GC229 Hip Arthritis
Degenerative or inflammatory disease of the hip joint characterized by cartilage loss, pain, stiffness, and progressive limitation of mobility.
Hip Arthritis — GC 229 Comprehensive Exam-Ready Notes
This lecture by Professor Henry Fu (GC 229) is a case-based tour through the major causes of hip arthritis. Rather than covering one disease, the deck walks through five clinical cases, each illustrating a distinct hip pathology:
| Case | Patient | Diagnosis |
|---|---|---|
| 1 | M/55, construction worker, drinker | Avascular Necrosis (AVN) of Femoral Head |
| 2 | M/50, ex-kickboxer, Caucasian | Primary Osteoarthritis (OA) of Hip |
| 3 | M/45, IVDU | Septic Arthritis of Hip |
| 4 | F/50, childhood hip infection | Secondary OA from DDH / Old Infection |
| 5 | M/22, stiff hip | Ankylosing Spondylitis with Hip Ankylosis |
Additionally, the lecture covers Developmental Dysplasia of the Hip (DDH) classification and management, and introduces robotic-arm assisted Total Hip Arthroplasty (THA).
Learning Objectives [1]
Formulate differential diagnosis for patients with hip pain Know how to take history for patients with hip problems Recognize radiological features of common hip disorders Formulate suitable management plan
Part 1: Hip Anatomy & Blood Supply — The Foundation for Understanding AVN
The femoral head has a precarious blood supply. Understanding the vascular anatomy explains why certain traumas (femoral neck fractures, hip dislocations) and certain systemic conditions (steroid use, alcohol) lead to AVN.
Blood Supply to the Femoral Head [1]:
- 1. Profunda Femoris Artery
- 2. Medial Femoral Circumflex Artery (MFCA)
- 3. Ligamentum teres artery (from obturator artery)
- 4. Ascending branch of medial circumflex artery
60% of patients have medial and lateral femoral circumflex arteries originating from the Profunda Femoral Artery
The Profunda Femoris Artery gives rise to both the medial and lateral femoral circumflex arteries in the majority (60%) of patients [1] Majority of blood supply comes from the Medial Femoral Circumflex Artery and its retinacular branches These run posteriorly and superiorly along the femoral neck MFCA and its branches are the MAIN blood supply
Why this is important: The retinacular branches of the MFCA are end-arteries that run along the posterior-superior femoral neck. They are vulnerable to disruption in:
- Displaced femoral neck fractures (capsule disrupted → vessels torn)
- Hip dislocations (vessels stretched/torn)
- Increased intramedullary pressure (steroid/alcohol → fat emboli → vessel occlusion)
The ligamentum teres artery is small and unreliable — it cannot salvage the femoral head if the MFCA is disrupted.
Broken Shenton's Line [1]
Shenton's line is a smooth arc drawn on an AP pelvis X-ray from the inferior border of the superior pubic ramus to the medial border of the femoral neck.
What the annotated pelvis film shows: a yellow arc along Shenton’s line that is discontinuous on the abnormal hip — use it as a quick “is the head–neck–pelvis relationship right?” check before listing OA/AVN features. [1]
A broken (disrupted) Shenton's line indicates:
- Femoral neck fracture
- Hip subluxation/dislocation
- DDH
- Any displacement of the femoral head relative to the acetabulum
Part 2: Case 1 — Avascular Necrosis (AVN) of the Femoral Head
M/55, construction site worker, good past health, 3-month right groin pain, unable to work. Drinker (2 cans beer/day).
Etiology: Trauma, Nature of work, Drug/alcohol Function: Walking (level ground/stairs), Sitting tolerance, Limp, Shoes and socks, Cutting toenails, Getting on/off public transport Harris Hip Score
High Yield — Harris Hip Score
The Harris Hip Score (max 100) is the standard functional outcome measure for hip conditions. It assesses Pain (44 points), Function (47 points: gait 33, activity 14), and ROM (9 points). You should know this exists and what it measures. [1][2]
Harris Hip Score — Detailed Breakdown [1]:
| Variable | Criterion | Points |
|---|---|---|
| Pain | None, or ignores it | 44 |
| Slight, occasional | 40 | |
| Mild pain, rarely moderate | 30 | |
| Moderate pain | 20 | |
| Marked pain | 10 | |
| Totally disabled, pain in bed | 0 | |
| Function – Limp | None | 11 |
| Slight | 8 | |
| Moderate | 5 | |
| Severe | 0 | |
| Function – Support | None | 11 |
| Cane, long walks | 7 | |
| Cane, most of the time | 5 | |
| One crutch | 3 | |
| Two canes | 2 | |
| Two crutches / Not able to walk | 0 | |
| Distance walked | Unlimited | 11 |
| Six blocks | 8 | |
| Two to three blocks | 5 | |
| Indoors only | 2 | |
| Bed and chair | 0 | |
| Stairs | Normally without railing | 4 |
| Normally with railing | 2 | |
| In any manner | 1 | |
| Unable to do | 0 | |
| Shoes and socks | With ease | 4 |
| With difficulty | 2 | |
| Unable | 0 | |
| Sitting | Ordinary chair for 1 h | 5 |
| High chair for 1 h | 3 | |
| Unable to sit in any chair | 0 | |
| Public transport | Able to use | 1 |
| Unable to use | 0 |
This patient's functional status [1]:
- Mechanical right hip pain
- Walks with stick, walking tolerance 15 minutes
- Limping+
- Stairs step by step
- Sitting tolerance 30 minutes in high chair
- Difficulty putting on shoes and socks
- Drinker, 2 cans of beer everyday
| Right | Left | |
|---|---|---|
| Flexion | 90° | 130° |
| FFD (Fixed Flexion Deformity) | 10° | 0° |
| Abduction | 20° | 40° |
| Adduction | 10° | 30° |
| External rotation | 20° | 40° |
| Internal rotation | 10° | 30° |
| True LLD | 1cm shorter | — |
Key points:
- All movements restricted on the affected (right) side
- Internal rotation and abduction are typically the first and most restricted movements in hip pathology (because the capsule is tightest in these positions)
- Fixed flexion deformity of 10° (detected by Thomas' test)
- True leg length discrepancy — femoral head collapse causes shortening
Avascular necrosis is a result of impairment of circulation to the femoral head → subsequent bone death and repair → bone disease
The key concept: bone is living tissue that requires blood supply. When blood supply is interrupted, osteocytes die. The body attempts to repair the dead bone by:
- Resorption of necrotic bone (→ cysts, lucency on X-ray)
- Creeping substitution — new bone laid down on dead trabecular scaffolding (→ sclerosis on X-ray)
- If the reparative process cannot keep up with mechanical loading, the subchondral bone collapses (→ crescent sign, femoral head flattening)
- Eventually, joint incongruity leads to secondary OA
Trauma (femoral neck fracture 15-50%, hip dislocation 10-25%) Alcohol abuse Steroid ( > 20mg/day increases the risk) Caisson disease Sickle cell anaemia
| Risk Factor | Mechanism |
|---|---|
| Trauma | Direct vessel disruption (MFCA retinacular branches) |
| Alcohol | Fat infiltration of marrow → ↑ intramedullary pressure → vascular compression; direct toxic effect on osteocytes |
| Steroids | Fat hypertrophy in marrow → ↑ intramedullary pressure; fat emboli; direct osteocyte apoptosis |
| Caisson disease | Nitrogen gas bubbles form in blood during rapid decompression → vessel occlusion |
| Sickle cell | Sickled RBCs occlude small vessels in femoral head |
Additional causes (from senior notes [2]): SLE, osteomyelitis, septic arthritis, radiation.
Exam Trap — Steroid Dose
The lecture specifies > 20 mg/day prednisolone increases AVN risk. This is a commonly tested threshold. Also remember: AVN is bilateral in many cases — always image the contralateral hip.
X-ray findings:
- Cyst (resorption of dead bone + replacement with fibrous & granulation tissue)
- Sclerosis (thickened trabeculae due to direct deposition of new bone onto dead bone)
- Crescent sign (subchondral collapse of the necrotic segment)
What the AVN radiographs show: patchy femoral-head sclerosis, flattened superior contour, and (in trauma cases) neck screws or bilateral deformed heads — X-ray stages collapse; MRI still needed for pre-collapse disease. [1]
MRI: 99% sensitivity and specificity
Why MRI is so important: X-rays are often NORMAL in early AVN (Ficat Stage 1). MRI detects marrow edema and the characteristic "double-line sign" on T2-weighted images (outer dark line = sclerotic bone, inner bright line = granulation tissue) before any structural collapse occurs [2].
MRI of contralateral hip — because AVN is frequently bilateral (especially in steroid/alcohol users), always scan both sides [1].
| Ficat Stage | Criteria | X-ray Features | Treatment |
|---|---|---|---|
| I | Normal X-ray, changes only on MRI | Normal | Core decompression |
| II | Sclerotic and cystic changes, Crescent sign (subchondral radiolucency) | Sclerosis, cysts, crescent sign | Core decompression / Vascularized bone graft |
| III | Femoral head collapse, Normal joint space | Head collapse but joint space preserved | Vascularized bone graft / THR |
| IV | Secondary OA | OA changes (joint space narrowing + osteophytes) | THR |
High Yield — Ficat Stage 3 vs 4
The critical distinction: Stage 3 has femoral head collapse but normal joint space (the acetabular cartilage is still intact). Stage 4 has secondary OA changes (joint space narrowing, osteophytes). This distinction determines whether joint-preserving surgery might still be attempted.
Treatment of AVN [1]
Conservative:
- Risk factor modification (alcohol, steroid)
- Avoid heavy weight bearing (running)
- Walking aids
- Drugs: bisphosphonate (treat osteoporosis, lacking RCT evidence)
- Regeneration of bone is very slow
Core Decompression:
- Rationale: Increased intra-medullary pressure → drilling relieves pressure → allows re-vascularization and bone regeneration
Bone Graft:
- Debridement of necrotic bone
- Autograft, allograft, or artificial bone graft
Why core decompression works: In AVN, dead marrow + reactive edema increase intraosseous pressure, which further compresses the already compromised vessels. Drilling a channel into the necrotic zone releases this pressure, allows blood vessel ingrowth, and may delay or prevent collapse.
Total Hip Replacement
- Quick and reliable procedure
- Improving implant survivorship
Part 3: Case 2 — Primary Osteoarthritis of the Hip
M/50, Caucasian, bilateral mechanical hip pain for 6 months, constant non-remitting, requires 2 elbow crutches, daily analgesics. Previously professional kickboxer.
Radiological features (remember: LOSS)
- Osteophyte
- Subchondral sclerosis
- Subchondral bone cyst
- Narrowing of joint space
WEIGHT BEARING X-rays Kellgren & Lawrence scoring system
High Yield — LOSS Mnemonic for OA X-ray
Loss of joint space (earliest sign) Osteophytes Subchondral Sclerosis Subchondral cysts
Weight-bearing X-rays are essential because joint space narrowing may not be apparent on non-weight-bearing films (the cartilage is not compressed). This is a classic exam point. [1]
Why each feature occurs:
- Joint space narrowing: Loss of articular cartilage → bones get closer together
- Osteophytes: Attempted repair/stabilization at joint margins → new bone growth
- Subchondral sclerosis: With cartilage loss, bone bears more load → thickens in response
- Subchondral cysts: Synovial fluid forced through cracks in denuded bone → cyst formation; OR ischemic necrosis of subchondral bone
Primary/Idiopathic:
- Uncommon in Chinese population
Secondary:
- Trauma
- Infection (e.g., old TB hip)
- Inflammatory joint diseases (e.g., RA)
- Crystal deposition diseases (e.g., gout)
- Neuropathic (e.g., Charcot joint)
- Metabolic/endocrine
High Yield — Primary Hip OA Uncommon in Chinese
This is a lecture-specific point that examiners can test. Primary (idiopathic) hip OA is uncommon in the Chinese population compared to Caucasians. When a Chinese patient presents with hip OA, always think about secondary causes (DDH, old infection, AVN, etc.). [1]
Management of Hip OA [1]
The lecture references the AAOS Evidence-Based Clinical Practice Guideline for Management of OA of the Hip (2017) [1].
The lecture presents OA management as a tiered pyramid (from base to apex) [1]:
- Information & advice (all patients) — education, weight loss, exercise, lifestyle alterations
- Self-help — simple analgesics, topical agents, nutraceuticals
- Simple non-surgical interventions (supervised) — NSAIDs, other drugs, physiotherapy/OT, orthoses
- Advanced non-surgical interventions — injections
- Surgery (few patients) — joint-preserving surgery (osteotomy, resurfacing) or partial/total joint replacement
The pyramid is widest at the base (applicable to all patients) and narrowest at the top (applicable to few patients). Upper levels are supervised interventions.
Understand the disease, Lifestyle modification, Weight loss, Walking aids
Muscle strengthening, Range of motion exercise, Cardiopulmonary function and endurance
AAOS Evidence Strength: Strong evidence supports the use of physical therapy to improve function and reduce pain for patients with hip OA and mild to moderate symptoms (two or more "High" quality studies) [1].
Limited evidence supports the use of pre-operative physical therapy to improve early function following THA [1].
Not affect natural history
- Paracetamol (Panadol): FIRST LINE
- Tramadol: non-narcotic, combine with paracetamol for synergistic effect; use if contraindication to NSAIDs
- Opioids: CNS depression, addiction — NO routine use
Pain relief + Anti-inflammatory (synovitis, bone marrow lesions) Not affect natural history Non-selective COX-I inhibitor:
- GI toxicity: gastritis, ulceration
- Nephrotoxicity: impair renal function
AAOS Evidence Strength: Strong evidence supports that NSAIDs improve short-term pain, function, or both in patients with symptomatic hip OA (two or more "High" quality studies) [1].
Celecoxib (Celebrex) or Etoricoxib (Arcoxia) Reduced GI toxicity (~50%) Cardiovascular toxicity:
- Inhibit vasodilation → hypertension → heart attack
- Reduce anti-platelet function of Aspirin Indication: COX-I contraindication (GI bleeding), patients on Warfarin
Exam Trap — COX-II Inhibitors
COX-II inhibitors reduce GI side effects but INCREASE cardiovascular risk. This is the key trade-off. They are indicated when COX-I inhibitors are contraindicated (e.g., history of GI bleeding or concurrent warfarin use). Know the AHA/ACC guideline reference from the lecture. [1]
Components of articular cartilage (glucosamine = amino sugar, chondroitin = proteoglycan) Dietary supplement ? Cartilage regeneration, decrease degradation — evidence uncertain Side effects uncommon: GI (gas, soft stool, nausea, diarrhoea, abdominal pain)
AAOS Evidence Strength: Moderate evidence does not support the use of glucosamine sulfate — it did not perform better than placebo for improving function, reducing stiffness, or decreasing pain in hip OA [1].
Anti-inflammatory effect Increases risk of infection if surgery within 3 months
AAOS Evidence Strength: Strong evidence supports the use of intra-articular corticosteroids to improve function and reduce pain in the short-term for hip OA [1].
High Yield — IA Steroid Before Surgery
If a patient has received an intra-articular steroid injection, total hip replacement should ideally be delayed at least 3 months to reduce perioperative infection risk. This is a commonly tested point. [1]
Viscosupplementation. AAOS Evidence Strength: Strong evidence does not support the use of intra-articular hyaluronic acid — it does not perform better than placebo for function, stiffness, and pain in hip OA [1].
The definitive treatment for end-stage hip OA when conservative measures have failed. Provides excellent pain relief and functional improvement.
Part 4: Case 3 — Septic Arthritis of the Hip
M/45, unemployed, known IVDU, sudden onset left groin pain. Previous groin pseudoaneurysm, Fournier's gangrene with skin grafting.
Tenderness in left groin Localized swelling with discharge Hip held in flexion, abduction and external rotation Hip joint irritable, resisting all passive movements
Why this position? The hip capsule has maximum volume in flexion, abduction, and external rotation. When there is an effusion or pus in the joint, the hip assumes this position to minimize intracapsular pressure and pain. This is a classic examination finding for septic arthritis of the hip.
Blood tests: WBC, CRP, ESR Image-guided Hip Aspiration:
- Cell count
- Gram smear
- Bacterial / fungal / AFB cultures
- ± Crystals Blood cultures Imaging
| Colour | Clarity | WBC/mm³ | Polymorph % | |
|---|---|---|---|---|
| Normal | Straw | Translucent | < 200 | < 25% |
| Traumatic | Blood stained | Translucent | < 5000 (RBC) | < 75% |
| Rheumatoid Arthritis | Yellow | Cloudy | 15,000–80,000 | 75% |
| Septic Arthritis | Purulent | Turbid | > 100,000 | > 75% |
| Periprosthetic Joint Infection (TKA/THA) | Purulent | Turbid | > 3,000 | > 80% |
High Yield — Synovial Fluid Thresholds
Learn the WBC cutoffs: Normal < 200, Inflammatory 2,000–100,000, Septic > 50,000–100,000. For periprosthetic joint infection, the threshold is much LOWER ( > 3,000 WBC, > 80% PMN) because the prosthetic environment alters the immune response. This difference is frequently tested. [1]
X-rays: soft-tissue swelling, hip joint capsular distension (widening of joint space or subluxation), proximal femoral metaphysis changes → osteomyelitis MRI: most useful test to distinguish proximal femoral osteomyelitis from septic arthritis Radioisotope scan
Antibiotics — AFTER joint fluid/synovium obtained for culture, unless hemodynamic instability Early initiation of antibiotics before obtaining specimens risks negative culture → affects antibiotic regime
Surgical Drainage:
- Anterior approach in young to preserve blood supply
- Posterior approach when hip destruction not salvageable (need for replacement)
- Surgical drainage with antibiotic cement spacer
Critical Principle — Culture Before Antibiotics
In septic arthritis, ALWAYS obtain joint aspirate for culture BEFORE starting antibiotics (unless the patient is hemodynamically unstable). Starting antibiotics first may sterilize the culture and you lose the opportunity to identify the organism and target therapy. [1]
Secondary OA Pain due to joint incongruency and chondral damage Stiffness due to ankylosis and soft tissue contracture (flexion and adduction contracture) Deformity: angulation, coxa vara, shortening Instability, dislocation Leg length discrepancy
Part 5: Case 4 — Secondary OA from DDH / Old Infection
F/50, right hip pain for many years. Childhood right hip infection → cast for 1 year. Right femoral osteotomy in Shanghai as teenager. Now: significant right hip pain, walks with stick, 30min walking tolerance, daily analgesics, difficulty with shoes/socks, significant LLD and back pain.
- True LLD: -4cm (right shorter)
- Right hip: Flexion 110°, FFD 0°, Abduction 30°, Adduction 20°, ER 30°, IR 20°
- Old ischium scar
Unstable, poor functioning hip Significant leg length discrepancy Proximal femur deformity Management: Total Hip Replacement
Joint: Restore pain-free stable joint Bone:
- Acetabular side: Restore anatomical hip centre
- Femoral side: Correct femoral side deformity Soft tissue:
- Contracted muscles, ligaments and joint capsule
- Sciatic nerve (risk of stretch injury with leg lengthening)
- Femoral shortening (to protect nerve)
The lecture demonstrates robotic-arm assisted THA and 3D-printed metal cutting jig for proximal femur wedge osteotomy — these are advanced techniques used for complex cases with significant deformity [1].
Part 6: Developmental Dysplasia of the Hip (DDH) — Classification
Radiological Measurements [1]
Normal: > 25° Dysplastic: < 20°
This angle measures the coverage of the femoral head by the acetabulum. A small angle means inadequate coverage → the femoral head is not properly contained → subluxation → secondary OA.
Normal: < 10° Dysplastic: > 10°
The Tönnis angle measures the inclination of the acetabular weight-bearing surface. A steep (high) angle means the weight-bearing force is directed laterally rather than medially → poor containment.
Dysplasia → Low Dislocation → High Dislocation
This classifies the severity of DDH in adults for surgical planning.
Based on percentage of proximal migration of medial neck-neck junction from inferior margin of acetabulum (teardrop)
The migration percentage is calculated as: L (%) = D / (H/5), where D = vertical migration distance from the teardrop to the medial femoral neck junction, and H = total pelvic height [1].
- Crowe I: < 50%
- Crowe II: 50-75%
- Crowe III: 75-100%
- Crowe IV: > 100%
Assumes femoral head height is 20% of pelvic height
Periacetabular Osteotomy (PAO):
- Indication: Symptomatic dysplasia in young adult with concentrically reduced hip and congruent joint space
- Before OA changes develop
Total Hip Replacement:
- Secondary OA changes
- Hip subluxation
High Yield — PAO vs THR Decision
PAO is for young patients with dysplasia but no OA changes yet — the goal is to improve acetabular coverage and prevent/delay OA. Once OA has developed, PAO is no longer appropriate and THR is needed. [1]
Part 7: Case 5 — Ankylosing Spondylitis with Hip Involvement
M/22, referred for "left hip AVN". Left hip stiffness for 3 years. Walking with stick 30 min, limping, difficulty sitting in normal chair, cannot manage shoes and socks. Minimal hip pain or back pain.
| Right | Left | |
|---|---|---|
| Flexion | 130° | 40° |
| FFD | 0° | 40° |
| Abduction | 40° | 15° |
| Adduction | 30° | -15° |
| ER | 30° | 15° |
| IR | 10° | -15° |
Left hip ankylosed at 40° flexion, 15° abduction, 15° external rotation Left hip abductor contraction palpable Schober test: excursion only 5mm (normal > 5cm) Chest expansion: 2cm (normal > 5cm)
Why Schober's test and chest expansion matter: These are screening tests for ankylosing spondylitis (AS). Reduced Schober's excursion indicates lumbar spine fusion; reduced chest expansion indicates costovertebral joint involvement. This patient was misdiagnosed as "AVN" — but the findings point to AS with hip ankylosis.
Clinical photographs [1]: The patient demonstrates a markedly stooped posture with forward flexion of the trunk on lateral view, with flexed hips and knees while standing. The frontal view shows trunk asymmetry/tilting. These postural findings are characteristic of advanced AS with loss of lumbar lordosis and fixed hip flexion deformity.
Multidisciplinary approach: Rheumatologist:
- Diagnosis of Ankylosing Spondylitis
- Medical treatment
- Screening of associated disorders Orthopaedic Surgeon:
- Hip (conversion to THR)
- Spine
Total hip replacement — conversion of ankylosed hip
Part 8: Total Hip Replacement — Key Concepts
THR involves replacing both the acetabular and femoral sides of the joint:
- Acetabular component: Metal shell + polyethylene or ceramic liner (reamed into the acetabulum)
- Femoral component: Metal stem inserted into the femoral canal + head (metal or ceramic)
GT (Greater Trochanter), Head, Acetabulum — these are the landmarks to identify on post-op X-rays.
- Cemented: Polymethylmethacrylate (PMMA) cement bonds implant to bone. Better for elderly/osteoporotic bone.
- Uncemented (press-fit): Implant has porous coating for bone ingrowth. Better for young, active patients with good bone quality.
- Hybrid: Cemented stem + uncemented cup (or vice versa).
| Early | Late |
|---|---|
| Infection | Aseptic loosening (most common late complication) |
| Dislocation | Periprosthetic fracture |
| DVT/PE | Wear and osteolysis |
| Nerve injury (sciatic) | Periprosthetic infection |
| Leg length discrepancy | Heterotopic ossification |
| Periprosthetic fracture | Implant failure |
The hip joint consists of acetabular side, articular surface and femoral side — describe radiological features by location Common hip disorders [AVN, OA, Septic Arthritis, DDH, AS]
Epidemiology of Hip Disorders Requiring THR (lecture data) [1]:
| Disorder | Total | Male | Female |
|---|---|---|---|
| Osteonecrosis | 41.2% | 50.9% | 33.0% |
| Osteoarthritis | 12.5% | 5.1% | 18.8% |
| Post-traumatic | 12.5% | 8.5% | 15.8% |
| Ankylosing spondylitis | 10.4% | 19.5% | 2.5% |
| Rheumatoid arthritis | 6.3% | 2.5% | 9.4% |
| Dysplasia | 6.3% | 4.1% | 8.0% |
| Past TB infection | 1.8% | 0.9% | 2.5% |
| Others | 9.2% | 8.5% | 9.9% |
Note: Osteonecrosis (AVN) is the most common indication for THR in this population, especially in males. Primary OA is relatively uncommon, consistent with the lecture point that primary hip OA is uncommon in the Chinese population.
Early referral for specialist care can significantly improve patient's function Total hip replacement is a reliable and durable treatment option for patients with end-stage arthritis
Exam Intelligence
| Trap | How to Avoid |
|---|---|
| Confusing AVN stages — "crescent sign = Stage 4" | Crescent sign = Stage 2 (subchondral radiolucency). Stage 3 = femoral head collapse. Stage 4 = secondary OA. |
| Primary hip OA in a Chinese patient | Uncommon — always look for secondary causes |
| Starting antibiotics before joint aspiration in septic arthritis | Culture FIRST (unless hemodynamically unstable) |
| Septic arthritis joint aspiration threshold WBC for native vs prosthetic joint | Native: > 100,000; Prosthetic: > 3,000 |
| IA steroid injection before THR | Delay surgery ≥ 3 months to reduce infection risk |
| Confusing PAO vs THR indication in DDH | PAO = young, no OA, congruent joint. THR = OA changes or subluxation. |
| Missing AS in a young patient with "hip stiffness" | Check Schober's test and chest expansion |
| COX-II "safer than COX-I" | Safer for GI, but MORE cardiovascular risk |
| Paracetamol vs NSAIDs as first-line for OA | Paracetamol is FIRST LINE per lecture |
| Condition | Age | Key History | Key Exam | Key Investigation |
|---|---|---|---|---|
| AVN | 30-60 | Steroid/alcohol/trauma | ↓ROM, LLD | MRI (99% sens/spec), Ficat staging |
| Primary OA | > 50 | Mechanical pain, occupation | Crepitus, ↓ROM | Weight-bearing XR (LOSS) |
| Septic Arthritis | Any | IVDU, fever, acute onset | Flexion/abduction/ER, irritable hip | Joint aspiration (WBC > 100k) |
| DDH with secondary OA | 30-50 | Childhood hip problem | LLD, Trendelenburg +ve | CE angle < 20°, Tönnis > 10° |
| AS | 15-40 | Back stiffness, morning stiffness | Schober's ↓, chest expansion ↓, hip ankylosis | HLA-B27, sacroiliac XR/MRI |
- GC 074 (Multiple Joint Pain) [10]: Provides the framework for differentiating inflammatory vs degenerative arthritis, seropositive vs seronegative arthritis — important for Case 5 (AS).
- GC 075 (Painful Red Joint) [11]: Covers septic arthritis approach in detail, including Kocher criteria for pediatric septic arthritis vs transient synovitis — relevant to Case 3.
- GC 237 (MSK Infection) [12]: Updated 2025 lecture on musculoskeletal infection — septic arthritis management, antibiotic choices.
- CFB OT04 (Reconstruction) [13]: Covers THR in more detail — implant types, approaches, complications.
- GC 228 (Knee OA Parts A & B) [14]: OA management principles are largely shared between hip and knee — the analgesic ladder, physiotherapy, and surgical thresholds are similar.
High Yield Summary
-
AVN
- Precarious blood supply (MFCA main supply) → steroid/alcohol/trauma → Ficat staging (I-IV) → Stage 1-2: core decompression ± bone graft; Stage 3-4: THR. MRI 99% sensitive. Always image contralateral hip.
-
Hip OA
- LOSS on weight-bearing XR (Loss of joint space, Osteophytes, Subchondral Sclerosis/cysts).
- Primary uncommon in Chinese.
- Management ladder: education → PT → paracetamol (first line) → NSAIDs (GI/renal toxicity) → COX-II (CV risk) → IA steroid (delay THR ≥ 3 months) → THR.
-
Septic Arthritis
- EMERGENCY. Hip held in flexion/abduction/ER. Aspirate BEFORE antibiotics. WBC > 100,000 ( > 3,000 for prosthetic joints). Surgical drainage essential.
-
DDH
- CE angle < 20° = dysplastic. Young + no OA → PAO. OA/subluxation → THR.
-
Ankylosing Spondylitis
- Young male, hip ankylosis, ↓ Schober's, ↓ chest expansion. MDT approach (rheumatology + orthopaedics). THR for ankylosed hip.
-
Harris Hip Score
- Pain (44) + Function (47) + ROM (9) = 100. Standard outcome measure.
-
IA steroid before THR
- Wait ≥ 3 months (infection risk).
Active Recall - Hip Arthritis (GC 229)
[1] Lecture slides: GC 229. Hip Arthritis.pdf (all pages cited throughout) [2] Senior notes: Maksim Surgery Notes.pdf (pp. 254-255, 270, 283) [3] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (pp. 1663-1673) [10] Lecture slides: GC 074. Multiple joint pain.pdf [11] Lecture slides: GC 075. Pain red joint.pdf [12] Lecture slides: GC 237. Musculoskeletal infection [Updated in 2025].pdf [13] Lecture slides: CFB (OT04) Reconstruction.pdf [14] Lecture slides: GC 228. Knee Osteoarthritis_Part A.pdf / Part B.pdf
GC228 Knee Osteoarthritis: Part B
Knee osteoarthritis is a degenerative joint disease involving progressive cartilage loss, subchondral bone changes, and inflammation of the knee, with Part B focusing on its clinical management, rehabilitation, and surgical treatment options.
GC230 Knee Sport Injuries: Part 1
Knee sport injuries encompass a spectrum of traumatic musculoskeletal conditions—including ligament tears (ACL, MCL, PCL, LCL), meniscal injuries, and patellar dislocations—commonly resulting from high-impact or pivoting athletic activities.