---

ORTHOPAEDICS - COMPREHENSIVE NOTES

---

1. OSTEOMYELITIS

Definition

---

ACUTE OSTEOMYELITIS

Aetiology / Causative Organisms

• Most common: Staphylococcus aureus (including MRSA - Panton-Valentine leukocidin [PVL] gene increases morbidity)
• Neonates: S. aureus, Group B Streptococcus, Gram-negative organisms
• Sickle cell disease: Salmonella species (classically)
• Immunocompromised: Gram-negative organisms, fungi
• Post-traumatic / post-surgical: S. aureus, Gram-negatives, Pseudomonas

Pathogenesis

• Infection usually arrives via haematogenous spread (most common)
• May also be via: direct inoculation (open fracture, surgery), or contiguous spread from adjacent soft tissue
• In children, infection seeds in the metaphysis of long bones - the slow, turbulent blood flow through looped metaphyseal vessels + microtrauma encourages bacterial seeding during bacteraemia
• Inflammation follows; if purulent material forms, abscess pressure leads to bony destruction
• Pus passes through cortical bone, elevates the periosteum (rendering cortical bone avascular) and stimulates new bone formation

Pathological Progression

1. Haematogenous seeding in metaphysis
2. Inflammatory exudate forms - raises intraosseous pressure
3. Periosteum elevated - cortex becomes avascular
4. Dead bone = sequestrum
5. Periosteum forms new bone surrounding the dead bone = involucrum ("bone-within-a-bone" appearance)
6. Pus may track through cortex and periosteum to form a subperiosteal abscess, then a soft tissue abscess, and may discharge through a sinus

In the neonate, vascular channels cross the physis connecting metaphysis to epiphysis - proximal femoral osteomyelitis and septic arthritis are essentially the same condition in neonates.

Clinical Features

• Systemic: Fever, malaise, rigors, raised WBC, CRP, ESR
• Local: Swelling, tenderness, warmth, erythema over affected bone
• Refusal to use limb (pseudoparalysis in infants)
• A sympathetic joint effusion may occur with metaphyseal osteomyelitis - differentiation from primary septic arthritis can be difficult

Investigations

• Blood: FBC (leukocytosis), CRP, ESR, blood cultures (positive in ~50%)
• X-ray: Normal in first 7-10 days. Periosteal reaction, lytic lesions appear later
• Bone scan (Tc-99m): Increased uptake - sensitive but not specific; useful early when X-ray normal
• MRI: Most sensitive and specific - shows marrow oedema, periosteal elevation, soft tissue extension
• Ultrasound: Detects subperiosteal abscess, joint effusion; guides aspiration
• Bone biopsy / aspiration: Organism identification and sensitivity - gold standard for diagnosis

Management

• Appropriate antibiotics - guided by culture; empirical IV anti-staphylococcal (e.g. flucloxacillin; vancomycin if MRSA risk)
• Initial IV, then step-down to oral once clinically improving and inflammatory markers falling
• Duration: typically 4-6 weeks total (2 weeks IV + oral); varies by region and organism
• Treat underlying conditions (e.g. sickle cell, malnutrition)

• Rest and splintage of affected limb
• Analgesia

• Drain pus when present (subperiosteal or soft tissue abscess)
• Surgical decompression if no improvement with antibiotics within 24-48 hours

Complications

• Septic arthritis (especially when metaphysis is intracapsular - e.g. hip)
• Pathological fracture
• Physeal damage → growth disturbance (especially in neonates due to trans-physeal vessels)
• Chronic osteomyelitis
• Septicaemia, metastatic infection

---

CHRONIC OSTEOMYELITIS

Definition

Aetiology

• Inadequately treated acute haematogenous osteomyelitis
• Post-traumatic (especially open fractures)
• Post-surgical
• Contiguous spread (e.g. diabetic foot, pressure sores)
• Rarely, haematogenous in adults (usually vertebral)

Pathology

• Sequestrum: Avascular dead bone, surrounded by pus; acts as foreign body, perpetuates infection
• Involucrum: Periosteal new bone surrounding sequestrum
• Cloaca: Openings in involucrum through which pus discharges
• Sinus tract: Chronic discharging sinus to skin surface
• Brodie's abscess: Subacute form - radiographic appearance of a sclerotic-walled cyst; cultures may be negative; classic location: metaphysis of tibia

Clinical Features

• History of prior bone infection or open fracture/surgery
• Chronic discharging sinus - intermittent or persistent
• Pain, swelling, tenderness over the affected area
• Systemic features may be minimal or absent
• Recurrent acute exacerbations (fever, increased pain, increased discharge)

Investigations

• X-ray: Shows sclerosis, periosteal thickening, lytic areas, sequestrum, involucrum
• CT: Better delineates sequestrum and cortical destruction
• MRI: Most sensitive for marrow involvement and soft tissue extent
• Bone scan: Useful but non-specific
• Sinogram: Injection of contrast into sinus tract to map extent
• Microbiology: Swab of sinus discharge (often colonised, not representative), deep tissue biopsy is better
• Histology: Rules out malignancy (Marjolin's ulcer - squamous cell carcinoma arising in chronic sinus)

Management

• Prolonged antibiotic therapy based on deep culture sensitivities
• Usually 6-12 weeks, sometimes indefinitely (suppressive therapy)

• Sequestrectomy: Removal of dead bone (sequestrum)
• Saucerisation (saucerization): Unroofing the cavity, creating a saucer shape to allow drainage and granulation
• Dead space management: Cancellous bone graft, antibiotic-impregnated beads (PMMA), Masquelet technique (induced membrane technique)
• Soft tissue coverage: Muscle flap or free flap for large defects
• External fixation / bone transport: If segmental bone loss (Ilizarov method)

Special Types

• Chronic relapsing/recurrent multifocal osteomyelitis (CRMO): Radiographic features suggest chronic osteomyelitis but cultures are negative. This is an inflammatory (not infective) condition. Non-specific histopathology.
• Brodie's abscess: Sclerotic walled cyst on imaging; represents subacute/chronic low-virulence infection; common in children/adolescents

---

2. FRACTURES AND FRACTURE HEALING

Definition

Classification of Fractures

• By skin integrity: Closed (simple) vs. Open (compound - bone communicates with external environment)
• By pattern: Transverse, oblique, spiral, comminuted (>2 fragments), segmental, avulsion, impacted
• By cause: Traumatic, stress (fatigue fracture from repeated loading), pathological (through diseased bone)
• By location: Epiphyseal, metaphyseal, diaphyseal; intra-articular vs. extra-articular
• In children: Greenstick (incomplete, one cortex intact), buckle/torus (cortex buckles, not disrupted), physeal (Salter-Harris classification)

• Type I: Through physis only
• Type II: Through physis + metaphysis (most common)
• Type III: Through physis + epiphysis
• Type IV: Through metaphysis + physis + epiphysis
• Type V: Crush injury to physis (worst prognosis)

Clinical Features of Fractures

• Pain, tenderness at fracture site
• Deformity, shortening, abnormal posture
• Swelling, bruising
• Loss of function, abnormal movement
• Crepitus (do not elicit deliberately)
• Neurovascular compromise (distal pulse, sensation, motor function)

Diagnosis

• Clinical examination
• X-ray: minimum 2 views (AP + lateral); joint above and below
• CT: complex fractures, intra-articular, spinal
• MRI: stress fractures, occult fractures, soft tissue injury

---

FRACTURE HEALING

Mechanisms

• Occurs when fracture ends are in cortical apposition with absolute stability and no movement at the fracture site
• No callus formation
• Osteoclastic cutting cones cut across the fracture line; osteoblasts lay down lamellar bone
• Analogous to normal bone remodelling
• Achieved by rigid internal fixation (e.g., compression plating)

• Most common form of fracture healing
• Requires some movement (strain) at the fracture site
• Involves callus formation - transition from one tissue type to another:
  1. Haematoma fills the fracture gap
  2. Fibrous tissue (granulation tissue)
  3. Soft callus (fibrocartilage)
  4. Hard callus (woven bone - calcified)
  5. Remodelling to lamellar bone

• Strain at fracture site determines tissue type:

  • 100% strain → fibrous tissue

  • ~10% → soft callus
  • <2% → hard callus and mineralisation
• A little movement is good; too much movement prevents healing

Factors Affecting Fracture Healing

• Blood supply to bone (periosteum + nutrient artery)
• Soft tissue injury (open fractures → poor perfusion)
• Infection
• Systemic disease: diabetes (microvascular), peripheral vascular disease
• Age (children heal faster)
• Nutritional status, smoking, medications (NSAIDs, steroids)

• Stability at fracture site
• Degree of displacement/comminution
• Bone-on-bone contact

Terminology of Fracture Healing

Non-Union Types

• Hypertrophic: Adequate vascularity but inadequate stability (elephant foot, horse hoof appearances on X-ray); treated by stabilisation
• Atrophic: Inadequate vascularity; no callus; treated by bone grafting + stabilisation
• Infected non-union: Requires infection control + bone reconstruction

Principles of Fracture Treatment (Apley's 4 Rs)

1. Reduce - Restore anatomy (closed or open reduction)
   • Intra-articular fractures: anatomical reduction mandatory
   • Extra-articular: mechanical alignment adequate
2. Hold - Maintain reduction (cast, traction, external fixation, internal fixation - plates, nails, screws)
3. Heal - Optimise biological and mechanical environment
4. Rehabilitate - Restore function

---

3. UPPER LIMB FRACTURES

---

4. SHOULDER DISLOCATION

Anatomy

---

ANTERIOR SHOULDER DISLOCATION

Mechanism

• Most common type (>95% of shoulder dislocations)
• FOOSH, abduction + external rotation force
• Head displaces anteriorly - most commonly subcoracoid (below coracoid process)
• Also subglenoid, subclavicular

Clinical Features

• Severe pain; arm held in slight abduction, supported by other hand
• Loss of normal rounded shoulder contour - flat, squarish appearance (deltoid flattening)
• Anterior fullness below coracoid
• Loss of normal shoulder profile - "straight line from acromion"
• Arm cannot be adducted to chest

Neurovascular Complications

• Axillary nerve injury (most common) - sensory loss over deltoid insertion ("regimental badge" area), deltoid weakness; usually recovers in weeks
• Brachial plexus injury (rare)
• Axillary artery injury (rare, especially in elderly)

Investigations

• AP X-ray: Humeral head displaced anteroinferiorly; subcoracoid position
• Axillary lateral / Y-view: Confirms anterior displacement; essential
• Post-reduction X-ray mandatory

Associated Lesions

• Bankart lesion: Tear of anteroinferior labrum (most common, ~85% of dislocations) - predisposes to recurrence
• Hill-Sachs lesion: Posterolateral compression fracture of humeral head (from impaction against glenoid rim)
• Bony Bankart: Fracture of anteroinferior glenoid rim
• HAGL lesion: Humeral avulsion of glenohumeral ligament

Reduction Techniques

1. Hanging arm method (Stimson technique): Patient prone, arm hangs over edge of couch with weight attached; muscle relaxation allows gravity reduction
2. Hippocratic method: Patient supine; traction on arm + countertraction (operator's foot in axilla - removing shoe); gentle external rotation helps reduction
3. Kocher's method: External rotation with elbow at 90° → forward flexion → internal rotation (risk of fracture, less commonly used now)
4. Cunningham technique / FARES method: Traction + gentle manipulation without sedation

• Reduction is easier the sooner it is carried out
• Adequate analgesia/sedation mandatory

Post-reduction Management

• Confirm reduction with X-ray
• Broad arm sling for 2-3 weeks
• Physiotherapy for rotator cuff strengthening
• Young, active patients have high recurrence rates

Recurrent Dislocation

• Subsequent dislocations require less force
• Positive apprehension sign (pain/apprehension on abduction-external rotation)
• Surgery: Bankart repair (labral reattachment, arthroscopic or open) + capsular tightening
• Significant bone loss: Latarjet procedure (coracoid transfer)

---

POSTERIOR SHOULDER DISLOCATION

Mechanism

• Uncommon (<5%)
• Classic mechanisms: electric shock, epileptic fit, severe shoulder restraint (half-Nelson)
• Forced internal rotation; arm driven posteriorly

Clinical Features

• May be subtle and frequently missed (on AP X-ray can look normal to the unwary)
• Arm held in internal rotation and adduction
• Patient post-ictal or recovering from electric shock (difficult to examine)

Investigations

• AP X-ray: May appear near-normal - "lightbulb sign" (head appears spherical due to internal rotation)
• Axillary lateral view is critical - confirms posterior displacement clearly
• CT: If fracture-dislocation suspected

Associated Lesions

• Reverse Hill-Sachs (McLaughlin lesion): Anterior impaction fracture of humeral head
• Posterior labral tear

Treatment

• Often requires general anaesthesia
• Closed reduction: gentle axial traction + external rotation while maintaining traction
• Locked posterior dislocation (posterior glenoid embedded in humeral head): requires open reduction
• Post-reduction: immobilise in neutral/external rotation brace

---

INFERIOR DISLOCATION (Luxatio Erecta)

• Rarest type
• Arm held fully elevated above head
• Often associated with rotator cuff and neurovascular injury
• Reduction by traction in line with arm, then arc down to side

---

5. HIP DISLOCATION

Anatomy

---

POSTERIOR HIP DISLOCATION

Mechanism

• High-energy trauma - motor vehicle collision (>95% have associated injuries)
• Force applied to flexed knee, pushing femur posteriorly - classic "dashboard injury"
• Associated injuries: acetabular fracture, femoral neck/shaft fracture, knee ligament injury

Clinical Features

• Limb shortened, adducted, internally rotated (key distinguishing feature from femoral neck fracture which is externally rotated)
• Severe pain; patient unable to move hip
• Posterior prominence palpable

Neurovascular Complications

• Sciatic nerve injury (~10%): foot drop, sensory loss
• Vascular injury (rare)

Investigations

• AP + lateral pelvis X-ray: Femoral head displaced posteriorly, appears smaller than opposite side
• CT: To identify associated acetabular fractures and loose fragments (intra-articular)
• Pre- and post-reduction CT recommended

Management

• Orthopaedic emergency - reduce within 6 hours (ideally <4 hours)
• Risk of AVN increases: <10% if reduced promptly → ~25% if reduced after 10-15 hours; nearly doubles further after 15 hours
• Closed reduction under procedural sedation (Allis manoeuvre - most common):
  • Patient supine, pelvis stabilised by assistant
  • Hip and knee flexed to 90°
  • In-line traction + internal rotation → femoral head levers back into acetabulum
  • Bigelow's manoeuvre: traction + circumduction (flexion → abduction → external rotation)
  • Stimson technique: patient prone, leg hangs off table, downward pressure on popliteal fossa
• Post-reduction: AP + lateral X-ray to confirm; CT to assess joint congruency and loose bodies
• If closed reduction fails or inadequate: open reduction in theatre
• Skin traction after reduction; early mobilisation when comfortable

Complications

• Avascular necrosis (AVN) of femoral head - most serious; risk proportional to time to reduction
• Post-traumatic osteoarthritis
• Sciatic nerve palsy (10%)
• Recurrent dislocation (if large acetabular fracture)

---

ANTERIOR HIP DISLOCATION

Mechanism

• Forced abduction + external rotation
• Femoral head levers out through anterior capsular tear
• Superior (pubic/iliac): Abduction + extension → head in front of acetabulum, superiorly
• Inferior (obturator): Abduction + flexion → head in obturator foramen

Clinical Features

• Superior type: Limb in extension, external rotation, slight abduction
• Inferior (obturator) type: Limb in marked flexion, abduction, external rotation - very characteristic appearance
• Femoral vessels and nerve at risk

Investigations

• AP pelvis X-ray: femoral head anterior to acetabulum
• CT confirms

Management

• Reduction under general anaesthesia in theatre (all anterior dislocations mandate operating room reduction)
• Closed reduction: traction in line with deformity, then internal rotation and adduction
• Open reduction if closed fails

---

6. POTT'S SPINE (TUBERCULOSIS OF THE SPINE)

Definition

Epidemiology

• Globally common; endemic in developing countries
• Most common site of osteoarticular TB (spine involved in ~50% of skeletal TB)
• Thoracic spine most commonly affected (T10-L1), followed by lumbar, then cervical

Pathogenesis

• Primary focus usually in lung; haematogenous spread to spine
• Bacteria seed the anterior vertebral body adjacent to the disc (anterior vertebral metaphysis - richly vascularised)
• Spreads under anterior longitudinal ligament to adjacent vertebrae
• Disc is avascular, so disc involvement is secondary - disc space narrows
• Caseous necrosis, vertebral body collapse
• Paravertebral abscess forms (cold abscess - no heat/redness)
• Abscess may track under ligaments (psoas abscess in lumbar TB, parapharyngeal abscess in cervical TB)

Clinical Features

• Insidious onset - weeks to months of:
  • Constitutional: malaise, weight loss, low-grade fever, night sweats
  • Back pain - localised, persistent, worse at night
  • Muscle spasm and rigidity
  • Gibbus deformity - angular kyphosis (pathognomonic) due to anterior vertebral collapse
  • Paraplegia (Pott's paraplegia) - from cord compression by abscess, granulation tissue, or collapsed vertebra

Pott's Paraplegia

• Early onset (healing disease): Due to abscess/granulation tissue - responds well to treatment
• Late onset (healed disease): Due to bony damage (sequestrum, deformity) - requires surgery

Investigations

• Blood: ESR raised, CRP raised; Mantoux/IGRA positive (not specific)
• Chest X-ray: May show pulmonary TB
• X-ray spine:
  • Narrowed disc space
  • Vertebral body destruction (anterior wedging)
  • Angular kyphosis (gibbus)
  • Paravertebral shadow (cold abscess)
  • Calcification in chronic cases
• MRI spine (gold standard): Shows extent of vertebral involvement, disc involvement, cord compression, abscess extent
• CT: Bony detail, abscess
• Biopsy: CT-guided biopsy for histology (caseating granuloma with Langerhans giant cells) and culture (ZN stain + AFB culture) - confirms diagnosis
• Sputum smear/culture if pulmonary lesion present

Management

Medical (cornerstone of treatment)

• Anti-tubercular therapy (ATT) - standard 4-drug regimen:
  • 2 months HRZE (Isoniazid + Rifampicin + Pyrazinamide + Ethambutol) - intensive phase
  • 4-7 months HR (Isoniazid + Rifampicin) - continuation phase
  • Total duration: 6-9 months (may extend to 12-18 months for complex/drug-resistant cases)
• Immobilisation with spinal orthosis (brace)
• Nutritional support

Surgical

1. Neurological deficit (paraplegia)
2. Abscess not resolving with medical treatment
3. Progressive deformity (kyphosis)
4. Instability
5. Failure of medical treatment / diagnostic uncertainty

• Abscess drainage (cold abscess: percutaneous or open)
• Anterior debridement - removal of diseased bone and disc
• Spinal stabilisation - anterior/posterior instrumented fusion
• Decompression if cord compressed

Complications

• Pott's paraplegia (neurological compromise)
• Progressive kyphosis/gibbus
• Psoas abscess (L-spine) - may track to groin/thigh
• Chronic discharging sinuses
• Spinal instability
• Rarely: SCC arising in sinus tract (Marjolin's ulcer)

---

7. DEVELOPMENTAL DYSPLASIA OF THE HIP (DDH)

Definition

• In joint but dysplastic/shallow acetabulum
• Subluxable (Barlow positive - can be pushed out with pressure)
• Reducible dislocation (Ortolani positive - dislocated at rest but can be reduced)
• Irreducible dislocation (Ortolani negative)

Epidemiology

• Incidence: Neonatal instability ~20 per 1000 live births; true dislocation ~2 per 1000 live births
• Many hips stabilise spontaneously
• Left hip more commonly affected (fetal position - left occipito-anterior)

Aetiology / Risk Factors

Pathology

• Shallow, sloped acetabulum (dysplasia)
• Stretched joint capsule
• Secondary changes with chronicity: soft tissue and bony adaptations making reduction harder with increasing age

Clinical Diagnosis

Neonatal Screening

• Ortolani test: Flex and abduct hip; examiner's finger behind greater trochanter lifts it forward - a soft clunk (not click) indicates reduction of a dislocated hip = Ortolani positive = reducible dislocation
• Barlow test: Hip flexed and adducted, downward pressure applied to knee - if hip dislocates with pressure = Barlow positive = subluxable/dislocatable hip

In Older Children (walking age)

• Short limb (apparent or real)
• Galeazzi sign: With hips and knees flexed, affected knee is lower (femoral shortening)
• Limping / Trendelenburg gait - abductor weakness
• Late presenting: bilateral DDH may cause waddling gait
• Adults: groin pain, secondary osteoarthritis

Investigations

• Ultrasound (birth - 6 months): Investigation of choice in infants (ossific nucleus not visible on X-ray until ~4-6 months)
  • Graf classification based on α angle (bony coverage) and β angle
  • Morin index: % femoral head covered by acetabulum (normal >50%)
  • Dynamic assessment: Barlow and Ortolani manoeuvres under US
• X-ray (>4-6 months): Once ossific nucleus appears
  • Hilgenreiner's line: Horizontal through triradiate cartilages
  • Perkins' line: Vertical from lateral edge of acetabulum
  • Normal: ossific nucleus in inner/lower quadrant
  • DDH: ossific nucleus in outer/upper quadrant
  • Shenton's line: Smooth arc along femoral neck and obturator foramen - disrupted in dislocation
  • Acetabular index: Normal <30°; DDH >30° at birth
• MRI / arthrogram: Intra-articular assessment pre/post reduction, under GA

Management

Neonates (0-6 months)

• Many unstable hips stabilise spontaneously by 6 weeks
• Pavlik harness (most widely used): Maintains hips in flexion and abduction (human position), allows controlled movement while achieving reduction
  • Success rate >90% for reducible dislocations
  • Risk of AVN - monitor with serial ultrasound
  • Must not be used if hip cannot be reduced (irreducible) as pressure can cause AVN
• Fixed splints (Von Rosen, etc.) - more rigid, higher AVN risk

6-18 months

• Closed reduction under GA + arthrogram + hip spica cast
• If closed reduction fails: open reduction
• Followed by hip spica cast for 3-6 months

18 months - 3 years

• Open reduction + spica cast
• May need femoral osteotomy (to improve stability)
• Acetabulum usually remodels if adequate reduction achieved

>3-4 years (late presenting)

• More likely to need combined surgery:
  • Open reduction
  • Femoral osteotomy (derotation/shortening)
  • Pelvic osteotomy - reshapes/redirects acetabulum (e.g., Salter innominate osteotomy, Pemberton, Dega, Ganz periacetabular osteotomy for adults)
• Acetabular remodelling potential decreases significantly after 3-4 years

Complications of DDH and Its Treatment

• Avascular necrosis (AVN) of femoral head - most feared; caused by pressure (Pavlik, splints) or over-aggressive reduction
• Redislocation
• Trochanteric overgrowth (following AVN) → Trendelenburg limp
• Leg length discrepancy
• Residual dysplasia → secondary osteoarthritis (leading cause of hip replacement in 4th-5th decade)
• Femoral nerve palsy (from harness)

---