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Here are model answers for your Pre-University Orthopaedics examination (MVASMC Basti):

Pre University Examination - Orthopaedics: Model Answers


Q1. Clostridial Gas Gangrene (Clostridial Myonecrosis) [10 marks]

Definition

Gas gangrene is a rapidly progressive, life-threatening soft-tissue infection characterised by widespread muscle necrosis, gas production in tissues, and severe systemic toxaemia. It is most commonly caused by Clostridium perfringens.

Etiopathogenesis

Causative Organisms:
  • Clostridium perfringens - most common (80-90%)
  • Clostridium septicum, C. bifermentans, C. sporogenes
  • Non-clostridial gas-producing organisms (coliforms) are co-isolated in 60-85% of cases
Predisposing Conditions:
  • Crushing injuries, missile/gunshot wounds
  • Compound fractures with devitalised muscle
  • Ischaemic/vascular injuries
  • Bowel surgery (spontaneous gas gangrene from C. septicum)
  • Premature wound closure
Pathogenesis:
  1. Devitalised (ischaemic) tissue creates the anaerobic environment needed for spore germination
  2. Incubation period: usually <24 hours (range: 1 hour to 6 weeks)
  3. C. perfringens produces multiple exotoxins:
    • Alpha-toxin (lecithinase) - most important; destroys RBCs, WBCs, platelets, fibroblasts, and muscle cells
    • Phi-toxin - causes myocardial suppression
    • Kappa-toxin - destroys connective tissue and blood vessels
  4. A vicious cycle ensues: bacteria multiply -> exotoxins cause local necrosis and vascular thrombosis -> further anaerobic spread -> gas (CO2, H2, N2) tracks along muscle planes
  5. Systemic exotoxins cause severe haemolysis, leading to hypotension, shock, AKI, and ARDS

Clinical Features

Local Signs:
  • Pain - earliest symptom; rapidly increases in severity (disproportionate to wound appearance)
  • Tense, woody swelling of the limb
  • Wound exudes serosanguineous (brownish, "dishwater") discharge
  • Skin turns bronze/brown, then blue-black
  • Haemorrhagic bullae (blisters)
  • Soft-tissue crepitus on palpation (gas in tissue planes)
  • Characteristic sickly-sweet odour
Systemic Signs:
  • High-grade fever, tachycardia, tachypnoea
  • Altered mental status (restlessness, anxiety, then delirium)
  • Hypotension progressing to septic shock
  • Jaundice (from haemolysis)
  • Oliguria/anuria (AKI)

Investigations

  • X-ray/CT scan - feathery gas shadows within muscle planes
  • Gram stain of exudate - large Gram-positive bacilli, notably WITHOUT neutrophils (neutrophils are destroyed by the toxins)
  • Blood tests - haemolytic anaemia, leucocytosis, metabolic acidosis, raised creatinine
  • Culture - anaerobic culture of wound discharge confirms organism

Differential Diagnosis

ConditionDistinguishing Features
Necrotising fasciitisFascia necrosis, not primarily muscle; mixed organisms; less rapid gas
CellulitisNo gas, no crepitus, less systemic toxicity
Non-clostridial crepitant myositisColiforms, slower; less toxaemia
Clostridial cellulitisGas in subcutaneous tissue, muscle not involved; less toxic
Streptococcal myonecrosisS. pyogenes; incubation 3-4 days; less rapid
Diabetic foot infectionGas from facultative anaerobes; less acute onset

Management

1. Resuscitation (ICU admission):
  • IV fluid resuscitation, inotropes for shock
  • Monitor urine output, ABG, renal function
  • Blood transfusion for haemolytic anaemia
2. Antibiotics (IV, high-dose):
  • Penicillin G (high dose) - first-line
  • Clindamycin - inhibits toxin production (key adjunct)
  • Third-generation cephalosporins added for polymicrobial cover
3. Surgery - EMERGENCY:
  • Radical surgical debridement - all necrotic muscle must be excised
  • Amputation - in established gas gangrene with systemic toxicity, amputation is life-saving and must not be delayed
  • Wound is left OPEN (no closure); packed with saline-soaked gauze
  • Re-exploration at 24-48 hours
4. Hyperbaric Oxygen (HBO):
  • Recommended in severe cases if facilities available
  • Inhibits bacterial growth in high O2 environment; may limit extent of debridement needed
5. Anti-gas gangrene serum - of limited evidence; rarely used now
Prognosis: Mortality 20-30%; higher with truncal/bowel involvement


Q2A. Classical Hand Deformities in Rheumatoid Arthritis [5 marks]

The inflamed rheumatoid synovium (pannus) destroys ligaments, tendons, and articular cartilage, producing characteristic deformities.

1. Ulnar Deviation/Drift at MCPJs

  • Most characteristic deformity of RA
  • Pannus destroys the MCPJ capsule and collateral ligaments
  • Flexor tendons bowstring towards the ulnar side
  • Results in ulnar deviation of fingers at the MCPJs with radial deviation of the wrist (zig-zag deformity)

2. Swan Neck Deformity

  • Hyperextension at PIPJ + Flexion at DIPJ
  • Caused by: MCPJ synovitis -> intrinsic muscle tightness -> PIP hyperextension; or FDS tendon rupture
  • Resembles a swan's neck in profile
Swan neck deformity diagram

3. Boutonniere Deformity

  • Flexion at PIPJ + Hyperextension at DIPJ
  • Caused by: attenuation/rupture of the central slip of extensor tendon -> lateral bands sublux volar to PIPJ axis -> PIPJ stuck in flexion, DIPJ hyperextends
Boutonniere deformity diagram

4. Z-deformity of Thumb (Hitchhiker's Thumb)

  • Flexion of IPJ + Hyperextension of MCPsJ (or vice versa)
  • Three types (Nalebuff classification)

5. Caput Ulnae Syndrome

  • Dorsal subluxation of the distal ulna due to DRUJ destruction
  • The prominent ulnar head ("caput ulnae") can rupture the extensor tendons of the little finger first, progressing radially (Vaughan-Jackson syndrome)

6. Extensor Tendon Ruptures

  • Begin with the little finger (EDM, EDC5), progressing radially (Vaughan-Jackson)
  • Unable to actively extend the involved fingers

7. Mallet Finger

  • Loss of active DIP extension due to extensor tendon attrition over a dorsal osteophyte


Q2B. Bursitis Around the Knee [5 marks]

A bursa is a synovium-lined sac that reduces friction between structures. Multiple bursae surround the knee joint.

1. Prepatellar Bursitis ("Housemaid's Knee")

  • Location: Subcutaneous, in front of the lower patella and upper patellar ligament
  • Cause: Repeated kneeling (carpet layers, roofers, clergy)
  • Features: Tender, fluctuant swelling directly over the patella; knee flexion is painful; joint itself is not involved
  • Treatment: Rest, aspiration, anti-inflammatory drugs; surgical excision for chronic/recurrent cases

2. Infrapatellar Bursitis ("Clergyman's Knee")

  • Superficial infrapatellar bursa: Between skin and patellar ligament below the tibial tuberosity
  • Deep infrapatellar bursa: Between patellar ligament and the tibia
  • Cause: Kneeling in a more upright position (prayer)
  • Features similar to prepatellar bursitis but lower in position

3. Suprapatellar Bursa

  • Located between the femur and the quadriceps tendon
  • Normally communicates with the knee joint cavity
  • Becomes distended in any knee joint effusion; best detected as a horseshoe-shaped swelling above the patella

4. Semimembranosus Bursa (Baker's Cyst precursor)

  • Located posteromedially, between semimembranosus and medial head of gastrocnemius
  • Becomes prominent and tense on knee extension
  • More common in children; usually resolves spontaneously

5. Baker's Cyst (Popliteal Cyst)

  • A herniation of the posterior synovial membrane through the oblique popliteal ligament
  • Located in the midline of the popliteal fossa, slightly below the joint line
  • Prominent on extension; disappears on flexion
  • Often associated with intra-articular pathology (OA, RA, TB)
  • On examination: transilluminates; Foucher's sign (becomes tense on extension, soft on flexion)
  • Rupture can mimic DVT (pseudothrombophlebitis)

6. Pes Anserinus Bursitis

  • Located medially, deep to the conjoined insertion of sartorius, gracilis, and semitendinosus
  • Common in obese women with OA; pain on the medial side of the knee

7. Iliotibial Band Bursa

  • Between the iliotibial band and the lateral femoral condyle
  • Common in runners ("runner's knee")


Q2C. Hangman's Fracture [5 marks]

Definition

A hangman's fracture is a traumatic spondylolisthesis of the axis (C2) - bilateral fractures through the pars interarticularis (isthmus) of C2, with forward displacement of C2 on C3.

Mechanism

  • Primary mechanism: Hyperextension + axial loading of the cervical spine
  • Classically described in judicial hanging (the noose forces hyperextension)
  • In modern practice: high-energy trauma - road traffic accidents, diving injuries, falls
  • Some patterns involve flexion-distraction

Classification (Levine-Edwards - Most Widely Used)

TypeDisplacementAngulationDisc/LigamentStability
Type I<3 mm<11°IntactStable
Type IaAtypical; distractionAngulationVariableUnstable
Type II>3 mm>11°C2/3 disc disruptedUnstable
Type IIaMinimalSevere angulationDisruptedVery unstable
Type III>3 mm + facet dislocationMarkedFully disruptedVery unstable
  • Starr-Eismont variant: Fracture extends into the posterior body of C2; higher rate of neurological injury; needs halo vest or surgery

Clinical Features

  • Neck pain, tenderness over C2
  • Torticollis
  • Neurological deficit is LESS common than expected because the bilateral pars fracture actually decompresses the spinal canal (the vertebral body shifts forward, widening the canal)
  • However, severe displacement or disc herniation can cause cord injury

Investigations

  • Plain X-ray: lateral view shows forward displacement of C2 body on C3; fracture through the pars
  • CT scan (gold standard): precise fracture characterisation
  • MRI: disc/ligament injury, cord signal changes

Management

Non-operative:
  • Type I and Type II without severe angulation: Rigid cervical collar or halo vest immobilisation for 8-12 weeks
  • Halo vest complications (especially in elderly): pin site infection, loosening, dysphagia
Operative:
  • Type IIa, Type III, and Starr-Eismont variant: Surgical stabilisation
  • Posterior C2-C3 fusion (most common)
  • Anterior C2-C3 discectomy and fusion (for disc disruption)
Prognosis: Generally good; most patients achieve bony union with non-operative treatment


Q2D. Pathoanatomy of CTEV (Congenital Talipes Equinovarus) Foot [5 marks]

Definition

Congenital Talipes Equinovarus (CTEV / Club Foot) is a complex three-dimensional congenital foot deformity that is fixed (not postural). The deformity has four components, remembered by the mnemonic CAVE or CAVE-S:

The Four Components of CTEV Deformity (CAVE)

ComponentDeformityLevel
C - CavusHigh arch of medial footMidfoot
A - AdductusForefoot adduction/medial deviationTarsometatarsal joints
V - VarusHindfoot inversion/varusSubtalar joint
E - EquinusPlantarflexion of hindfootAnkle joint

Detailed Pathoanatomy

1. Bony Changes:
  • Talus: The head and neck of the talus are deviated medially and plantarward (the talar neck is short and internally rotated)
  • Calcaneus: In equinus (plantarflexed) and varus (inverted) position; the posterior part is pulled up by the shortened tendo-Achilles, making the heel feel "empty"
  • Navicular: Displaced medially with respect to the talar head (talonavicular subluxation) - the most consistent pathological finding
  • Cuboid: Displaced medially with respect to the calcaneus
2. Soft-Tissue Changes (Medial and Posterior):
  • Ligaments: Calcaneofibular ligament and plantar calcaneonavicular (spring) ligament are shortened and thickened
  • Tendons and sheaths: Posterior tibial tendon sheath, tendo-Achilles, tibialis posterior, flexor hallucis longus, and flexor digitorum longus are contracted
  • Tendon sheaths contain contractile myofibroblasts (fibroblastic component)
  • The lateral structures (peroneal tendons and their sheaths) are elongated
3. Muscular Changes:
  • Gastrocsoleus and posterior tibial muscles are smaller than normal
  • Reduced myofibrils, increased connective tissue (possibly due to neuromuscular abnormality)
  • Evertors (peronei) are weak
4. Vascular Changes:
  • The dorsalis pedis artery may be diminished in calibre
  • Contributes to difficulty with healing post-surgery
5. Skin:
  • Deep medial crease and single posterior crease are characteristic
  • All children have a smaller calf and foot on the affected side

Key Pathological Distinction

  • In postural CTEV (intrauterine moulding): deformity is correctable and fully reducible; no structural joint/bone change
  • In structural idiopathic CTEV: deformity is fixed; underlying bony and soft-tissue changes as above

Clinical Appearance

The foot shows: hindfoot equinus + varus, midfoot cavus + adductus, giving the appearance of forefoot cavus. The forefoot appears supinated but is actually pronated relative to the hindfoot.

Classification

  • Pirani score (0-6): based on 6 clinical signs; guides Ponseti treatment
  • Dimeglio classification (Grade I-IV): grades reducibility and severity

Sources: Bailey and Love's Short Practice of Surgery 28th Ed; Campbell's Operative Orthopaedics 15th Ed 2026; S. Das Manual on Clinical Surgery 13th Ed
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