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TEERTHANKER MAHAVEER MEDICAL COLLEGE

General Surgery - Final MBBS (3rd Prof Part II) - Complete Answers

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Q1. Wound Healing Phases, Classification of Surgical Wounds, and Factors Affecting Wound Healing (3+3+4 = 10 marks)

Part A: Phases of Wound Healing (3 marks)

Flowchart: Phases of Wound Healing

TISSUE INJURY
     │
     ▼
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
PHASE 1: HEMOSTASIS (Immediate - 0 to few hours)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
• Vasoconstriction (immediate)
• Platelet adhesion to exposed collagen (via vWF, GPIIb-IIIa)
• Platelet activation → release of alpha granules
  (PDGF, TGF-β, IGF-1, fibronectin)
• Dense bodies → serotonin → vasodilation + permeability
• Coagulation cascade → fibrin clot formation
• Provisional wound matrix (fibrin scaffold)
     │
     ▼
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
PHASE 2: INFLAMMATION (Day 1–5)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
Early (Day 1-2): NEUTROPHILS dominate
  • PMNs recruited by chemotaxis (IL-8, C5a, LTB4)
  • Phagocytosis of bacteria and debris
  • Release of proteases, ROS
  • Non-essential for wound healing (sterile wounds heal without PMNs)

Late (Day 2-5): MACROPHAGES dominate (MASTER CELLS of wound healing)
  • Derived from blood monocytes
  • Essential for wound healing
  • Release PDGF, TGF-α, TGF-β, IL-1, TNF-α
  • Recruit fibroblasts
  • M1 phenotype: host defense (TNF-α, NO, IL-6)
  • M2 phenotype: wound healing, angiogenesis
     │
     ▼
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
PHASE 3: PROLIFERATION (Day 4–21)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
3 key events:
  1. FIBROPLASIA
     • Fibroblasts migrated from wound edges
     • Collagen synthesis (Type III initially → later Type I)
     • Stimulated by PDGF, TGF-β, EGF, FGF

  2. ANGIOGENESIS
     • New capillary formation (VEGF-driven)
     • Granulation tissue = fibroblasts + new capillaries + macrophages

  3. EPITHELIALIZATION
     • Keratinocytes migrate over moist wound bed
     • Contact inhibition stops migration when wound closed
     • Growth factors: EGF, TGF-α, KGF (FGF-7)
     │
     ▼
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
PHASE 4: MATURATION/REMODELING (Day 21 → 2 years)
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
• Type III collagen replaced by Type I collagen
• Cross-linking by lysyl oxidase
• Collagenase (MMP-1) degrades excess collagen
• Max tensile strength = 80% of original (never 100%)
• Wound contraction by myofibroblasts (α-SMA positive)
• Vascularity decreases → scar becomes avascular, pale, flat

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Part B: Classification of Surgical Wounds (3 marks)

CDC Classification of Surgical Wounds

Classification by Depth

• Superficial incisional SSI: Skin + subcutaneous tissue only
• Deep incisional SSI: Fascia and muscle layers
• Organ/space SSI: Any organ/space opened during operation

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Part C: Factors Affecting Wound Healing (4 marks)

FACTORS AFFECTING WOUND HEALING
         │
    ┌────┴────┐
    ▼         ▼
 LOCAL      SYSTEMIC
FACTORS     FACTORS

LOCAL:
┌─────────────────────────────────────┐
│ Promoting Healing    Impairs Healing │
│ • Moist environment  • Infection    │
│ • Good blood supply  • Ischemia     │
│ • Debridement done   • Foreign body │
│ • Wound closure      • Desiccation  │
│                      • Haematoma    │
│                      • Radiation    │
└─────────────────────────────────────┘

SYSTEMIC FACTORS:
┌──────────────────────────────────────────────────┐
│ Factor              Effect                        │
│────────────────────────────────────────────────── │
│ Diabetes mellitus   ↓ PMN function, microangiopathy│
│ Malnutrition        ↓ Collagen synthesis (↓ Vit C) │
│ Corticosteroids     ↓ Inflammation, ↓ fibroplasia  │
│ Chemotherapy        ↓ Cell proliferation           │
│ Jaundice            Impairs collagen synthesis      │
│ Uraemia             Impairs PMN function            │
│ Anaemia/Hypoxia     ↓ Collagen hydroxylation        │
│ Old age             ↓ All healing phases            │
│ Obesity             Poor vascularity of fat         │
│ Zinc deficiency     ↓ Epithelialization             │
│ Vit C deficiency    ↓ Collagen cross-linking        │
│ Vit A deficiency    ↓ Epithelialization             │
└──────────────────────────────────────────────────┘

• Vitamin C: Hydroxylation of proline/lysine for collagen synthesis
• Zinc: DNA synthesis, cell proliferation
• Vitamin A: Epithelialization, counteracts steroid effects
• Protein: Substrate for collagen; negative nitrogen balance impairs healing

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Q2. Donor Criteria, Massive Blood Transfusion, and Complications (2.5+2.5+5 = 10 marks)

Part A: Donor Criteria for Blood Transfusion (2.5 marks)

Inclusion Criteria (NACO/WHO Guidelines)

Exclusion Criteria

• HIV positive / high-risk sexual behaviour
• Hepatitis B or C carrier
• Syphilis / gonorrhoea
• Malaria (within past 3 years or living in endemic area)
• Recent vaccination (defer 2 weeks for live vaccines)
• Pregnancy / recent delivery (defer 6 months)
• Major surgery in last 6 months
• Diabetes on insulin
• Cancer (absolute)
• Epilepsy
• Drug addiction
• Unexplained weight loss >5 kg in 3 months

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Part B: Massive Blood Transfusion (MBT) (2.5 marks)

Indications

• Major trauma with haemorrhagic shock
• Ruptured aortic aneurysm
• Obstetric catastrophe (PPH, placenta praevia)
• Major hepatic/vascular surgery

Massive Transfusion Protocol (MTP)

• 1:1:1 ratio: pRBC : Fresh Frozen Plasma (FFP) : Platelets
  • Mimics whole blood
  • Prevents dilutional coagulopathy
• Tranexamic acid: Give ASAP (within 3 hours of trauma) - CRASH-2 trial
• Avoid crystalloids/colloids as primary resuscitation fluids
• Calcium supplementation: Each unit of blood contains citrate (chelates Ca²⁺)
• Warm all blood products (prevent hypothermia)
• Monitor with TEG (Thromboelastography) or ROTEM

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Part C: Complications of Blood Transfusion (5 marks)

Flowchart: Complications

COMPLICATIONS OF BLOOD TRANSFUSION
              │
    ┌─────────┴──────────┐
    ▼                    ▼
IMMUNOLOGICAL         NON-IMMUNOLOGICAL

IMMUNOLOGICAL:
├── HAEMOLYTIC REACTIONS
│   ├── Acute (<24 hrs): ABO incompatibility
│   │   • Fever, chills, back/loin pain
│   │   • Haemoglobinuria (red/brown urine)
│   │   • Shock, DIC, acute renal failure
│   │   • Action: STOP transfusion immediately
│   │     → Saline flush, IV fluids, O2, furosemide
│   └── Delayed (1-14 days): Anamnestic reaction
│       • Mild haemolysis, anaemia, jaundice
│
├── FEBRILE NON-HAEMOLYTIC TRANSFUSION REACTION
│   • Fever >1°C rise, rigors
│   • Due to cytokines from donor WBCs
│   • Tx: Paracetamol, slow/stop transfusion
│
├── ALLERGIC / ANAPHYLACTIC
│   • Urticaria, bronchospasm, hypotension
│   • Tx: Chlorpheniramine, adrenaline, steroids
│
└── TRANSFUSION-RELATED ACUTE LUNG INJURY (TRALI)
    • Commonest cause of transfusion mortality
    • Non-cardiogenic pulmonary oedema
    • Within 6 hrs of transfusion (usually FFP)
    • Tx: O2, ventilatory support

NON-IMMUNOLOGICAL:
├── INFECTIONS
│   ├── Bacterial (faulty storage)
│   ├── Viral: HIV, Hep B, Hep C, CMV, EBV
│   ├── Parasitic: Malaria, Chagas disease
│   └── Prion: vCJD
│
├── MASSIVE TRANSFUSION COMPLICATIONS
│   ├── Coagulopathy (dilutional)
│   ├── Hypocalcaemia (citrate toxicity)
│   ├── Hyperkalaemia (from old stored blood)
│   ├── Hypokalaemia (later phase)
│   ├── Hypothermia
│   ├── Metabolic alkalosis (citrate → bicarbonate)
│   └── TACO (Transfusion Associated Circulatory Overload)
│       • Pulmonary oedema in elderly/cardiac patients
│       • Tx: Slow rate, furosemide
│
├── IRON OVERLOAD (repeated transfusions, e.g. thalassaemia)
│   • ~250 mg elemental iron/unit pRBCs
│   • Tx: Desferrioxamine
│
├── AIR EMBOLISM
└── THROMBOPHLEBITIS

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Q3. SSI: Definition, Organisms, Classification, Prevention and Management (1+1+3+3+2 = 10 marks)

Part A: What is SSI? (1 mark)

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Part B: Organisms Causing SSI (1 mark)

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Part C: Classification of SSI (3 marks)

CLASSIFICATION OF SSI (CDC Definition)
              │
    ┌─────────┼──────────┐
    ▼         ▼           ▼
SUPERFICIAL  DEEP      ORGAN/SPACE
INCISIONAL  INCISIONAL    SSI

SUPERFICIAL INCISIONAL SSI:
• Within 30 days of surgery
• Involves SKIN + SUBCUTANEOUS tissue only
• At least ONE of:
  - Purulent discharge from wound
  - Positive culture from wound fluid
  - Pain, tenderness, swelling, redness + wound opened by surgeon
  - Diagnosis by surgeon/physician

DEEP INCISIONAL SSI:
• Within 30 days (or 1 year if implant)
• Involves FASCIA + MUSCLE layers
• At least ONE of:
  - Purulent discharge from deep incision
  - Spontaneous dehiscence or opened by surgeon
    (when patient has fever >38°C, pain/tenderness)
  - Abscess on direct examination, re-operation, imaging

ORGAN/SPACE SSI:
• Any part of body OPENED or MANIPULATED during surgery
• E.g.: intraabdominal abscess after bowel surgery
• Pus from drain placed into organ/space
• Positive culture from organ/space specimen

• Minor SSI: Discharges pus/infected serous fluid; no systemic signs; no delay in discharge
• Major SSI: Significant pus; systemic signs (tachycardia, pyrexia, raised WBC); delayed discharge; needs secondary procedure

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Part D: Prevention of SSI (3 marks)

PREVENTION OF SSI
        │
   ┌────┴────┐
   ▼         ▼
PREOPERATIVE  INTRAOPERATIVE  POSTOPERATIVE

PREOPERATIVE:
• Treat remote infections before elective surgery
• HbA1c control in diabetics (<7%)
• Smoking cessation (at least 30 days before)
• Nutritional optimization
• Reduce preoperative hospital stay
• Skin decolonization: chlorhexidine body wash
• Hair removal: clippers NOT razors (razors ↑ SSI)
• Shower with antiseptic soap on night before surgery

ANTIBIOTIC PROPHYLAXIS:
• Give within 60 minutes before incision
• Cefazolin is first line (or based on flora)
• Single dose usually sufficient (repeat if surgery >4 hrs)
• NO routine postoperative antibiotics

INTRAOPERATIVE:
• Surgical hand scrub (5 min brushing)
• Sterile gloves + gown
• Maintain surgical site haemostasis
• Gentle tissue handling; avoid devitalized tissue
• Minimize dead space
• Appropriate suture selection
• Irrigation with warm saline
• Maintain normothermia (warming blanket)
• Maintain normoglycaemia (target BSL <10 mmol/L)
• High-flow O2 delivery (FiO2 0.8) intraoperatively
• Minimize operative time

POSTOPERATIVE:
• Aseptic wound dressings
• Remove drains early
• Protect wound for 48 hours (epithelialized by then)
• Monitor glucose, temperature
• Educate patient on wound care

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Part E: Management of SSI (2 marks)

MANAGEMENT OF SSI
       │
       ├── MINOR SSI
       │   ├── Open wound (remove sutures/staples)
       │   ├── Drain pus
       │   ├── Wound swab for C&S
       │   └── Dressings (moist/saline-soaked)
       │       Usually NO antibiotics needed
       │
       └── MAJOR SSI
           ├── Open + debride wound
           ├── Wound swab → C&S
           ├── IV antibiotics based on organism/sensitivity
           │   (empiric: Cefuroxime + Metronidazole for abdominal)
           ├── Source control (drain abscesses)
           ├── Nutritional support
           ├── Consider vacuum-assisted closure (VAC) for large wounds
           └── Secondary closure once wound is clean
               (granulation tissue present, no infection)

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Q4. Shock: Types, Pathophysiology and Management of Septic Shock (1+2+3+4 = 10 marks)

Part A: What is Shock? (1 mark)

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Part B: Types of Shock (2 marks)

CLASSIFICATION OF SHOCK
          │
    ┌─────┼──────┬────────┐
    ▼     ▼      ▼        ▼
HYPO-  CARDIO- DISTRIBU- OBSTRUCTIVE
VOLAEMIC GENIC  TIVE

1. HYPOVOLAEMIC SHOCK
   Cause: ↓ Circadian volume
   ├── Haemorrhagic (trauma, GI bleed, AAA rupture)
   └── Non-haemorrhagic (burns, vomiting, diarrhoea, third spacing)
   Haemodynamics: ↓CO, ↑SVR, ↑HR, ↓CVP

2. CARDIOGENIC SHOCK
   Cause: Pump failure (>40% myocardium infarcted)
   ├── MI (most common)
   ├── Arrhythmia
   └── Cardiomyopathy
   Haemodynamics: ↓CO, ↑SVR, ↑CVP, ↑PCWP

3. DISTRIBUTIVE SHOCK (vasogenic)
   Cause: Abnormal vasodilation → maldistribution of flow
   ├── Septic shock (most common)
   ├── Anaphylactic shock
   ├── Neurogenic shock (spinal cord injury)
   └── Addisonian crisis
   Haemodynamics: ↑CO (early), ↓SVR, ↓CVP

4. OBSTRUCTIVE SHOCK
   Cause: Mechanical obstruction to flow
   ├── Tension pneumothorax
   ├── Cardiac tamponade
   └── Massive pulmonary embolism
   Haemodynamics: ↓CO, ↑SVR, ↑CVP

Classification of Haemorrhagic Shock (ATLS)

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Part C: Pathophysiology of Septic Shock (3 marks)

PATHOPHYSIOLOGY OF SEPTIC SHOCK

SOURCE OF INFECTION
(Gram-negative: LPS/Endotoxin | Gram-positive: Teichoic acid, Peptidoglycan)
         │
         ▼
PATTERN RECOGNITION RECEPTORS
(Toll-like receptors on macrophages, monocytes)
         │
         ▼
CYTOKINE STORM
TNF-α, IL-1β, IL-6, IL-8, IL-10, PAF
         │
    ┌────┴──────────────┐
    ▼                   ▼
VASODILATION         ENDOTHELIAL DAMAGE
(iNOS → ↑↑ NO)          │
    │               Capillary leak → Third spacing
    ▼                   │
↓SVR (↓ afterload)       ▼
↑CO early              HYPOVOLAEMIA
    │                   │
    ▼                   ▼
WARM/HYPERDYNAMIC ←→ COLD/HYPODYNAMIC
PHASE (early)           PHASE (late)
• Warm skin           • Cold, clammy skin
• Bounding pulse      • Thready pulse
• ↑CO                 • ↓CO
• ↑HR                 • Oliguria, MODS

    ┌────────┬──────────┬─────────┐
    ▼        ▼          ▼         ▼
CARDIAC    RENAL     HEPATIC   PULMONARY
DEPRESSION FAILURE   FAILURE   FAILURE
(TNF-α,              (elevated  (ARDS)
 IL-1β,              LFTs)
 iNOS)
         │
         ▼
MULTIPLE ORGAN DYSFUNCTION SYNDROME (MODS)
         │
         ▼
         DEATH
         (40-60% mortality with MODS)

THREE CORE MECHANISMS in Septic Shock:
1. HYPOVOLAEMIA - relative + absolute (capillary leak, sweating, poor intake)
2. MYOCARDIAL DEPRESSION - TNF-α, IL-1β, NO impair contractility
3. SYSTEMIC INFLAMMATION - microvascular + mitochondrial dysfunction

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Part D: Management of Septic Shock (4 marks)

Surviving Sepsis Campaign / Bundle (Hour-1 Bundle)

MANAGEMENT OF SEPTIC SHOCK
         │
    ┌────┴─────┐
    ▼          ▼
IMMEDIATE   DEFINITIVE
(1st hour)   (Ongoing)

IMMEDIATE - THE "SEPSIS 6" (complete within 1 hour):
1. MEASURE LACTATE (target <2 mmol/L)
2. BLOOD CULTURES (×2 sets) BEFORE antibiotics
3. IV BROAD-SPECTRUM ANTIBIOTICS (within 1 hour of recognition)
   • Empiric: Piperacillin-tazobactam ± Vancomycin
   • Or: Meropenem/Imipenem for high-risk/ICU
4. IV FLUID RESUSCITATION: 30 mL/kg crystalloid (Ringer's lactate preferred)
   • Target MAP ≥65 mmHg
5. VASOPRESSORS if MAP <65 mmHg despite fluid:
   • NOREPINEPHRINE = first-line vasopressor
     (0.1–0.3 mcg/kg/min, titrate)
   • Add VASOPRESSIN if refractory (0.03 units/min)
   • Add EPINEPHRINE as third line
6. SUPPLEMENTAL O2 / INTUBATION if SpO2 <94%

MONITORING:
• Urine output (target >0.5 mL/kg/hr)
• CVP, MAP monitoring
• Serial lactate every 2 hours
• ScvO2 (target >70%)

SUPPORTIVE CARE:
• SOURCE CONTROL (drain abscess, remove infected device)
• STEROIDS: Hydrocortisone 200–300 mg/day IV
  (only if refractory to fluids + vasopressors)
• TIGHT GLYCAEMIC CONTROL (target 7.8–10 mmol/L)
• Lung-protective ventilation if ARDS (TV 6 mL/kg)
• DVT + stress ulcer prophylaxis
• Early enteral nutrition
• Renal replacement therapy if acute kidney injury

ANTIBIOTICS:
• Reassess and de-escalate after 48–72 hrs based on cultures
• Duration: typically 7–10 days (procalcitonin-guided)

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Q5. Burns Case (Medico-legal + Management) (2+2+6 = 10 marks)

Part A: Should you inform the police? And why? (2 marks)

1. Medicolegal Case (MLC): Burns from fire in young married women fall under the category of a Medico-Legal Case (MLC). Section 174 CrPC (now BNSS) mandates reporting of all suspicious injuries.
2. Dowry Death / Domestic Violence: Under Section 498A IPC (now BNS) and Section 304B IPC (Dowry Death), burns in newly married women within 7 years of marriage are presumed to be dowry-related until proven otherwise.
3. Dying Declaration: As the patient is conscious, a dying declaration should be recorded in her own words in the presence of a magistrate (if available) or doctor, as it is admissible as evidence even if she recovers.
4. Doctor cannot be neutral in suspected domestic violence/dowry harassment cases. The patient's consent or refusal does NOT absolve the doctor of the reporting duty.
5. Section 302/307 IPC: If criminal act suspected, reporting is compulsory under CrPC.

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Part B: Will you delay treatment if police cannot come? (2 marks)

1. Doctor's primary duty is to the patient (Hippocratic Oath, NMC guidelines).
2. Delay in treatment of burns is life-threatening - every minute matters in airway management and fluid resuscitation.
3. Indian law does not permit withholding treatment in an emergency for medicolegal formalities.
4. MLC paperwork can be completed simultaneously with/after initiating treatment.
5. Inform the police telephonically/via hospital record, and the treatment must start immediately without waiting for police arrival.

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Part C: Management of 25% Burns (6 marks)

BURNS MANAGEMENT FLOWCHART

INITIAL ASSESSMENT: ABC + STOP THE BURNING PROCESS
         │
    ┌────┴────┐
    ▼         ▼
PRIMARY     SECONDARY
SURVEY      SURVEY

PRIMARY SURVEY (ABCDE):
A - AIRWAY
  • Assess for inhalation injury signs:
    - Singed nasal hairs, eyebrows
    - Hoarseness, stridor
    - Carbonaceous sputum
    - Burns in enclosed space
  • If inhalation injury suspected → EARLY INTUBATION
    (airways swell rapidly → late intubation is dangerous)
  • High-flow O2 via NRB mask (100% O2 counteracts CO poisoning)

B - BREATHING
  • Assess chest wall expansion
  • Circumferential chest burns → escharotomy

C - CIRCULATION
  • 2 large-bore IV lines (in unburned skin if possible)
  • IV fluid resuscitation (PARKLAND FORMULA):
    ┌─────────────────────────────────────────────────────┐
    │ PARKLAND FORMULA:                                   │
    │ Total 24-hr fluid = 4 mL × Weight (kg) × %BSA burn │
    │ (Only TBSA >20% calculated, 2nd and 3rd degree only)│
    │                                                     │
    │ This patient: 4 × 55 kg × 25% = 5,500 mL           │
    │                                                     │
    │ Distribution:                                       │
    │ • FIRST 8 hours: Give 1/2 = 2,750 mL               │
    │   (from TIME OF BURN, not hospital arrival)         │
    │ • NEXT 16 hours: Give 1/2 = 2,750 mL               │
    │                                                     │
    │ Fluid: Ringer's Lactate (NOT normal saline)         │
    └─────────────────────────────────────────────────────┘
  • Foley catheter → target UO: 0.5-1 mL/kg/hr (adults)
  • Blood pressure monitoring

D - DISABILITY (Neurological status)
  • GCS (patient is conscious here)
  • Analgesia: IV morphine (titrated doses)

E - EXPOSURE / ENVIRONMENT
  • Remove all clothing and jewellery
  • Prevent hypothermia (warm blankets, warm IV fluids)

BURNS ASSESSMENT:
┌──────────────────────────────────────────────┐
│ % BSA CALCULATION - "RULE OF NINES" (Wallace) │
│                                               │
│ Head + Neck      = 9%                         │
│ Each arm         = 9% (×2 = 18%)              │
│ Front of trunk   = 18%                        │
│ Back of trunk    = 18%                        │
│ Each leg         = 18% (×2 = 36%)             │
│ Perineum         = 1%                         │
│ TOTAL            = 100%                       │
│                                               │
│ Palm of patient's hand = 1% BSA               │
│ (useful for scattered burns)                  │
└──────────────────────────────────────────────┘

DEPTH OF BURNS:
┌────────────────┬────────────┬──────────────────────────┐
│ Depth          │ Old Name   │ Features                 │
├────────────────┼────────────┼──────────────────────────┤
│ Superficial    │ 1st degree │ Erythema, no blister     │
│ Partial thick. │ 2nd degree │ Blisters, painful, moist │
│ (superficial)  │            │ Heals in 14 days         │
│ Partial thick. │ 2nd degree │ Pale/red mottled, less   │
│ (deep)         │            │ painful, >21 days        │
│ Full thickness │ 3rd degree │ Leathery, insensate,     │
│                │            │ no healing without graft │
│ 4th degree     │ 4th degree │ Bone/muscle involved     │
└────────────────┴────────────┴──────────────────────────┘

WOUND CARE:
• Clean burns: Chlorhexidine solution
• Apply Silver sulfadiazine (SSD) cream (Flamazine)
• OR Mafenide acetate (penetrates eschar)
• Non-adherent dressings
• Tetanus prophylaxis (Tetanus toxoid ± TIG)

NUTRITION:
• Burns are hypermetabolic (↑↑ energy needs)
• Calorie = 25 kcal/kg + 40 kcal/% burn
• Protein = 1-3 g/kg/day
• Start enteral nutrition within 6 hrs
• Curling's ulcer prophylaxis: Ranitidine/PPI

SURGICAL MANAGEMENT:
• Escharotomy: For circumferential full-thickness burns
  (chest, limbs) → releases compartment pressure
• Early excision and grafting (within 3-5 days)
  - Split-thickness skin graft (STSG)
  - Donor sites: thigh, back
• For 25% TBSA: needs ICU admission + multidisciplinary care

SPECIAL CONSIDERATIONS (Kerosene burns):
• Kerosene burns are chemical + thermal
• Remove contaminated clothing
• Wash affected areas copiously with water
• Kerosene can cause aspiration pneumonitis if ingested

CRITERIA FOR BURNS UNIT TRANSFER:
• >10% TBSA partial thickness (adults)
• Any full-thickness burns
• Burns of face, hands, feet, genitalia, perineum
• Inhalation injury
• Chemical/electrical burns
• Circumferential burns of extremities

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Q6. Short Notes (4 × 5 = 20 marks)

(a) Refeeding Syndrome

Pathophysiology Flowchart

PROLONGED STARVATION
         │
         ▼
Body switches to fat/protein catabolism
Intracellular electrolytes (P, K, Mg) depleted
(but serum levels remain normal due to shifts)
         │
REFEEDING BEGINS (↑ Carbohydrates)
         │
         ▼
↑ Insulin secretion
         │
    ┌────┴───────────────┐
    ▼                    ▼
PHOSPHATE            POTASSIUM & MAGNESIUM
shifts intracellular  shift intracellular
         │
         ▼
HYPOPHOSPHATAEMIA (KEY ABNORMALITY)
(also: Hypokalaemia, Hypomagnesaemia)
         │
    ┌────┴──────────────────────┐
    ▼                           ▼
↓ ATP production           ↓ Cardiac contractility
↓ 2,3-DPG in RBCs          (arrhythmias)
(impaired O2 delivery)
         │
         ▼
CARDIAC FAILURE, RESPIRATORY FAILURE,
HAEMOLYTIC ANAEMIA, SEIZURES, RHABDOMYOLYSIS

At-risk Groups

• Anorexia nervosa
• Alcoholism
• Prolonged NPO
• Cancer cachexia
• Post-operative malnourished patients

Prevention and Management

---

(b) TPN (Total Parenteral Nutrition)

Composition of TPN

Indications

INDICATIONS FOR TPN
├── GI TRACT NON-FUNCTIONAL
│   ├── Short bowel syndrome (<100 cm remaining)
│   ├── High-output fistula (>500 mL/day)
│   ├── Prolonged ileus
│   ├── Severe Crohn's disease / IBD
│   └── Necrotising enterocolitis
├── GI TRACT INACCESSIBLE
│   ├── Oesophageal obstruction
│   └── Post-oesophagectomy
└── GI TRACT MUST REST
    ├── Acute pancreatitis (severe)
    └── Post radiation enteritis

Complications of TPN

COMPLICATIONS OF TPN
    │
    ├── CATHETER-RELATED (Central line)
    │   ├── Pneumothorax, haemothorax (at insertion)
    │   ├── Air embolism
    │   ├── Catheter-related bloodstream infection (CRBSI)
    │   │   (most common serious complication)
    │   └── Subclavian/superior vena cava thrombosis
    │
    ├── METABOLIC
    │   ├── Hyperglycaemia (most common)
    │   ├── Hypoglycaemia (abrupt stopping)
    │   ├── Refeeding syndrome
    │   ├── Electrolyte imbalances
    │   ├── Hyperlipidaemia
    │   └── Essential fatty acid deficiency
    │
    └── ORGAN-RELATED
        ├── TPN-associated liver disease
        │   (steatosis → fibrosis → cirrhosis)
        ├── Cholestasis (no enteral stimulation of bile)
        ├── Acalculous cholecystitis
        └── Metabolic bone disease

---

(c) Abdominal Compartment Syndrome (ACS)

Pathophysiology

CAUSE (Bowel oedema, haemoperitoneum, massive fluid resuscitation,
       burns, packing, ileus)
          │
          ▼
↑ INTRA-ABDOMINAL PRESSURE (IAP)
          │
    ┌─────┼──────────┬────────┐
    ▼     ▼          ▼        ▼
RESPIRATORY  RENAL    CARDIAC  HEPATIC/GUT
                            SPLANCHNIC
RESPIRATORY:               RENAL:
• Diaphragm pushed up      • Renal vein compression
• ↑ Airway pressures       • ↓ Renal perfusion
• ↓ FRC, atelectasis       • Oliguria → anuria
• Hypoxia + hypercarbia    • Acute tubular necrosis

CARDIAC:                   GUT:
• IVC compression          • Bowel ischaemia
• ↓ Venous return          • Bacterial translocation
• ↓ Cardiac output         • Worsens sepsis

IAP Grading (WSACS)

Measurement

• Measured via urinary bladder (intravesical pressure)
• Instil 25 mL saline, measure at end expiration, patient supine
• Abdominal Perfusion Pressure (APP) = MAP - IAP (target >60 mmHg)

Management

MEDICAL MANAGEMENT:
• NG decompression
• Enemas + prokinetics (metoclopramide)
• Diuretics + colloids to remove third-space fluid
• Neuromuscular blockade (paralysis reduces abdominal tone)
• Paracentesis (if ascites/free fluid)

SURGICAL MANAGEMENT:
• DECOMPRESSIVE LAPAROTOMY = definitive treatment
• Midline incision, leave abdomen OPEN
• Temporary abdominal closure:
  - Bogota bag (IV bag sutured to fascia)
  - Vacuum-assisted closure (VAC) / ABThera
• Re-exploration every 48 hrs; close abdomen when swelling resolved

---

(d) Buerger's Disease (Thromboangiitis Obliterans)

Key Facts

Pathology

• Segmental acute + chronic inflammation in smaller arteries (both upper and lower limbs)
• Initial arterial inflammation → extends to adjacent veins and nerves (all three together = hallmark)
• Fibrous encasement of the neurovascular bundle
• Phlebitis migrans: painful, tender nodules over peripheral artery with reduced/absent pulse

Diagnostic Criteria (Olin's Criteria)

1. Smoking history
2. Onset before age 50
3. Infrapopliteal arterial occlusion
4. Either upper limb involvement OR phlebitis migrans
5. Absence of atherosclerotic risk factors (other than smoking)

Clinical Features

BUERGER'S DISEASE - CLINICAL FEATURES

LOWER LIMBS (more common):
• Foot/instep claudication (infrapopliteal occlusion)
• Absent foot pulses (normal femoral + popliteal pulses)
• Intense rubor with dependency
• Ischaemic ulcers on toes/fingers

UPPER LIMBS:
• Hand claudication (bilateral, symmetrical)
• Fingertip ulcers
• Digital artery involvement > radial/ulnar

RAYNAUD'S PHENOMENON:
• ~50% patients
• Triphasic colour response (white → blue → red)

PHLEBITIS MIGRANS:
• Early in disease
• Superficial thrombophlebitis
• Tender, red, nodular streaks

Management

MANAGEMENT OF BUERGER'S DISEASE

MOST IMPORTANT: COMPLETE TOBACCO ABSTINENCE
(Only intervention that changes disease course)
         │
    ┌────┴────┐
    ▼         ▼
STOPS      CONTINUES SMOKING
DISEASE    → Relentless progression
ACTIVITY   → Rest pain → Tissue loss → AMPUTATION

MEDICAL:
• Aspirin (antiplatelet)
• Prostanoids: IV Iloprost/Prostaglandin E1
  (most effective pharmacological treatment)
• Calcium channel blockers (for Raynaud's)
• Epidural analgesia for intractable pain

SURGICAL:
• Sympathectomy (lumbar/cervical)
  → Relieves vasospasm, promotes healing of ulcers
• Bypass surgery: limited (distal vessels affected)
• Omental transposition (for neovascularization)
• Amputation: as last resort (good healing capacity means limb salvage often possible)

PROGNOSIS: If smoke-free → benign course
            If continues → 43% amputation rate

---

(e) Phylloides Tumour

Clinical Features

Classification (Histological)

PHYLLOIDES TUMOUR CLASSIFICATION

Based on MITOTIC RATE per 10 High-Power Fields (HPF):

BENIGN             BORDERLINE          MALIGNANT
Mitotic rate       Mitotic rate        Mitotic rate
< 4/10 HPF         4–9/10 HPF          ≥ 10/10 HPF
     │                  │                   │
     ▼                  ▼                   ▼
Good prognosis     Monitor closely    Can metastasise
Local recurrence   10-15% recur       Via BLOODSTREAM
possible           May progress       (NOT lymphatics)
Wide local         Wide local         MASTECTOMY
excision           excision           ± Radiotherapy

Histopathology

• Leaf-like intracanalicular projections into cleft-like spaces (Greek: "phyllodes" = leaf-like)
• Cellular stroma with varying atypia
• Both epithelial AND stromal components
• NOT a pure sarcoma (contains epithelium)

Management

TREATMENT OF PHYLLOIDES TUMOUR

1. BENIGN/BORDERLINE:
   Wide Local Excision (WLE) with 2-cm clear margins
   (including overlying skin + underlying pectoralis fascia)
   - High local recurrence if margins inadequate

2. MALIGNANT / LARGE / RECURRENT:
   Simple Mastectomy (no axillary clearance needed - lymph node spread rare)
   ± Postoperative radiotherapy (for malignant/recurrent)
   ± Systemic chemotherapy (for malignant phyllodes)

AXILLARY SURGERY: NOT routine (lymph node metastases rare)
FOLLOW-UP: Regular (10-year follow-up; late recurrence possible)

---

---

Q7. Thyroid Carcinoma: Classification, Papillary Thyroid Carcinoma (2+1+2+5 = 10 marks)

Part A: Classification of Thyroid Carcinoma (2 marks)

CLASSIFICATION OF THYROID CARCINOMA
              │
    ┌─────────┼──────────┬──────────┐
    ▼         ▼          ▼          ▼
WELL-      MEDULLARY  UNDIFFEREN-  LYMPHOMA
DIFFERENTIATED         TIATED       (rare)
    │         │         (Anaplastic)
    ├── PTC   │              │
    │  (80%)  │         Worst prognosis
    │         │         6% of thyroid Ca
    └── FTC   │
       (10%)  │
              │
       C-cell origin
       (parafollicular)
       Calcitonin ↑
       RET proto-oncogene
       MEN 2A & 2B

ORIGIN SUMMARY:
┌────────────────┬─────────────────────────────────┬────────────┐
│ Type           │ Cell of Origin                  │ % of cases │
├────────────────┼─────────────────────────────────┼────────────┤
│ Papillary (PTC)│ Follicular cell                 │ 80%        │
│ Follicular (FTC│ Follicular cell                 │ 10%        │
│ Hurthle cell   │ Follicular cell (oncocytic)     │ 3-5%       │
│ Medullary (MTC)│ Parafollicular C-cell           │ 5-8%       │
│ Anaplastic     │ Follicular cell (dedifferentiated│ 1-2%      │
│ Lymphoma       │ Lymphocytes                     │ <1%        │
└────────────────┴─────────────────────────────────┴────────────┘

SPECIAL ASSOCIATIONS:
• PTC: BRAF V600E mutation (most common), RET/PTC rearrangement
• FTC: RAS mutations, PAX8-PPARγ rearrangement
• MTC: RET proto-oncogene mutation (hereditary: MEN 2A, 2B)
• Anaplastic: TP53 mutation, often from dedifferentiated PTC/FTC
• Lymphoma: Associated with Hashimoto's thyroiditis

---

Part B: Clinical Features of Papillary Thyroid Carcinoma (1 mark)

Clinical Features

• Solitary thyroid nodule: Most common presentation - painless, firm, mobile lump in thyroid
• Cervical lymphadenopathy: Very common (30–80%) - especially young patients; nodes may present before the primary
• Slow-growing, often asymptomatic for years
• Rarely: hoarseness (RLN involvement), dysphagia, dyspnoea
• Rare distant metastases (lung, bone)
• Associated with: Prior radiation exposure (Chernobyl), childhood radiation to neck

---

Part C: Histopathology of PTC (2 marks)

Hallmark Nuclear Features of PTC (PATHOGNOMONIC)

HISTOPATHOLOGY OF PAPILLARY THYROID CARCINOMA

ARCHITECTURE:
• Papillary fronds with fibrovascular cores
  (true papillae = fibrovascular stalk covered by neoplastic epithelium)
• May show follicular areas

NUCLEAR FEATURES (DIAGNOSTIC - any 2 of these is diagnostic):
┌─────────────────────────────────────────────────────────────┐
│ 1. "ORPHAN ANNIE EYE" NUCLEI (Ground-glass/clear nuclei)   │
│    → Empty-looking nuclei with marginated chromatin         │
│    → Most characteristic feature                           │
│                                                             │
│ 2. NUCLEAR GROOVES                                          │
│    → Longitudinal grooves (nuclear bars)                   │
│                                                             │
│ 3. NUCLEAR PSEUDO-INCLUSIONS                               │
│    → Cytoplasmic invaginations into nucleus                 │
│    → Round, eosinophilic intranuclear inclusions           │
│                                                             │
│ 4. Nuclear crowding and overlapping                        │
│ 5. Large irregular nuclei                                  │
└─────────────────────────────────────────────────────────────┘

PSAMMOMA BODIES:
• Laminated calcified concentric rings
• Pathognomonic of PTC (present in ~50%)
• Represent calcified foci of infarcted papillary tips

IMMUNOHISTOCHEMISTRY:
• TTF-1 positive (thyroid transcription factor)
• Thyroglobulin positive
• CK19 positive (cytokeratin)
• HBME-1 positive
• BRAF V600E staining

VARIANTS OF PTC:
• Classic PTC (most common)
• Follicular variant (lymph node mets less common)
• Tall cell variant (aggressive)
• Diffuse sclerosing variant (young patients, bilateral)
• Columnar cell variant
• Micropapillary (<10 mm, usually indolent)

---

Part D: Management of Papillary Thyroid Carcinoma (5 marks)

Risk Stratification (ATA Guidelines)

Management Flowchart

DIAGNOSIS OF PTC
(FNAC/Core biopsy + USS + CT/MRI neck + TFTs + Thyroglobulin)
         │
         ▼
STAGING (TNM system):
T - Primary tumour size + extrathyroidal extension
N - Regional lymph node status
M - Distant metastases

         │
    ┌────┴────┐
    ▼         ▼
MICROCARCINOMA   CLINICALLY SIGNIFICANT PTC
(<10 mm)         (≥10 mm or symptomatic)
    │                       │
    ▼                       ▼
CONTROVERSIAL:         TOTAL THYROIDECTOMY
- Active surveillance       │
  (Japan: 2/3 do not    ┌───┴────────────────────┐
  progress)             ▼                        ▼
- OR hemithyroidectomy  LOW RISK                HIGH RISK
                        │                        │
                    Hemithyroidectomy        Total thyroidectomy +
                    (lobectomy) if           Central neck dissection
                    unifocal, <4 cm,         (Level VI)
                    no ETE, no mets          ±
                                             Lateral neck dissection
                                             (if N1b - level II-V)

SURGICAL DETAILS:
• Total thyroidectomy = removal of both lobes + isthmus
• AVOID injury to:
  - Recurrent laryngeal nerve (RLN) - hoarseness
  - External laryngeal nerve (ELN) - voice pitch loss
  - Parathyroid glands (4) - hypocalcaemia
• Intraoperative neuromonitoring of RLN

POST-SURGICAL MANAGEMENT:

RADIOACTIVE IODINE (RAI / I-131):
• Remnant ablation: destroys remaining thyroid tissue
• Allows use of thyroglobulin as tumour marker
• Required for: High-risk, intermediate-risk PTC
• NOT required for: Low-risk PTC
• Preparation: Stop T4 for 4-6 weeks (or give recombinant TSH)
• Dose: 30–150 mCi depending on risk

TSH SUPPRESSION THERAPY:
• Levothyroxine (T4) given at doses to suppress TSH
• Rationale: TSH is a growth factor for thyroid cancer cells
• Target TSH:
  - High risk: <0.1 mU/L (suppressed)
  - Low risk: 0.5–2.0 mU/L (normal)

SURVEILLANCE:
• Serum thyroglobulin (Tg) levels - tumour marker
  (should be undetectable post total thyroidectomy + RAI)
• Anti-Tg antibodies
• Neck USS (6-12 monthly)
• Whole body scan if Tg rises

PROGNOSIS:
• Excellent: 10-year survival >95% for low-risk PTC
• Worse in: Elderly, large tumour, ETE, distant mets
• Lymph node mets in young patients do NOT worsen prognosis
  (unique feature of PTC - unlike other cancers)

TARGETED THERAPY (for advanced/refractory disease):
• Sorafenib (BRAF/VEGFR inhibitor)
• Lenvatinib (multi-kinase inhibitor)
• Dabrafenib + Trametinib (for BRAF V600E-positive)
• External beam radiotherapy (for unresectable/palliative)

---

Summary Table - AMES / MACIS Prognostic Scoring for PTC

---

Sources: Sabiston Textbook of Surgery (wound healing); Bailey & Love's Short Practice of Surgery 28th Edition (SSI, blood transfusion, phylloides, thyroid); Rosen's Emergency Medicine (shock, septic shock, Buerger's disease); Robbins & Kumar Basic Pathology (thyroid carcinoma histopathology)