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Quick Reference Summary

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SECTION 7: HAND

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Q1. Anatomy of Fascial Spaces of Palm & Types of Hand Infections ⭐⭐⭐ (2017, 2018 - HIGHEST WEIGHTAGE)

FASCIAL SPACES OF THE PALM

1. Thenar space
2. Midpalmar space
3. Hypothenar space
4. Interdigital web spaces (×3 - between index-middle, middle-ring, ring-little fingers)

Thenar Space

• Bounded: anteriorly by flexor tendons of index finger; posteriorly by 1st dorsal interosseous; radially by 1st metacarpal; ulnarly by vertical septum from palmar fascia to 3rd metacarpal
• Contains: index finger lumbrical muscle
• Infection: swelling of thenar eminence + dorsal thumb web; index/middle finger held semiflexed; thumb abducted and extended

Midpalmar Space

• Bounded: anteriorly by flexor tendons to middle/ring/little; posteriorly by metacarpals 3-5 and interossei; radially by same vertical septum separating from thenar space
• Contains: middle and ring finger lumbrical muscles
• Infection: loss of palmar concavity (hallmark); dorsal swelling of hand (NOT to be mistaken for infection site); restricted middle and ring finger motion; systemic sepsis can be severe

Surgical Drainage

• Thenar space: incision along thenar crease on radial side
• Midpalmar space: incision through palm via longitudinal incision along middle metacarpal, or through dorsal web space
• Always drain in operating room under GA by hand surgeon; CT scan helpful to confirm extent

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TYPES OF HAND INFECTIONS

1. Paronychia (Most Common Hand Infection)

• Definition: Infection of the perionychium (nail fold)
• Acute: <6 weeks; abscess formation around nail fold/base
• Chronic: >6 weeks; fungal (Candida), seen in dishwashers/diabetics
• Organism: Staphylococcus aureus (MRSA increasingly common >10% prevalence)
• Treatment: Acute - Freer elevator to elevate 25% of nail + gauze packing; if abscess - incision + drainage; chronic - antifungals

2. Felon (Pulp Space Infection)

• Definition: Closed-space infection of the distal finger pulp
• Mechanism: Penetrating trauma → infection tracks through fibrous septa creating "collar-stud" abscesses
• Features: Tense, throbbing pain; digital pulp hard and tender; pressure on distal phalanx
• Complications: Osteomyelitis of distal phalanx, flexor tenosynovitis
• Treatment: Fishmouth incision or lateral longitudinal incision; NOT a transverse volar incision (divides sensory nerves and vessels)

3. Suppurative Flexor Tenosynovitis (Most Dangerous Hand Infection)

• Definition: Infection within the flexor tendon synovial sheath
• Most common cause: Penetrating trauma; also hematogenous spread
• Organism: S. aureus; Gram-negative in drug users/diabetics/immunocompromised
• Kanavel's 4 Cardinal Signs (1925):
  1. Exquisite tenderness over the path of the flexor sheath
  2. Symmetrical sausage-shaped swelling of the digit
  3. Flexed posturing of the affected finger
  4. Pain on passive extension of the involved finger
• Communication: Little finger sheath → Ulnar bursa; Thumb flexor sheath → Radial bursa; Both communicate at wrist (horseshoe abscess potential)
• Treatment:
  • Early (<24-48 hrs): IV antibiotics, immobilization, elevation
  • Late/failure: Surgical - open incision + irrigation of tendon sheath under GA by hand surgeon
  • Delayed treatment → tendon adhesions, scarring, permanent loss of digital function

4. Palmar Deep Space Infections

• Occur in 5-15% of all hand infections
• Organisms: S. aureus and Streptococcus spp.
• CT scan to confirm + delineate extent
• Surgical drainage by hand surgeon in OR
• Thenar space vs. midpalmar space (see anatomy section above)

5. Web Space (Collar-Button) Abscess

• Subfascial infection of the web space between fingers
• Presents as dumbbell-shaped or "collar-stud" abscess (dorsal + palmar components connected through web)
• Both components must be drained (dorsal and volar incisions)

6. Herpetic Whitlow

• Viral infection (Herpes simplex) of the finger pulp
• Healthcare workers and dentists at risk
• Vesicular eruption; NO incision (draining spreads virus)
• Treatment: Acyclovir; self-limiting

7. Human/Animal Bite Infections

• Human bite (clenched-fist injury over MCP joint): Eikenella corrodens, Streptococcus; highly morbid; joint inoculation common
• Animal bite: Pasteurella multocida, Capnocytophaga
• Treatment: debridement, NO primary closure, broad-spectrum antibiotics (amoxicillin-clavulanate)

8. Mycobacterial Infections

• Nontuberculous mycobacteria (M. marinum from fish tanks); chronic tenosynovitis

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Q2. Surgical Anatomy of Palmar Spaces (10 marks)

• Guyon's canal: ulnar nerve and vessels at wrist between pisiform and hook of hamate
• Carpal tunnel: bounded by flexor retinaculum anteriorly, carpal bones posteriorly; contains 9 flexor tendons + median nerve
• The palmar aponeurosis divides superficial from deep spaces; its vertical septa create the compartments
• Radial bursa (thumb FPL sheath) + Ulnar bursa (little finger flexor sheath) communicate at Parona space at the wrist → explains horseshoe abscess when both bursae communicate

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Q3. Principles of Management of Infection of the Hand (10 marks)

General Principles

1. Elevation of hand (reduces edema, pain)
2. Empiric antibiotics: cover S. aureus (including MRSA if prevalence >10%): TMP-SMX, clindamycin, or doxycycline; hospital-acquired: Vancomycin IV
3. Do NOT incise prematurely: early infections may resolve with antibiotics alone
4. Surgical drainage: once fluctuance or abscess confirmed - non-negotiable
5. Appropriate incisions: avoid neurovascular bundles; avoid transverse volar incisions in digits
6. Splinting: in position of function (wrist 30° extension, MCPs 70° flexion, IPs extended) after surgery
7. Early hand therapy/physiotherapy: prevent adhesions and stiffness
8. Serial wound inspection: open packing, delayed closure

Indications for Surgery

• Established abscess with fluctuance
• Kanavel's signs (tenosynovitis)
• Failure to improve with 24-48 hours of IV antibiotics
• Palmar deep space infection
• Joint sepsis

Position of Safe Immobilization (POSI)

• Wrist: 30° extension
• MCPs: 60-70° flexion (prevents collateral ligament contracture)
• IPs: full extension
• Thumb: palmar abduction

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SECTION 8: LEGS - VASCULAR SURGERY

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Q1. Recent Modalities for Management of Varicose Veins ⭐⭐⭐ (2017 - HIGH WEIGHTAGE)

Pathophysiology

• Varicose veins = abnormally dilated, tortuous superficial veins due to incompetent valves
• Great Saphenous Vein (GSV) incompetence most common; originates at saphenofemoral junction (SFJ)

Classification (CEAP)

Clinical Tests for Varicose Veins

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Treatment Modalities

A. Conservative

• Compression stockings (class II, 23-32 mmHg): first-line for symptomatic relief
• Weight loss, exercise, limb elevation
• Indications: mild symptoms, contraindication to invasive treatment

B. Sclerotherapy

• Mechanism: sclerosant destroys venous endothelium → inflammatory response → fibrosis and obliteration
• Agents:
  • Hypertonic saline (11.7-23.4%)
  • Sodium tetradecyl sulfate (STS, 0.125-3%)
  • Polidocanol (0.5-3%)
• Foam sclerotherapy: air/CO₂ mixed with liquid sclerosant to create microfoam → more effective as larger contact surface area with endothelium; used for larger veins under ultrasound guidance
• Compression applied after for 3-5 days (continuous) then stockings for 2 weeks
• Complications: allergic reaction, hyperpigmentation, thrombophlebitis, DVT, skin necrosis, visual disturbances (foam)
• Indications: telangiectasias, spider veins, small varicosities; residual veins after surgery

C. Endovenous Thermal Ablation (Modern Gold Standard)

• Wavelengths: 810-1470 nm; newer 1470 nm targets water in vein wall
• Mechanism: laser energy → thermal injury → vein wall destruction → fibrosis
• Technique: under LA/tumescent anesthesia + ultrasound guidance; puncture GSV at distal thigh/upper calf; advance fiber to 2 cm below SFJ; tumescent anesthetic (dilute lignocaine+adrenaline) injected pericatheter; laser fired as catheter withdrawn
• Advantages: day-case procedure; faster recovery than open surgery; lower recurrence than SFJ ligation alone
• Complications: DVT (2-3%), ecchymosis, saphenous nerve injury (15-30%), phlebitis, skin burns

• Mechanism: radiofrequency energy delivered via catheter → resistive heating 120°C → collagen contraction → vein wall fibrosis
• Technique: same as EVLA; catheter withdrawn in 6.5 cm segments with each segment treated for 20 seconds
• Advantages: less postprocedural pain and bruising than EVLA; equally effective
• Complications: similar to EVLA - DVT, nerve injury, skin thermal burns

• Cyanoacrylate glue (VenaSeal): medical-grade glue injected into vein; no tumescent required; no nerve injury risk; good for anticoagulated patients
• Mechanochemical ablation (MOCA/ClariVein): rotating wire causes mechanical endothelial damage + simultaneous liquid sclerosant injection; no tumescent; no thermal injury

D. Surgical Treatment

• SFJ flush ligation at groin (flush with common femoral vein) + stripping of GSV from groin to knee using invagination stripper
• GSVs >2 cm diameter (too large for thermal ablation)
• Ambulatory phlebectomy (Muller's technique): avulsion of residual branch varicosities through 2 mm stab incisions using phlebectomy hook
• Complications: hematoma, lymphocele, DVT, wound infection, saphenous nerve injury, recurrence (30% at 5 years)

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Q2. Recent Advances in Investigation & Treatment of Lower Limb Varicose Veins

• Duplex ultrasound: gold standard; maps reflux, identifies incompetent perforators, assesses deep system patency; mandatory before any intervention
• Air/photoplethysmography: assesses venous refill time
• Venography (ascending/descending): now largely replaced by duplex

• RFA (ClosureFast, ClosureRFS)
• EVLA (various wavelengths including 1470nm)
• MOCA (ClariVein)
• Cyanoacrylate (VenaSeal)
• Percutaneous ambulatory phlebectomy under LA
• Ultrasound-guided foam sclerotherapy (UGFS)

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Q4. Anatomical Basis for Various Tests for Varicose Veins of Lower Limb

• Hunterian perforator (lower thigh): connects GSV to femoral vein
• Dodd's perforator (upper calf): connects GSV to popliteal vein
• Boyd's perforator (upper calf): below knee medially
• Cockett's perforators (lower calf, I, II, III): posterior medial - most commonly incompetent; associated with venous ulcers (gaiter area)

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Q5. Complications of Varicose Vein Surgery

• Injury to femoral artery/vein at SFJ
• Lymphatic injury → lymphocele/lymphoedema
• Injury to saphenous nerve (paresthesia of medial leg)
• Injury to sural nerve (SSV stripping)

• Hematoma (most common)
• Wound infection
• DVT (1-3%)

• Recurrence (30% at 5 years - most common late complication)
• Residual telangiectasias
• Saphenous nerve injury - paresthesia along medial leg/foot
• Lymphedema of leg
• Groin scar complications

• EVLA: saphenous nerve injury (15-30%); thermal skin burns
• RFA: same but less nerve injury
• Foam: visual disturbances (transient), DVT, pigmentation

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Q6. Pathology of DVT

Virchow's Triad (1856)

1. Stasis (altered blood flow)
2. Endothelial injury (vessel wall damage)
3. Hypercoagulability (altered blood constituents)

Pathogenesis

• Initiating site: Soleal sinuses of the calf (most common site) - stasis in these valve pockets
• Platelet adhesion → fibrin deposition → propagation of thrombus
• Thrombus propagates in the direction of blood flow (proximally)
• Acute thrombus: red (fibrin + RBCs) = initial, soft, poorly adherent
• Older thrombus: white, organized, adherent to vessel wall

Hypercoagulable States

Classification

• Distal DVT: calf veins only (tibial, peroneal, muscular) - lower PE risk, usually resolves
• Proximal DVT: popliteal, femoral, iliac, IVC - high PE risk
• Phlegmasia Alba Dolens: massive DVT with arterial vasospasm; white, cold, painful leg
• Phlegmasia Cerulea Dolens: massive DVT blocking all venous outflow; blue, painful, swollen leg; venous gangrene risk; emergency

Complications of DVT

1. Pulmonary Embolism (PE) - most serious; dyspnea, chest pain, hypoxia → pulmonary hypertension → RV failure → death
2. Post-thrombotic syndrome (PTS) - chronic venous insufficiency; edema, pain, hyperpigmentation, lipodermatosclerosis, venous ulceration (Years later)
3. Phlegmasia cerulea dolens → venous gangrene
4. Recurrent DVT

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Q7. Preventive Measures for Post-Operative DVT

Risk Stratification (Caprini Score / Rogers Score)

• Very low risk (<0.5%): Caprini 0 - early ambulation only
• Low risk (<1.5%): Caprini 1-2 - mechanical prophylaxis
• Moderate risk (3%): Caprini 3-4 - LMWH/UFH OR mechanical
• High risk (6%): Caprini ≥5 - LMWH/UFH + mechanical combined

Mechanical Methods

Pharmacological Methods

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Q8. Clinical Features of DVT + Pharmacological Bases of Drugs Used for Its Management ⭐⭐ (2016, 2015)

Clinical Features

• Calf/limb pain and tenderness
• Swelling (unilateral edema)
• Heaviness
• Warmth and erythema over the affected vein

• Pitting edema of the limb
• Dilated superficial veins
• Homans sign: calf pain on dorsiflexion of foot - classic but non-specific; positive in only 50% (NOT pathognomonic)
• Low-grade fever
• Calf diameter difference >3 cm (between legs at 10 cm below tibial tuberosity)
• Moses sign: calf pain on AP compression (vs. lateral compression)

• Score ≥2 = DVT likely; <2 = DVT unlikely

• D-dimer: Sensitive (>95%) but not specific; negative D-dimer effectively rules out DVT (NPV 97-99%); not useful post-op (always elevated)
• Duplex ultrasound: Gold standard; non-compressible vein = DVT
• CT venography (CTV): For pelvic/iliac vein/IVC extension
• MR venography: Non-invasive; best for proximal/pelvic veins
• Contrast venography (DSA): Rarely used; gold standard historically; useful for iliac/IVC assessment before thrombolysis
• Impedance plethysmography: Measures venous capacitance; not useful for calf DVT

Pharmacological Management of DVT

1. Unfractionated Heparin (UFH)

• Mechanism: binds antithrombin III → dramatically potentiates AT III activity → inhibits thrombin (IIa) and Factor Xa (1:1 ratio); also inhibits IXa, XIa, XIIa
• Monitoring: aPTT (target 1.5-2.5x normal = 60-80 seconds)
• Reversal: Protamine sulfate (1 mg per 100 IU heparin)
• Complications: Bleeding; HIT (Heparin-Induced Thrombocytopenia) - immune mediated, platelet fall >50% by day 5-10, paradoxically thrombogenic; treat with argatroban/lepirudin
• Advantage: Short half-life; reversible; safe in renal failure

2. Low Molecular Weight Heparin (LMWH)

• Examples: Enoxaparin, dalteparin, tinzaparin
• Mechanism: Predominantly anti-Xa activity (3:1 ratio anti-Xa:anti-IIa); also activates AT III
• Monitoring: Not routinely required; anti-Xa levels in renal failure, pregnancy, obesity
• Reversal: Protamine (partial, ~60%)
• Advantages: Predictable dose response; once/twice daily SC; lower HIT risk; can be outpatient

3. Warfarin (Vitamin K Antagonist - VKA)

• Mechanism: Inhibits Vitamin K epoxide reductase → reduces carboxylation of Vitamin K-dependent clotting factors (II, VII, IX, X) and proteins C and S
• Monitoring: INR (target 2.0-3.0)
• Reversal: Vitamin K (slow); Fresh Frozen Plasma (FFP) (fast); PCC (prothrombin complex concentrate) (fastest)
• Onset: 48-72 hours (protein C falls first → transient hypercoagulable state → need to overlap with heparin for 5 days until INR therapeutic)
• Duration: First DVT + transient risk factor: 3 months; unprovoked DVT: ≥3 months, consider long-term; recurrent/cancer: indefinite LMWH

4. Direct Oral Anticoagulants (DOACs)

• Advantages: No monitoring needed; predictable response; oral; fewer drug interactions than warfarin

5. Thrombolysis (Catheter-Directed Thrombolysis - CDT)

• Indicated for: massive iliofemoral DVT, phlegmasia cerulea dolens, acute limb-threatening DVT
• Agents: Alteplase (tPA), streptokinase, urokinase
• Reduces post-thrombotic syndrome better than anticoagulation alone

6. IVC Filter

• Indicated when anticoagulation contraindicated but PE risk high
• Retrievable preferred; should be removed when anticoagulation safe to restart

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Q9. Recent Advances in PVD (Peripheral Vascular Disease)

Investigations

• Ankle-Brachial Index (ABI): >0.9 normal; 0.5-0.9 claudication; <0.5 rest pain; <0.3 gangrene
• Duplex ultrasound: initial imaging; identifies stenosis/occlusion
• CT angiography (CTA): gold standard preoperative imaging; identifies calcified vessels
• MR angiography (MRA): no radiation; excellent for run-off vessels
• DSA (Digital Subtraction Angiography): gold standard; allows simultaneous intervention; "road-map" for surgical planning

Management Advances

• Aggressive risk factor modification: statins, antihypertensives, smoking cessation, antiplatelet (aspirin/clopidogrel)
• Cilostazol (PDE-3 inhibitor): improves claudication distance
• Supervised exercise programs

• Percutaneous transluminal angioplasty (PTA): balloon dilation of stenoses
• Stenting: bare metal, drug-eluting, covered stents (iliac > femoral)
• Atherectomy devices: directional, orbital, rotational; debulk plaque
• Drug-coated balloons (DCB): paclitaxel-coated; reduce restenosis in femoral-popliteal disease
• Covered endoprostheses (EVAR/FEVAR): for aorto-iliac disease

• Aorto-bifemoral bypass (best long-term patency for iliac disease)
• Femoro-popliteal bypass (above or below knee)
• Femoro-distal bypass (to tibial/peroneal for CLI)
• Conduit: autologous great saphenous vein = GOLD STANDARD (10-year patency 60-70%)

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Q10. Recent Advances in Management of Diabetic Foot

Classification (Wagner)

IDSA/IWGDF Classification of Infection Severity

• Uninfected: No inflammation; Grade 1 (PEDIS)
• Mild: Local infection, <2 cm erythema; Grade 2
• Moderate: Systemic non-threatening, >2 cm; Grade 3
• Severe: Systemic sepsis; Grade 4

Principles of Management (Multidisciplinary - MDT)

1. Off-loading: Total Contact Cast (TCC) = gold standard; removes mechanical trauma; most important for neuropathic ulcers
2. Debridement: sharp surgical debridement of necrotic/infected tissue; gold standard for wound bed preparation
3. Infection control: superficial - oral antibiotics (amoxicillin-clavulanate); deep/systemic - IV broad-spectrum (Tazocin, meropenem); guided by tissue culture (NOT swab)
4. Wound care: moist environment; saline/NPWT (Vacuum-Assisted Closure); bioengineered skin substitutes (Apligraf, Dermagraft)
5. Vascular assessment: ABI; if ischemic - revascularization BEFORE debridement
6. Osteomyelitis: MRI gold standard; 6 weeks IV antibiotics ± surgical resection
7. Glycemic control: Tight control accelerates healing; target HbA1c <7%
8. Amputation: when revascularization impossible and non-healing; most distal possible: toe → ray resection → transmetatarsal → Symes → BKA → AKA

Recent Advances

• Negative pressure wound therapy (NPWT/VAC): accelerates healing; reduces edema; promotes granulation tissue
• Growth factors: PDGF (becaplermin gel) - FDA approved for neuropathic DFU
• Hyperbaric oxygen therapy (HBOT): increases tissue O₂ tension; indicated for Wagner grade 3-4
• Bioengineered skin substitutes: Apligraf, Dermagraft, Integra
• Stem cell therapy and PRP: under investigation

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Q11. Role of Lumbar Sympathectomy in Treatment of PVD

Indications

• Inoperable PVD with rest pain when bypass not feasible
• Painful diabetic neuropathy
• Hyperhidrosis of the lower limb
• Causalgia/CRPS of lower limb
• Raynaud's phenomenon (lower limb)
• Buerger's disease (TAO) - particularly useful

Mechanism

• Interrupts sympathetic innervation to lower limb
• Causes cutaneous vasodilation (blood flow to skin increases)
• Does NOT increase blood flow to ischemic muscle (muscle vessels are under metabolic autoregulation)
• Benefit therefore is for skin perfusion → helps heal digital/heel ulcers and reduces rest pain at night

Technique

• 3 ports; clips/harmonic scalpel used
• L2, L3, L4 ganglia removed
• Shorter hospital stay; lower morbidity

• CT/fluoroscopy-guided injection of phenol or alcohol into L2-L4 ganglia
• For poor operative candidates
• Shorter duration of effect than surgical

Limitations

• Duration of benefit: 6-12 months (develops sympathetic denervation supersensitivity)
• No benefit in calcified vessels (arteriosclerosis obliterans - already maximally dilated)
• Useful mainly in inflammatory/spastic conditions (Buerger's disease, Raynaud's)

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Q12. Ingrown Toenail (2015)

Definition

Pathogenesis

• Incorrect nail cutting (curved instead of straight across)
• Tight footwear
• Abnormal nail curvature (pincer nail)
• Excessive sweating, poor hygiene

Classification (Heifetz)

Management

• Stage I: Conservative: warm soaks, correct nail cutting, wider shoes, cotton wool under nail edge (Natarajan technique)
• Stage II: Partial nail avulsion under LA (ring block); phenolization of nail matrix (80% phenol applied to matrix of avulsed portion to prevent regrowth)
• Stage III: Zadik's procedure (total nail ablation with matrix excision) or Wedge excision (excision of lateral 25% nail + matrix under LA)
• Recurrence: 2-10% after phenolization; near 0% after full Zadik's

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Q13. Trench Foot (Immersion Foot)

• Definition: Non-freezing cold injury from prolonged exposure to cold, wet conditions (0-15°C)
• Mechanism: Sustained vasoconstriction → ischemia → nerve/vascular damage
• Three Phases:
  1. Ischemic phase (during exposure): cold, numb, pale/mottled, no pulses
  2. Hyperemic phase (on rewarming): hot, red, severe burning/throbbing pain, blistering; DVT risk
  3. Late phase: hyperhidrosis, cold sensitivity, chronic pain, hyperesthesia
• Management: Passive rewarming; elevate limb; IV analgesia; anticoagulation during hyperemic phase; no rubbing; no heat application
• Military significance: Common in WWI; affects soldiers in cold wet trenches

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Q14. Madura Foot (Multiple Sinuses in Right Foot)

Definition

Etiology

Clinical Features

• Rural areas; barefoot workers; endemic in Africa, India, Latin America
• Starts as small, painless, firm subcutaneous nodule over dorsum of foot (after thorn prick)
• Progressive invasion of deep tissues; destruction of muscle and bone
• Triad: swelling + sinuses + grains (sulfur granules)
• Eventually entire foot destroyed; systemic spread rare

Diagnosis

• X-ray: honey-comb cavities in bone; sclerosis; periosteal reaction
• MRI: "dot-in-circle" sign = gold standard for diagnosis
• Culture and histopathology of biopsy/grain
• FNAC of nodule

Management

• Co-trimoxazole 12 mg/kg TMP/day for months-years
• Dapsone 100 mg BD
• Amikacin + co-trimoxazole for resistant cases

• Itraconazole 400 mg/day (drug of choice)
• Voriconazole as alternative
• Longer treatment (1-3 years); less response than actinomycetoma
• Surgery: excision of localized lesions; amputation only when extensive bony involvement

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Q15. Elephantiasis / Filariasis in Lower Limb ⭐

Definition

Etiology in Lower Limb - Classification

• Milroy's disease: Congenital hereditary lymphedema from birth; mutation in VEGFR3
• Meige's disease: Lymphedema praecox (puberty - 35 years)
• Lymphedema tarda: >35 years

Filariasis - Pathophysiology

• Wuchereria bancrofti (90% of cases); Brugia malayi/timori
• Vector: Culex mosquito (Wuchereria bancrofti)
• Microfilariae in lymphatics → adult worms → inflammatory response → lymphatic obstruction + dilation → lymphoedema
• Nocturnal periodicity: microfilariae circulate at night (when Culex bites)

Clinical Features of Elephantiasis

1. Lymphedema: Non-pitting initially, becomes non-pitting and brawny as fibrosis progresses
2. Skin changes: Thickening, warty plaques, hyperkeratosis, papillomatosis
3. Gross limb enlargement (can weigh 50+ kg)
4. Scrotal/genital involvement: Hydrocele, scrotal lymphedema in males
5. Chyluria: passage of milky urine (chyle in urine) from lymphatics into urinary tract

Diagnosis

• Peripheral blood smear (midnight sample): microfilariae
• ICT (Immunochromatographic test): antigen detection; can be done anytime
• Ultrasound: "filarial dance sign" - motile adult worms in dilated lymphatics

Management of Elephantiasis

• Diethylcarbamazine (DEC): drug of choice; kills microfilariae + adult worms
• Ivermectin + Albendazole: mass drug administration (MDA) for control
• Lymphedema treatment: Complete Decongestive Therapy (CDT):
  • Manual Lymphatic Drainage (MLD)
  • Multilayer bandaging
  • Compression garments (life-long)
  • Skin care

• Indicated for severe lymphedema unresponsive to conservative treatment
• Charles procedure: Excision of skin and subcutaneous tissue down to deep fascia; skin graft applied; radical but effective; results in abnormal limb appearance
• Homan's procedure: Excision of skin and subcutaneous tissue; buried dermal flap
• Lymphaticovenular anastomosis (LVA): Microsurgical shunt; early disease; relieves lymph stasis
• Vascularized lymph node transfer (VLNT): Transfers lymph nodes from neck/groin to affected limb; creates new lymphatic drainage

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Q16. Unilateral vs Bilateral Lower Limb Edema

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Q17. Lower Limb Ischemia (Acute and Chronic)

Acute Limb Ischemia - 6 P's

1. Pain
2. Pallor
3. Pulselessness
4. Paresthesia (sensory loss = severe ischemia)
5. Paralysis (motor loss = impending gangrene)
6. Perishing cold

• Class I: Viable (no sensory/motor loss) - anticoagulate, plan surgery
• Class IIa: Marginally threatened (sensory loss only) - urgent revascularization
• Class IIb: Immediately threatened (sensory + motor loss) - emergency revascularization
• Class III: Irreversible (profound anesthesia + paralysis) - primary amputation

• IV heparin bolus immediately
• Emergency embolectomy (Fogarty catheter) if embolic
• Bypass surgery if thrombotic/occlusive
• Thrombolysis (CDT) for acute/subacute if non-critical ischemia

Chronic Limb Ischemia

• Fontaine Classification: I (asymptomatic) → II (claudication: IIa >200m, IIb <200m) → III (rest pain) → IV (gangrene)
• Leriche syndrome: Aorto-iliac occlusion → bilateral buttock claudication + erectile dysfunction + absent femoral pulses

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Q18. Ilizarov's Technique in Buerger's Disease ⭐ (2023)

Buerger's Disease (Thromboangiitis Obliterans - TAO)

• Nonatherosclerotic, segmental inflammatory disorder affecting small and medium-sized arteries, veins, and nerves
• Typically young males (<50 years) who smoke/chew tobacco/cannabis
• Affects distal vessels: tibial, radial, ulnar, digital arteries

• Digital ischemia, distal claudication (arch of foot/calf/arm)
• Digital ulcerations

• 40% have Raynaud's phenomenon

• Abnormal Allen test
• Absent peripheral pulses
• Arteriography: corkscrew collaterals (characteristic but not pathognomonic)

1. Complete tobacco abstinence - cornerstone; urinary cotinine testing
2. Antiplatelet: aspirin 81-325 mg/day (modest benefit)
3. Iloprost (prostacyclin analogue): 1 ng/kg/min IV for 6 hrs/day × 28 days - superior to aspirin; improves pain and wound healing
4. Lumbar sympathectomy (see Q11)
5. Bosentan (endothelin receptor antagonist): emerging role
6. Spinal cord stimulation: variable success
7. Ilizarov technique/bone marrow angiogenesis: osteotomy stimulates neovascularization
8. Angioplasty if suitable lesion
9. Amputation: when revascularization impossible + non-healing + unrelenting pain

Ilizarov's Technique in PVD/Buerger's Disease

• Concept: Ilizarov discovered that controlled distraction osteogenesis stimulates bone and soft tissue regeneration (Law of Tension-Stress)
• In PVD/Buerger's disease: Tibial cortex osteotomy (corticotomy) is performed; Ilizarov circular external fixator applied; slow distraction at 1 mm/day
• Mechanism of benefit: Distraction stimulates neovascularization/angiogenesis → new blood vessel formation in the ischemic zone → increased perfusion → ulcer healing + pain relief
• Published results show improvement in ABI, wound healing, and pain scores in selected patients with critical limb ischemia

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Q19. Psoas Abscess - Etiology, Investigation, Management (10 marks)

Definition

Classification & Etiology

• Primary: S. aureus; gram-negative rods
• Secondary: M. tuberculosis (most common secondary cause globally); Enterobacteriaceae; Bacteroides

Pathology

• Infection within psoas muscle sheath → pus tracks along muscle → presents in groin/thigh as a cold abscess (TB) or hot abscess (pyogenic)
• Spinal TB (Pott's disease): paradiscal caries → bony destruction → pus tracks anteriorly within psoas sheath → present in femoral triangle (iliac fossa/groin) or down to lesser trochanter

Clinical Features

• Fever, malaise
• Psoas sign (positive): pain on extending hip with patient lateral position
• Hip held in flexion (relieves pain by relaxing psoas)
• Low back pain / flank pain
• Groin swelling (fluctuant, cystic)
• In spinal TB: gibbus deformity; paraplegia; kyphosis at thoracolumbar junction

Investigations

• CBC: leukocytosis (pyogenic) or lymphocytosis/normal (TB)
• ESR/CRP elevated
• Ultrasound: initial screen; shows fluid collection
• CT scan (abdomen/pelvis): investigation of choice; defines extent; guides drainage; shows spine involvement; "cottage-loaf" sign of large psoas abscess
• MRI spine: for spinal TB assessment
• Mantoux test, IGRA (for TB)
• Pus culture and sensitivity; AFB smear + culture; PCR for TB

Management

• Empiric: IV Tazocin/Meropenem; modify per culture
• TB: RHEZ (Rifampicin, Isoniazid, Ethambutol, Pyrazinamide) for 2 months, then RH for 4 months

• CT/ultrasound-guided percutaneous drainage: first line for both pyogenic and TB psoas abscess; safe and effective; avoids surgery
• Open surgical drainage: when percutaneous fails; complex multiloculated; large spinal TB abscess

• Anterior decompression + fusion (Hodgson's approach) for significant kyphosis/instability/paraplegia
• Posterior instrumented fusion for stability

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Q20. Popliteal Cyst (Baker's Cyst)

Definition

Pathogenesis

• Increased intra-articular pressure → herniation of knee joint capsule posteriorly
• Usually secondary to intra-articular pathology: osteoarthritis (most common adult cause), rheumatoid arthritis, meniscal tears, ACL tears, chondral lesions
• Primary (idiopathic) in children - communicates with knee via one-way valve

Clinical Features

• Posterior knee swelling; may extend down calf
• Mild ache; stiffness on knee extension
• Fouche's sign: disappears on full knee extension (pathognomonic)
• Transillumination: positive (cystic)

Complications

• Rupture: ruptured cyst causes acute calf pain/swelling - mimic DVT ("pseudothrombophlebitis"); Crescent sign on plain X-ray (crescent of dissected fluid); confirmed by USS
• Compression of popliteal vessels/tibial nerve
• Infection of cyst

Investigations

• Ultrasound: investigation of choice; differentiates cyst from DVT, lipoma, popliteal aneurysm
• MRI knee: defines cyst + intra-articular pathology
• Arthrography: injection of contrast into knee appears in cyst

Management

• Treat underlying cause: arthroscopic meniscectomy/repair if meniscal tear; RA disease-modifying therapy
• Aspiration: under USS guidance + corticosteroid injection; high recurrence
• Surgical excision: open; for symptomatic large cysts not responding to conservative treatment; recurrence if intra-articular pathology not addressed

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Q21. Filariasis in Lower Limb

• Wuchereria bancrofti (90%), Brugia malayi, Brugia timori
• Culex mosquito vector
• "Filarial dance sign" on USG
• DEC = drug of choice
• MDA with DEC + ivermectin + albendazole for elimination programs
• Charles procedure for severe elephantiasis

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Priority Summary Table

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SECTION: BURNS

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Pre-Q: Fluid Therapy in Burns (10 marks) ⭐⭐⭐ (2018 - HIGHEST WEIGHTAGE)

Why Fluid Resuscitation is Needed

• Release of vasoactive mediators (histamine, prostaglandins, bradykinin, reactive oxygen species)
• Loss of oncotic pressure as proteins leak from vasculature
• Evaporative losses from denuded skin
• Result: Burn shock = hypovolemic + distributive shock

Monitoring Adequacy of Resuscitation

Fluid Resuscitation Formulas

• Volume = 4 mL × Weight (kg) × %TBSA burned
• Only second- and third-degree burns counted (NOT first-degree)
• Half given in first 8 hours (from time of burn, NOT from time of arrival)
• Remaining half over next 16 hours
• Fluid: Ringer's Lactate (crystalloid of choice)

• Total = 4 × 70 × 40 = 11,200 mL in 24 hrs
• First 8 hrs: 5,600 mL = 700 mL/hr
• Next 16 hrs: 5,600 mL = 350 mL/hr

• 2 mL × Weight (kg) × %TBSA in 24 hrs (RL)
• Half in first 8 hrs, half in next 16 hrs
• Tends to result in less fluid overload than Parkland

• 1 mL × kg × %TBSA (colloid: NS) + 1 mL × kg × %TBSA (crystalloid: NS) + 2000 mL 5% dextrose in 24 hrs
• Max 10,000 mL/24 hrs

Second 24 Hours

• Replace evaporative + insensible losses
• Add colloid (albumin/FFP): 0.5-1 mL × kg × %TBSA
• Reduce crystalloid to maintain UO
• Start enteral nutrition within 6-12 hours of burn

"Fluid Creep" Problem

• Over-resuscitation → abdominal compartment syndrome, pulmonary edema, extremity compartment syndrome, conversion of partial to full-thickness burns
• Modern approach: restrict to minimum effective volume; vitamin C (66 mg/kg/hr × 24 hrs) may reduce capillary leak and total fluid requirement

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Pre-Q: Non-Thermal Burns / Non-Thermal Injury (10 marks) ⭐⭐ (2018)

1. Chemical Burns (3% of burn admissions)

• Sulfuric acid, nitric acid, hydrochloric acid
• Coagulative necrosis - self-limiting (eschar limits penetration)
• HF acid (hydrofluoric acid): special case - penetrates deeply; binds Ca²⁺/Mg²⁺; causes hypocalcemia, cardiac arrhythmias; treatment = calcium gluconate gel topically + IV calcium gluconate; intra-arterial calcium gluconate for digit burns; cardiac monitoring mandatory

• Cement, lime, NaOH, potassium hydroxide
• Liquefactive necrosis - no self-limitation → penetrates deeply; MORE dangerous than acids
• Saponification of fats + protein denaturation

1. Dry chemical: brush off first (do NOT apply water before brushing - thermal reaction)
2. Liquid chemical: copious water irrigation for minimum 30 minutes (most important first step)
3. Do NOT use neutralizing agents (exothermic reaction causes more damage)
4. Specific antidotes for special chemicals (HF → calcium gluconate)
5. Systemic monitoring for absorbed chemicals (formic acid → hemolysis/hemoglobinuria; HF → hypocalcemia)

2. Electrical Burns (3% of burn admissions)

• Low voltage (<1000V): household current; local entry/exit wounds; less systemic effects
• High voltage (>1000V): industrial; massive internal tissue destruction; iceberg phenomenon (small surface but deep coagulation necrosis)
• Lightning injury: instantaneous; flashover effect; usually survives; but serious cardiac/neurological complications

• Current follows path of least resistance (nerves, vessels)
• Deep tissue necrosis out of proportion to surface burns
• Heat generated = I²R × time (Joule heating)

• Cardiac arrhythmias (most common cause of immediate death): ECG mandatory in all electrical burns; normal ECG + low-voltage = may not need admission
• Rhabdomyolysis + myoglobinuria → acute renal failure
• Compartment syndrome in extremities
• Cataract development (long-term; high voltage)
• Neurological sequelae (long-term)

• Vigorous IV fluid resuscitation (increase UO to 1-2 mL/kg/hr to clear myoglobin)
• Urine alkalinization (sodium bicarbonate) if myoglobinuria
• Fasciotomy/escharotomy early, even with moderate clinical suspicion
• ECG + cardiac monitoring
• Ophthalmology + neurology review

3. Radiation Burns

• Ionizing radiation (nuclear accidents, radiation therapy overdose)
• Acute radiation syndrome stages: prodromal → latent → manifest illness → recovery/death
• Local radiation injury: latent period → erythema → desquamation → ulceration
• Management: supportive; colony-stimulating factors (G-CSF) for bone marrow suppression; surgical debridement and flap coverage for radiation ulcers

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Q1. Assess Depth and Wound of Burns & Clinical Significance

Assessment of Burn Depth

1. Zone of Coagulation (center): maximal damage; protein coagulation; frankly necrotic; requires excision and grafting; corresponds to full-thickness burn
2. Zone of Stasis (middle): ischemia from vasoconstriction + impaired perfusion; potentially salvageable; corresponds to deep partial-thickness; can convert to full-thickness with infection, poor perfusion, or inadequate resuscitation
3. Zone of Hyperemia (periphery): inflammatory vasodilation; heals spontaneously; corresponds to superficial burns

• Distinguishing partial from full-thickness determines surgical vs. conservative management
• Deep partial-thickness burns benefit from early excision + grafting (at 3-5 days)
• Zone of stasis can be converted to coagulation zone by infection, poor resuscitation, or edema - emphasizing importance of early aggressive treatment
• Laser Doppler imaging: most accurate non-invasive tool for burn depth (sensitivity 83%, specificity 97%); predicts healing potential at 48-72 hours

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Q: Methods of Assessment of Area of Burns (10 marks) ⭐⭐ (2018)

1. Rule of Nines (Wallace, 1951)

2. Rule of Palm (Palmar Method)

• Patient's own palmar surface (palm + closed fingers) = approximately 1% TBSA
• Useful for: irregular, patchy, or small burns
• Quick and practical in field/emergency

3. Lund and Browder Chart ⭐ (Most Accurate)

• Pre-drawn body diagram; specific body regions assigned age-adjusted % TBSA
• Accounts for changing proportions with age (especially head vs. legs)
• Fills in chart area by area
• Recommended for: children, any burn where accuracy matters
• Most accurate method for calculating %TBSA in both children and adults

4. Computerized/Digital Methods

• 3D imaging software
• Smartphone apps (e.g., Mersey Burns, BurnCase 3D)
• More accurate than bedside methods, especially for large/complex burns

Clinical Significance of TBSA Assessment

• Guides fluid resuscitation (Parkland formula uses %TBSA)
• Determines referral to burn center (>10% partial thickness; >5% full thickness)
• Predicts mortality (Baux score = age + %TBSA; >100 = high mortality)
• Determines nutritional requirements (Curreri formula: 25 kcal/kg + 40 kcal × %TBSA)

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Q2. Recent Advances in Management of Burns

1. Early Excision and Grafting (Major Advance)

• Tangential excision of burn wound at 3-5 days (not delayed weeks as historically done)
• Reduces: wound infection, hospital stay, hypertrophic scarring, systemic sepsis
• Followed by split-thickness skin grafting (STSG) or biological dressings

2. Negative Pressure Wound Therapy (NPWT)

• Applied over meshed skin grafts → improves graft take
• Also used for wound bed preparation before grafting

3. Biological and Synthetic Skin Substitutes

4. Inhalation Injury Management Advances

• High-frequency oscillatory ventilation (HFOV)
• Prone positioning
• Nebulized N-acetylcysteine + heparin alternating to prevent cast formation
• Bronchoscopy: assess + washout carbonaceous deposits
• CO poisoning: 100% O₂ via NRB (reduces CO half-life from 4-5 hrs to 60-90 min); hyperbaric O₂ for severe cases

5. Nutritional Support Advances

• Early enteral feeding within 6-12 hours
• Curreri formula: 25 kcal/kg/day + 40 kcal × %TBSA burned
• High protein: 1.5-2 g protein/kg/day
• Anabolic agents: oxandrolone (testosterone analogue) reduces catabolism in major burns
• Insulin: tight glycemic control (glucose 140-180 mg/dL)

6. Pharmacological Advances

• Vitamin C (ascorbic acid 66 mg/kg/hr × 24 hrs): reduces free radical-mediated capillary leak; reduces total fluid requirement
• Propranolol: blocks hypermetabolic response; reduces muscle catabolism
• Recombinant human growth hormone: preserves lean body mass

7. Scar Management

• Pressure garments (23 hours/day for 12-18 months): reduce hypertrophic scarring
• Silicone gel sheets: applied over healed burns
• Intralesional triamcinolone injection
• Laser therapy (fractional CO₂, pulsed-dye laser)
• ReCell device: spray-on autologous skin cells from a 1 cm² biopsy to cover large areas

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Q3. Various Methods for Assessment of Area of Burns (10 marks)

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Q4. Clinical Scenario - 24-year-old Female, Suicidal Burns, 40% TBSA, Legal Steps

Complete Management

1. Airway: Check for inhalation injury (singed nasal hair, carbonaceous sputum, hoarse voice, facial burns); if present → early intubation before airway edema occludes
2. Breathing: 100% O₂ via NRB mask (rule out CO poisoning)
3. Circulation: 2 large-bore IV lines (antecubital or through burn if necessary); blood for CBC, electrolytes, coagulation, group and cross-match, carboxyhemoglobin, beta-hCG (pregnancy)

• Parkland formula: 4 × 60 kg (assume) × 40 = 9,600 mL RL in 24 hrs
• Half (4,800 mL) in first 8 hrs from time of burn
• Half in next 16 hrs
• Urinary catheter: target UO 0.5-1 mL/kg/hr

• Remove all clothing/jewelry
• Clean debris; wash gently with chlorhexidine
• Classify depth; estimate %TBSA accurately (Lund-Browder preferred)
• Photograph burns for documentation
• Cover with sterile dressings; do NOT apply ice or cold water to large burns (worsens hypothermia)

• IV morphine/fentanyl titrated
• Benzodiazepines for anxiety (cautious use)

• Escharotomy if circumferential full-thickness burns of extremities/chest (impairs circulation/breathing)
• Early referral to burn center (>40% TBSA, 24 yrs old - burn center criteria met)
• Early excision + grafting when stable

• Check for other injuries (suicidal context: drug ingestion? trauma?)
• Beta-hCG (positive? - 2 months amenorrhea noted in Q4 - likely pregnant; impacts management decisions)

• Psychiatric assessment mandatory post-stabilization
• Suicide risk assessment; safeguarding measures

Legal Steps (Medico-Legal Aspects) - CRITICAL FOR EXAM

• Thorough, contemporaneous, dated, legible documentation of all findings, conversations, and decisions
• Photograph burns with ruler/scale marker for medicolegal record
• Document patient's mental status on arrival

• If patient competent (conscious, oriented): explain treatment, obtain written informed consent
• If patient unconscious/incompetent: treat in best interests under doctrine of implied consent; document reason for proceeding without formal consent

• Patient cannot refuse life-saving treatment while acutely suicidal (lacks capacity)
• Detain under relevant mental health legislation if needed
• Notify psychiatry for assessment and formal detention if necessary

• Notify police if suspicious circumstances (e.g., if injury could be due to assault despite suicidal history)
• Police will interview once stable

• Confirm with beta-hCG/USS
• If pregnant: obstetric consultation; modify drug choices (avoid teratogenic agents); fetal monitoring
• Burns in pregnancy carry higher mortality for both mother and fetus (premature labor risk if >25% TBSA)

• Burns consistent with suicidal history? (distribution, depth, pattern)
• Witness statement from paramedics/family
• Any evidence suggesting homicidal burning? - report to police

• Suicide risk: duty of care to protect patient from herself; confidentiality secondary to safety

• If there are children in household: notify social services/child protection
• Financial, social, and psychological support initiated

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Q5. Clinical Features & Management of Adult 40% Burns (2014) / Q6. Pathophysiology of Burns & Management of 50% Burns in 60-year-old Female (2021) ⭐⭐⭐

Pathophysiology of Burns

Local Response

• Three zones (Jackson): coagulation → stasis → hyperemia
• Zone of stasis: salvageable with optimal treatment; destroyed by inadequate resuscitation, infection, edema

Systemic Response (Major Burns >20% TBSA)

• Immediate: massive cytokine release (histamine, TNF-α, IL-1, IL-6) → capillary leak → Burns shock (hypovolemic + distributive)
• Cardiac depression: direct myocardial depressant factor released
• Hemoconcentration initially → later hemodilution after resuscitation

• Inhalation injury (above glottis): heat injury → mucosal edema → upper airway obstruction (critical 12-24 hrs post-burn)
• Below glottis: steam or chemical injury; bronchospasm, cast formation, chemical tracheobronchitis
• CO poisoning: CO binds hemoglobin (affinity 240× > O₂) → shifts oxyhemoglobin dissociation curve left → tissue hypoxia
• CN poisoning: inhibits cytochrome oxidase → histotoxic hypoxia; treat with hydroxocobalamin

• Hypovolemia → acute tubular necrosis
• Myoglobin/hemoglobin precipitate in tubules → renal failure (especially electrical burns)

• Splanchnic vasoconstriction → mucosal ischemia
• Bacterial translocation → sepsis
• Curling's ulcer: stress ulcer; prophylaxis with PPI/H2-blocker mandatory
• Ileus

• Burn wound itself = most common source of sepsis
• Immunosuppression: reduction in cell-mediated and humoral immunity
• Loss of skin barrier → entry for organisms
• Most common organisms: S. aureus (early), Gram-negative bacilli (Pseudomonas aeruginosa - particularly dangerous, late), fungi (Candida, Aspergillus in prolonged cases)

• Resting metabolic rate can increase by 2-3× in major burns - most hypermetabolic state of any injury
• Protein catabolism: massive nitrogen loss
• Hyperglycemia (insulin resistance)
• Temperature set-point raised to 38-38.5°C; patient shivering at normal temperatures
• Lipolysis exceeds lipogenesis → fatty infiltration of liver

• Early: hemoconcentration; late: anemia (hemolysis + reduced RBC production)
• Thrombocytopenia
• DIC (in major burns)

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Complete Management of 40-50% Burns in Adults

• Time of burn, mechanism, enclosed space (→ inhalation injury), loss of consciousness (→ CO)
• Past medical history, tetanus status, medications, allergies

• Facial burns + any of: stridor, hoarse voice, singed nasal/eyebrows, carbonaceous sputum, enclosed space history → early intubation (within 4-6 hrs before edema)
• Do NOT wait for respiratory distress to develop

• 100% O₂ via NRB (CO poisoning); minimum 6 hours
• Check SpO₂ (may be falsely normal with CO poisoning - use co-oximetry)
• Circumferential chest burns → escharotomy (bilateral anterior chest)

• Parkland formula (RL): 4 mL × kg × %TBSA; half in 8 hrs, half in 16 hrs
• Urinary catheter + strict UO monitoring
• Monitor for fluid overload (pulmonary edema, abdominal compartment syndrome)

• Accurate depth and area assessment
• IV analgesia + sedation
• NGT: early enteral feeding within 6-12 hrs; Curling ulcer prophylaxis (PPI)
• Tetanus prophylaxis
• Wound photography, documentation
• Decision on escharotomy (circumferential burns)
• Referral to burn center

• Tangential excision at 3-5 days post-burn (ideally)
• Blood loss can be massive: each 1% TBSA = approx. 250 mL blood loss
• Split-thickness skin grafting (STSG):
  • Donor sites: thighs, back (most common)
  • Meshed STSG (1:2, 1:4, 1:6 ratio): expands donor skin to cover larger areas; ideal for large burns
  • Sheet STSG for face/hands (cosmetic areas)
• Biologic dressings (Integra, allografts) as temporary cover when donor sites insufficient

• Partial-thickness >10% TBSA
• Burns involving face, hands, feet, genitalia, perineum, major joints
• Full-thickness burns of any size
• Electrical, chemical, inhalation burns
• Age <10 or >50 years with major burns
• Patients with comorbidities

• Physiotherapy (prevent contractures)
• Occupational therapy
• Pressure garments, splinting
• Psychological support (PTSD, depression, body image issues)
• Nutritional rehabilitation: oxandrolone, high calorie/protein diet

• Baux score: age + %TBSA; >100 = high mortality
• 60-year-old female with 50% burns: Baux = 110 → high mortality (~50-70%)
• Inhalation injury doubles mortality

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SECTION: OBESITY

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Q1-4. Bariatric Surgery - Indications, Procedures, Complications, Principles ⭐⭐⭐ (2013, 2017, 2014 - HIGHEST WEIGHTAGE)

Definitions

• Overweight: BMI 25-29.9 kg/m²
• Obese: BMI ≥30 kg/m²
• Morbid obesity: BMI ≥40 kg/m² (or ≥35 + comorbidities)
• Super-morbid obesity: BMI ≥50 kg/m²
• Super-super obese: BMI ≥60 kg/m²

Indications for Bariatric Surgery (NIH Consensus 1991, still applicable)

1. BMI ≥40 kg/m² regardless of comorbidities, OR
2. BMI 35-39.9 kg/m² + at least one significant obesity-related comorbidity:
   • Type 2 diabetes mellitus
   • Hypertension
   • Obstructive sleep apnea (OSA)
   • Obesity-hypoventilation syndrome
   • Severe osteoarthritis
   • Non-alcoholic steatohepatitis (NASH)
   • Dyslipidemia

• Failure of non-surgical weight loss attempts (>6 months)
• Psychologically stable; understand risks and long-term commitment
• No untreated psychiatric illness, active substance abuse
• Able to participate in long-term follow-up

• BMI ≥30 + inadequately controlled T2DM (metabolic surgery)

Contraindications

• Uncontrolled psychiatric illness (active psychosis, bulimia nervosa)
• Active substance/alcohol abuse
• Non-compliant patient
• Pregnancy
• Irreversible organ failure (unless bridging to transplant)
• Inability to tolerate general anesthesia

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Classification of Bariatric Surgery Procedures

1. Restrictive: reduces gastric capacity → reduces food intake
2. Malabsorptive: bypasses absorptive small bowel
3. Combined (restrictive + malabsorptive): most effective for weight loss and metabolic benefits

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A. Laparoscopic Roux-en-Y Gastric Bypass (LRYGB) - Gold Standard

1. Create small gastric pouch (~30 mL) from proximal stomach using linear stapler along lesser curve (bougie 32F guide)
2. Divide proximal jejunum at 30-75 cm from ligament of Treitz
3. Roux limb (alimentary limb): brought up to gastric pouch as antecolic-antegastric orientation; gastrojejunostomy created (~12 mm diameter)
4. Biliopancreatic limb (proximal jejunum): anastomosed to alimentary limb 100-150 cm distal to gastrojejunostomy → jejuno-jejunostomy (Y-junction)

• Food → gastric pouch → Roux limb directly (bypasses majority of stomach + proximal bowel where carbohydrates, proteins absorbed)
• Bile/pancreatic juice: travel down biliopancreatic limb and mix with food only at common channel
• GLP-1 ↑: glucoincretin effect → T2DM remission (70% complete remission)

• T2DM: 70-80% complete remission (sometimes before significant weight loss)
• HTN: 50-75% resolution
• OSA: 80-85% resolution
• Dyslipidemia: 70% improvement

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B. Laparoscopic Sleeve Gastrectomy (LSG) - Currently Most Performed Globally ⭐

1. Divide short gastric vessels along greater curve (LigaSure/Harmonic)
2. 40F bougie placed along lesser curve as guide
3. Linear cutting stapler applied parallel to bougie from 6 cm proximal to pylorus to angle of His → resects lateral 80% of stomach
4. Creates tubular "sleeve" 32-40F diameter
5. Fundus (ghrelin-producing) is removed → appetite suppression

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C. Laparoscopic Adjustable Gastric Band (LAGB)

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D. Biliopancreatic Diversion (BPD) with Duodenal Switch (DS)

1. Sleeve gastrectomy (restrictive component)
2. Division of duodenum 2 cm distal to pylorus
3. Alimentary limb (ileum) anastomosed to duodenum (duodenoileostomy) at 250 cm from ileocecal valve
4. Biliopancreatic limb anastomosed at 100 cm from ileocecal valve → only 100 cm common channel

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Comparison Table

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Complications of Bariatric Surgery

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Physiological Changes in Obesity (Q5)

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SECTION: INJURY / TRAUMA

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Q1. Golden Hour & Emergency Medical Services Reducing Morbidity and Mortality

The "Golden Hour" Concept (R. Adams Cowley, 1970s)

• The critical 60 minutes after major trauma during which definitive surgical/medical intervention can save lives and prevent death from reversible injuries
• Concept based on observation that trauma patients treated within 1 hour had significantly better outcomes
• Modern interpretation: a philosophy urging urgency rather than a strict 60-minute cutoff

Why the Golden Hour Matters

1. Immediate deaths (seconds-minutes): unsurvivable brain/aortic injuries; cannot be prevented
2. Early deaths (minutes-hours): hemorrhage (most common), airway obstruction, tension pneumothorax, cardiac tamponade; PREVENTABLE with rapid intervention = target of Golden Hour
3. Late deaths (days-weeks): sepsis, multi-organ failure; prevention requires early effective care in first hour

How EMS Reduces Morbidity/Mortality

• Rapid extrication + airway management
• Hemorrhage control (tourniquet, wound packing)
• C-spine immobilization
• IV access + fluid resuscitation en route
• Rapid transport ("scoop and run" vs. "stay and play" - generally scoop and run for penetrating trauma; more stabilization for blunt)

• Trauma team activation
• Primary survey (ABCDE) and simultaneous resuscitation
• Identification of immediately life-threatening injuries
• Operative hemorrhage control
• Damage control resuscitation (blood products from the start)

• Tension pneumothorax (needle thoracostomy)
• Cardiac tamponade (pericardiocentesis/thoracotomy)
• Airway obstruction (intubation, surgical airway)
• External hemorrhage (direct pressure, tourniquets)
• Internal hemorrhage (emergency surgery)

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Q2. Damage Control Surgery (DCS) for Trauma ⭐⭐

Concept

1. Hypothermia (<35°C → coagulopathy; <32°C → cardiac arrhythmias)
2. Acidosis (pH <7.2 → impairs coagulation cascade, cardiac contractility)
3. Coagulopathy (dilutional, consumptive, hypothermia-induced)

Stages of Damage Control Surgery

1. Stop hemorrhage: packing (liver, pelvis), ligation of bleeding vessels, temporary intravascular shunts (for major vessels)
2. Control contamination: stapling bowel ends (without anastomosis); drain hollow viscus; pack contaminated areas
3. Temporary closure: abdomen NOT closed definitively

• Techniques: Bogota bag, OPSITE sandwich (Vac-Pac), Wittmann patch
• Once done → transfer to ICU

• Warm patient (forced-air warming, warm IV fluids)
• Correct coagulopathy: FFP:pRBC:platelets = 1:1:1 (massive transfusion protocol)
• Correct acidosis (hemorrhage control + resuscitation)
• Mechanical ventilation, vasopressors if needed
• Repeat point-of-care coagulation testing (TEG/ROTEM-guided)
• Abdominal surveillance (re-explore if deterioration)

• When: temperature >36°C, pH >7.35, coagulopathy corrected, lactate normalized
• Definitive: anastomoses, vascular reconstruction, hernia repair, abdominal closure

• Primary fascial closure if possible
• If not: sequential closure with mesh
• Prolonged open abdomen → planned ventral hernia repair later

Damage Control Resuscitation (DCR)

• Permissive hypotension (MAP 50-65 mmHg for penetrating trauma until hemorrhage controlled) - avoids "popping the clot"
• 1:1:1 ratio: pRBC:FFP:platelets (hemostatic resuscitation)
• TXA (Tranexamic acid): within 3 hours of injury (CRASH-2 trial); 1 g IV bolus + 1 g infusion; reduces mortality from hemorrhage by 15%
• Minimize crystalloid (causes hemodilution, worsens coagulopathy)
• Calcium replacement (transfused blood contains citrate → hypocalcemia)

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Q3. Advanced Trauma Life Support (ATLS) ⭐⭐

Philosophy

Primary Survey - ABCDE

• Airway obstruction
• Tension pneumothorax
• Open pneumothorax
• Massive hemothorax
• Flail chest
• Cardiac tamponade

Secondary Survey

• Head-to-toe examination AFTER primary survey and initial resuscitation
• AMPLE history: Allergies, Medications, Past history, Last meal, Events/Environment
• Adjuncts: ECG, chest X-ray, pelvis X-ray, FAST scan

FAST (Focused Assessment with Sonography in Trauma)

• Looks for free fluid in: pericardial sac, Morrison's pouch (hepatorenal), splenorenal space, pelvis (pouch of Douglas/retrovesical)
• Extended FAST (eFAST): adds bilateral lung apices (pneumothorax detection)
• Takes 2-3 minutes; bedside; no radiation; immediately available
• Positive FAST + hemodynamic instability = emergency laparotomy

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Q4. Triage ⭐

Definition

Goals

• Do the most good for the greatest number
• Identify who needs immediate life-saving intervention
• Prevent death from treatable conditions
• Appropriate allocation of resources

Simple Triage and Rapid Treatment (START) System

Mass Casualty Incident (MCI) vs. Multiple Casualty Incident

• MCI: resources overwhelmed by number of casualties
• Multiple: many casualties but resources adequate

Hospital Triage Systems

• Manchester Triage System (MTS): flowchart-based; 5 priorities (Immediate/Urgent/Standard/Non-urgent/Walking)
• Emergency Severity Index (ESI): 5-level; based on resource utilization
• Triage Revised Trauma Score (RTS): GCS + SBP + RR; predicts mortality

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Q5. Management of Blunt Abdominal Trauma + Renal Injury

Initial Assessment

• FAST scan (initial)
• CT abdomen/pelvis with IV contrast (gold standard if hemodynamically stable)
• Diagnostic peritoneal lavage (DPL): if FAST inconclusive; positive if >100,000 RBC/mm³ or >500 WBC/mm³ or bacteria/bowel contents

Hemodynamically Unstable Patient + FAST Positive

Hemodynamically Stable Patient

Organ-Specific Management

• AAST Grade I-III: non-operative management (NOM) in 80-90%; angioembolization for arterial blush on CT
• Grade IV-V: laparotomy; hepatic packing; Pringle maneuver; angioembolization adjunct

• Most common intra-abdominal organ injured in blunt trauma
• AAST Grade I-II: NOM (>90% success)
• Grade III+: angioembolization or splenectomy
• NOM failure signs: ongoing hemorrhage, hemodynamic instability

• Delayed presentation (12-24 hrs); peritonitis
• Requires operative repair

• Zone 1 (central): always explore
• Zone 2 (flank): explore if penetrating; observe if blunt + stable
• Zone 3 (pelvic): explore only if penetrating; pelvic packing/angioembolization for blunt

Renal Injury (Mentioned in Q5)

• Grade I-III: NOM; bed rest; hydration; monitor hematuria
• Grade IV: NOM attempted; angioembolization; ureteric stenting for extravasation
• Grade V: operative (nephrectomy/vascular repair)

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Q6. Protocol for Polytrauma Patient

Definition

Protocol (Sequential)

• ABCDE assessment; airway protection; hemorrhage control
• Trauma team pre-alert; activate massive transfusion protocol (MTP)
• Scoop and run for penetrating; limited stabilization en route

• Primary survey (ABCDE) with simultaneous interventions
• 2 large-bore IVs + blood draw (group, XM, CBC, coag, BMP, lactate, ABG)
• Initiate MTP (1:1:1 ratios)
• FAST scan, chest X-ray, pelvis X-ray (trauma triad X-rays)
• Urinary catheter + NGT
• Monitoring: SpO₂, ETCO₂, ECG, continuous BP

• TXA within 3 hrs of injury
• Permissive hypotension for penetrating injury
• Minimize crystalloids; blood product-based resuscitation

• Continue resuscitation; correct coagulopathy/hypothermia/acidosis
• TEG/ROTEM-guided product administration
• Early enteral nutrition within 24-48 hrs
• DVT prophylaxis once hemorrhage controlled
• Tight glycemic control
• Lung-protective ventilation (TV 6 mL/kg IBW; PEEP 5-8; FiO₂ to keep SpO₂ >92%)

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Q7. Management of Warfare Injuries

Classification

• Blast injuries (IED, explosive): primary (overpressure wave), secondary (fragments), tertiary (thrown), quaternary (burn/crush)
• Penetrating ballistic injuries
• Blast lung (primary blast injury): bilateral pulmonary contusions; hemoptysis; does NOT need PPV unless essential (worsens)
• Traumatic amputation: tourniquet → DCS → staged reconstruction

Damage Control in Military Context

• Combat Application Tourniquet (CAT): lifesaving for extremity hemorrhage; apply 2-3 inches above wound; note time
• Wound packing: with hemostatic gauze (Combat Gauze - kaolin-impregnated)
• TXA: CRASH-2 and MATTERS trial evidence for prehospital use within 3 hours
• Permissive hypotension in austere/prolonged field care until definitive surgery
• Delayed primary closure: war wounds NOT closed primarily (contamination)
• Forward Surgical Team (FST): damage control surgery within 1-2 hrs
• Role 1/2/3/4 evacuation chain

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Q8. Scoring Systems for Polytrauma (2018) ⭐⭐

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Q9. ACS - Abdominal Compartment Syndrome ⭐

Definition

Causes

• Massive fluid resuscitation (burns, trauma, sepsis) - most common
• Abdominal hemorrhage/hematoma
• Bowel edema/ileus
• Abdominal packing (post-DCS)
• Ascites

Pathophysiology

• Renal: compression of renal veins + parenchyma → oliguria/anuria → AKI (most sensitive indicator)
• Respiratory: diaphragmatic elevation → ↓ lung compliance → ↑ peak airway pressures → hypoxia, hypercapnia
• Cardiovascular: IVC compression → ↓ venous return → ↓ CO → shock
• GI: mesenteric ischemia → bacterial translocation
• Intracranial: ↑ abdominal/thoracic pressure → ↑ ICP

Measurement of IAP

• 25 mL saline instilled into empty bladder via Foley catheter
• Pressure transducer zeroed at mid-axillary line at iliac crest
• Measure at end-expiration
• Reliable, easy, reproducible bedside measurement

Management

• Decompress GI tract (NGT, rectal tube)
• Improve abdominal wall compliance: adequate analgesia, sedation, neuromuscular blockade
• Reduce fluid intake; diuresis; hemofiltration if needed
• Body positioning (reverse Trendelenburg)

• Decompressive laparotomy (midline incision): if IAP >25 mmHg + new organ dysfunction; or IAP 20-25 mmHg + not responding to medical
• Temporary abdominal closure (Bogota bag, NPWT Vac-Pac)
• When swelling resolves (5-10 days): staged abdominal closure
• Delayed: planned ventral hernia repair

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Q10. Metabolic Response to Injury ⭐ (2017 - HIGH WEIGHTAGE)

Two Phases (Cuthbertson, 1932)

• Shock/hypoperfusion phase
• ↓ Metabolic rate; ↓ O₂ consumption
• Sympathetic activation; vasoconstriction
• Oliguria; hypothermia
• Purpose: conserve energy; redirect blood to vital organs

• Hypermetabolic phase
• ↑ Metabolic rate (up to 2-3× normal in major burns)
• ↑ O₂ consumption; ↑ CO₂ production
• Hyperglycemia; fever
• Net protein catabolism
• Two sub-phases:
  • Catabolic sub-phase (days to weeks): negative nitrogen balance; muscle wasting
  • Anabolic sub-phase: gradual recovery; restoration of body composition

Mediators of Metabolic Response

Metabolic Consequences

• Hepatic glycogenolysis (early; depleted within 24 hrs)
• Gluconeogenesis ↑↑ (amino acids, lactate, glycerol as substrates)
• Peripheral insulin resistance (cortisol + catecholamines antagonize insulin)
• Result: Hyperglycemia ("stress diabetes"); even in non-diabetics
• Persistent hyperglycemia → impaired immune function, increased infection risk

• Negative nitrogen balance (protein catabolism > synthesis)
• Skeletal muscle most affected (vast protein reservoir)
• Proteolysis releases amino acids → liver for gluconeogenesis (glucogenic amino acids: alanine, glutamine)
• Urinary nitrogen losses: 15-30 g/day in major trauma (normal = 8-10 g/day)
• Consequences: muscle wasting, impaired wound healing, immune dysfunction

• Lipolysis ↑↑ (catecholamines + cortisol activate hormone-sensitive lipase)
• Free fatty acids + glycerol released from adipose
• FFAs = major energy source for cardiac, skeletal muscle in flow phase
• Ketone bodies produced in liver from FFAs
• "Autocannibalism" - body literally consuming itself

• Resting Energy Expenditure (REE): ↑ proportional to severity
• Elective surgery: ↑ 5-10%
• Major trauma: ↑ 20-30%
• Major burns: ↑ 100-200% (most hypermetabolic state)

• Liver produces acute phase proteins: CRP (↑), fibrinogen (↑), complement (↑), SAA (↑)
• Negative acute phase proteins: albumin (↓), transferrin (↓), pre-albumin (↓)
• Fever: IL-1, IL-6, TNF-α reset hypothalamic thermostat via PGE₂

Clinical Implications

1. Nutritional support: early enteral nutrition (within 24-48 hrs); high protein 1.5-2 g/kg/day; 25-30 kcal/kg/day
2. Glycemic control: tight control 140-180 mg/dL reduces morbidity
3. Anabolic agents: oxandrolone (burns), insulin infusions
4. Immunonutrition: glutamine, arginine, omega-3 fatty acids
5. Minimally invasive surgery: reduces magnitude of stress response vs. open surgery
6. Epidural analgesia: blunts neuroendocrine axis → reduces catabolic response to surgery

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Priority Summary Table