring THA in the 30s–40s.
Slipped Capital Femoral Epiphysis (SCFE)
SCFE involves posterior–inferior slippage of the femoral head through the growth plate (physis) relative to the femoral neck. It is the most common hip disorder in adolescents, with peak incidence between ages 10–16 years. In Australia, SCFE is more prevalent in Pacific Islander, Māori, and Indigenous Australian populations.
SCFE is an orthopaedic emergency. Delayed diagnosis increases the risk of avascular necrosis (AVN) and chondrolysis. Any adolescent with hip, groin, or knee pain should have the hip examined and an X-ray performed. Weight-bearing must be restricted immediately.
Classification
Stable
Stable SCFE
Patient can bear weight (with or without crutches). Accounts for ~90% of cases. Lower AVN risk (~10%).
Urgent surgical pinning (in-situ)
Unstable
Unstable SCFE
Patient cannot bear weight even with crutches. ~10% of cases. AVN risk up to 50%. Acute on chronic.
Emergency surgical stabilisation
Risk Factors
- Obesity (most children with SCFE are above the 90th percentile for weight)
- Endocrine disorders: hypothyroidism, growth hormone deficiency, panhypopituitarism, hypogonadism — bilateral SCFE in a non-obese child mandates endocrine workup
- Male sex (M:F = 2:1), left side more common
- Bilateral in 20–40% (both may present simultaneously or sequentially)
Clinical Features
- Insidious hip, groin, or referred knee pain (knee pain is the presenting complaint in 15–50% of cases)
- Limp, externally rotated leg, limited internal rotation
- Obligate external rotation on passive hip flexion
- Acute exacerbation on a background of chronic symptoms (acute-on-chronic = most unstable)
Investigations
- X-ray pelvis AP + frog-leg lateral: the frog-leg lateral view is most sensitive. Look for Klein's line (a line drawn along the superior femoral neck should intersect the epiphysis; if it does not, SCFE is likely — Trethowan sign). Widened, irregular physis. Posterior–medial displacement of the epiphysis.
- MRI: if X-rays are equivocal; also assesses AVN.
Management
- In-situ pinning with a single cannulated screw is the standard treatment for stable SCFE. The pin is placed centrally in the femoral head under fluoroscopic guidance. Weight-bearing is restricted post-operatively (non-weight-bearing → partial → full over 6–8 weeks).
- Unstable SCFE: gentle reduction and pinning within 24 hours. Controversy exists regarding the role of urgent reduction — some centres perform hip capsulotomy to decompress intracapsular haematoma and reduce AVN risk.
- Prophylactic pinning of the contralateral hip is controversial but may be considered in high-risk patients (pre-pubertal, endocrine disorder, obesity).
- Long-term: risk of premature OA (50% by age 50), FAI from remodelling, and AVN. Regular orthopaedic follow-up until skeletal maturity.
Hip Pain in Adults & Elderly
Hip Osteoarthritis (OA)
Hip OA is the most common cause of hip pain in adults over 50 years and is the leading cause of hip pain requiring total hip replacement in Australia. Over 50,000 primary total hip replacements were performed in Australia in 2022 (AOANJRR). Risk factors include increasing age, obesity, previous hip injury or surgery, occupational overuse, and family history. Aboriginal and Torres Strait Islander Australians have a higher burden of OA and may present at a younger age.
Clinical Features
- Pain: anterior groin pain radiating to the thigh and knee; worse with weight-bearing, stairs, rising from sitting
- Stiffness: morning stiffness <30 minutes (distinguishes from inflammatory arthritis); "start-up" stiffness
- Reduced range of motion: internal rotation is the first movement lost; fixed flexion deformity
- Functional limitation: difficulty with shoes/socks, getting out of low chairs, walking
- Crepitus on movement
Diagnostic Criteria (ACR Clinical Criteria)
Hip OA can be diagnosed clinically if hip pain is present plus at least 2 of the following 3:
- ESR <20 mm/h
- Radiographic osteophytes
- Joint space narrowing on X-ray
Radiographic Features
- Joint space narrowing (superior > medial)
- Osteophytes (acetabular and femoral)
- Subchondral sclerosis and cyst formation
- Kellgren–Lawrence grading (Grade 0–4) guides severity and management decisions
Management — Stepped Approach
1
Education & Self-Management
Disease education, activity modification, weight loss (target BMI <30), use of assistive devices. Arthritis Australia resources. OARSI strongly recommends patient education.
2
Exercise Therapy
Supervised land-based or aquatic exercise programs (≥12 weeks). Strengthens peri-articular muscles, improves function. Referred via GP Management Plan (GPMP, Item 721) to physiotherapist. Medicare rebate for 5 allied health visits/year.
3
Pharmacotherapy
Paracetamol (1 g QID, max 4 g/day) as first-line. Oral NSAIDs (short course, with PPI cover) if paracetamol insufficient. Topical NSAIDs for localised symptoms. Intra-articular corticosteroid injection for flares (evidence for short-term benefit only).
4
Weight Management
Every 5 kg of weight loss reduces knee/hip OA symptoms by ~20%. Low-calorie diet + exercise is the most effective conservative combination. Consider referral to dietitian (GPMP Item 10950).
5
Total Hip Arthroplasty (THA)
Indicated when conservative measures fail for ≥3–6 months and functional impairment significantly affects quality of life. Referral to orthopaedic surgeon for assessment. Australia's 10-year prosthesis survival rate exceeds 95% (AOANJRR).
Pharmacotherapy Detail
Paracetamol
Panadol® · Dymadon® · Simple analgesic
Adult dose
500–1000 mg PO QID (max 4 g/day); modified-release 665 mg TDS
Renal adjustment
No adjustment required
PBS status
✔ PBS General Benefit
Naproxen
Naprosyn® · Naprogesic® · NSAID
Adult dose
250–500 mg PO BD with food; use lowest effective dose for shortest duration
Paediatric dose
5–7 mg/kg PO BD (Juvenile Idiopathic Arthritis)
Renal adjustment
eGFR <30 mL/min: avoid
PBS status
✔ PBS General Benefit
Celecoxib
Celebrex® · Selective COX-2 inhibitor
Adult dose
200 mg PO daily (100–200 mg BD); lower CV risk than non-selective NSAIDs
Renal adjustment
eGFR <30 mL/min: avoid
PBS status
✔ PBS General Benefit
Omeprazole
Losec® · Proton pump inhibitor (gastroprotection)
Adult dose
20 mg PO daily (concurrent with NSAID for GI protection)
PBS status
✔ PBS General Benefit
Duloxetine
Cymbalta® · SNRI (for OA pain with central sensitisation)
Adult dose
30 mg PO daily for 1 week, then 60 mg PO daily
PBS status
✔ PBS Authority Required
Triamcinolone acetonide (IA injection)
Kenacort® · Corticosteroid
Adult dose
40 mg intra-articular under ultrasound guidance; may repeat after ≥3 months
PBS status
✔ PBS General Benefit
OARSI/EULAR Key Recommendations: Exercise therapy and weight loss are the strongest evidence-based conservative treatments for hip OA. Paracetamol alone has modest efficacy; NSAIDs are more effective but require gastroprotection. Intra-articular hyaluronic acid and PRP injections are not routinely recommended (insufficient evidence). Opioids should be avoided in chronic OA management.
Greater Trochanteric Pain Syndrome (GTPS)
GTPS encompasses trochanteric bursitis, gluteal tendinopathy, and external coxa saltans (snapping hip). It affects 10–25% of the general population, is more common in women aged 40–60 years, and is the most common cause of lateral hip pain. The underlying pathology is now understood to be predominantly gluteal tendinopathy (tendinosis of gluteus medius and/or minimus) rather than isolated bursitis.
Clinical Features
- Lateral hip pain over the greater trochanter
- Worse with lying on the affected side at night, prolonged walking, climbing stairs
- Tenderness on palpation of the greater trochanter
- Positive single-leg stance test (30-second single-leg stand reproduces lateral hip pain)
- Resisted hip abduction may be painful (gluteus medius involvement)
- FABER test may be negative (helps distinguish from intra-articular hip pathology)
Investigations
- Diagnosis is primarily clinical. Imaging is not required in typical presentations.
- Ultrasound: first-line imaging if diagnosis uncertain. Shows gluteal tendinopathy (tendon thickening, hypoechoic change, partial tears) and/or trochanteric bursal fluid.
- MRI: for refractory cases or when intra-articular pathology is suspected. Identifies gluteal tendon tears and bone oedema at the greater trochanter.
Management
1
Activity Modification
Avoid prolonged single-leg stance, crossing legs, lying on the affected side. Sleep with pillow between knees.
2
Physiotherapy (First-line)
Eccentric loading program for gluteal tendons. Isometric hip abduction exercises. Progressive strengthening over 12+ weeks. Lateral hip drop exercises. This has the strongest evidence base.
3
Corticosteroid Injection
Ultrasound-guided trochanteric bursal injection with 40 mg triamcinolone + 5 mL 1% lidocaine. Short-term benefit (4–12 weeks) but recurrence rate ~50%. Best used as an adjunct to physiotherapy, not as standalone treatment.
4
Shockwave Therapy
Extracorporeal shockwave therapy (ESWT) may benefit patients who fail physiotherapy. Moderate evidence. Available at select physiotherapy practices.
5
Surgical Referral
For refractory cases: gluteal tendon repair, trochanteric bursectomy, or iliotibial band release. Rarely required.
Avascular Necrosis (AVN) & Aortoiliac Occlusion
Avascular Necrosis of the Femoral Head
Avascular necrosis (osteonecrosis) of the femoral head results from disruption of blood supply, leading to bone cell death and eventual femoral head collapse. It accounts for approximately 5–12% of total hip replacements in Australia. Bilateral involvement occurs in 40–80% of non-traumatic cases.
Aetiology
| Category | Causes |
|---|---|
| Traumatic | Femoral neck fracture, hip dislocation (most common cause; AVN risk 10–30% with fracture, up to 70% if dislocation not reduced within 6 hours) |
| Corticosteroids | Most common non-traumatic cause. Risk increases with cumulative dose (>2 g prednisolone equivalent) and prolonged use. Cushing syndrome. |
| Alcohol excess | >400 mL ethanol/week significantly increases risk. Lipid-mediated vascular occlusion mechanism. |
| Systemic disease | SLE, antiphospholipid syndrome, sickle cell disease, Gaucher disease, HIV, decompression sickness (Caisson disease) |
| Iatrogenic | Post-radiation, organ transplant (up to 20% incidence in renal transplant recipients) |
| Idiopathic | 10–20% of cases have no identifiable risk factor |
Clinical Features
- Insidious onset of groin or hip pain, often worse at rest and at night (distinguishing from OA)
- May be bilateral at presentation (always image both hips)
- Reduced internal rotation and hip flexion
- Classically affects patients aged 20–50 years (younger than typical OA)
- Rapid progression if untreated; femoral head collapse within 6–36 months
Investigations
- MRI: gold-standard for early detection. Sensitivity >99%. Shows bone marrow oedema, serpiginous double-line sign on T2-weighted images. Can detect AVN months before X-ray changes appear.
- X-ray: may be normal in early stages (Ficat Stage I). Crescent sign (subchondral fracture) is a hallmark of Stage II. Femoral head flattening/collapse in Stage III–IV.
- Blood tests: FBC, LFTs, lipid profile, coagulation screen, autoimmune panel (ANA, anti-dsDNA, antiphospholipid antibodies), haemoglobin electrophoresis if indicated.
Ficat–Arlet Staging
Stage I
Early
Normal X-ray. MRI abnormal (bone marrow oedema). Mild hip pain.
Core decompression (best outcomes)
Stage II
Subtle Changes
Sclerosis, cyst formation on X-ray. Crescent sign. Femoral head still round.
Core decompression ± bone graft
Stage III
Collapse
Femoral head flattening/collapse (crescent sign). Articular surface irregularity.
Core decompression or THA (depending on age/extent)
Stage IV
Advanced
Femoral head collapse with secondary OA. Joint space narrowing. Acetabular changes.
Total hip arthroplasty
Management
- Core decompression: indicated in Ficat I–II (pre-collapse). Involves drilling into the necrotic zone to reduce intraosseous pressure and promote revascularisation. Success rates 60–80% in early disease.
- Bone grafting: vascularised fibular graft or autologous bone graft may be combined with core decompression.
- Total hip arthroplasty: the definitive treatment for Ficat III–IV or failed joint-preserving procedures. Cemented or uncemented depending on age and bone quality.
- Bisphosphonates: IV pamidronate or oral alendronate have been trialled as adjunctive therapy to slow bone resorption, but evidence is limited and not routinely recommended.
- Address underlying cause: reduce/cease corticosteroids if possible, alcohol cessation, treat underlying systemic disease.
- Weight-bearing restriction: protected weight-bearing with crutches is recommended while the femoral head is at risk of collapse.
Aortoiliac Occlusive Disease (Leriche Syndrome)
Leriche syndrome describes the clinical triad of aortoiliac occlusive disease caused by atherosclerotic narrowing or occlusion of the distal aorta and/or common iliac arteries. It is an under-recognised cause of hip and buttock pain that must be considered in patients over 50 years with cardiovascular risk factors.
Classic Leriche triad:
- Bilateral buttock and thigh claudication
- Absent or diminished femoral pulses bilaterally
- Erectile dysfunction in males
Clinical Features
- Claudication: bilateral buttock, hip, and thigh pain on walking that resolves with rest. Distinguishing feature from hip OA: pain is activity-dependent and completely resolves at rest.
- Fontaine classification:
- Stage I: asymptomatic
- Stage IIa: claudication >200 m; IIb: claudication <200 m
- Stage III: rest pain (especially at night, relieved by hanging leg over bed)
- Stage IV: tissue loss/gangrene
- Examination: absent or weak femoral pulses, bruit over the aorta/iliac arteries, skin pallor on elevation, delayed capillary refill, trophic changes (hair loss, shiny skin), impotence in males
Investigations
- Ankle-brachial pressure index (ABPI): first-line non-invasive test. Normal 0.9–1.3. <0.9 confirms PAD. <0.5 suggests critical limb ischaemia. May be falsely elevated in diabetics due to medial calcification.
- Duplex ultrasound: identifies level and severity of stenosis.
- CT angiography (CTA): gold-standard for surgical planning. Defines anatomy of stenosis, calcification, and run-off vessels.
- MR angiography: alternative to CTA if contrast allergy or renal impairment. MBS Item 59313 (Medicare-rebatable).
- Cardiovascular risk assessment: lipid panel, HbA1c, blood pressure, ECG, echocardiography. Patients with aortoiliac disease have high rates of concurrent coronary and cerebrovascular disease.
Management
1
Cardiovascular Risk Reduction
Smoking cessation (most important modifiable risk factor), statin therapy (atorvastatin 80 mg), antiplatelet (aspirin 100 mg or clopidogrel 75 mg), BP control (target <130/80), HbA1c <7% in diabetics. Supervised exercise program (30 min × 3/week for ≥12 weeks).
2
Supervised Exercise Therapy
Exercise training improves claudication distance by 50–200%. Structured program with treadmill walking to near-maximal claudication pain, rest, repeat. Hospital-based programs are available in most Australian metropolitan centres.
3
Endovascular Intervention
Percutaneous transluminal angioplasty (PTA) ± stenting of iliac stenoses. Preferred for short-section stenoses. Minimal access, faster recovery. TASC A/B lesions.
4
Surgical Bypass
Aortobifemoral or iliofemoral bypass grafting for extensive occlusions (TASC C/D). High long-term patency rates. Reserved for failed endovascular treatment or extensive disease.
Pharmacotherapy for PAD
Aspirin
Cartia® · Cardiprin® · Antiplatelet
Adult dose
100 mg PO daily
PBS status
✔ PBS General Benefit
Clopidogrel
Plavix® · Iscover® · Antiplatelet
Adult dose
75 mg PO daily
PBS status
✔ PBS General Benefit
Atorvastatin
Lipitor® · Statin
Adult dose
40–80 mg PO daily (high-intensity for PAD)
PBS status
✔ PBS General Benefit
Cilostazol
Pletal® · Phosphodiesterase III inhibitor
Adult dose
100 mg PO BD (improves claudication distance)
PBS status
✔ PBS Authority Required
Investigations Summary
Essential
X-ray pelvis AP + lateral/frog-leg
First-line imaging for all age groups. Assess for fracture, SCFE, Perthes, OA, AVN changes. MBS Item 55704. Available in all Australian practices.
Available
Hip ultrasound (Paediatric)
Graf method for DDH screening (4–6 weeks). Guided aspiration for suspected septic arthritis. MBS Item 55800. Available in metropolitan and regional centres.
Essential
MRI hip (with/without contrast)
Gold-standard for AVN, Perthes staging, labral tears, stress fractures, occult fractures, soft tissue pathology. MBS Item 63551 (with contrast), 63554 (without). Available in most metro hospitals; regional via telehealth referral to imaging hubs.
Available
CT angiography (aortoiliac)
Gold-standard for Leriche syndrome planning. MBS Item 57359. Available in metro and large regional hospitals.
Available
Ankle-brachial pressure index (ABPI)
Non-invasive PAD screening. Can be performed in GP rooms with Doppler. MBS Item 11300 (if performed in vascular lab).
Essential
Blood tests: FBC, CRP, ESR
Inflammatory markers for septic arthritis, osteomyelitis, polymyalgia rheumatica, malignancy. Available in all Australian pathology services (MBS bulk-billed).
Specialist
Bone scan (SPECT)
Occult fractures, metastatic disease, Perthes staging. Less commonly used now with MRI availability. MBS Item 61306.
Specialist
Diagnostic hip injection (image-guided)
Intra-articular local anaesthetic injection to confirm hip joint as pain source. Performed under fluoroscopy or ultrasound. MBS Item 55054.
Special Populations
Pregnancy
Pelvic girdle pain / symphysis pubis dysfunction: Affects up to 20% of pregnant women. Hormonal laxity of the SIJ and pubic symphysis. Manage with physiotherapy, pelvic belt, and simple analgesia (paracetamol is safe).
Avoid NSAIDs in the third trimester (risk of premature ductus arteriosus closure). Short-term NSAID use in the second trimester is permissible if benefits outweigh risks.
Avascular necrosis: Rare but reported in pregnancy (possibly related to fat embolism or hypercoagulability). MRI is safe in pregnancy (no gadolinium in first trimester).
Paediatrics
DDH screening at birth (Ortolani/Barlow) and selective ultrasound at 4–6 weeks for risk factors. Failure to screen is a common source of delayed diagnosis.
A limping child is an orthopaedic emergency until proven otherwise. Exclude septic arthritis and fracture before considering transient synovitis.
NSAIDs in children: Ibuprofen 5–10 mg/kg PO 8-hourly is preferred. Avoid aspirin in children <16 years (Reye syndrome risk). Always use weight-based dosing.
SCFE: Bilateral in 20–40%. Endocrine workup (thyroid function, growth hormone) is mandatory for bilateral or atypical SCFE.
Elderly
Intracapsular neck of femur fracture: Most common fragility fracture in the elderly. Urgent surgical fixation (<48 hours) reduces mortality. Assess bone health (DEXA, calcium, vitamin D, PTH) and commence antiresorptive therapy.
Insufficiency fractures: Sacral and pubic rami fractures in osteoporotic patients. MRI is the investigation of choice (X-rays may be normal initially).
Polymyalgia rheumatica: Presents with bilateral hip and shoulder girdle pain/stiffness in patients >50 years. ESR typically >40 mm/h. Responds dramatically to low-dose prednisolone (15–25 mg daily).
Metastatic disease: Prostate, breast, lung, kidney, and thyroid cancers commonly metastasise to the proximal femur and pelvis. Bone scan or whole-body MRI for staging.
Falls risk: Hip pain itself increases falls risk. Multifactorial falls assessment and home safety modifications are essential.
Renal Impairment
Avascular necrosis is more common in dialysis patients and renal transplant recipients (up to 20% incidence). Steroid-sparing immunosuppression strategies reduce risk.
NSAIDs: Contraindicated if eGFR <30 mL/min. Use paracetamol as first-line. Tramadol requires dose reduction in CKD (eGFR <30: max 100 mg/day).
Renal osteodystrophy: Secondary hyperparathyroidism and adynamic bone disease increase fracture risk. Coordinate with nephrology.
Gadolinium-based MRI contrast: Avoid gadolinium-based agents if eGFR <30 mL/min (nephrogenic systemic fibrosis risk). Use non-contrast MRI protocols.
Hepatic Impairment
Alcohol-related AVN: Significant alcohol consumption is a major risk factor. Counselling and alcohol cessation support are essential components of management.
Paracetamol: Maximum 2 g/day in chronic liver disease (4 g/day is hepatotoxic in the setting of cirrhosis or heavy alcohol use).
NSAIDs: Use with caution; increased risk of GI bleeding and hepatorenal syndrome in cirrhosis. Celecoxib has lower GI bleeding risk but is not hepatically safe.
Immunocompromised
Atypical infections: Consider fungal osteomyelitis, mycobacterial infection, and opportunistic pathogens in immunocompromised patients with hip pain (HIV, transplant recipients, biologic therapy).
Steroid-induced AVN: Cumulative corticosteroid dose >2 g prednisolone equivalent is a significant risk factor. MRI screening may be warranted in high-risk patients on prolonged corticosteroid therapy.
Septic arthritis: May present atypically with blunted inflammatory response. Maintain a high index of suspicion and lower the threshold for joint aspiration.
Post-arthroplasty infection: Prosthetic joint infection (PJI) presents with pain, swelling, and loosening. Requires microbiological diagnosis and two-stage revision in most cases. Coordinate with infectious diseases.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
Recommendations for practice:
- Engage Aboriginal Health Workers and Aboriginal Liaison Officers early in the care pathway for all Indigenous patients with hip pain.
- Use telehealth for specialist consultations where possible to reduce travel burden (MBS telehealth items available).
- Ensure all DDH screening programs in remote communities have culturally appropriate education materials in local languages.
- Consider the social and emotional wellbeing framework in chronic pain management rather than a purely biomedical model.
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📚 References
- 1. Australian Orthopaedic Association National Joint Replacement Registry (AOANJRR). Hip, Knee & Shoulder Arthroplasty: Annual Report 2023. Adelaide: AOA; 2023.
- 2. Royal Australian College of General Practitioners (RACGP). Guidelines for Preventive Activities in General Practice (Red Book). 9th edn. Melbourne: RACGP; 2018. DDH screening recommendations.
- 3. Australian Institute of Health and Welfare (AIHW). Arthritis and other musculoskeletal conditions. Canberra: AIHW; 2023. Cat. no. PHE 285.
- 4. National Health and Medical Research Council (NHMRC). Clinical Practice Guideline for the Management of Hip and Knee Osteoarthritis. Canberra: NHMRC; 2018.
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- 8. Herring JA, Kim HT, Browne R. Legg-Calvé-Perthes disease. Part II: Prospective multicenter study of the effect of treatment on outcome. J Bone Joint Surg Am. 2004;86(10):2121–2134.
- 9. Loder RT, Skopelja EN. The epidemiology and demographics of slipped capital femorphysis. ISRN Orthop. 2011;2011:486512.
- 10. Cibulka MT, White DM, Woehrle J, et al. Hip pain and mobility deficits — hip osteoarthritis: clinical practice guidelines linked to the International Classification of Functioning, Disability, and Health from the Orthopaedic Section of the APTA. J Orthop Sports Phys Ther. 2009;39(4):A1–A25.
- 11. National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand. Peripheral arterial disease – diagnosis and management. Melbourne: NHFA; 2018.
- 12. Ficat RP. Idiopathic bone necrosis of the femoral head. Early diagnosis and treatment. J Bone Joint Surg Br. 1985;67(1):3–9.
- 13. Royal Australasian College of Physicians (RACP). Australian Clinical Guideline for Hip and Knee Osteoarthritis. Sydney: RACP; 2018.
- 14. Friedman RJ, Wysocki RW. Avascular necrosis of the femoral head. J Am Acad Orthop Surg. 2022;30(16):e1083–e1094.
- 15. Grissom LE, Harcke HT. Ultrasonography in the diagnosis and management of developmental dysplasia of the hip. Pediatr Radiol. 2023;53(4):627–638.