Hip Osteoarthritis

Hip osteoarthritis is a degenerative joint disease characterized by progressive loss of articular cartilage, subchondral bone remodeling, and osteophyte formation in the hip joint, leading to pain, stiffness, and impaired mobility.

2. Epidemiology

3. Risk Factors

Risk Factor	Mechanism
Age (> 60y)	Cumulative cartilage wear + reduced chondrocyte regenerative capacity + senescent cell accumulation
Female sex	Post-menopausal oestrogen decline → reduced chondroprotection; ligamentous laxity
Genetics / Family history	Polymorphisms in collagen type II (COL2A1), GDF5, and other structural genes
Ethnicity	Primary hip OA less common in Chinese/Asian populations vs. Caucasians
Hip morphology	Acetabular dysplasia (DDH), cam/pincer FAI → abnormal contact stresses

Risk Factor	Mechanism
*Obesity* ^[4]	Increased mechanical load on weight-bearing joints; adipokines (leptin, adiponectin) promote a pro-inflammatory catabolic state in cartilage
*Previous trauma* ^[2]^[4]	Direct cartilage damage → focal loss of cartilage → altered joint biomechanics → progressive degeneration
*Occupation* ^[4]	Repetitive loading (e.g., farming, heavy manual labour) → chronic microtrauma to cartilage
Muscle weakness	Weak hip abductors/extensors → poor dynamic joint stabilisation → increased cartilage contact pressures
Steroid use	Predisposes to AVN → secondary OA
Alcohol	Predisposes to AVN → secondary OA
Low bone density	Paradoxically, some evidence suggests low BMD may be protective against OA (less stiff subchondral bone); however, the relationship is complex

The 'Defective Load vs. Defective Cartilage' Framework

A useful way to conceptualise secondary OA aetiology ^[2]:

Defective Load (abnormal forces on normal cartilage):

Force: obesity, occupational overuse
Area: joint dysplasia (e.g., DDH) — same force over a smaller contact area = higher stress per unit area

Defective Cartilage (normal forces on abnormal cartilage):

Damage: trauma, haemophilia (recurrent haemarthroses)
Disease: inflammatory (RA), metabolic (gout), infection (septic arthritis, TB)
Unsupported: AVN (dead subchondral bone → cartilage loses its structural foundation → collapse)

4. Anatomy and Function of the Hip Joint

Understanding the anatomy is essential for understanding why hip OA presents the way it does and why certain surgical approaches carry specific risks.

Superficial muscles: gluteus medius and minimus (abductors; superior gluteal nerve) ^[2]:

These are the primary hip abductors.
They are critical for the Trendelenburg mechanism: during single-leg stance (as in walking), the abductors on the stance side contract to keep the pelvis level. If they are weak or their lever arm is shortened (e.g., by femoral head collapse in OA, or by a shortened femoral neck), the pelvis drops on the contralateral side → Trendelenburg sign positive → Trendelenburg gait (waddling gait).

Deep muscles: piriformis (at the exit of the sciatic nerve) ^[2]:

Clinically relevant because the sciatic nerve exits the pelvis below the piriformis (in most people), so piriformis pathology can cause sciatica-like symptoms.

Hip Muscles Summary ^[2]:

Compartment	Muscles	Action	Nerve
Anterior	Quadriceps femoris, Sartorius, Pectineus, Iliopsoas	Knee extension (quads); Hip flexion (iliopsoas, sartorius)	Femoral nerve (L2–L4)
Medial	Adductor magnus/longus/brevis, Gracilis, Obturator externus	Hip adduction	Obturator nerve (L2–L4)
Posterior	Hamstrings (biceps femoris, semitendinosus, semimembranosus)	Hip extension, Knee flexion	Sciatic nerve (L4–S3)
Lateral/gluteal	Gluteus medius & minimus	Hip abduction	Superior gluteal nerve (L4–S1)
Lateral/gluteal	Gluteus maximus	Hip extension, external rotation	Inferior gluteal nerve (L5–S2)

Why does the hip adopt an externally rotated posture in OA?

Externally rotated limb on supine position ^[2]: In hip OA, inflammation and effusion increase intra-articular pressure. The hip joint capsule has its greatest volume in slight flexion, abduction, and external rotation — this is the position of maximum capsular relaxation and least intra-articular pressure. The patient therefore subconsciously holds the hip in this position for pain relief. Over time, the capsule contracts in this position, leading to a fixed flexion and external rotation deformity.

5. Etiology (Focus on Hong Kong)

Secondary causes are the dominant aetiology in Hong Kong. The lecture slides provide a classification ^[1]:

Category	Examples	Relevance to Hong Kong
*Trauma*	Femoral neck fractures, acetabular fractures, hip dislocations	Post-traumatic OA in young adults
*Infection*	Septic arthritis, *old TB hip*	TB hip is specifically highlighted; historically significant in HK
*Inflammatory joint diseases*	*e.g., Rheumatoid Arthritis*	RA causes cartilage destruction → secondary OA
*Crystal deposition diseases*	*e.g., Gout*	Gout can affect the hip (uncommon but recognised)
*Neuropathic*	*e.g., Charcot joint*	Seen in diabetic neuropathy, tabes dorsalis (tertiary syphilis)
*Metabolic/Endocrine*	Haemochromatosis, acromegaly, hyperparathyroidism	Less common but examinable
Developmental	DDH (developmental dysplasia of the hip)	Significant in Chinese population — shallow acetabulum → increased contact stress → early OA
AVN	Steroid use, alcohol, SLE, sickle cell, caisson disease, trauma	Very relevant in HK: SLE common in Chinese women → steroid use → AVN → OA

6. Pathophysiology

Understanding the pathophysiology of OA is fundamental. The lecture slides provide an excellent diagram of the molecular biology ^[3].

7. Classification

Type	Description
Primary (Idiopathic)	No identifiable underlying cause; age-related degeneration; *uncommon in Chinese*
Secondary	Identifiable predisposing cause (see Etiology section above)

This is the most widely used radiological grading system for OA severity:

Grade	Findings	Clinical Correlation
0	Normal	No OA
1	Doubtful: possible osteophytic lipping	Questionable OA
2	Minimal: definite osteophytes, possible joint space narrowing	Mild OA
3	Moderate: moderate osteophytes, definite joint space narrowing, some sclerosis	Moderate OA
4	Severe: large osteophytes, marked joint space narrowing, severe sclerosis, bone deformity	Severe OA (bone-on-bone)

8. Clinical Features

Symptom	Description	Pathophysiological Basis
*Pain*	Deep groin pain, often radiating to the *anterior thigh and knee* ^[2]. *Aggravated by weight-bearing and exertion, relieved by rest* ^[2]. In advanced OA, rest pain and night pain develop.	Early: Subchondral bone microfractures, synovitis (inflammatory mediators activate nociceptors). Cartilage itself is aneural — it has no nerve endings — so cartilage loss alone does not cause pain. Pain comes from: (1) subchondral bone (richly innervated periosteum exposed), (2) synovitis, (3) capsular stretching/fibrosis, (4) periarticular muscle spasm, (5) osteophyte impingement.
*Morning stiffness*	*< 30 minutes* after immobility ^[2]. Short-lived compared to inflammatory arthritis (which typically has > 60 min). *More prominent in hip OA than knee OA* ^[2].	During rest, synovial fluid redistributes away from the joint surfaces, and the inflamed/thickened capsule stiffens. With gentle movement, fluid returns and the capsule "loosens up." In RA, ongoing active inflammation means it takes much longer for stiffness to resolve.
Stiffness / Loss of range	Progressive difficulty with certain movements — particularly internal rotation (lost earliest), abduction, and flexion. Difficulty putting on shoes and socks, cutting toenails ^[1].	Osteophyte formation at joint margins physically blocks movement. Capsular fibrosis and thickening limit range. The capsule is tightest in internal rotation and extension → these are lost first.
Swelling	*Intermittent (effusion) or continuous (capsule thickening)* ^[2]	Effusion: inflammatory mediators increase synovial fluid production. Capsule thickening: chronic low-grade synovitis → fibrosis. Hip effusion is deep and rarely visible (unlike knee), but may be detected on ultrasound.
Deformity	Progressive external rotation, flexion, and adduction posture of the affected limb → apparent leg-length discrepancy.	Capsular contracture in the position of maximum volume (flexion, external rotation, slight abduction initially → then adduction as adductors tighten). Fixed flexion deformity tilts the pelvis → compensatory lumbar lordosis.
Loss of function	Difficulty walking, climbing stairs, using public transport, sitting for prolonged periods ^[1].	Combination of pain, stiffness, mechanical block, and muscle weakness.
Limp	Two types: (1) *Antalgic gait* — short stance phase on affected side (pain avoidance); (2) *Trendelenburg gait* — trunk sways over affected side (abductor weakness) ^[2].	Antalgic: pain causes the patient to spend less time weight-bearing on the affected leg. Trendelenburg: gluteus medius/minimus weakness (from disuse atrophy, or shortened lever arm due to femoral head migration) → pelvis drops on the contralateral side during single-leg stance → compensatory trunk lean towards the affected side.
*Referred knee pain*	Hip pathology presenting as knee pain, especially in children (Perthes, SCFE).	*Hilton's Law*: obturator nerve (L2–L4) supplies both hip and knee joints → convergence of afferent signals in the dorsal horn of the spinal cord → brain misinterprets origin ^[2].

Pain Pattern in Hip OA

The classic pattern is groin pain radiating to the anterior thigh and sometimes to the knee. Buttock pain is less typical of hip OA and should make you think of sacroiliac joint pathology, lumbar spine disease, or piriformis syndrome. Lateral hip pain suggests trochanteric bursitis or gluteus medius tendinopathy rather than intra-articular hip OA.

Sign	Description	Pathophysiological Basis
*Externally rotated limb on supine position* ^[2]	The affected leg lies in external rotation when the patient is supine.	The hip capsule has its greatest volume in slight flexion, abduction, and external rotation → this is the "resting position" of least intra-articular pressure → patient splints the hip here. Chronic capsular contracture maintains this position.
*Antalgic gait* ^[2]	Shortened stance phase on the affected side; the patient "hurries off" the painful leg.	Pain avoidance mechanism — minimising time spent loading the affected hip.
*Trendelenburg gait* ^[2]	Trunk lurches towards the affected side during stance phase; pelvis drops on the contralateral side.	Hip abductor (gluteus medius/minimus) insufficiency — from disuse atrophy, pain inhibition, or mechanical disadvantage (shortened femoral neck from OA, femoral head migration → reduced abductor lever arm).
Positive Trendelenburg test	When standing on the affected leg, the contralateral pelvis drops (normally it should rise or stay level).	Same mechanism as Trendelenburg gait — tests abductor function.
*Painful passive movement with reduced ROM* ^[2]	Internal rotation is lost first, followed by extension, abduction, and then flexion. Pain at end-range.	Osteophytes and capsular contracture limit movement. The capsule is most taut in internal rotation and extension → these are restricted earliest. Pain is from periosteal nociceptors on osteophytes, capsular stretch, and subchondral bone.
Crepitus	Grating/grinding sensation felt on passive movement.	Irregular, roughened articular surfaces (fibrillated/eroded cartilage, exposed bone) rubbing against each other.
*Fixed flexion deformity (Thomas test positive)* ^[2]	*End-stage* finding. The hip cannot be fully extended. Thomas test: flex the contralateral hip fully to flatten the lumbar lordosis → the affected hip will flex up off the bed if a fixed flexion deformity is present.	Chronic capsular contracture in flexion. The patient compensates by increasing lumbar lordosis (which masks the flexion deformity during casual observation — Thomas test eliminates this compensation).
Apparent leg-length discrepancy	The affected leg appears shorter despite equal true leg lengths.	Fixed adduction contracture → functional shortening. Fixed abduction contracture → apparent lengthening. True shortening can occur if the femoral head migrates superiorly (bone loss, cartilage loss).
Muscle wasting	Wasting of gluteal muscles and quadriceps on the affected side.	Disuse atrophy from pain-limited activity and reduced joint loading. Gluteal wasting exacerbates the Trendelenburg mechanism.

Examination Sequence — Hip OA

Look (gait, posture, deformity, muscle wasting, scars, leg-length discrepancy) → Feel (tenderness over groin/greater trochanter, warmth) → Move (active → passive ROM: flexion, extension, abduction, adduction, internal rotation, external rotation; note pain, crepitus, and end-feel) → Special tests (Thomas test for fixed flexion deformity, Trendelenburg test for abductor function, leg-length measurement) → Neurovascular (distal pulses, sensation, motor power)

This is a commonly tested comparison ^[2]:

Feature	*Degenerative (OA)*	*Inflammatory (RA)*
*Joint involvement*	*Weight-bearing joints: knee, hip, L-spine, C-spine; Small hand joints: 1st CMC, IPJ*	*Any joint (especially MCP, PIP, wrist)*
*Bone density*	*Preserved*	*Juxta-articular osteopenia*
*Periarticular bony erosion*	No	*Yes*
*Reactive bony changes*	*Yes (osteophytes, sclerosis)*	No
Morning stiffness	< 30 min	> 60 min
Swelling	Bony (osteophytes)	Soft, boggy (synovial thickening)
Systemic features	Absent	Present (fatigue, fever, weight loss)
Lab findings	Normal ESR/CRP (or mildly elevated)	Elevated ESR/CRP, RF+, anti-CCP+

Before confirming hip OA, exclude other causes of hip pain ^[2]:

Condition	Key Distinguishing Features
Femoral neck fracture	Acute onset after trauma/fall; shortened, externally rotated leg; unable to weight-bear
AVN of femoral head	Younger patient; risk factors (steroids, alcohol, SLE); MRI shows double-line sign; early: limited IR and abduction with pain
Sciatica (lumbar radiculopathy)	Pain radiates below the knee, follows dermatomal distribution; positive SLR; neurological deficit
Trochanteric bursitis / Greater trochanteric pain syndrome	Lateral hip pain over the greater trochanter; tender on palpation; pain lying on affected side
Gluteus medius tendinopathy	Similar to trochanteric bursitis; lateral hip pain; difficulty side-lying
Septic arthritis	Acute onset; fever; very painful, hot, swollen joint; elevated WCC/CRP; joint aspiration diagnostic
Inflammatory arthritis (RA, AS)	Prolonged morning stiffness (> 60 min); systemic features; young patient (AS: HLA-B27+, sacroiliitis)
Referred pain from lumbar spine	Back pain with radicular component; neurological signs; no hip ROM restriction
DDH (in young adults)	Groin pain in young women; X-ray shows acetabular dysplasia; history of childhood hip problems
Perthes disease / SCFE	Children/adolescents; limited IR; specific X-ray findings

Pathological Process	Clinical Feature(s)
Cartilage loss → bone-on-bone contact	Pain on weight-bearing, crepitus
Synovitis (inflammatory mediators)	Effusion, pain, morning stiffness
Capsular fibrosis/contracture	Reduced ROM (IR lost first), fixed flexion deformity
Subchondral bone stress	Rest pain, night pain (advanced)
Osteophyte formation	Mechanical block, pain at end-range, bony enlargement
Abductor dysfunction	Trendelenburg sign/gait
Pain avoidance	Antalgic gait
Obturator nerve convergence	Referred knee pain

High Yield Summary

Hip OA = joint failure — involves cartilage, subchondral bone, synovium, capsule, and periarticular muscles.
Primary hip OA is uncommon in the Chinese population — always think secondary causes in Hong Kong.
Secondary causes to know: DDH, AVN (steroids > 20 mg/day, alcohol, trauma, SLE, caisson disease, sickle cell), infection (old TB hip), inflammatory arthritis (RA), crystal deposition (gout), neuropathic (Charcot), metabolic/endocrine.
AVN risk factors: Trauma (femoral neck fracture 15–50%, hip dislocation 10–25%), alcohol, steroids, caisson disease, sickle cell.
Radiological features (LOSS): Loss of joint space (earliest), Osteophytes, Subchondral sclerosis, Subchondral cysts.
Key symptoms: Deep groin pain aggravated by weight-bearing, morning stiffness < 30 min, stiffness (difficulty with shoes/socks), loss of function (walking, stairs, public transport).
Key signs: Externally rotated limb at rest, antalgic gait, Trendelenburg gait (end-stage), painful limited ROM (IR lost first), fixed flexion deformity (Thomas test +), muscle wasting.
Internal rotation is the first movement lost — because the capsule is tightest in IR.
Hip pain can be referred to the knee (Hilton's Law; obturator nerve L2–L4) — always examine the hip when a patient presents with knee pain.
DDH management: Periacetabular osteotomy if congruent joint space preserved and no OA; THR if secondary OA established.
Natural history: Molecular → Pre-radiographic (MRI) → Radiographic (X-ray) → End-stage (joint replacement). Intervene early for best outcomes.
Harris Hip Score evaluates pain, function (walking, stairs, shoes/socks, sitting, public transport), deformity, and ROM.
OA vs RA: OA = weight-bearing joints, preserved bone density, osteophytes, no erosions. RA = any joint, juxta-articular osteopenia, erosions, no reactive bony changes.

Active Recall - Hip Osteoarthritis (Pre-DDx/Dx/Mx)

Differential Diagnosis of Hip Pain

The first learning outcome of the hip arthritis lecture is to formulate differential diagnosis for patients with hip pain ^[1]. This is critical because "hip pain" is a symptom, not a diagnosis — and many conditions masquerade as hip OA. Your job is to systematically work through the possibilities, guided by the patient's age, pain location, onset, and associated features.

Systematic Differential Diagnosis by Category

Condition	Key Distinguishing Features	Why It Mimics OA
Hip OA (the index diagnosis)	Chronic groin pain, mechanical pattern (worse with activity, better with rest), morning stiffness < 30 min, LOSS on X-ray	—
Avascular necrosis (AVN)	Younger patient; risk factors (steroids > 20 mg/day, alcohol, trauma — femoral neck fracture 15–50%, hip dislocation 10–25%, caisson disease, sickle cell) ^[1]; insidious groin pain; limited abduction and internal rotation ^[5]; X-ray: osteopenia → sclerosis → crescent sign; MRI: double-line sign on T2W ^[5]	Both cause deep groin pain with restricted ROM. AVN may progress to secondary OA, so early AVN can look identical. The key is the risk factor profile and MRI findings before X-ray changes appear.
Inflammatory arthritis (RA, AS)	RA: morning stiffness > 60 min, polyarticular, systemic features (fatigue, fever), RF+/anti-CCP+, juxta-articular osteopenia and erosions on X-ray. AS: young male (< 40), insidious back pain improving with exercise, HLA-B27+, fusion of SI joint on X-ray ^[2]; bilateral hip involvement common	Inflammatory arthritis can cause secondary hip OA. Distinguished by prolonged morning stiffness, systemic features, and lab/imaging findings.
Infection — septic arthritis / old TB hip ^[1]	Septic arthritis: acute onset, fever, very painful joint held in flexion/ER, unable to weight-bear, elevated WCC/CRP/ESR, joint aspiration is diagnostic (purulent fluid, WCC > 50,000, culture +). Old TB hip: chronic, indolent; may present with secondary OA changes years later; look for soft-tissue swelling, joint capsular distension (with widening of joint space or even subluxation), and radiographic changes in proximal femoral metaphysis suggesting osteomyelitis on X-ray ^[6]; MRI may be the most useful test to distinguish proximal femoral osteomyelitis from septic arthritis ^[6]	Septic arthritis is an emergency — don't confuse acute joint pain for an OA flare. TB hip is historically important in HK and causes chronic destruction mimicking OA.
Crystal deposition — gout / pseudogout ^[1]	Acute flares of severe pain, swelling, erythema. Gout: elevated urate, needle-shaped negatively birefringent crystals on aspirate. Pseudogout (CPPD): chondrocalcinosis on X-ray, rhomboid-shaped weakly positively birefringent crystals	Crystal arthropathy can cause acute-on-chronic hip pain. The hip is an unusual site for gout but is recognised.
Neuropathic arthropathy (Charcot joint) ^[1]	Grossly destructive joint changes with relatively less pain than expected (pain-sensation mismatch). Causes: diabetes (most common in foot), tabes dorsalis (syphilis — hip/knee), syringomyelia	Loss of proprioception and pain → unregulated mechanical stress → rapid joint destruction. X-ray shows dramatic destruction with debris, subluxation, and disorganisation.
Acetabular labral tear	Young active adults; mechanical symptoms (clicking, catching, giving way); groin pain worse with pivoting/twisting; positive anterior impingement test (FADIR: Flexion-Adduction-Internal Rotation reproduces groin pain); MR arthrogram diagnostic	Can coexist with early OA or FAI. Pain pattern overlaps with early OA but the mechanical symptoms (clicking/catching) are a key distinguishing feature.
Femoroacetabular impingement (FAI)	Young adults; cam type (femoral head asphericity) or pincer type (acetabular over-coverage); groin pain with prolonged sitting and activity; positive FADIR test; alpha angle > 55° on X-ray/MRI	FAI is a pre-arthritic condition that predisposes to OA. Important to identify early because corrective surgery may delay OA.
DDH (in adults)	Young women; groin pain; X-ray shows hip dysplasia (inadequate acetabular coverage) ^[2], broken Shenton's line, subluxation; may present with early secondary OA	DDH causes secondary OA through increased contact stress over a smaller area. Management: periacetabular osteotomy before OA changes; THR if secondary OA established ^[1].
Fractures ^[2]	Femoral neck fracture: elderly with osteoporosis (fragility fracture) or young with high-energy trauma; acute onset; shortened, abducted, externally rotated leg ^[7]; unable to weight-bear; disrupted Shenton's line on X-ray. Stress/insufficiency fracture: insidious onset in runners or osteoporotic elderly; normal X-ray initially → MRI diagnostic	Acute fracture is usually obvious. Beware the occult/stress fracture with insidious onset that may be mistaken for OA — if X-ray is normal but suspicion is high, get an MRI.
Perthes disease / SCFE (paediatric)	Perthes: boys aged 5–10, hip pain, limited IR and abduction, X-ray: flattening/sclerosis/fragmentation of femoral epiphysis ^[8]. SCFE: obese boys aged 10–15, hip pain radiating to knee, loss of IR/abduction/flexion, X-ray: posterior displacement of epiphysis ^[8]	In children/adolescents with hip pain — always think of these. Both can present with referred knee pain. Perthes leads to deformed femoral head → secondary OA in adulthood.

Condition	Key Distinguishing Features	Why It's in the DDx
Trochanteric bursitis / Greater trochanteric pain syndrome (GTPS) ^[2]	Lateral hip pain over the greater trochanter; tenderness on direct palpation of the greater trochanter; pain lying on the affected side at night; full hip ROM on examination (unlike OA where ROM is restricted); no groin pain	This is one of the most common conditions confused with hip OA. The key differentiator is pain location — lateral (trochanteric) vs. groin (intra-articular OA) — and preserved ROM.
Gluteus medius tendinopathy ^[2]	Very similar to trochanteric bursitis; lateral hip pain; may have weakness of hip abduction (resisted abduction reproduces pain); often seen in middle-aged women	Now considered part of the GTPS spectrum. Distinguished from OA by lateral (not groin) pain and preserved passive ROM. Can coexist with hip OA.
Iliopsoas bursitis/tendinopathy	Anterior groin pain worse with hip flexion against resistance; may have snapping ("snapping hip" — the iliopsoas tendon flicks over the iliopectineal eminence)	The groin pain can mimic hip OA, but ROM is usually preserved and pain is specifically reproduced by resisted flexion.
Adductor strain	Medial thigh/groin pain; tenderness over adductor origin (pubic tubercle); pain on resisted adduction	Common in athletes. Pain location overlaps with hip OA but onset is usually acute/subacute after a sporting event.

Condition	Key Distinguishing Features	Why It's in the DDx
Sciatica / Lumbar radiculopathy ^[2]^[9]	Pain radiates below the knee, follows a dermatomal distribution (L4/L5/S1); numbness, tingling; positive straight leg raise (SLR); may have neurological deficit (weakness, reflex changes); hip ROM is full	Sciatica is a non-specific term describing a variety of leg and back symptoms ^[9]. Radiculopathy at L5–S1 from a herniated disc causes sharp or burning pain that radiates down the posterior or lateral aspect of the leg, usually to the foot or ankle ^[9]. The key is that hip examination is normal — full ROM, no groin tenderness.
Lumbar spinal stenosis	Neurogenic claudication: bilateral leg heaviness/pain with walking, relieved by sitting or leaning forward (flexion opens the spinal canal); often elderly	Can mimic the "activity-related leg pain" of hip OA. Distinguished by the positional relief (flexion) and bilateral symptoms.
Sacroiliac joint dysfunction	Posterior buttock pain; tenderness over SI joint; positive SI joint provocation tests (FABER/Patrick test, compression, distraction); associated with AS, post-partum	Pain is posterior, not groin. FABER test: Flexion-Abduction-External Rotation — SI joint pain is at the posterior SI joint, not the groin (though this test also stresses the hip).
Meralgia paraesthetica	Burning/tingling over the anterolateral thigh; caused by compression of the lateral femoral cutaneous nerve (L2–L3) at the inguinal ligament; risk factors: obesity, tight belts, diabetes	Purely sensory — no motor deficit, no hip ROM restriction. The anterolateral thigh location and paraesthetic quality distinguish it from OA pain.
Vascular claudication	Calf pain (not usually hip/groin) on walking, relieved by standing still; absent/diminished peripheral pulses; atherosclerotic risk factors (smoking, diabetes, hypertension)	Distinguished from hip OA by the pain pattern (calf, not groin), relief by standing (not by sitting as in neurogenic claudication), and vascular examination findings.
Intra-abdominal/pelvic pathology	Inguinal hernia, femoral hernia, ovarian pathology, ectopic pregnancy, psoas abscess, retroperitoneal tumour, nephrolithiasis	These are important "don't miss" diagnoses. A psoas abscess (TB!) can present with hip flexion pain and a flexed posture of the hip.

Don't Forget: Referred Pain from the Lumbar Spine

Mechanical back pain accounts for 97% of lower back pain ^[10]. The lumbar spine is an extremely common source of referred hip/buttock pain. Always examine the lumbar spine when assessing a patient with hip pain — check for back tenderness, SLR, neurological deficit. If hip ROM is full and the pain pattern follows a dermatomal distribution, the problem is likely the spine, not the hip.

This is particularly useful in clinical practice and exams. The patient's age dramatically narrows the differential ^[8]:

Age Group	Differential Diagnoses to Consider
0–5 years	DDH, septic arthritis, transient synovitis ("irritable hip")
5–10 years	Perthes disease, septic arthritis, osteomyelitis, transient synovitis
10–16 years	SCFE, avulsion fracture, infection (osteomyelitis/septic arthritis), malignancy (osteosarcoma, Ewing's sarcoma)
Young adults (16–40)	FAI, labral tear, DDH (secondary OA), AVN, inflammatory arthritis (AS, RA), stress fracture, infection (TB)
Middle-aged (40–65)	Primary or secondary OA, AVN, GTPS/gluteus medius tendinopathy, inflammatory arthritis, referred spinal pain
Elderly ( > 65)	Primary OA, femoral neck fracture (fragility), metastatic disease, Paget's disease, spinal stenosis

Feature	Hip OA	AVN	Septic Arthritis	GTPS	Lumbar Radiculopathy
Pain location	Groin → anterior thigh/knee	Groin	Groin (deep)	Lateral hip (GT)	Buttock → posterior thigh → below knee
Onset	Chronic, insidious	Subacute/chronic	Acute (hours)	Subacute/chronic	Acute or chronic
Systemic features	None	None	Fever, ↑WCC, ↑CRP	None	None
ROM	Restricted (IR first)	Restricted (IR, abduction)	Severely restricted, held in flexion/ER	Full (passive ROM normal)	Full hip ROM
Key investigation	X-ray (LOSS)	MRI (double-line sign)	Joint aspiration	Clinical diagnosis ± US	MRI lumbar spine
Age peak	Elderly (primary); any age (secondary)	30–50 (steroid/alcohol); any age (trauma)	Any age	Middle-aged women	30–50 (disc); elderly (stenosis)

The 3 Questions That Narrow Your DDx Fastest

Where exactly is the pain? Groin = intra-articular. Lateral = periarticular (GTPS). Buttock/radiating below knee = referred (spine).
What is the patient's age? This alone narrows the list dramatically (see age-based table above).
Is passive ROM restricted? Yes = intra-articular pathology (OA, AVN, septic arthritis, inflammatory arthritis). No = periarticular or referred.

When you see OA changes on X-ray, look for clues to the underlying aetiology ^[2]:

Underlying Cause	Additional X-ray Features
DDH	Hip dysplasia (inadequate acetabular coverage), subluxation, broken Shenton's line ^[2]
AVN	Osteopenia → sclerosis → crescent sign (subchondral collapse) → secondary OA ^[5]
AS	Fusion of SI joint ^[2], syndesmophytes, "bamboo spine"
RA	Juxta-articular osteopenia, erosions, symmetrical joint space narrowing (no osteophytes)
TB hip	Joint space widening (effusion) → destruction; soft-tissue swelling, capsular distension ^[6]; periarticular osteopenia ("Phemister triad": juxta-articular osteoporosis, marginal erosions, gradual joint space narrowing)
Gout	Punched-out erosions with overhanging edges, preserved joint space until late
Paget's disease	Coarsened trabecular pattern, cortical thickening, bone enlargement

Imaging Tip from Lecture Slides

The hip joint consists of acetabular side, articular surface and femoral side — describe the radiological features by location ^[1]. This systematic approach ensures you don't miss pathology. When reporting a hip X-ray: (1) Acetabular side: coverage, depth, osteophytes, protrusio. (2) Joint space: width, symmetry. (3) Femoral side: head shape, neck-shaft angle, osteophytes, cysts, sclerosis.

The senior notes provide a systematic approach to orthopaedic differential diagnosis ^[11]:

TIN: Trauma, Infection, Neoplasm — always consider first (urgent/dangerous) Then: Inflammatory, Metabolic Then: Degenerative, Vascular, Congenital

Applied to hip pain:

T — Fracture (NOF, acetabular, stress), dislocation
I — Septic arthritis, osteomyelitis, TB hip
N — Primary bone tumour (osteosarcoma in young), metastatic disease (elderly — breast, lung, prostate, kidney, thyroid)
Inflammatory — RA, AS, psoriatic arthritis, reactive arthritis
Metabolic — Gout, pseudogout, Paget's disease
Degenerative — OA (primary or secondary)
Vascular — AVN
Congenital — DDH, FAI (cam/pincer morphology)

High Yield Summary — DDx of Hip Pain

Pain location is the single most useful discriminator: Groin = intra-articular; Lateral = periarticular (GTPS); Buttock/radiating below knee = referred (spine).
Hip OA DDx from senior notes: fractures, sciatica, trochanteric bursitis, gluteus medius tendinopathy.
Age guides the differential: Child (Perthes, DDH, septic arthritis, SCFE) → Young adult (AVN, DDH, FAI, labral tear, AS) → Elderly (primary OA, fracture, metastasis, spinal stenosis).
Passive ROM is the key sign: Restricted = intra-articular. Full = periarticular or referred.
AVN is a major secondary cause in HK — risk factors: steroids > 20 mg/day, alcohol, trauma (NOF 15–50%, dislocation 10–25%), caisson disease, sickle cell.
Septic arthritis is the emergency "don't miss" — acute, febrile, very painful, restricted ROM; aspirate urgently. MRI distinguishes osteomyelitis from septic arthritis.
TB hip is historically significant in Hong Kong — chronic destruction, X-ray shows capsular distension, joint space widening, then destruction.
Always examine the lumbar spine when assessing hip pain — referred pain from the spine is extremely common.
On X-ray, describe features by location (acetabular side, articular surface, femoral side) and look for clues to secondary causes (DDH: dysplasia; AVN: crescent sign; AS: SI fusion; TB: Phemister triad).

Active Recall - Differential Diagnosis of Hip Pain

References

^[1] Lecture slides: GC 229. Hip Arthritis (1).pdf (pp. 2, 32, 81, 103) ^[2] Senior notes: maxim.md (section 6.3 OA hip) ^[5] Senior notes: maxim.md (section 6.4 AVN of hip) ^[6] Lecture slides: GC 229. Hip Arthritis (1).pdf (p. 53 — Imaging for septic arthritis) ^[7] Senior notes: maxim.md (section 6.2 Hip trauma — fracture neck of femur) ^[8] Senior notes: maxim.md (sections on SCFE, Perthes disease) ^[9] Senior notes: felixlai.md (section on differential diagnosis of intermittent claudication — sciatica) ^[10] Lecture slides: GC 226. Lumbar Spine Pathology_Part E (2).pdf (p. 2) ^[11] Senior notes: maxim.md (section 1.2 History taking — differential diagnosis tiers)

Diagnostic Criteria, Diagnostic Algorithm & Investigations for Hip Osteoarthritis

1. Diagnostic Criteria — How Do We Actually Diagnose Hip OA?

Unlike many medical conditions, hip OA does not have a single pathognomonic lab test. The diagnosis is fundamentally clinical + radiological. Let's work through this from first principles.

Feature	Suggests NOT OA — Think Instead
Morning stiffness > 60 min	Inflammatory arthritis (RA, AS)
Markedly elevated ESR/CRP	Infection (septic arthritis), inflammatory arthritis, malignancy
Fever, hot swollen joint	Septic arthritis (emergency)
Erosions on X-ray	RA, gout
Juxta-articular osteopenia	RA
Normal passive ROM with lateral hip pain	Greater trochanteric pain syndrome (periarticular, not intra-articular)
Neurological deficit	Lumbar radiculopathy (referred, not hip joint)

3. Investigation Modalities — Detailed Breakdown

3.1 Plain Radiographs (X-rays) — The First-Line Investigation

Plain X-ray is the cornerstone investigation for hip OA ^[1]^[12]. It is cheap, widely available, and provides the key diagnostic information.

View	What It Shows	Why It's Important
AP pelvis (weight-bearing if possible)	Both hips for comparison; acetabular coverage; joint space width; alignment; pelvic symmetry	Allows comparison of affected vs. unaffected hip. Weight-bearing compresses the joint, making joint space narrowing more apparent.
Lateral view of affected hip (frog-leg lateral or cross-table lateral)	Femoral head shape; anterior/posterior osteophytes; crescent sign in AVN	The frog-leg view (abducted, externally rotated) is particularly useful for detecting crescent sign in AVN ^[5] and cam morphology in FAI.

The hallmarks of osteoarthritis: joint space narrowing, subchondral sclerosis, marginal osteophytes, subchondral cysts ^[13]

Feature	What It Looks Like	Pathophysiology	Clinical Significance
Loss of joint space (joint space narrowing)	Asymmetric narrowing, typically superolateral in hip OA (where maximal weight-bearing occurs); compare with contralateral hip	Represents cartilage loss — the cartilage is radiolucent (invisible on X-ray), so as it thins, the apparent gap between the femoral head and acetabulum narrows	Earliest radiographic change ^[2]. Superolateral narrowing is typical of primary OA; medial/axial narrowing suggests RA or inflammatory arthritis.
Osteophytes	Bony spurs at the margins of the joint — along the acetabular rim and femoral head-neck junction	Reactive new bone formation at the periosteum, driven by TGFβ and BMPs; the joint's attempt to increase surface area and redistribute load	Most reliable radiographic feature for diagnosing OA. Look for them on both the acetabular and femoral sides.
Subchondral sclerosis	Increased whiteness (radiodensity) of bone directly beneath the damaged cartilage	Exposed subchondral bone bears increased stress → osteoblast activation → increased bone density. The stiffened bone is less shock-absorbing → further damages cartilage (vicious cycle).	Indicates areas of maximal mechanical stress and cartilage loss.
Subchondral cysts (geodes)	Well-defined lucent (dark) areas in the subchondral bone	Two theories: (1) synovial fluid forced through microfractures in the subchondral plate; (2) focal bone necrosis with cyst formation	Can be large and dramatic; may mimic other pathology. Seen in more advanced OA.

When you see OA changes, always look for clues to a secondary cause:

Secondary Cause	Specific X-ray Features
DDH	Hip dysplasia (inadequate acetabular coverage); shallow acetabulum; broken Shenton's line; femoral head subluxation ^[2]
AVN	Osteopenia → sclerosis → crescent sign ^[2]^[5]; cyst (resorption of dead bone + replacement with fibrous and granulation tissue); sclerosis (thickened trabeculae due to direct deposition of new bone onto dead bone); crescent sign (subchondral collapse of the necrotic segment) ^[14]
AS	Fusion of SI joint ^[2]; protrusio acetabuli (medial migration of femoral head)
RA	Symmetrical joint space narrowing; juxta-articular osteopenia; erosions; no osteophytes; protrusio
TB hip	Soft-tissue swelling or hip joint capsular distension (with widening of the joint space or even subluxation); radiographic changes in the proximal femoral metaphysis: osteomyelitis ^[6]
Paget's disease	Coarsened trabecular pattern; cortical thickening; bone enlargement ("picture frame" vertebra if spine)

Systematic X-ray Reporting for the Hip — Lecture Slide Approach

The hip joint consists of acetabular side, articular surface and femoral side — describe the radiological features by location ^[12]:

Acetabular side: coverage/depth, osteophytes, sclerosis, cysts, protrusio, dysplasia
Articular surface (joint space): width (narrowed?), symmetry (superolateral vs medial), Shenton's line
Femoral side: head shape (spherical? collapsed? flattened?), osteophytes, cysts, sclerosis, crescent sign, neck-shaft angle, femoral offset

This systematic approach prevents you from missing pathology and is explicitly what the lecturers expect ^[12].

This is the standard radiological grading system for OA severity, used for both knee and hip:

Kellgren and Lawrence scoring system ^[1]

Grade	Description	Key Feature
0	Normal	No OA features
1	Doubtful	Possible osteophytic lipping, doubtful joint space narrowing
2	Minimal	Definite osteophytes, possible joint space narrowing
3	Moderate	Moderate osteophytes, definite joint space narrowing, some sclerosis, possible cysts
4	Severe	Large osteophytes, marked joint space narrowing (bone-on-bone), severe sclerosis, bone deformity

Why does grading matter? It guides management decisions:

KL 1–2: Conservative management, lifestyle modification, physiotherapy
KL 3: Conservative ± consider surgical options (osteotomy if appropriate)
KL 4: Usually requires arthroplasty (THR) if symptoms warrant

3.2 MRI — The Gold Standard for Soft Tissue and Early Disease

MRI is not routinely needed for diagnosing established hip OA (X-ray is sufficient). It is indicated when:

X-ray is normal but clinical suspicion is high (pre-radiographic OA, occult fracture, early AVN)
Suspected AVN — MRI has 99% sensitivity and specificity ^[14] for AVN
Suspected labral tear or FAI — MR arthrogram (with intra-articular gadolinium) is the investigation of choice
Distinguishing osteomyelitis from septic arthritis — MRI may be the most useful test to distinguish proximal femoral osteomyelitis from septic arthritis of the hip ^[6]
Suspected occult fracture — stress fracture or insufficiency fracture with normal X-ray

Condition	MRI Findings	Explanation
Early/Pre-radiographic OA	Bone marrow oedema (BME), cartilage thinning/defects, early osteophytes, synovitis, effusion	Structural changes occur before symptoms and before X-ray changes ^[3]. MRI detects these earlier. BME on MRI correlates with pain in OA.
AVN	T2W: double-line sign — outer dark line (sclerosis/reactive bone) and inner bright line (granulation tissue/hyperaemia) ^[5]; T1W: low signal replacing normal fatty marrow	The double-line sign is pathognomonic for AVN. MRI detects AVN before X-ray changes appear (Ficat Stage 0–I). MRI should include bilateral hips because contralateral AVN is common ^[5].
Labral tear	Irregularity, cleft, or detachment of the acetabular labrum; best seen on MR arthrogram	The labrum is a fibrocartilaginous structure; tears appear as high signal within or detachment from the labrum.
Septic arthritis	Joint effusion, synovial thickening and enhancement, bone marrow oedema in adjacent bone; may show periosteal reaction (osteomyelitis)	Differentiates effusion from bone infection. Most useful to distinguish osteomyelitis from septic arthritis ^[6].
Occult fracture	Linear low-signal line on T1W with surrounding bone marrow oedema	Fractures that are invisible on X-ray (especially femoral neck stress fractures) are readily detected by MRI.

Hip OA itself does not have diagnostic blood tests. Bloods are used to exclude other conditions:

Test	Purpose	Expected in OA	Abnormal in
ESR ^[15]	Acute phase reactant	Normal (< 20 mm/hr) or mildly elevated	Elevated in RA, AS, septic arthritis, malignancy, TB
CRP ^[15]	Acute phase reactant	Normal or mildly elevated	Elevated in septic arthritis (markedly), RA, crystal arthropathy
WBC ^[15]	White cell count	Normal	Elevated in septic arthritis, osteomyelitis
RF (Rheumatoid Factor)	Screen for RA	Negative	Positive in ~70% of RA
Anti-CCP	Highly specific for RA	Negative	Positive in RA (more specific than RF)
Urate	Screen for gout	Normal	Elevated in gout (though can be normal during an acute flare)
HLA-B27	If AS suspected	Negative	Positive in ~90% of AS
Blood cultures ^[15]	If septic arthritis suspected	Negative	Positive in ~50% of septic arthritis

When to Order Bloods

Do NOT order a panel of inflammatory markers and autoantibodies for every patient with chronic hip pain and a classic OA presentation. Order them when:

The clinical picture is atypical (young patient, prolonged morning stiffness, systemic symptoms)
You need to exclude infection (acute onset, fever, elevated inflammatory markers)
You suspect an underlying inflammatory or metabolic cause (RA, AS, gout)

Modality	Indication	Findings
Ultrasound (US)	Detect hip effusion; guide aspiration; assess GTPS/gluteus medius tendinopathy	Effusion appears as anechoic fluid within the joint capsule. US is quick, bedside, and non-ionising — ideal for confirming effusion before aspiration.
CT scan	Preoperative planning for complex THR (e.g., DDH with significant bony deformity); acetabular fracture assessment	Better bony detail than MRI; useful for 3D planning of component positioning in THR.
Radioisotope bone scan ^[6]	Infection workup; suspected metastatic disease; Paget's disease	Increased uptake at areas of high bone turnover. Sensitive but non-specific. Can identify multiple sites of disease (metastases, polyostotic Paget's).
DEXA scan	If osteoporosis suspected (fragility fracture, AVN assessment)	T-score ≤ -2.5 = osteoporosis. Important for fracture risk assessment in elderly patients with hip OA.

When AVN is identified as the cause of secondary hip OA, staging guides treatment:

Ficat classification and treatment ^[14]:

Ficat Stage	Criteria	Treatment
I	Normal X-ray (MRI may show changes)	Core decompression
II	Sclerotic or cystic lesions	Core decompression / vascularised bone graft
III	Subchondral collapse (crescent sign)	Vascularised bone graft / THR
IV	OA changes (joint space collapse, acetabular changes)	THR

Why core decompression works in early AVN: The femoral head has a rigid bony shell. When infarction occurs, oedema and inflammation increase intraosseous pressure within this rigid compartment → further compromises blood flow (a vicious cycle, similar in concept to compartment syndrome). Core decompression involves drilling a channel into the femoral head → reduces intraosseous pressure → allows ingrowth of new blood vessels → may halt progression.

Why THR is needed in late AVN: Once subchondral collapse has occurred (Ficat III–IV), the articular surface is permanently deformed → incongruent joint → progressive OA. No amount of core decompression can restore a collapsed femoral head — the joint must be replaced.

Harris Hip Score (HHS) is the standard functional outcome tool for hip OA and is specifically used for follow-up after THR ^[16]:

Domain	Max Points	Components
Pain	44	Severity and impact on function
Function	47	Gait (33): limp, support (none/cane/crutch), distance walked. Activity (14): stairs, wear socks/shoes, sitting time, enter public transportation
Range of motion	5 (recorded as 9 in some versions)	Composite of flexion, abduction, adduction, ER, IR
Absence of deformity	4	Fixed flexion < 30°, fixed adduction < 10°, fixed IR < 10°, LLD < 3.2 cm

Total: 100 points

90–100 = Excellent
80–89 = Good
70–79 = Fair
< 70 = Poor

Exam Tip — Harris Hip Score

In an OSCE or clinical exam, mentioning that you would use the Harris Hip Score to quantify functional impairment and track outcomes after THR demonstrates sophisticated clinical thinking. The key components to remember: Pain (44) and Function (47) make up the vast majority of the score — pain relief and functional improvement are what matter most to patients ^[16].

Investigation	When to Order	Key Findings in Hip OA
Plain X-ray (AP pelvis + lateral hip)	First-line for all suspected hip OA	LOSS: joint space narrowing (superolateral), osteophytes, subchondral sclerosis, subchondral cysts
MRI hip	X-ray normal but suspicion high; suspected AVN, labral tear, occult fracture, infection	Pre-radiographic OA: BME, cartilage defects. AVN: double-line sign. Labral tear: cleft/detachment.
Blood tests (ESR, CRP, WCC)	Atypical presentation; exclude infection/inflammation	Normal in OA; elevated in septic arthritis, RA, AS
RF, anti-CCP, urate, HLA-B27	Suspected inflammatory/metabolic cause	Normal in OA; positive in RA, gout, AS respectively
Image-guided hip aspiration	Suspected septic arthritis or crystal arthropathy	Cell count, Gram stain, culture (bacterial/fungal/AFB), crystals
CT scan	Preoperative planning, complex bony anatomy	3D bony detail for THR planning
Ultrasound	Effusion detection, aspiration guidance, periarticular pathology	Effusion, tendinopathy, bursitis
Bone scan	Infection, metastasis, Paget's	Increased uptake at sites of bone turnover
Harris Hip Score	Baseline assessment and follow-up after THR	Quantifies pain, function, ROM, deformity

High Yield Summary — Diagnosis of Hip OA

Diagnosis is clinical + radiological — no specific lab test for OA.
ACR criteria: Hip pain + 2 of 3 (ESR < 20, osteophytes on X-ray, joint space narrowing).
First-line investigation: Plain X-ray (AP pelvis + lateral of affected hip).
Radiographic hallmarks (LOSS): Loss of joint space (earliest), Osteophytes (most reliable), Subchondral sclerosis, Subchondral cysts.
Describe X-ray by location: acetabular side, articular surface, femoral side.
Kellgren-Lawrence grading: Grade 0 (normal) to Grade 4 (bone-on-bone).
Always look for secondary causes on X-ray: DDH (dysplasia), AVN (crescent sign), AS (SI fusion), TB (capsular distension), RA (erosions/osteopenia).
MRI: 99% sensitive/specific for AVN (double-line sign); best for pre-radiographic OA, labral tears, and distinguishing osteomyelitis from septic arthritis.
Bloods are to exclude differentials, not to diagnose OA: ESR, CRP, WCC (infection); RF, anti-CCP (RA); urate (gout); HLA-B27 (AS).
Image-guided aspiration: urgent for suspected septic arthritis — cell count, Gram smear, bacterial/fungal/AFB culture, +/- crystals.
Ficat classification for AVN: I (normal X-ray) → core decompression; II (sclerotic/cystic) → core decompression/bone graft; III (subchondral collapse) → bone graft/THR; IV (OA changes) → THR.
Harris Hip Score: Pain (44) + Function (47) + ROM + Deformity = max 100. Used for baseline and post-THR follow-up.
Natural history: Molecular → Pre-radiographic (MRI/biomarkers) → Radiographic (X-ray) → End-stage. Intervene early.

Active Recall - Diagnosis & Investigations for Hip OA

References

^[1] Lecture slides: GC 229. Hip Arthritis (1).pdf (pp. 2, 29, 32) ^[2] Senior notes: maxim.md (sections 6.3 OA hip, 9.1 Osteoarthritis) ^[3] Lecture slides: GC 228. Knee Osteoarthritis_Part B (1).pdf (p. 13 — Natural History of OA) ^[5] Senior notes: maxim.md (section 6.4 AVN of hip) ^[6] Lecture slides: GC 229. Hip Arthritis (1).pdf (p. 53 — Imaging for septic arthritis) ^[7] Senior notes: maxim.md (section 7.4 OA knee — Kellgren-Lawrence classification) ^[12] Lecture slides: GC 229. Hip Arthritis (1).pdf (p. 103 — Take Home Messages) ^[13] Lecture slides: GC 228. Knee Osteoarthritis_Part A (1).pdf (p. 32 — Radiographic features) ^[14] Lecture slides: GC 229. Hip Arthritis (1).pdf (pp. 15, 20 — AVN investigations and Ficat classification) ^[15] Lecture slides: GC 229. Hip Arthritis (1).pdf (p. 51 — Investigations for septic arthritis) ^[16] Senior notes: maxim.md (section 6.3 — Harris Hip Score after THR)

Management of Hip Osteoarthritis

3. First-Line Treatment — Non-Pharmacological Core Treatment (ALL Patients)

This is the foundation of OA management. It should be offered to every single patient, regardless of disease severity.

4. Second-Line Treatment — Pharmacological and Adjunctive (SOME Patients)

Added when core treatments alone do not achieve adequate symptom control.

Analgesics do not affect the natural history of OA — they provide symptomatic relief only ^[22]. This is a critical concept: no currently available drug can reverse or halt cartilage degradation.

Agent	Role	Mechanism	Key Points from Lectures
Paracetamol (Panadol)	First-line analgesic ^[22]	Central analgesic effect (mechanism incompletely understood — may involve COX-3 inhibition, serotonergic pathways, endocannabinoid system). No anti-inflammatory effect.	Widely used but network meta-analysis shows paracetamol does not seem to confer any demonstrable effect or benefit in OA at any dose ^[23]. Side effects: liver function abnormalities; elderly people with impaired paracetamol clearance ^[23]. Despite weak evidence, still recommended as first-line because of safety profile relative to NSAIDs.
NSAIDs (e.g., ibuprofen, naproxen, diclofenac)	Second-line; proven benefit ^[7]	Inhibit cyclooxygenase (COX-1 and COX-2) → reduce prostaglandin synthesis → reduce inflammation and pain in the synovium.	More effective than paracetamol for OA pain. However, significant side effects: GI bleeding (COX-1 inhibition reduces protective gastric mucus), renal impairment (prostaglandins maintain renal blood flow in hypovolaemia), cardiovascular risk (especially COX-2 selective inhibitors). Use at lowest effective dose for shortest duration. Add PPI for GI protection in high-risk patients.
Tramadol	Non-narcotic ^[22]; combine with paracetamol for synergistic effect ^[22]; if contraindication to use NSAIDs ^[22]	Weak μ-opioid receptor agonist + inhibits serotonin and noradrenaline reuptake → dual analgesic mechanism. "Non-narcotic" in the sense that it is a weaker opioid, but it can still cause dependence.	Used when paracetamol alone is insufficient and NSAIDs are contraindicated (e.g., renal impairment, GI bleeding history, cardiovascular disease).
Opioids	No routine use ^[22]	Strong μ-opioid receptor agonists.	CNS depression, addiction ^[22]. Opioids offer only limited benefit for chronic OA pain and function ^[24]. Potentially serious adverse effects including drug abuse and addiction ^[24]. Elderly patients are at particular risk — sedation and dizziness which predispose to falls and fractures ^[24]. Pre-operative opioid use independently predicted greater opioid requirement post-surgery, prolonged hospital stay, greater risks of in-hospital complications, and early revision surgery ^[24]. Updated Australian GP guidelines do not recommend opioids as a treatment option ^[24].

The Opioid Trap

Do NOT routinely prescribe opioids for chronic OA pain. The evidence shows minimal benefit with significant harm — addiction, falls in the elderly, worse surgical outcomes. If a patient is on opioids pre-operatively for OA, they will have a harder time after THR, not an easier one ^[24]. This is a common exam question and a real-world clinical pitfall.

Injection	Evidence	Mechanism	Practical Points
Intra-articular corticosteroid	Moderate evidence for short-term pain relief ^[2]	Potent anti-inflammatory → suppresses synovitis, reduces effusion.	Hip injections must be done under image guidance (US or fluoroscopy) because the hip is deep. Provides weeks to months of relief. Repeated injections (> 3–4/year) may accelerate cartilage loss. Useful as a "bridge" while optimising conservative measures or awaiting surgery.
Intra-articular hyaluronic acid	Strong evidence DOES NOT support its use ^[25]	"Viscosupplementation" — hyaluronic acid is a normal component of synovial fluid; injection aims to restore viscoelastic properties.	Strong evidence does not support the use of intraarticular hyaluronic acid because it does not perform better than placebo for function, stiffness, and pain in patients with symptomatic osteoarthritis of the hip ^[25]. Strength of Recommendation: Strong Evidence (3 stars) ^[25]. Despite ongoing commercial promotion, the evidence is clear — it doesn't work for hip OA.
Platelet-rich plasma (PRP)	?evidence ^[2]	Contains growth factors (PDGF, TGFβ, VEGF) that theoretically promote tissue repair.	Evidence is mixed and mostly low quality. Not currently recommended as standard treatment. Mentioned in senior notes as having uncertain evidence ^[2].

Exam Point — Hyaluronic Acid for Hip OA

Strong evidence AGAINST intra-articular hyaluronic acid for hip OA ^[25]. This is a common exam question — students often mistakenly think viscosupplementation is a reasonable treatment option. For the hip specifically, the AAOS clinical practice guideline (cited in the lecture slides ^[26]) recommends AGAINST it.

5. Third-Line Treatment — Surgery (FEW Patients)

Indications for operative management ^[2]:

Patient factors: age, functional status, comorbidities, expectations
Disease factors: severe impairment to ADL, pain despite conservative treatment

The key question is: joint-preserving surgery vs. joint replacement?

5.1 Joint-Preserving Surgery

Osteotomy: correct deformity and relieve joint pressure ^[2]^[27]:

Feature	Details
Indication	Young (< 60y) with preservation of articular cartilage. Pre-requisite: single compartment ^[27]
Contraindications	Severe articular damage, ligament laxity, severe varus deformities ^[27]
For the hip	Hip osteotomy ^[27] — redirect the femoral head or acetabulum to improve coverage and redistribute load

Types of osteotomy for the hip:

Periacetabular osteotomy (PAO) ^[1]:
- Indication: Symptomatic dysplasia in young adult with concentrically reduced hip and congruent joint space — before OA changes ^[1]
- Mechanism: the acetabulum is cut and reoriented to provide better coverage of the femoral head → more even load distribution → delays/prevents OA
- Requires a skilled surgeon; technically demanding; significant rehabilitation
Femoral osteotomy (valgus or varus):
- Redirects the femoral head within the acetabulum
- Used in specific deformities (e.g., post-Perthes, post-SCFE)

5.2 Joint Replacement — The Definitive Treatment for End-Stage Hip OA

Total hip replacement is a reliable and durable treatment option for patients with end stage arthritis ^[12].

Different surgical approaches defined relative to gluteus medius ^[2]:

Approach	Advantage	Disadvantage
Posterior — most common	Preserve abductor mechanism → Rapid rehab	Sciatic nerve injury; Risk of hip joint dislocation
Anterolateral (modified Hardinge)	Detach abductor mechanism → Good exposure	Superior gluteal nerve injury
Anterior (Smith-Petersen) — rare	For open washout of infected hip	Limited exposure; learning curve

Why does the posterior approach risk dislocation? The posterior approach involves detaching the short external rotators (piriformis, obturator internus, gemelli) and the posterior capsule. These structures normally resist posterior dislocation. After surgery, if the patient flexes, adducts, and internally rotates the hip (e.g., sitting on a low chair, crossing legs), the femoral head can dislocate posteriorly through the unhealed posterior capsule.

Why does the posterior approach risk sciatic nerve injury? The sciatic nerve exits the pelvis below the piriformis and runs posterior to the hip joint — it is directly in the surgical field during the posterior approach.

Why does the anterolateral approach risk superior gluteal nerve injury? The approach splits or detaches the gluteus medius (innervated by the superior gluteal nerve). The nerve enters the muscle from its deep surface, approximately 5 cm proximal to the greater trochanter — surgical dissection beyond this "safe zone" can damage the nerve → hip abductor weakness → Trendelenburg gait.

Direct Anterior Approach — Modern Trend

The direct anterior approach (DAA) — distinct from the traditional Smith-Petersen — is gaining popularity. It is truly intermuscular and internervous (passes between sartorius/TFL laterally and rectus femoris medially), preserving the abductors and posterior capsule. Advantages: lower dislocation rate, faster recovery, fewer hip precautions. Disadvantage: steep learning curve, risk of lateral femoral cutaneous nerve injury (meralgia paraesthetica), wound complications in obese patients.

Cause	Specific Management Considerations
DDH	PAO if congruent joint space, before OA changes; THR if secondary OA or subluxation ^[1]. THR in DDH is technically challenging: shallow acetabulum, abnormal anatomy, potential need for femoral shortening, sciatic nerve at risk with limb lengthening.
AVN	Ficat I–II: core decompression ± bone graft; Ficat III: bone graft/THR; Ficat IV: THR ^[14]. Address underlying cause (stop steroids if possible, alcohol cessation).
Inflammatory arthritis (RA, AS)	Multidisciplinary approach ^[30]: Rheumatologist (diagnosis, medical treatment, screening of associated disorders) + Orthopaedic Surgeon (hip, spine) ^[30]. Medical treatment (DMARDs, biologics) must be optimised before considering THR.
Infection (TB hip)	Treat the infection first (anti-TB regimen for TB: 6–9 months of combination therapy). THR can be performed once infection is eradicated, but has higher complication rates. Anterior (Smith-Petersen) approach: for open washout of infected hip ^[2].

Stage	Clinical Picture	Management
Mild (KL 1–2)	Mild pain, minimal functional limitation	Core treatment: education, exercise, weight loss. Paracetamol ± topical NSAIDs.
Moderate (KL 3)	Moderate pain, reduced ROM, some ADL limitation	Core treatment + oral NSAIDs (shortest duration), walking aids, PT escalation, intra-articular steroid. Consider osteotomy if young with correctable deformity.
Severe (KL 4)	Bone-on-bone, severe pain, significant ADL impairment, failed conservative Rx	Core treatment + THR (gold standard for end-stage).
Young with secondary OA	Early secondary OA from DDH, AVN, post-traumatic	Joint-preserving surgery first: PAO (DDH), core decompression/bone graft (AVN), osteotomy (deformity correction). THR if joint-preserving options exhausted.

The lecture slides reference the AAOS Management of Osteoarthritis of the Hip Evidence-Based Clinical Practice Guideline ^[26]. Key recommendations:

Intervention	AAOS Recommendation	Strength
Physical therapy	Strongly recommended for mild-moderate symptoms	Strong
Preoperative PT	Limited evidence supports early function improvement post-THR	Limited
Intra-articular hyaluronic acid	NOT recommended — does not outperform placebo	Strong (against)
NSAIDs	Recommended for pain relief	Strong
Opioids	Not routinely recommended	Against
Weight loss	Recommended	Moderate
THR	Recommended for end-stage disease	Strong

High Yield Summary — Management of Hip OA

First-line = Education, Exercise, Weight Control (ALL patients) — NOT analgesics, NOT surgery.
OA Treatment Pyramid: Core non-pharmacological (all) → Pharmacological + adjuncts (some) → Surgery (few).
Physiotherapy — Strong evidence for improving function and reducing pain in mild-moderate hip OA.
Analgesics do NOT affect natural history — symptomatic relief only.
Paracetamol = first-line analgesic but network meta-analysis shows no demonstrable benefit in OA at any dose; used for safety profile relative to NSAIDs.
NSAIDs have proven benefit but GI, renal, and cardiovascular side effects limit their use.
Tramadol: non-narcotic, synergistic with paracetamol, use if NSAIDs contraindicated.
Opioids: NO routine use — limited benefit, serious adverse effects (addiction, falls in elderly, worse surgical outcomes).
Intra-articular hyaluronic acid: Strong evidence AGAINST — does not outperform placebo for hip OA.
Intra-articular steroid: short-term relief, image-guided, useful as bridge.
Surgical indications: severe ADL impairment + pain despite conservative treatment.
Joint-preserving: Osteotomy (young < 60, preserved cartilage), PAO (DDH before OA), Core decompression (AVN Ficat I–II).
THR = reliable and durable for end-stage arthritis. Surgical approaches relative to gluteus medius: Posterior (most common, preserves abductors but risk of dislocation/sciatic nerve injury), Anterolateral/Hardinge (good exposure but superior gluteal nerve injury), Anterior/Smith-Petersen (rare, for infected hip washout).
THR goals: restore pain-free stable joint, restore anatomical hip centre (acetabular), correct femoral deformity, address soft tissue contractures, protect sciatic nerve.
Harris Hip Score for pre- and post-operative assessment.
Multidisciplinary approach for inflammatory causes (rheumatologist + orthopaedic surgeon).

Active Recall - Management of Hip OA

References

^[1] Lecture slides: GC 229. Hip Arthritis (1).pdf (p. 81 — Management of DDH) ^[2] Senior notes: maxim.md (sections 6.3 OA hip, 9.1 Osteoarthritis — Management) ^[7] Senior notes: maxim.md (sections 6.2 Hip trauma, 7.4 OA knee — KL classification, surgical options) ^[11] Senior notes: maxim.md (section 1.3 Management overview — ERAS, walking aids) ^[12] Lecture slides: GC 229. Hip Arthritis (1).pdf (p. 103 — Take Home Messages) ^[14] Lecture slides: GC 229. Hip Arthritis (1).pdf (p. 20 — Ficat classification and treatment) ^[17] Lecture slides: GC 228. Knee Osteoarthritis_Part A (1).pdf (pp. 35–36 — OA Treatment Pyramid) ^[18] Lecture slides: GC 228. Knee Osteoarthritis_Part B (1).pdf (p. 30 — First-line management question) ^[19] Lecture slides: GC 228. Knee Osteoarthritis_Part A (1).pdf (p. 42 — COME programme) ^[20] Lecture slides: GC 228. Knee Osteoarthritis_Part B (1).pdf (p. 29 — Conclusion) ^[21] Lecture slides: GC 229. Hip Arthritis (1).pdf (pp. 37–38 — Physiotherapy evidence) ^[22] Lecture slides: GC 229. Hip Arthritis (1).pdf (p. 39 — Analgesics) ^[23] Lecture slides: GC 228. Knee Osteoarthritis_Part B (1).pdf (p. 8 — Paracetamol evidence) ^[24] Lecture slides: GC 228. Knee Osteoarthritis_Part B (1).pdf (p. 10 — Opioids) ^[25] Lecture slides: GC 229. Hip Arthritis (1).pdf (p. 44 — Intra-articular hyaluronic acid) ^[26] Lecture slides: GC 229. Hip Arthritis (1).pdf (p. 34 — AAOS guideline reference) ^[27] Senior notes: maxim.md (section 9.1 — Osteotomy vs Arthroplasty table) ^[28] Lecture slides: GC 228. Knee Osteoarthritis_Part B (1).pdf (p. 18 — Limited role of arthroscopy) ^[29] Lecture slides: GC 229. Hip Arthritis (1).pdf (p. 64 — Management goals for THR) ^[30] Lecture slides: GC 229. Hip Arthritis (1).pdf (p. 92 — Multidisciplinary approach for AS)

Complications of Hip Osteoarthritis

Complications of hip OA fall into two broad categories: (A) complications of the disease itself (untreated or progressive OA), and (B) complications of treatment (particularly surgical). Both are high-yield for exams. Let's work through each systematically, explaining the "why" from first principles.

Part A: Complications of the Disease Itself

Part B: Complications of Treatment

Treatment	Complications	Mechanism
Paracetamol	Liver function abnormalities; elderly with impaired clearance ^[23]	Hepatotoxicity from NAPQI metabolite (normally conjugated by glutathione; overwhelmed in overdose or chronic use/impaired metabolism)
NSAIDs	GI bleeding/ulceration; renal impairment; cardiovascular events (MI, stroke); fluid retention, hypertension	COX-1 inhibition → reduced protective gastric prostaglandins; COX-mediated prostaglandins maintain renal blood flow; COX-2 inhibition shifts thromboxane/prostacyclin balance → prothrombotic state
Opioids	CNS depression, addiction ^[22]; sedation and dizziness predisposing to falls and fractures in elderly ^[24]; pre-operative opioid use predicts: greater opioid requirement post-surgery, prolonged hospital stay, greater in-hospital complications, early revision surgery ^[24]	μ-opioid receptor activation → respiratory depression, sedation, constipation, tolerance, physical dependence. Opioid-induced hyperalgesia paradoxically worsens pain with chronic use.
Intra-articular steroid	Cartilage degradation with repeated injections; infection (rare, ~1 in 50,000); post-injection flare; systemic glucose spike (in diabetics); soft tissue atrophy	Corticosteroids are catabolic to cartilage (inhibit proteoglycan synthesis, promote chondrocyte apoptosis). Repeated injections > 3–4/year may accelerate joint destruction.
Bisphosphonates (for AVN)	Osteonecrosis of the jaw (ONJ) ^[5]	Bisphosphonates suppress osteoclast-mediated bone resorption → impaired bone remodelling → jaw bone (which has high turnover due to dental stress) cannot heal → necrosis. Risk increased with IV formulations, dental procedures, and prolonged use.

B2. Complications of Total Hip Replacement (THR)

These are extremely high-yield and explicitly listed in the senior notes ^[2]^[33]:

Specific complications of THR: thromboembolism, dislocation, infection of prosthesis, leg length discrepancy ^[2]

The senior notes provide a temporal classification ^[33]:

Complication	Mechanism	Details
Bone fracture ^[33]	Intraoperative: reaming of the acetabulum or femoral canal; impaction of uncemented components into osteoporotic bone	Periprosthetic fracture — particularly of the femoral shaft during stem insertion. More common with uncemented stems in osteoporotic bone. Classified by Vancouver classification (A: trochanteric; B: around/just below stem; C: well below stem).
Vascular injury (femoral artery in THR) ^[33]	The femoral artery and vein lie anterior to the hip joint. Retractors placed on the anterior acetabular wall can compress or lacerate the external iliac/femoral vessels.	Rare but catastrophic. More common in revision surgery or with anterior approaches. Presents with acute haemorrhage or post-operative swelling/shock.
Nerve injury (sciatic nerve in THR) ^[33]	Sciatic nerve injury ^[2] — the sciatic nerve runs posterior to the hip joint, directly in the field of the posterior approach. Risk increased with limb lengthening > 4 cm (stretch injury).	Presents with foot drop (common peroneal component most vulnerable — superficial and wrapped around fibular neck). Superior gluteal nerve injury with the anterolateral (modified Hardinge) approach ^[2] → abductor weakness → Trendelenburg gait.
Bleeding	Surgical trauma to periarticular vessels; bone cut surfaces ooze	May require transfusion. Minimised by tranexamic acid (anti-fibrinolytic — blocks plasmin-mediated clot breakdown).

Complication	Mechanism	Details
DVT / PE (Thromboembolism) ^[2]	Virchow's triad: (1) Venous stasis (immobility post-op), (2) Endothelial injury (surgical trauma, heat from cement polymerisation), (3) Hypercoagulability (post-operative inflammatory response, tissue factor release)	DVT affects up to 40–60% of patients without prophylaxis. PE is the most feared complication — can be fatal. Prophylaxis: mechanical (TED stockings, intermittent pneumatic compression, early mobilisation) + pharmacological (LMWH e.g. enoxaparin, or DOACs e.g. rivaroxaban, for 28–35 days post-op).
Infection (early) ^[33]	Bacterial inoculation at the time of surgery; haematogenous seeding from distant sites (UTI, dental)	Infection is difficult to detect and treat ^[33]. Early infection (< 4 weeks): acute pain, wound erythema, discharge, fever, elevated CRP. Commonest organisms: Staphylococcus aureus, coagulase-negative staphylococci. Prevention: laminar flow theatres, prophylactic IV antibiotics (e.g., cefazolin at induction), MRSA screening ^[11].
Cement reaction (Bone Cement Implantation Syndrome — BCIS)	PMMA cement polymerisation → exothermic reaction + monomer toxicity + fat/marrow embolisation → acute hypotension, hypoxia, cardiac arrest	Occurs during cemented femoral stem insertion. The pressurised cement forces fat, marrow, and cement particles into the venous system → emboli → cardiopulmonary compromise. Can be fatal. Prevention: lavage and suction of femoral canal before cementing, slow insertion, maintain intravascular volume.

Complication	Mechanism	Details
Dislocation ^[2]	Femoral head dislocates from the acetabular cup. Most common direction: posterior (especially with posterior approach — posterior capsule and short external rotators are divided).	Risk factors: posterior approach, component malpositioning (excessive anteversion/retroversion), soft tissue laxity, non-compliance with hip precautions, neuromuscular disease. Prevention post-op: do not squat / cross legs / flex hip > 90°, abduction pillow, high-low chair ^[7]. Incidence: 2–5% (posterior approach); lower with anterior approach. If recurrent, may need revision surgery with constrained liner or dual-mobility cup.
Prosthesis infection (periprosthetic joint infection — PJI) ^[2]	Early PJI (< 4 weeks): direct surgical contamination. Delayed PJI (4 weeks – 1 year): low-virulence organisms (e.g., Cutibacterium acnes). Late PJI ( > 1 year): haematogenous seeding from distant infection (dental, urinary, skin). Biofilm formation on the prosthesis surface protects bacteria from antibiotics and host immunity.	Most devastating complication. Diagnosis: joint aspiration (cell count, culture), CRP, ESR, intra-operative histology. Management: debridement + antibiotic exchange (DAIR) for early infection with well-fixed components; two-stage revision (explant → antibiotic spacer → 6–12 weeks IV antibiotics → reimplant) for chronic infection; one-stage revision (explant and reimplant in single sitting) gaining evidence. Lifelong precautions: antibiotic prophylaxis before dental procedures (controversial but commonly practised).
Leg length discrepancy (LLD) ^[2]	Intentional or unintentional lengthening/shortening during THR. The surgeon adjusts component positioning and femoral offset, but achieving perfect leg length equality is challenging.	Must counsel patients beforehand ^[33]. Perceived LLD > 1 cm is often symptomatic. May cause: gait asymmetry, back pain, patient dissatisfaction, sciatic nerve stretch (if lengthened excessively). Prevention: intra-operative measurement, templating, and fluoroscopy. Management: shoe raise for residual LLD.
Aseptic loosening	The most common reason for revision surgery. Wear particles (polyethylene, metal, ceramic) are phagocytosed by macrophages → release pro-inflammatory cytokines (TNFα, IL-1, IL-6) → activate osteoclasts → periprosthetic osteolysis → component loosening.	Presents with gradually increasing pain years after surgery (cf. infection which has a more acute presentation with systemic features). X-ray: progressive radiolucent lines around the prosthesis, component migration. Management: revision THR (exchange worn components + bone grafting for osteolytic defects).
Wear and bearing failure	Articulating surfaces wear over time. Polyethylene → particulate debris → osteolysis (as above). Metal-on-metal → metallosis (cobalt/chromium ions → pseudotumour, ALVAL — adverse local tissue reaction). Ceramic → fracture (rare).	Survival of replacement (not requiring revision surgery): 15–20 years ^[33]. This is why THR is preferably performed in older patients — fewer lifetime years of wear = lower chance of needing revision. Younger, more active patients wear out prostheses faster.
Heterotopic ossification (HO)	Abnormal bone formation in periarticular soft tissues after surgical trauma. Ectopic bone forming in muscle/capsule restricts hip ROM.	Risk factors: male sex, ankylosing spondylitis, previous HO, extensive surgical dissection. Prevention: single-dose radiation therapy (700 cGy within 24 hours post-op) or indomethacin for 6 weeks (COX inhibition reduces osteoblast differentiation). Grading: Brooker classification (I–IV).
Periprosthetic fracture	Fracture of the femur around a prosthetic stem, usually from a fall or minor trauma in osteoporotic bone.	Classified by Vancouver system: Type A (trochanteric — often conservative), Type B (around/below stem — may need revision ± ORIF), Type C (below stem — treat as standard fracture).

The Big Four Complications of THR to Always Mention

When asked about complications of THR in an exam, the four you must mention (as per the senior notes ^[2]) are:

Thromboembolism (DVT/PE)
Dislocation
Infection of prosthesis
Leg length discrepancy

Then add: nerve injury (sciatic — posterior approach; superior gluteal — anterolateral), periprosthetic fracture, aseptic loosening, and heterotopic ossification for extra marks.

Procedure	Specific Complications
Osteotomy	Non-union, malunion, delayed union, neurovascular injury, conversion to THR may be technically more difficult if osteotomy fails
Core decompression (for AVN)	Femoral fracture through the drill tract (weakened cortex), haematoma, infection, failure to halt progression
Arthroscopy	DVT (0.4%), PE (0.1%), death (0.03%) ^[28]; increases rate of progression of OA; shortens time to joint replacement ^[28] — this is why arthroscopic debridement has a very limited role in OA

Timing	Complications
Disease-related	Progressive disability, fixed deformity (flexion/ER/adduction contracture), Trendelenburg gait, secondary OA of adjacent joints, falls/fractures, cardiovascular/psychological/sleep complications
Immediate (intra-op)	Bone fracture, vascular injury (femoral artery), nerve injury (sciatic, superior gluteal), cement reaction (BCIS)
Early (days–weeks)	DVT/PE, wound infection, early PJI, dislocation
Late (months–years)	Aseptic loosening (most common cause of revision), chronic PJI, wear/osteolysis, LLD, heterotopic ossification, periprosthetic fracture

High Yield Summary — Complications of Hip OA and THR

OA is a serious disease: increased risk of cardiovascular/respiratory disorder, psychological disorder, sleep disturbance, and mortality.
Disease complications: progressive disability, fixed flexion/ER/adduction deformity, Trendelenburg gait, secondary OA of adjacent joints, falls.
Late complications of hip pathology (from lecture slides): secondary OA, stiffness/ankylosis/contracture, deformity (angulation, coxa vara, shortening), instability/dislocation, leg length discrepancy.
The Big Four THR complications: thromboembolism (DVT/PE), dislocation, prosthesis infection, leg length discrepancy.
Nerve injury by approach: Posterior → sciatic nerve; Anterolateral → superior gluteal nerve.
Dislocation prevention: no squatting, no crossing legs, no hip flexion > 90°, abduction pillow, high-low chair.
Aseptic loosening is the most common reason for revision THR — caused by wear particle-induced osteolysis.
PJI is the most devastating complication — biofilm formation makes eradication difficult; often requires two-stage revision.
Prosthesis survival: 15–20 years without revision.
Opioid complications in OA: limited benefit, addiction, falls in elderly, worse surgical outcomes — NOT recommended routinely.
Arthroscopy in OA: very limited role; increases rate of OA progression and shortens time to joint replacement.

Active Recall - Complications of Hip OA and THR

References

^[2] Senior notes: maxim.md (section 6.3 OA hip — specific complications) ^[5] Senior notes: maxim.md (section 6.4 AVN of hip — bisphosphonates and ONJ) ^[7] Senior notes: maxim.md (section 6.2 Hip trauma — dislocation prevention post-THR) ^[11] Senior notes: maxim.md (section 1.3 Management overview — ERAS protocol) ^[12] Lecture slides: GC 229. Hip Arthritis (1).pdf (p. 103 — Take Home Messages) ^[16] Senior notes: maxim.md (section 6.3 — Harris Hip Score) ^[22] Lecture slides: GC 229. Hip Arthritis (1).pdf (p. 39 — Analgesics) ^[23] Lecture slides: GC 228. Knee Osteoarthritis_Part B (1).pdf (p. 8 — Paracetamol) ^[24] Lecture slides: GC 228. Knee Osteoarthritis_Part B (1).pdf (p. 10 — Opioids) ^[28] Lecture slides: GC 228. Knee Osteoarthritis_Part B (1).pdf (p. 18 — Arthroscopy complications) ^[31] Lecture slides: GC 228. Knee Osteoarthritis_Part A (1).pdf (p. 5 — OA is a serious disease) ^[32] Lecture slides: GC 229. Hip Arthritis (1).pdf (p. 55 — Late complications) ^[33] Senior notes: maxim.md (section 9.1 — Specific complications of total replacement)

High Yield Summary

Hip OA = joint failure — involves cartilage, subchondral bone, synovium, capsule, and periarticular muscles.
Primary hip OA is uncommon in the Chinese population — always think secondary causes in Hong Kong.
Secondary causes to know: DDH, AVN (steroids > 20 mg/day, alcohol, trauma, SLE, caisson disease, sickle cell), infection (old TB hip), inflammatory arthritis (RA), crystal deposition (gout), neuropathic (Charcot), metabolic/endocrine.
AVN risk factors: Trauma (femoral neck fracture 15–50%, hip dislocation 10–25%), alcohol, steroids, caisson disease, sickle cell.
Radiological features (LOSS): Loss of joint space (earliest), Osteophytes, Subchondral sclerosis, Subchondral cysts.
Key symptoms: Deep groin pain aggravated by weight-bearing, morning stiffness < 30 min, stiffness (difficulty with shoes/socks), loss of function (walking, stairs, public transport).
Key signs: Externally rotated limb at rest, antalgic gait, Trendelenburg gait (end-stage), painful limited ROM (IR lost first), fixed flexion deformity (Thomas test +), muscle wasting.
Internal rotation is the first movement lost — because the capsule is tightest in IR.
Hip pain can be referred to the knee (Hilton's Law; obturator nerve L2–L4) — always examine the hip when a patient presents with knee pain.
DDH management: Periacetabular osteotomy if congruent joint space preserved and no OA; THR if secondary OA established.
Natural history: Molecular → Pre-radiographic (MRI) → Radiographic (X-ray) → End-stage (joint replacement). Intervene early for best outcomes.
Harris Hip Score evaluates pain, function (walking, stairs, shoes/socks, sitting, public transport), deformity, and ROM.
OA vs RA: OA = weight-bearing joints, preserved bone density, osteophytes, no erosions. RA = any joint, juxta-articular osteopenia, erosions, no reactive bony changes.

High Yield Summary — DDx of Hip Pain

Pain location is the single most useful discriminator: Groin = intra-articular; Lateral = periarticular (GTPS); Buttock/radiating below knee = referred (spine).
Hip OA DDx from senior notes: fractures, sciatica, trochanteric bursitis, gluteus medius tendinopathy.
Age guides the differential: Child (Perthes, DDH, septic arthritis, SCFE) → Young adult (AVN, DDH, FAI, labral tear, AS) → Elderly (primary OA, fracture, metastasis, spinal stenosis).
Passive ROM is the key sign: Restricted = intra-articular. Full = periarticular or referred.
AVN is a major secondary cause in HK — risk factors: steroids > 20 mg/day, alcohol, trauma (NOF 15–50%, dislocation 10–25%), caisson disease, sickle cell.
Septic arthritis is the emergency "don't miss" — acute, febrile, very painful, restricted ROM; aspirate urgently. MRI distinguishes osteomyelitis from septic arthritis.
TB hip is historically significant in Hong Kong — chronic destruction, X-ray shows capsular distension, joint space widening, then destruction.
Always examine the lumbar spine when assessing hip pain — referred pain from the spine is extremely common.
On X-ray, describe features by location (acetabular side, articular surface, femoral side) and look for clues to secondary causes (DDH: dysplasia; AVN: crescent sign; AS: SI fusion; TB: Phemister triad).

High Yield Summary — Diagnosis of Hip OA

Diagnosis is clinical + radiological — no specific lab test for OA.
ACR criteria: Hip pain + 2 of 3 (ESR < 20, osteophytes on X-ray, joint space narrowing).
First-line investigation: Plain X-ray (AP pelvis + lateral of affected hip).
Radiographic hallmarks (LOSS): Loss of joint space (earliest), Osteophytes (most reliable), Subchondral sclerosis, Subchondral cysts.
Describe X-ray by location: acetabular side, articular surface, femoral side.
Kellgren-Lawrence grading: Grade 0 (normal) to Grade 4 (bone-on-bone).
Always look for secondary causes on X-ray: DDH (dysplasia), AVN (crescent sign), AS (SI fusion), TB (capsular distension), RA (erosions/osteopenia).
MRI: 99% sensitive/specific for AVN (double-line sign); best for pre-radiographic OA, labral tears, and distinguishing osteomyelitis from septic arthritis.
Bloods are to exclude differentials, not to diagnose OA: ESR, CRP, WCC (infection); RF, anti-CCP (RA); urate (gout); HLA-B27 (AS).
Image-guided aspiration: urgent for suspected septic arthritis — cell count, Gram smear, bacterial/fungal/AFB culture, +/- crystals.
Ficat classification for AVN: I (normal X-ray) → core decompression; II (sclerotic/cystic) → core decompression/bone graft; III (subchondral collapse) → bone graft/THR; IV (OA changes) → THR.
Harris Hip Score: Pain (44) + Function (47) + ROM + Deformity = max 100. Used for baseline and post-THR follow-up.
Natural history: Molecular → Pre-radiographic (MRI/biomarkers) → Radiographic (X-ray) → End-stage. Intervene early.

High Yield Summary — Management of Hip OA

First-line = Education, Exercise, Weight Control (ALL patients) — NOT analgesics, NOT surgery.
OA Treatment Pyramid: Core non-pharmacological (all) → Pharmacological + adjuncts (some) → Surgery (few).
Physiotherapy — Strong evidence for improving function and reducing pain in mild-moderate hip OA.
Analgesics do NOT affect natural history — symptomatic relief only.
Paracetamol = first-line analgesic but network meta-analysis shows no demonstrable benefit in OA at any dose; used for safety profile relative to NSAIDs.
NSAIDs have proven benefit but GI, renal, and cardiovascular side effects limit their use.
Tramadol: non-narcotic, synergistic with paracetamol, use if NSAIDs contraindicated.
Opioids: NO routine use — limited benefit, serious adverse effects (addiction, falls in elderly, worse surgical outcomes).
Intra-articular hyaluronic acid: Strong evidence AGAINST — does not outperform placebo for hip OA.
Intra-articular steroid: short-term relief, image-guided, useful as bridge.
Surgical indications: severe ADL impairment + pain despite conservative treatment.
Joint-preserving: Osteotomy (young < 60, preserved cartilage), PAO (DDH before OA), Core decompression (AVN Ficat I–II).
THR = reliable and durable for end-stage arthritis. Surgical approaches relative to gluteus medius: Posterior (most common, preserves abductors but risk of dislocation/sciatic nerve injury), Anterolateral/Hardinge (good exposure but superior gluteal nerve injury), Anterior/Smith-Petersen (rare, for infected hip washout).
THR goals: restore pain-free stable joint, restore anatomical hip centre (acetabular), correct femoral deformity, address soft tissue contractures, protect sciatic nerve.
Harris Hip Score for pre- and post-operative assessment.
Multidisciplinary approach for inflammatory causes (rheumatologist + orthopaedic surgeon).

High Yield Summary — Complications of Hip OA and THR

OA is a serious disease: increased risk of cardiovascular/respiratory disorder, psychological disorder, sleep disturbance, and mortality.
Disease complications: progressive disability, fixed flexion/ER/adduction deformity, Trendelenburg gait, secondary OA of adjacent joints, falls.
Late complications of hip pathology (from lecture slides): secondary OA, stiffness/ankylosis/contracture, deformity (angulation, coxa vara, shortening), instability/dislocation, leg length discrepancy.
The Big Four THR complications: thromboembolism (DVT/PE), dislocation, prosthesis infection, leg length discrepancy.
Nerve injury by approach: Posterior → sciatic nerve; Anterolateral → superior gluteal nerve.
Dislocation prevention: no squatting, no crossing legs, no hip flexion > 90°, abduction pillow, high-low chair.
Aseptic loosening is the most common reason for revision THR — caused by wear particle-induced osteolysis.
PJI is the most devastating complication — biofilm formation makes eradication difficult; often requires two-stage revision.
Prosthesis survival: 15–20 years without revision.
Opioid complications in OA: limited benefit, addiction, falls in elderly, worse surgical outcomes — NOT recommended routinely.
Arthroscopy in OA: very limited role; increases rate of OA progression and shortens time to joint replacement.

Hip Osteoarthritis

1. Definition

2. Epidemiology

Global

Hong Kong / Chinese Population — Critical Distinction

3. Risk Factors

3.1 Non-modifiable Risk Factors

3.2 Modifiable Risk Factors

4. Anatomy and Function of the Hip Joint

4.1 Bony Anatomy

4.2 Neurovascular Supply

4.3 Gluteal Muscles and Hip Biomechanics

5. Etiology (Focus on Hong Kong)

5.1 Primary (Idiopathic) OA

5.2 Secondary OA

5.3 Avascular Necrosis (AVN) as a Cause of Secondary Hip OA

5.4 Developmental Dysplasia of the Hip (DDH) as a Cause of Secondary Hip OA

6. Pathophysiology

6.1 Normal Joint Homeostasis

6.2 Pathological Cascade in OA

6.3 Subchondral Bone Changes

6.4 Natural History

7. Classification

7.1 By Aetiology [1][2]

7.2 Radiological Grading — Kellgren-Lawrence Classification

7.3 Functional Assessment — WOMAC Score

7.4 Harris Hip Score [1]

7.5 Radiological Features of OA — The "LOSS" Mnemonic [2]

8. Clinical Features

8.1 History Taking — The Approach

8.2 Symptoms (with Pathophysiological Basis)

8.3 Signs (with Pathophysiological Basis)

8.4 Distinguishing OA from Inflammatory Arthritis (RA)

9. Differential Diagnosis of Hip Pain (Brief Overview)

10. Summary Table — Linking Pathophysiology to Clinical Features

Active Recall - Hip Osteoarthritis (Pre-DDx/Dx/Mx)

References

The Approach — Think Anatomically, Then by Aetiology

Systematic Differential Diagnosis by Category

A. Intra-articular Causes (Pain from Within the Hip Joint)

B. Periarticular Causes (Pain from Around the Hip)

C. Referred Pain (Distant Pathology Projecting to the Hip)

Age-Based Approach to Differential Diagnosis

Decision Flowchart — Approach to Hip Pain DDx

Key Distinguishing Features — Summary Table for Exams

Distinguishing X-ray Features by Underlying Cause of Secondary Hip OA

Septic Arthritis — A "Don't Miss" Diagnosis

Differential Diagnosis in the Broader Context — The "TIN" Framework

Active Recall - Differential Diagnosis of Hip Pain

1. Diagnostic Criteria — How Do We Actually Diagnose Hip OA?

1.1 The ACR (American College of Rheumatology) Clinical Classification Criteria for Hip OA

1.2 Why These Criteria Make Sense — First Principles

1.3 What Hip OA is NOT

2. Diagnostic Algorithm

3. Investigation Modalities — Detailed Breakdown

3.1 Plain Radiographs (X-rays) — The First-Line Investigation

Required Views

The Four Hallmarks of OA on X-ray — LOSS [2][12][13]

X-ray Features of Underlying Causes (Secondary OA) [2]

Kellgren-Lawrence (KL) Classification [1][7]

3.2 MRI — The Gold Standard for Soft Tissue and Early Disease

Key MRI Findings

Natural History — MRI Detects Disease Earlier Than X-ray [3]

3.3 Blood Investigations — To Exclude Differential Diagnoses

3.4 Joint Aspiration — When Infection or Crystal Arthropathy Is Suspected

3.5 Other Imaging Modalities

3.6 Staging of AVN — The Ficat Classification [14]

4. The Harris Hip Score — Functional Assessment [2][16]

5. Summary — Putting It All Together

Active Recall - Diagnosis & Investigations for Hip OA

1. Management Principles — The Big Picture

2. Management Algorithm

3. First-Line Treatment — Non-Pharmacological Core Treatment (ALL Patients)

3.1 Education and Self-Management

3.2 Exercise and Physiotherapy

3.3 Weight Reduction

4. Second-Line Treatment — Pharmacological and Adjunctive (SOME Patients)

4.1 Analgesics

4.2 Topical Treatments

4.3 Intra-articular Injections