SURGERY

Comprehensive Surgical Notes

Based on Bailey & Love's Short Practice of Surgery and SRB's Manual of Surgery
1. SHOCK
Definition
Shock is defined as a state of acute circulatory failure with inadequate tissue perfusion resulting in
cellular hypoxia and dysfunction. It is a life-threatening condition where the cardiovascular system
fails to maintain adequate perfusion of vital organs, leading to cellular and metabolic derangements.
(Bailey & Love)

Pathophysiology
Shock results in inadequate oxygen delivery to tissues. The cellular response includes:
• Switch from aerobic to anaerobic metabolism → lactic acidosis
• Failure of Na-K ATPase pump → cellular oedema
• Release of inflammatory mediators (TNF, IL-1, IL-6)
• Activation of complement and coagulation cascades
• Microcirculatory dysfunction (distributive failure)
• End-organ damage if prolonged: ARDS, ATN, DIC, MOF

Classification / Types of Shock

Type Mechanism Examples Haemodynamic
Profile
Hypovolaemic Reduced circulating Haemorrhage, burns, ↓CO, ↑SVR, ↓CVP
volume dehydration, GI losses
Cardiogenic Pump failure AMI, arrhythmia, ↓CO, ↑SVR, ↑CVP
cardiomyopathy,
tension pneumothorax
Distributive – Septic Maldistribution of blood Gram-negative ↑CO (early), ↓SVR,
flow bacteraemia, peritonitis ↓CVP
Distributive – IgE-mediated Drug reactions, insect ↑CO, ↓SVR, ↓CVP
Anaphylactic vasodilation stings, blood products
Distributive – Loss of sympathetic Spinal cord injury ↑CO, ↓SVR, ↓CVP,
Neurogenic tone above T6 Bradycardia
Obstructive Mechanical obstruction PE, cardiac ↓CO, ↑SVR, ↑CVP
to flow tamponade, tension
pneumothorax

Classes of Haemorrhagic Shock (ATLS Classification)

Parameter Class I Class II Class III Class IV
Blood loss (mL) <750 750–1500 1500–2000 >2000
Blood loss (%) <15% 15–30% 30–40% >40%
Heart rate (bpm) <100 100–120 120–140 >140
BP Normal Normal ↓ ↓↓
Pulse pressure Normal ↓ ↓ ↓↓
Respiratory rate 14–20 20–30 30–40 >35
Urine output >30 20–30 5–15 Negligible
(mL/hr)
Mental status Alert Anxious Confused Lethargic/Unconscious
Fluid Crystalloid Crystalloid Crystalloid + Blood + crystalloid
replacement blood
Clinical Features
General features common to all types of shock:
• Hypotension: systolic BP <90 mmHg or MAP <65 mmHg
• Tachycardia (except neurogenic shock which has bradycardia)
• Tachypnoea
• Cold, clammy, mottled skin (warm in distributive shock)
• Reduced urine output (<0.5 mL/kg/hr)
• Altered mental status – anxiety, confusion, obtundation
• Metabolic acidosis (lactic acid >2 mmol/L)

Management of Hypovolaemic/Haemorrhagic Shock

Follows ATLS principles – ABCDE approach:
A – Airway: Secure with cervical spine control if trauma
B – Breathing: High-flow O₂ (15 L/min via non-rebreather mask)
C – Circulation:
• Two large-bore IV cannulae (14–16G) in antecubital fossae
• Send bloods: FBC, U&E, LFTs, coagulation, cross-match, ABG, lactate
• Intraosseous access if IV access fails
• Initial fluid resuscitation: 1–2 L warm crystalloid (Hartmann's or 0.9% NaCl) in adults
• Reassess after each fluid bolus (BP, HR, urine output, skin perfusion)
• Transfuse packed RBCs if Class III/IV or persistent haemodynamic instability
• Damage control resuscitation: 1:1:1 ratio – pRBC: FFP: Platelets
• Permissive hypotension (target systolic 80–90 mmHg) until surgical haemostasis in penetrating
trauma
• Tranexamic acid 1g IV within 3 hours of injury (CRASH-2 trial)
D – Disability: GCS, pupils
E – Exposure and Environment: Full examination, prevent hypothermia

Management of Septic Shock

Follows Surviving Sepsis Campaign Guidelines (Hour-1 Bundle):
• Measure lactate; re-measure if initial lactate >2 mmol/L
• Blood cultures before antibiotics
• Broad-spectrum antibiotics within 1 hour of recognition
• 30 mL/kg crystalloid IV for hypotension or lactate ≥4 mmol/L
• Vasopressors (noradrenaline first-line) to maintain MAP ≥65 mmHg
• Source control: drain abscesses, remove infected devices, debridement
• Vasopressin 0.03 units/min as second agent if noradrenaline dose escalating
• Hydrocortisone 200 mg/day IV if vasopressor-refractory septic shock
• Monitor with CVP, arterial line, ScvO₂
• Mechanical ventilation: low tidal volume 6 mL/kg ideal body weight
• DVT prophylaxis, stress ulcer prophylaxis, glucose control (target 6–10 mmol/L)
• Corticosteroids only in refractory shock

Management of Cardiogenic Shock

• Identify and treat cause: PCI for STEMI, pericardiocentesis for tamponade
• Inotropic support: dobutamine (first-line), dopamine, adrenaline
• Vasopressors: noradrenaline to maintain MAP ≥65 mmHg
• Careful fluid administration (avoid fluid overload)
 • Intra-aortic balloon pump (IABP): reduces afterload, augments diastolic BP
• Mechanical circulatory support (LVAD, ECMO) in refractory cases
• Diuretics if pulmonary oedema once haemodynamically stable
• Avoid negative inotropes

Management of Anaphylactic Shock

• Remove/stop trigger agent immediately
• Adrenaline (epinephrine) IM 0.5 mg (0.5 mL of 1:1000) into anterolateral thigh – FIRST AND MOST
IMPORTANT
• Lay patient flat, raise legs if BP low (unless breathing difficulty)
• High-flow O₂ (15 L/min)
• IV access, rapid fluid resuscitation (500–1000 mL crystalloid bolus)
• Antihistamine: chlorphenamine 10 mg IV slow
• Corticosteroid: hydrocortisone 200 mg IV (prevents biphasic reaction)
• Bronchospasm: nebulised salbutamol, IV aminophylline
• Monitor: 6–12 hours observation (risk of biphasic reaction)
• Prescribe self-injectable adrenaline pen on discharge

Management of Neurogenic Shock

• Spinal immobilisation and C-spine protection
• Fluid resuscitation: judicious – avoid fluid overload
• Vasopressors: phenylephrine or noradrenaline to restore SVR
• Bradycardia: atropine, external pacing if severe
• Target MAP >85 mmHg in spinal cord injury (to maintain cord perfusion)
• Methylprednisolone: controversial; not routinely recommended
• Treat associated injuries

Monitoring in Shock
• Basic: HR, BP, RR, SpO₂ , urine output (catheterise), temperature
• Advanced: CVP (normal 5–10 cmH₂ O), arterial line (continuous BP monitoring)
• Biochemical: serial ABGs, lactate, bicarbonate, base excess
• Cardiac output: pulmonary artery catheter, transpulmonary thermodilution (PiCCO), cardiac echo
• ScvO₂ >70% (goal-directed therapy)
• FAST ultrasound in trauma

Complications of Shock
• Acute Tubular Necrosis (ATN) → Acute Kidney Injury
• Acute Respiratory Distress Syndrome (ARDS)
• Disseminated Intravascular Coagulation (DIC)
• Multiple Organ Failure (MOF) / Multi-Organ Dysfunction Syndrome (MODS)
• Acute Liver Failure
• Intestinal ischaemia → bacterial translocation → further sepsis
• Ischaemic heart disease / myocardial depression
• Cerebral hypoperfusion → brain death
2. STAGES OF WOUND HEALING
Definition
Wound healing is a complex, dynamic biological process of restoring cellular structures and tissue
layers after injury. It involves a highly orchestrated sequence of cellular and molecular events. (Bailey
& Love)

Types of Wound Healing

• Primary intention (First intention): Wound edges are approximated, minimal scarring (e.g., surgical
incision)
• Secondary intention: Wound left open, heals by granulation tissue, contraction and epithelialisation
(e.g., abscess cavity)
• Tertiary intention (Delayed primary closure): Wound initially left open, closed after 3–5 days once
infection controlled (e.g., contaminated wounds)

Phases of Wound Healing

Wound healing proceeds through four overlapping phases:

Phase 1: Haemostasis (Immediate – Minutes to Hours)

• Vasoconstriction (immediate, reflex)
• Platelet aggregation and plug formation (primary haemostasis)
• Coagulation cascade activation → fibrin clot formation (secondary haemostasis)
• Clot provides scaffold for cell migration
• Platelets release growth factors: PDGF, TGF-β, EGF
• Duration: Seconds to hours

Phase 2: Inflammatory Phase (Days 1–4)

• Vasodilation and increased vascular permeability (mediated by histamine, prostaglandins)
• Polymorphonuclear neutrophils (PMNs) first to arrive (peak at 24–48 hours): phagocytose bacteria
and debris
• Monocytes arrive by Day 2–3, mature into macrophages (peak at 48–72 hours)
• Macrophages: key orchestrators – phagocytosis, cytokine release (TNF-α, IL-1, IL-6, PDGF, TGF-β,
FGF, VEGF)
• Classic signs: rubor, calor, tumor, dolor, functio laesa
• Lymphocytes arrive last: modulate immune response
• In absence of macrophages → impaired wound healing

Phase 3: Proliferative Phase (Days 4–21)

Three key events:
• 1. Angiogenesis: New capillary formation stimulated by VEGF, FGF; endothelial cells migrate into
wound
• 2. Fibroplasia/Granulation tissue formation:
- Fibroblasts migrate in (from Day 3, peak Days 7–14)
- Fibroblasts produce collagen (initially Type III, replaced by Type I)
- Collagen cross-linking by lysyl oxidase
- Granulation tissue: pink, granular, highly vascular, fills wound
• 3. Epithelialisation:
- Keratinocytes migrate from wound edges and skin appendages
- Occurs within 24–48 hours in primary intention wounds
- Complete epithelialisation seals the wound surface
- Wound contraction: myofibroblasts (containing α-smooth muscle actin) contract the wound
Phase 4: Remodelling (Maturation) Phase (3 Weeks to 2 Years)
• Type III collagen progressively replaced by Type I collagen
• Collagen fibres reorient along lines of stress
• Tensile strength increases: reaches 80% of original strength by 3 months (never 100%)
• Maximum tensile strength ~80% at 6 months
• Vascularity decreases → scar becomes paler and flatter
• Scar undergoes maturation: red, raised, firm scar → white, flat, soft scar
• Excessive remodelling → hypertrophic scar or keloid

Growth Factors in Wound Healing

Growth Factor Source Function
PDGF Platelets, macrophages Fibroblast/smooth muscle cell
chemotaxis and proliferation
TGF-β Platelets, macrophages Collagen synthesis, fibroblast
proliferation
EGF Platelets, macrophages Epithelial cell proliferation
FGF Macrophages, endothelium Angiogenesis, fibroblast
proliferation
VEGF Macrophages, keratinocytes Angiogenesis
IGF-1 Liver, fibroblasts Cell proliferation and collagen
synthesis

Factors Affecting Wound Healing

Local factors:
• Blood supply (ischaemia impairs healing)
• Wound infection
• Foreign body
• Wound tension
• Wound type (sharp vs crush injury)
• Dead space, haematoma
Systemic factors:
• Age (elderly – delayed healing, reduced collagen synthesis)
• Nutritional status (protein, zinc, vitamins A and C deficiencies impair healing)
• Diabetes mellitus (impaired neutrophil function, microvascular disease, neuropathy)
• Corticosteroids and immunosuppressants
• Chemotherapy and radiotherapy
• Jaundice and uraemia
• Anaemia and hypoxia
• Obesity
• Smoking

Abnormal Wound Healing

• Hypertrophic scar: Raised, red scar confined to wound margins; may resolve spontaneously; treated
with compression, steroid injections
• Keloid: Scar extends beyond wound margins, does not regress; more common in darker skin;
treated with compression, intralesional steroids, excision + radiation
• Wound dehiscence: Superficial or deep; predisposed by infection, poor nutrition, obesity, steroids
• Wound contracture: Excessive contraction causing functional limitation (common after burns)
• Chronic wound/non-healing: Decubitus ulcer, venous ulcer, diabetic foot ulcer – impaired all phases
3. SURGICAL SITE INFECTION (SSI)
Definition
A Surgical Site Infection (SSI) is an infection occurring within 30 days of an operative procedure (or
within 90 days if an implant is in place) and involving the skin, subcutaneous tissue, deep soft tissue
(fascia, muscle), or organs/spaces opened or manipulated during the procedure. (CDC/NHSN
definition, endorsed by Bailey & Love)

Types of SSI
The CDC classifies SSIs into three types based on depth:

1. Superficial Incisional SSI

• Involves only skin and subcutaneous tissue
• Within 30 days of surgery
• Presents with: purulent discharge, pain, swelling, redness, warmth at incision
• Diagnosis: clinical (no culture needed for superficial infection)
• Management: wound opening, drainage, dressings; antibiotics if cellulitis present

2. Deep Incisional SSI

• Involves deep soft tissues (fascial and muscle layers) of the incision
• Within 30 days (or 90 days if implant)
• Presents with: deeper pain, fever, purulent discharge from deep incision, dehiscence
• Management: opening and debridement of deep tissues, wound VAC may be needed

3. Organ/Space SSI
• Involves any organ or space (other than incised body wall) opened/manipulated during procedure
• Examples: intra-abdominal abscess, empyema, anastomotic leak
• Requires: drainage (radiological or surgical), antibiotics, source control

Classification of Surgical Wounds (Altemeier Classification)

Class Definition SSI Rate Examples
Class I – Clean Non-inflamed, no break <2% Thyroid surgery, hernia
in sterile technique, no repair, breast surgery,
hollow viscus entered mastectomy
Class II – Clean- Hollow viscus entered 5–10% Elective bowel surgery,
Contaminated under controlled cholecystectomy,
conditions; no spillage appendicectomy (non-
inflamed)
Class III – Acute inflammation, 15–20% Perforated appendix,
Contaminated major break in stab wound, traumatic
technique, spillage wound <4h
from hollow viscus
Class IV – Established infection, >30% Faecal peritonitis,
Dirty/Infected pus, perforated viscus, traumatic wound >4h,
faecal contamination abscess drainage

Microbiology
Common causative organisms:
• Staphylococcus aureus (including MRSA): most common – skin flora, clean wounds
• Coagulase-negative Staphylococci: implant-related
• Escherichia coli and Enterobacteriaceae: abdominal surgery
 • Enterococcus spp.
• Bacteroides spp. (anaerobes): colorectal surgery
• Pseudomonas aeruginosa: burns, ICU patients
• Streptococcus spp.

Risk Factors
Patient-related:
• Diabetes mellitus, obesity, malnutrition
• Immunosuppression (steroids, HIV, chemotherapy)
• Age extremes
• Pre-existing remote infection
• MRSA carrier status
• Smoking, jaundice, anaemia
Procedure-related:
• Emergency vs elective surgery
• Duration >2 hours
• Contaminated wound class
• Use of drains, foreign material
• Poor surgical technique (dead space, haematoma, excessive diathermy)
Peri-operative:
• Inadequate antibiotic prophylaxis
• Shaving >6 hours before surgery (vs clipping)
• Hyperglycaemia intraoperatively
• Hypothermia
• Inadequate skin preparation

Prevention of SSI
Preoperative:
• Identify and treat remote infections
• MRSA screening and decolonisation (chlorhexidine wash, nasal mupirocin)
• Optimise nutrition, blood glucose control, smoking cessation
• Correct anaemia
• Bowel preparation only for specific colorectal procedures
• Antibiotic prophylaxis: appropriate agent, correct dose, 60 minutes before incision
Intraoperative:
• Hair removal: clippers (not shaving) on the day of surgery
• Skin antisepsis: chlorhexidine + alcohol (superior to povidone-iodine)
• Maintain normothermia (warming blankets, warm IV fluids)
• Maintain blood glucose <11 mmol/L
• Adequate tissue oxygenation (FiO₂ 80% perioperatively)
• Meticulous surgical technique: gentle tissue handling, obliterate dead space, ensure haemostasis
Postoperative:
• Sterile wound dressing for 48 hours
• Closed suction drainage if needed (remove early)
• Monitor for early signs of infection
• Repeat antibiotic doses if procedure >3–4 hours

Management of SSI
• Superficial: wound opening + drainage, saline dressings, antibiotics if systemic signs
• Deep: explore wound, debride necrotic tissue, wound VAC therapy
• Organ/space: CT-guided drainage or surgical re-exploration, appropriate systemic antibiotics
• Antibiotic selection guided by culture and sensitivity
• Nutritional support, blood glucose optimisation
• Consider MRSA cover (vancomycin/teicoplanin) if risk factors present
4. TYPES OF SURGICAL WOUNDS
Classification by Contamination (Altemeier)
See SSI section above for detailed Altemeier classification (Clean, Clean-contaminated,
Contaminated, Dirty).

Classification by Mechanism of Injury

• Incised wound: Clean-cut wound from sharp instrument; minimal tissue destruction; heals well by
primary intention (e.g., surgical incision, knife wound)
• Laceration: Irregular wound caused by blunt trauma; tissue crushed/torn; more contamination; higher
infection risk
• Contused wound: Wound with significant bruising; intact or disrupted skin; underlying haematoma;
devitalised tissue
• Puncture wound: Small entry wound, deep tract; high risk of anaerobic infection (tetanus, gas
gangrene)
• Crush injury: Extensive soft tissue damage; compartment syndrome risk; myoglobinuria,
rhabdomyolysis
• Degloving injury: Shearing of skin from underlying fascia; devascularised skin flap
• Abrasion: Superficial wound involving epidermis only; heals by epithelialisation
• Avulsion: Tearing away of tissue from attachment; may require graft or flap coverage
• Bite wound: Animal or human bites; polymicrobial infection (Pasteurella, Eikenella,
Capnocytophaga); always leave open or delayed primary closure
• Missile wound (gunshot): Cavitation effect; tissue necrosis; metal fragments; staged debridement

Classification by Duration
• Acute wound: Heals in predictable phases; progresses through haemostasis → inflammation →
proliferation → remodelling; expected to close within expected time
• Chronic wound: Fails to heal in predictable manner and time (>6 weeks); stuck in inflammatory
phase; examples: pressure ulcers, venous leg ulcers, diabetic foot ulcers, arterial ulcers

Classification by Depth
• Superficial: Epidermis ± dermis
• Partial thickness: Through dermis; may involve skin appendages; can re-epithelialise
• Full thickness: Through entire dermis; requires grafting for large wounds
• Deep: Involves subcutaneous fat, fascia, muscle, bone, tendons, vessels, nerves

Wound Management Principles

• ATLS principles for traumatic wounds
• Haemostasis: direct pressure, tourniquets, surgical control
• Wound toilet: thorough irrigation with saline (high-pressure)
• Debridement: removal of devitalised, contaminated tissue (surgical or autolytic/enzymatic)
• Wound closure:
- Primary closure: clean wounds, minimal contamination, within 6 hours
- Delayed primary closure: contaminated wounds, closed at 3–5 days
- Secondary intention: highly infected, devitalised wounds
• Dressings: appropriate for wound type (wet, moist environment aids healing)
• Tetanus prophylaxis for all traumatic wounds
• Antibiotic prophylaxis for contaminated/bite wounds
5. ACTINOMYCOSIS
Aetiology
• Causative organism: Actinomyces israelii (most common), also A. naeslundii, A. viscosus
• Gram-positive, non-acid-fast, anaerobic/microaerophilic filamentous bacteria (not a true fungus)
• Normal commensal of oral cavity, GI tract, and female genital tract
• Not contagious; endogenous infection following mucosal breach

Pathology
• Chronic suppurative granulomatous infection
• Pathognomonic: "sulphur granules" – yellowish granules (colonies of Actinomyces) visible in pus
• Forms dense fibrotic masses with multiple sinuses
• Spreads by direct extension across tissue planes (ignores fascial barriers)
• Does NOT spread via lymphatics or bloodstream (early)
• Associated organisms: "companion bacteria" (Streptococci, Bacteroides, Fusobacterium) which may
enhance virulence

Types / Sites of Infection

• 1. Cervicofacial actinomycosis (55–60% – most common):
- Following dental extraction, jaw fracture, or oral trauma
- Presents as hard, indurated mass at angle of jaw ("wooden jaw" or "lumpy jaw")
- Multiple discharging sinuses on face/neck containing sulphur granules
- May involve mandible (actinomycotic osteomyelitis)
- Trismus may be present
• 2. Thoracic actinomycosis (15–20%):
- Following aspiration of oral material or direct spread from cervicofacial
- Presents as lung consolidation, cavitation, pleural effusion/empyema
- May erode through chest wall forming cutaneous sinuses
- Can cause rib destruction, pericarditis
- Must differentiate from pulmonary tuberculosis and malignancy
• 3. Abdominal/Pelvic actinomycosis (20–25%):
- Following appendicectomy (ruptured appendix), bowel perforation, abdominal trauma, IUCD
- Presents as hard, fixed abdominal mass often mimicking malignancy
- Can involve any abdominal organ: ileocaecal region most common
- Pelvic actinomycosis: associated with IUCD; presents as adnexal mass, chronic pelvic pain
- Perianal actinomycosis: perianal fistulae and sinuses
• 4. CNS actinomycosis: Rare; brain abscess
• 5. Musculoskeletal: Osteomyelitis, septic arthritis

Diagnosis
• Clinical: hard mass with sinuses, sulphur granules in discharge
• Gram stain: Gram-positive filaments with "ray-fungus" appearance
• Culture: anaerobic culture for 2–4 weeks (slow-growing); often negative
• Histology: sulphur granules with central basophilic zone and peripheral eosinophilic clubs ("ray
fungus")
• CT scan: mass with ring enhancement, sinus tracts
• FNAC/biopsy: may demonstrate characteristic granules
• PCR: increasingly used

Treatment
Medical (cornerstone of treatment):
• Penicillin G IV: 10–20 million units/day for 2–6 weeks (initial intensive phase)
• Followed by oral amoxicillin 500 mg TDS for 6–12 months
• Alternative: ampicillin, doxycycline, erythromycin, clindamycin
• Prolonged therapy essential to prevent relapse (minimum 3–6 months oral antibiotics)
Surgical:
• Drainage of abscesses
• Resection of fibrotic masses if medical treatment fails
• Excision of sinuses
• Debridement of involved bone
• Combination of surgery + antibiotics gives best results
6. GAS GANGRENE (CLOSTRIDIAL MYONECROSIS)
Definition
Gas gangrene (Clostridial myonecrosis) is a rapidly progressive, life-threatening infection of skeletal
muscle caused by toxin-producing Clostridium species, characterised by tissue necrosis, gas
production, and severe systemic toxicity.

Aetiology
Causative organisms (Clostridium spp.):
• Clostridium perfringens (welchii) – most common (80%)
• Clostridium novyi
• Clostridium septicum
• Clostridium histolyticum
• Gram-positive, spore-forming, obligate anaerobes
• Normal inhabitants of soil, GI tract, faeces
Predisposing conditions:
• Traumatic wounds (especially with devitalised muscle, soil contamination, missile injuries)
• Post-operative (especially lower GI surgery, amputation)
• Spontaneous (in immunocompromised, malignancy – especially C. septicum with colorectal cancer)
• Vascular insufficiency (ischaemia creates anaerobic environment)
• Diabetes mellitus
• IVDU (injection drug use)

Pathogenesis
• Spores germinate in anaerobic, devitalised, ischaemic tissue
• Bacteria produce exotoxins (especially alpha-toxin – lecithinase/phospholipase C)
• Alpha-toxin destroys cell membranes, causes haemolysis, platelet destruction
• Gas production: CO₂ and H₂ (fermentation of tissue carbohydrates)
• Rapidly spreads through fascial planes
• Severe systemic toxicity: shock, multi-organ failure, DIC

Clinical Features
Local features (rapid progression):
• Severe, disproportionate pain at wound site (early warning sign)
• Wound oedema with tense, discoloured skin (initially pale, then dusky bronze/dark)
• Thin, serous or serosanguineous discharge with sweetish, foul odour
• Crepitus (gas palpable in tissues) – pathognomonic
• Skin bullae containing dark fluid
• Gas in tissue on palpation/X-ray (feathery pattern in muscles)
• Muscle: greyish, non-contractile, non-bleeding when cut
Systemic features (early, severe):
• Tachycardia out of proportion to fever
• High fever or hypothermia
• Profound toxaemia, hypotension, shock
• Haemolytic anaemia, jaundice
• Renal failure, DIC
• Altered consciousness

Investigations
• Gram stain of wound discharge: Gram-positive rods, absence of PMNs (toxin kills neutrophils)
 • Culture: anaerobic culture (usually not needed urgently)
• X-ray: gas in soft tissues (feathery/mottled pattern within muscle)
• CT/MRI: extent of gas, muscle involvement (helpful for planning surgical margins)
• ABG: metabolic acidosis
• FBC: haemolytic anaemia, leukocytosis
• LFTs, renal function, coagulation (DIC screen)
• Blood cultures

Management
Emergency – requires immediate surgical intervention. Delay increases mortality.
Surgical (PRIMARY and MOST IMPORTANT):
• Emergency wide surgical debridement: all infected/necrotic tissue must be excised
• Fasciotomy to release compartment syndrome if present
• Amputation may be required for limb gas gangrene (life-saving)
• Wound left open, re-exploration at 24–48 hours (second-look laparotomy/debridement)
• All grey, non-bleeding, non-contracting muscle must be excised
Medical:
• High-dose penicillin G: 3–4 million units IV 4-hourly (drug of choice)
• Metronidazole 500 mg IV 8-hourly (anaerobic cover)
• Clindamycin: reduces toxin production (add to penicillin)
• Chloramphenicol: for penicillin-allergic patients
• Aggressive resuscitation: IV fluids, blood transfusion, vasopressors
• Treat DIC, acute renal failure, haemolytic anaemia
Hyperbaric oxygen (HBO):
• Adjunct therapy, NOT a substitute for surgery
• 100% O₂ at 3 atmospheres → inhibits Clostridial growth, limits toxin production
• 3 sessions in first 24 hours
• Reduces demarcation, may reduce extent of tissue loss
• Only available in selected centres; should not delay surgery
Antitoxin: No longer recommended (polyvalent antitoxin had high anaphylaxis risk)

Prognosis
• Mortality: 20–30% (higher with truncal involvement, spontaneous gas gangrene, delayed treatment)
• Rapid recognition and surgery are the key determinants of survival
• Limb loss common but life-saving
7. CARBUNCLE
Definition
A carbuncle is a deep-seated, interconnected group of infected hair follicles (furuncles) that form a
confluent mass of suppuration with multiple discharging sinuses/points through the skin. It represents
a more severe form of furuncle (boil). (Bailey & Love)

Aetiology
• Organism: Staphylococcus aureus (most common, often MRSA)
• Predisposing factors: Diabetes mellitus (most important), obesity, immunosuppression, poor
hygiene, malnutrition, renal failure, corticosteroid use, IVDU

Pathology
• Multiple adjacent hair follicles infected → furunculosis → coalesce into a single mass
• Infection extends through subcutaneous tissue
• Multiple small abscesses communicating with each other
• Skin overlying becomes necrotic with multiple openings ("pepper-pot" pattern)
• Common sites: nape of neck (most common), upper back, face, axilla, thigh, buttock

Clinical Features
• Large, painful, indurated, erythematous swelling
• Multiple pointing heads/sinuses ("honeycomb" or "cribriform" appearance)
• Purulent, blood-stained discharge from multiple openings
• Surrounding cellulitis
• Central slough/necrosis
• Systemic features: fever, rigors, malaise (more prominent than furuncle)
• Regional lymphadenopathy
• Danger of cavernous sinus thrombosis if on face (dangerous area of face: triangle from bridge of
nose to angle of mouth)

Investigations
• Blood glucose: always exclude diabetes mellitus
• FBC: leukocytosis
• Blood cultures: if systemic sepsis
• Swab for culture and sensitivity (MRSA screen)
• Urine glucose/HbA1c

Management
Medical:
• Systemic antibiotics (always required – unlike furuncle):
- Flucloxacillin 500 mg QDS for 5–7 days (first-line for Staphylococcus)
- Co-amoxiclav if broad-spectrum needed
- Clindamycin or vancomycin for MRSA
• Analgesics
• Diabetic control: strict blood glucose management essential for resolution
• Hot compresses (facilitate pointing and drainage)
Surgical:
• Incision and drainage: when fluctuant (DO NOT incise before pointing – spreads infection)
• Cruciate incision or elliptical excision of necrotic tissue
• Removal of all slough/necrotic material
• Wound left open and packed with saline-soaked or antiseptic dressings
 • Regular dressing changes
• Re-excision if incomplete drainage
NEVER squeeze a carbuncle on the face – risk of spreading infection to cavernous sinus
8. CLOSTRIDIAL INFECTIONS IN SURGERY
Overview
Clostridium are Gram-positive, spore-forming, obligate anaerobic bacilli found in soil and GI tract.
They cause several important surgical infections through production of potent exotoxins.

Classification of Clostridial Infections

• 1. Clostridial myonecrosis (Gas Gangrene) – C. perfringens (see Gas Gangrene section)
• 2. Tetanus – C. tetani
• 3. Botulism – C. botulinum
• 4. Pseudomembranous colitis – C. difficile
• 5. Clostridial cellulitis/wound infection
• 6. Clostridial septicaemia

Tetanus (Clostridium tetani)

Pathogenesis: Tetanus toxin (tetanospasmin) produced at wound → travels retrograde along nerves
→ blocks glycine/GABA release at spinal inhibitory interneurones → unopposed motor neurone
stimulation → spastic paralysis
Clinical features:
• Incubation: 3–21 days (shorter incubation = more severe disease)
• Trismus (lockjaw) – first symptom: masseter spasm
• Risus sardonicus: sardonic smile (facial muscle spasm)
• Opisthotonus: hyperextension of back (severe)
• Dysphagia, drooling
• Generalised muscle rigidity and spasms
• Autonomic instability: hypertension, tachycardia, sweating
• Laryngeal spasm → respiratory failure
Management:
• Wound debridement (remove source of toxin production)
• Human Tetanus Immunoglobulin (HTIG) 150–500 units IM: neutralise unbound toxin
• Metronidazole 500 mg IV/oral TDS for 7–10 days (or penicillin G)
• Diazepam/midazolam: muscle relaxants for spasms
• Mechanical ventilation for respiratory failure
• Magnesium sulphate: autonomic instability
• ICU management
• Active immunisation with tetanus toxoid (disease does not confer immunity)
Prevention:
• Universal immunisation: DTP series in childhood (3 doses at 2, 3, 4 months + boosters)
• Wound management: debridement, do not close heavily contaminated wounds
• Tetanus-prone wounds: puncture wounds, >6h old, devitalised tissue, soil/faeces contamination,
burns
• For tetanus-prone wound: HTIG + tetanus toxoid (if not immunised or immunisation uncertain)

Pseudomembranous Colitis (Clostridium difficile)

Pathogenesis: C. difficile overgrowth following antibiotic therapy → produces Toxin A (enterotoxin)
and Toxin B (cytotoxin) → mucosal damage, inflammation, pseudomembrane formation
Risk factors: Broad-spectrum antibiotics (especially clindamycin, ampicillin, cephalosporins,
fluoroquinolones), elderly, hospitalisation, PPI use, immunosuppression, IBD, previous C. difficile
infection
Clinical features:
• Watery diarrhoea (3+ loose stools/24h): hallmark
 • Abdominal cramps and pain
• Fever, leukocytosis
• Severe: toxic megacolon, colonic perforation, peritonitis, septic shock
Diagnosis:
• Stool C. difficile toxin A/B enzyme immunoassay (EIA): rapid, available
• Glutamate dehydrogenase (GDH) antigen test: screening
• PCR: most sensitive
• Stool culture: gold standard but slow
• Colonoscopy: yellowish-white pseudomembranes (not routinely needed)
• CT abdomen: thickened colon wall, ascites, pericolic stranding
Management:
• STOP the causative antibiotic immediately (if possible)
• Isolation of patient (contact precautions, hand washing with soap/water – NOT alcohol gel)
• Mild-moderate (first episode): oral vancomycin 125 mg QDS for 10 days OR fidaxomicin 200 mg BD
for 10 days (superior to metronidazole)
• Severe (WBC >15, AKI, ICU): oral vancomycin 125–500 mg QDS ± IV metronidazole
• Fulminant (toxic megacolon, peritonitis): urgent surgery – subtotal colectomy with ileostomy
• Recurrent infection: faecal microbiota transplant (FMT); bezlotoxumab (monoclonal antibody to Toxin
B) to prevent recurrence

Clostridial Cellulitis
• Localised infection of subcutaneous tissue (NOT muscle)
• Less severe than gas gangrene
• Organism: C. perfringens most common
• Gas in subcutaneous tissue but NO muscle involvement
• Less systemic toxicity
• Treatment: debridement + antibiotics (penicillin G + metronidazole)
• Must distinguish from gas gangrene (requires surgical exploration to assess muscle)
9. MADURA FOOT (MYCETOMA)
Definition
Madura foot (Mycetoma pedis) is a chronic, slowly progressive suppurative granulomatous infection
affecting the foot (and occasionally other body parts), characterised by tumefaction, draining sinuses,
and the presence of grains/granules in the discharge. (SRB's Surgery)

Aetiology
Two types based on causative organism:
• 1. Actinomycetoma (50–60%): Caused by filamentous bacteria (actinomycetes):
- Nocardia brasiliensis (most common in India)
- Actinomadura madurae
- Actinomadura pelletieri
- Streptomyces somaliensis
• 2. Eumycetoma (40–50%): Caused by true fungi:
- Madurella mycetomatis (most common worldwide)
- Madurella grisea
- Pseudallescheria boydii
Epidemiology:
• Endemic in tropical and subtropical regions: India, Africa, South America, Middle East
• "Mycetoma belt": 15°S–30°N
• Most common in agricultural workers
• Males affected more (3:1 ratio)
• Route of entry: traumatic inoculation through puncture wounds (thorns, splinters) in bare feet

Pathology
• Chronic progressive granulomatous infection
• Grains/granules: colonies of organisms embedded in cement-like matrix
• Colour of grains guides aetiology: white/yellow (Actinomadura, Nocardia), black (Madurella), red (A.
pelletieri)
• Spreads slowly through subcutaneous tissue, fascia, muscle, and bone
• Extensive fibrosis, abscess formation, multiple sinus tracts
• Bone destruction: cortical erosion, "punched-out" lesions, periosteal reaction
• Deformity of foot

Clinical Features
• Triad: tumefaction (swelling), sinuses, grains in discharge
• Initial: painless papule or nodule at site of inoculation
• Progressive swelling of foot (rarely painful despite extensive destruction)
• Multiple sinuses that open and close
• Purulent discharge with characteristic grains/granules
• Foot deformed, grossly enlarged
• Skin: hyperpigmented, nodular, indurated
• Usually no regional lymphadenopathy
• No systemic features (unless secondary bacterial infection)
• Progression over years to decades
• Late: bone involvement (osteomyelitis), extensive destruction

Investigations
• Identification of grains: colour and morphology guide organism
 • Gram stain/Ziehl-Neelsen: filamentous bacteria (actinomycetoma) vs fungal hyphae (eumycetoma)
• Culture: aerobic and anaerobic, fungal cultures (difficult, slow)
• X-ray foot: cortical bone erosion, periosteal reaction, "mottled" or "moth-eaten" bone
• MRI: gold standard – shows extent of soft tissue, muscle, bone involvement; "dot in circle" sign
• Ultrasound: hyperechoic grains surrounded by hypoechoic halo
• Histology of biopsy: granulomatous inflammation with grains
• PCR and sequencing: definitive species identification

Treatment
Actinomycetoma (bacterial):
• Co-trimoxazole (trimethoprim-sulphamethoxazole) + streptomycin: first-line combination
• Amikacin + co-trimoxazole for severe/resistant cases
• Prolonged treatment: 12–24 months
• High cure rates with medical therapy alone
• Surgery + chemotherapy for localised disease
Eumycetoma (fungal):
• Itraconazole 400 mg/day: first-line (for 12–24 months minimum)
• Voriconazole: second-line
• Medical treatment alone has limited efficacy for eumycetoma
• Surgery: wide local excision or amputation for localised, resistant, or advanced cases
• Combined medical + surgical approach gives best results
Surgical principles:
• Localised lesion without bone involvement: wide local excision
• Advanced with bone involvement: below-knee amputation (often necessary)
• All surgery supplemented with prolonged antifungal/antibacterial therapy
10. PRINCIPLES OF MINIMALLY INVASIVE SURGERY (MIS)
Definition
Minimally Invasive Surgery (MIS) refers to surgical techniques that minimise trauma to the patient
through small incisions or natural orifices, while achieving the same operative goals as open surgery,
with reduced morbidity and faster recovery.

Types of Minimally Invasive Surgery

• Laparoscopic surgery (most common)
• Thoracoscopic surgery (VATS – Video-Assisted Thoracoscopic Surgery)
• Robotic-assisted surgery (da Vinci system)
• Endoscopic surgery (ERCP, EUS, EMR, ESD)
• Natural Orifice Transluminal Endoscopic Surgery (NOTES)
• Single Incision Laparoscopic Surgery (SILS)
• Arthroscopic surgery
• Hysteroscopic and ureteroscopic surgery

Fundamental Principles of Laparoscopic Surgery

• 1. Pneumoperitoneum:
• Carbon dioxide (CO₂ ) insufflation into peritoneal cavity
• CO₂ chosen: cheap, non-combustible, rapidly absorbed, more soluble than air
• Pressure: 12–15 mmHg (optimal working space without haemodynamic compromise)
• Entry: Veress needle (closed technique) or Hasson technique (open/cut-down technique)
• Physiological effects: ↑ IVC compression → ↓ venous return → ↓ cardiac output; diaphragmatic
elevation → ↓ respiratory compliance; CO₂ absorption → hypercapnia
• 2. Trocar Placement:
• Camera port (10–12 mm): usually umbilical (most cosmetically acceptable scar)
• Working ports (5–12 mm): triangulation with target organ
• Patient positioning: Trendelenburg (head down) for pelvic surgery; reverse Trendelenburg for upper
GI
• Triangulation principle: camera and instruments form triangle with target at apex
• 3. Optics and Imaging:
• 0° or 30° laparoscopes (30° gives better views around structures)
• High-definition (HD) and 4K cameras
• Light source: LED/xenon
• 3D laparoscopy and robotic systems improve depth perception
• 4. Energy Sources:
• Monopolar diathermy: cutting and coagulation
• Bipolar diathermy: precise haemostasis, safer near structures
• Ultrasonic dissectors (Harmonic scalpel): combines cutting/haemostasis, less thermal spread, no
smoke
• Advanced bipolar (LigaSure): vessel sealing up to 7 mm diameter
• Plasma kinetic energy (PKS)

Physiological Effects of Pneumoperitoneum

Cardiovascular:
• Increased IAP → IVC compression → decreased venous return → decreased cardiac output
• Decreased renal blood flow → ↓ urine output (transient)
• Increased afterload (SVR)
Respiratory:
• Diaphragmatic elevation → decreased FRC, compliance, lung volumes
 • Hypercapnia from CO₂ absorption (controlled by hyperventilation)
• Increased airway pressures
Neuroendocrine:
• Increased catecholamines, vasopressin, renin-angiotensin activation
• Not clinically significant in healthy patients

Advantages of MIS over Open Surgery

• Smaller incisions → reduced wound complications (infection, hernia, dehiscence)
• Less pain → reduced analgesic requirements
• Shorter hospital stay
• Faster return to normal activities
• Reduced ileus (less bowel handling)
• Better cosmesis
• Reduced blood loss
• Lower risk of incisional hernia
• Reduced adhesion formation
• Improved vision (magnification 4–8×)
• Reduced immunosuppressive response to surgery

Disadvantages and Limitations

• Loss of tactile (haptic) feedback
• 2D vision (traditional laparoscopy – overcome by 3D/robotic)
• Limited instrument movement (fulcrum effect)
• Long learning curve (requires structured training)
• Risk of trocar site hernias
• CO₂ embolism (rare but fatal)
• Port site recurrence in cancer surgery (controversial)
• Longer operative time initially
• Equipment dependence (cost, setup)
• Physiological effects of pneumoperitoneum

Contraindications to Laparoscopic Surgery

Absolute contraindications (few):
• Inability to tolerate pneumoperitoneum (severe cardiorespiratory compromise)
• Uncorrected coagulopathy
• Intestinal obstruction with grossly distended bowel (relative)
Relative contraindications:
• Previous multiple abdominal surgeries (adhesions)
• Obesity (extreme BMI)
• Advanced pregnancy (beyond first trimester – Hasson technique preferred)
• Prior peritonitis with frozen abdomen

Robotic Surgery
• Three-component system: surgeon console, patient-side cart (robotic arms), vision cart
• Da Vinci Surgical System: most widely used
• Advantages over standard laparoscopy: 3D HD vision, EndoWrist articulation (7° freedom of
movement), tremor filtration, stable camera platform
• Applications: prostatectomy, hysterectomy, colorectal surgery, cardiac surgery
• Disadvantages: very high cost, no haptic feedback, bulky, longer setup time

Common Laparoscopic Procedures

• Laparoscopic cholecystectomy (gold standard for gallstone disease)
• Laparoscopic appendicectomy
• Laparoscopic fundoplication (Nissen)
• Laparoscopic inguinal hernia repair (TAPP/TEP)
• Laparoscopic colectomy/anterior resection
• Laparoscopic splenectomy
• Laparoscopic adrenalectomy
• Laparoscopic nephrectomy
• Laparoscopic bariatric surgery
11. CONGENITAL HYPERTROPHIC PYLORIC STENOSIS (CHPS)
Definition
Congenital Hypertrophic Pyloric Stenosis is a condition characterised by hypertrophy and
hyperplasia of the smooth muscle of the pylorus, causing progressive gastric outlet obstruction in
neonates and young infants.

Epidemiology
• Incidence: 2–4 per 1000 live births (most common surgical cause of non-bilious vomiting in infancy)
• Male:Female ratio: 4:1 (males predominantly affected)
• Firstborn children (especially firstborn male)
• Caucasians > Asian or African populations
• Family history: increased risk (5× if mother affected, 2× if father affected)
• Presents typically between 2–8 weeks of age (rarely before 2 weeks or after 12 weeks)

Aetiology
Exact cause unknown. Proposed mechanisms:
• Deficiency of nitric oxide synthase (loss of inhibitory innervation to pyloric muscle)
• Abnormal innervation of pylorus (reduced interstitial cells of Cajal)
• Genetic factors: multifactorial inheritance
• Association with maternal macrolide antibiotic use (erythromycin) in first 2 weeks of life

Pathology
• Pyloric muscle (circular layer) hypertrophied and hyperplastic
• Length: 2–3 cm (normal <1 cm); Width: >0.4 cm (normal <0.2 cm)
• "Olive-shaped" hard mass palpable in right epigastrium
• Mucosa and submucosa intact, prolapsed into duodenum
• Progressive obstruction → projectile vomiting → metabolic derangement

Clinical Features
Presentation:
• Non-bilious projectile vomiting: hallmark
- Vomiting begins at 2–6 weeks; progressively more forceful
- "Projectile" – may travel several feet
- Non-bilious (pylorus is proximal to ampulla of Vater)
- Hunger immediately after vomiting ("hungry baby" – feeds eagerly after vomiting)
• Failure to thrive: weight loss, poor weight gain
• Constipation (no stool reaching bowel)
• Dehydration: sunken fontanelle, dry mucous membranes, decreased skin turgor, decreased urine
output
• Visible gastric peristalsis: waves visible from left to right hypochondrium (if stomach full)
• Palpable pyloric "olive": firm, mobile, ovoid mass in right hypochondrium/epigastrium
- Best palpated after vomiting, while infant is feeding, with patient relaxed
- Pathognomonic when palpated (only 60–80% palpable)

Metabolic Consequences
• Hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria
- Loss of HCl in vomitus → ↓ H⁺ , ↓ Cl⁻ → metabolic alkalosis
- Kidneys attempt to compensate: excrete HCO₃ ⁻ with Na⁺ and K⁺ → hypokalaemia
- Dehydration → aldosterone release → further K⁺ loss
- Paradoxical aciduria: kidneys prefer to conserve Na⁺ by excreting H⁺ despite alkalosis
• Dehydration
• Hyponatraemia

Investigations
• Serum electrolytes (Na⁺ , K⁺ , Cl⁻ , HCO₃ ⁻ ): hypochloraemia, hypokalaemia, raised HCO₃ ⁻
• Blood gas: metabolic alkalosis (pH >7.45, HCO₃ elevated, normal or low pCO₂ )
• Ultrasound (investigation of choice):
- Pyloric muscle thickness >4 mm
- Pyloric channel length >17 mm
- Positive "doughnut sign" (transverse view) and "antrum sign"
- Sensitivity and specificity >95%
• Barium swallow (if ultrasound equivocal): "string sign" (thin trickle of contrast through narrow pyloric
channel); "shoulder sign"
• Blood glucose: hypoglycaemia common

Management
NOT a surgical emergency – metabolic correction must precede surgery.
Preoperative resuscitation (mandatory):
• NG tube: to decompress stomach
• IV fluid correction: 0.45% or 0.9% NaCl + KCl (20 mEq/L); do NOT use potassium until urine output
established
• Correct to: Na⁺ >130, Cl⁻ >90, K⁺ >3.0, pH <7.45, HCO₃ <28 before surgery
• Monitor urine output >1 mL/kg/hr
Surgical (Ramstedt's Pyloromyotomy):
• Procedure of choice: longitudinal incision through pyloric serosa and muscularis down to
submucosa, spreading muscle fibres (without entering mucosa)
• Approaches:
- Traditional open: right upper quadrant transverse/supraumbilical incision
- Laparoscopic pyloromyotomy (increasingly preferred): equivalent outcomes, better cosmesis
- Circumumbilical approach: better cosmesis
• Check for mucosal perforation after procedure: saline instilled via NG tube/air
• If mucosal perforation: suture, rotate myotomy 180°, re-perform
Postoperative care:
• Begin feeding 2–6 hours post-op (graduated regime)
• Some vomiting expected post-op (resolves within 24–48h)
• Discharge usually within 24–48 hours

Prognosis
• Excellent: mortality <0.5% in well-resourced settings
• Persistent vomiting occurs in ~25% post-op (due to oedema) – usually resolves
• Incomplete pyloromyotomy: rare, requires re-operation
12. HYPOSPADIAS
Definition
Hypospadias is a congenital anomaly characterised by the triad of:
1. Abnormally located urethral meatus (on the ventral surface of the penis, proximal to the normal
position at the tip of glans)
• 2. Ventral curvature of the penis (chordee)
• 3. Dorsal hooding (incomplete foreskin ventrally)

Incidence and Aetiology

• Incidence: 1 in 300 male births (one of the most common congenital abnormalities)
• Aetiology: multifactorial (genetic + hormonal + environmental)
• Failure of fusion of urethral folds (which normally fuse from perineum to glans)
• Associated with deficient androgen stimulation during development
• Associations: cryptorchidism (10%), inguinal hernia, upper urinary tract anomalies (3–5% if proximal)
• Risk higher with environmental oestrogen exposure, maternal progestogen therapy

Classification / Types (by Meatal Position)

Type Location of Meatus Frequency
Glanular On glans penis, just proximal to Most common
tip
Coronal At coronal sulcus
Penile (distal) Distal shaft of penis Together 70–75%
Penile (mid) Mid shaft of penis
Penile (proximal) Proximal shaft of penis
Penoscrotal Junction of penis and scrotum Together 25–30%
Scrotal On the scrotum
Perineal Perineum (severe) Most severe, consider DSD

Clinical Features
• Abnormal position of urethral meatus (ventral, proximal to tip)
• Chordee: ventral curvature of erect penis (absent in anterior forms)
• Dorsal hooding: skin bunched on dorsal surface, absent ventral foreskin
• Spraying/deflection of urinary stream
• Need to sit to urinate in severe forms
• Painful erections (due to chordee)
• Infertility (severe proximal hypospadias)
• Psychosexual issues in older children

Investigations
• Clinical examination: usually diagnostic
• Karyotype: if severe/perineal hypospadias + cryptorchidism → Disorders of Sexual Development
(DSD)
• Testosterone stimulation test: for severe cases to assess androgen responsiveness
• Micturating cystourethrogram (MCUG): if UTI or upper tract anomalies suspected
• Renal ultrasound: proximal hypospadias
• Endoscopy: to exclude prostatic utricle
Timing of Surgical Correction
• Optimal age: 6–18 months (before age 2 years)
• Before toilet training and before psychological awareness of genital appearance
• Testosterone stimulation: give testosterone ointment or IM injections 6–8 weeks before surgery to
increase penile size (especially for proximal cases)
• NEVER circumcise before surgical repair (prepuce may be needed for urethroplasty)

Surgical Treatment
Goals of surgery:
• 1. Place meatus at tip of glans (orthotopic position)
• 2. Correct chordee (straighten penis)
• 3. Achieve good cosmesis
• 4. Allow normal urinary stream
• 5. Allow normal sexual function
Principles:
• Release of chordee (if present): excision of fibrous tissue on ventral surface
• Urethroplasty: construction of neourethra using local skin flaps or grafts
• Glanuloplasty: creating a conical glans with neo-meatus at tip
• Skin coverage: rearrangement of penile skin
Common surgical techniques:
• MAGPI (Meatoplasty and Glanuloplasty Incorporated): for distal/coronal, no chordee
• Mathieu (Flip-flap): distal hypospadias
• Duckett (Transverse preputial island flap): mid/proximal hypospadias (single stage)
• Tubularized Incised Plate Urethroplasty (TIP / Snodgrass procedure): most popular; reliable, good
cosmesis; for distal and mid-penile with mild chordee
• Staged procedures (e.g., Bracka): for severe proximal, failed previous repairs; use buccal mucosa
graft
• Buccal mucosa urethroplasty: gold standard for complex/redo cases
Catheterisation:
• Urethral or suprapubic catheter left for 7–14 days postoperatively

Complications
• Urethrocutaneous fistula: most common (5–15%)
• Urethral stricture/meatal stenosis
• Wound dehiscence
• Diverticulum of neourethra
• Residual chordee
• Hair in urethra (if hair-bearing skin used)
• Balanitis xerotica obliterans (BXO)
• Psychological sequelae if repair delayed
13. SURGICAL AUDIT
Definition
A surgical audit is a systematic, critical analysis of the quality of surgical care, including procedures
and processes, use of resources, and the resulting outcome and quality of life for the patient. It
compares actual performance against agreed standards to identify areas for improvement. (Bailey
& Love)

Purpose and Importance

• Improve the quality of patient care
• Identify adverse outcomes and complications
• Ensure evidence-based practice
• Reduce complications and mortality
• Benchmarking against national/international standards
• Education and training evaluation
• Medico-legal documentation
• Resource allocation and cost-effectiveness

Types of Audit
• Structure audit: Examines resources available (staffing, facilities, equipment)
• Process audit: Examines how care is delivered (adherence to protocols, guidelines)
• Outcome audit: Examines results of care (morbidity, mortality, readmission rates)
• Retrospective audit: Reviews past records (most common in surgery)
• Prospective audit: Data collected going forward from a set point
• Concurrent audit: Ongoing real-time evaluation
• Peer review: Colleagues evaluate each other's practice
• Significant event audit: Detailed review of adverse events

The Audit Cycle

The audit cycle (also called the audit loop) has five steps:
• 1. Identify a problem or topic for audit
• 2. Set criteria and standards (evidence-based, from guidelines – e.g., NICE)
• 3. Measure current practice against standards (data collection, analysis)
• 4. Implement change (if performance below standard)
• 5. Re-audit to check improvement (close the loop)
Without re-audit and change implementation, the cycle is incomplete – this is the most common
failing.

National Surgical Audits and Databases

UK examples:
• National Surgical Quality Improvement Program (NSQIP): US-based, widely adopted
• National Emergency Laparotomy Audit (NELA): tracks outcomes for emergency laparotomy
• National Oesophago-Gastric Cancer Audit (NOGCA)
• National Bowel Cancer Audit (NBOCA)
• National Hip Fracture Database
• CEPOD (Confidential Enquiry into Perioperative Deaths) → now NCEPOD (National Confidential
Enquiry into Patient Outcome and Death)
• Mortality and Morbidity (M&M) meetings: regular departmental review of complications and deaths

Outcome Measures in Surgical Audit

Process measures:
 • Antibiotic prophylaxis rates
• VTE prophylaxis compliance
• Correct consent documentation
Outcome measures:
• 30-day mortality rate
• Readmission rate (30-day, 90-day)
• Reoperation rate
• Complication rates (specific and overall)
• Length of hospital stay
• Patient-reported outcome measures (PROMs)
• Patient-reported experience measures (PREMs)

Principles of Good Surgical Audit

• Should be anonymous (protect patient and surgeon identity in reporting)
• Must include all patients (no selection bias)
• Must be prospective when possible
• Clear criteria and standards must be set before data collection
• Findings must lead to actionable change
• Results must be disseminated (departmental meetings, publications)
• Completion of the audit loop is essential
• Ethics approval may be needed for prospective research audits

Audit vs Research
Feature Audit Research
Purpose Improve practice vs standard Generate new knowledge
Standard Pre-existing (guidelines) None (tests hypothesis)
Ethics approval Usually not needed Required
Randomisation Not used May use RCT
Generalisability Local/departmental Universal
Methodology Observational Experimental or observational
14. UNIVERSAL SAFETY PRECAUTIONS
Definition and Rationale
Universal (Standard) Precautions are a set of infection control practices applied to all patients
regardless of suspected or confirmed diagnosis, to prevent transmission of bloodborne pathogens
(HIV, Hepatitis B, Hepatitis C) and other infectious agents between patients and healthcare workers.
Introduced by CDC in 1987 following HIV epidemic.

Components of Universal Precautions

• 1. Hand hygiene:
• WHO 5 moments: before patient contact, before aseptic procedure, after body fluid exposure, after
patient contact, after touching patient surroundings
• Soap and water: for visibly soiled hands, C. difficile (alcohol ineffective against spores)
• Alcohol-based hand rub: for routine hand hygiene
• 2. Personal Protective Equipment (PPE):
• Gloves: for contact with blood, body fluids, mucous membranes, non-intact skin
• Gown/apron: for procedures likely to cause splashing
• Mask and eye protection/face shield: for procedures with risk of splashes/sprays to face
• Respiratory protection (N95/FFP3 masks): for airborne precautions (TB, COVID-19)
• 3. Safe handling and disposal of sharps:
• Never recap needles with both hands (use one-hand scoop technique if necessary)
• Do not remove needles from syringes by hand
• Immediately discard sharps into puncture-resistant sharps containers
• Do not overfill sharps containers (>3/4 full)
• Announce "sharp" when passing in theatre
• 4. Safe injection practices:
• Use single-use syringes and needles
• Single-dose vials where possible
• Do not reuse needles/syringes even for same patient
• 5. Respiratory hygiene and cough etiquette:
• Cover coughs/sneezes with tissue (dispose immediately)
• Mask febrile respiratory patients
• 6. Handling of patient care equipment:
• Decontaminate reusable equipment before reuse (clean, disinfect, sterilise as appropriate)
• 7. Environmental cleaning:
• Regular cleaning and disinfection of patient care areas and high-touch surfaces
• 8. Linen handling:
• Handle soiled linen as little as possible
• Bag at point of use
• 9. Safe waste disposal:
• Clinical waste (contaminated) → yellow bags → incineration
• Sharps → yellow sharps containers with black lid

Sharps Injury Management

Immediate actions:
• 1. Do NOT suck wound
• 2. Encourage bleeding (do not squeeze)
• 3. Wash immediately with soap and water
• 4. Cover with waterproof dressing
• 5. Report immediately to occupational health/Infection Control
• 6. Document: time, nature of injury, source patient details
 • 7. Risk assessment: source patient HIV, HBV, HCV status
• 8. Post-exposure prophylaxis (PEP):
- HIV PEP: within 72 hours (ideally <1 hour) – tenofovir/emtricitabine + raltegravir for 28 days
- HBV: HBIG + HBV vaccine if not immunised
- HCV: no effective PEP; monitor LFTs and HCV RNA at 6–8 weeks
• 9. Follow-up serology at 6 weeks, 3 months, 6 months

Transmission-Based Precautions (Additional Precautions)

In addition to standard precautions:
• Contact precautions: MRSA, VRE, C. difficile, skin infections → gloves + gown, single room
• Droplet precautions: influenza, meningococcal, mumps → surgical mask, single room
• Airborne precautions: TB, measles, chickenpox → FFP3/N95 respirator, negative-pressure room

WHO Surgical Safety Checklist

Three phases (Sign In, Time Out, Sign Out):
Sign In (before anaesthesia induction):
• Patient identity, procedure, site, consent verified
• Site marked
• Anaesthesia machine and equipment checked
• Pulse oximeter functioning
• Allergies, airway risk, blood loss risk assessed
Time Out (before incision):
• All team members introduced by name
• Confirm patient, procedure, and site (verbal)
• Antibiotic prophylaxis given <60 minutes prior
• Critical steps reviewed
• Equipment/implant availability confirmed
• Imaging displayed
Sign Out (before patient leaves theatre):
• Instrument, sponge, needle count correct
• Specimen labelled correctly
• Equipment issues documented
• Key concerns for recovery communicated
15. DIAGNOSTIC IMAGING IN SURGERY
Overview
Diagnostic imaging is integral to surgical practice, used for diagnosis, staging, treatment planning,
and intraoperative guidance. Selection is based on clinical question, availability, cost, radiation
exposure, and patient factors.

1. Plain X-Rays (Radiographs)

Principles: X-rays attenuated differentially by tissues (air/gas = black; fat = dark grey; soft tissue/fluid
= grey; bone/calcium = white; metal = white)
Surgical applications:
• Chest X-ray: pneumothorax, haemothorax, pleural effusion, pneumomediastinum, foreign bodies, rib
fractures, cardiomegaly
• Abdominal X-ray (AXR): bowel obstruction (dilated loops, air-fluid levels), perforation
(pneumoperitoneum – Rigler's sign in supine), volvulus (coffee-bean sign – sigmoid; whirl sign –
caecal), toxic megacolon
• Erect chest X-ray: best for pneumoperitoneum (air under diaphragm)
• Skeletal X-rays: fractures, bone tumours, osteomyelitis
• Limitations: low soft tissue contrast, 2D image, radiation

2. Ultrasound (USS)
Principles: High-frequency sound waves reflected at tissue interfaces; no ionising radiation; real-time
imaging
Advantages: No radiation, portable, cheap, real-time, can guide interventions, safe in pregnancy
Surgical applications:
• FAST (Focused Assessment with Sonography in Trauma): detect free fluid in peritoneal/pericardial
cavities
• Abdominal USS: gallstones, cholecystitis (wall thickening, pericholecystic fluid, positive Murphy's),
AAA, renal stones, liver lesions, appendicitis in paediatrics
• Vascular: duplex USS for DVT, carotid stenosis, peripheral arterial disease
• Breast: differentiate cyst from solid; guide FNAC
• Thyroid, parotid, lymph node assessment
• Endoscopic USS (EUS): staging of GI cancers
• Intraoperative USS: liver metastases, bile duct stones
• Interventional: USS-guided drainage, biopsy
Limitations: Operator-dependent; poor visualisation of gas-containing structures; limited in obese
patients; cannot penetrate bone

3. Computed Tomography (CT)

Principles: Multiple X-ray projections reconstructed into cross-sectional images; excellent soft tissue
contrast with contrast enhancement
Advantages: Fast, widely available, excellent anatomical detail, multiplanar reconstruction
Surgical applications:
• Trauma: CT trauma survey ("trauma pan-scan") – head, cervical spine, chest, abdomen, pelvis;
detect solid organ injuries, pneumothorax, haemothorax
• Abdominal pain: appendicitis, diverticulitis, pancreatitis, bowel obstruction (transition point)
• Cancer staging: TNM staging for GI, lung, renal, pancreatic cancers
• Vascular: CT angiography for AAA, aortic dissection, mesenteric ischaemia
• Acute abdomen: perforation, ischaemia, obstruction
• Interventional: CT-guided biopsy, drain placement
• Brain/spine: neurosurgical emergencies
Limitations: Radiation dose, contrast nephropathy, allergy, less sensitive for mucosal lesions,
artefact from metal

4. Magnetic Resonance Imaging (MRI)

Principles: Uses magnetic field and radiofrequency pulses; superior soft tissue contrast; no ionising
radiation
Surgical applications:
• Liver: characterise liver lesions (HCC, metastases, haemangioma, cysts)
• Rectal cancer staging: MRI pelvis is gold standard – assess tumour depth (T-stage), mesorectal
fascia involvement, nodal status
• Pancreatic disease: MRCP for bile duct/pancreatic duct stones, strictures
• Breast MRI: for implants, lobular cancer, post-treatment assessment
• Musculoskeletal: cartilage, soft tissue, bone marrow lesions
• Brain/spinal cord: superior to CT for posterior fossa, cord lesions
• Perianal fistulae: MRI pelvis for fistula mapping
• Madura foot: extent of infection
Limitations: Time-consuming, expensive, claustrophobia, incompatible with pacemakers/metallic
implants, motion artefact, poor in acute trauma

5. Nuclear Medicine Imaging

Principles: Radioisotope-labelled tracers taken up by specific tissues; detect functional/metabolic
activity
Types:
• Bone scan (Tc-99m MDP): bone metastases (more sensitive than X-ray), osteomyelitis
• HIDA scan (hepatobiliary iminodiacetic acid): acute cholecystitis (no GB filling), bile leak, biliary
dyskinesia
• PET-CT (Positron Emission Tomography-CT): F18-FDG; staging and restaging of lymphoma,
colorectal, lung, head and neck cancers; detect occult metastases
• Sentinel node mapping: Tc-99m-labelled nanocolloid + blue dye for sentinel node biopsy in breast
cancer/melanoma
• MIBG scan: phaeochromocytoma, neuroblastoma
• VQ scan: pulmonary embolism
• Octreotide scan/Ga-68 PET: NETs (neuroendocrine tumours)

6. Interventional Radiology
• Angiography and embolisation: GI bleeding, trauma, hepatic artery embolisation for HCC
• TIPSS (Transjugular Intrahepatic Portosystemic Shunt): portal hypertension, refractory variceal
bleeding
• Thrombolysis and thrombectomy: acute limb ischaemia, PE
• Percutaneous drainage: abscess, biloma, pleural effusion
• Stenting: ureteric, biliary, oesophageal, colonic stents
• Endovascular aneurysm repair (EVAR): AAA
• TACE (Transarterial Chemoembolisation): HCC
16. UPPER GI ENDOSCOPY (OGD)
Definition
Upper GI Endoscopy (Oesophago-Gastro-Duodenoscopy – OGD) is a procedure using a flexible
fibreoptic or videoendoscope to visualise the oesophagus, stomach, and first two parts of the
duodenum. It is the most commonly performed therapeutic endoscopic procedure.

Indications
Diagnostic:
• Dyspepsia/upper abdominal pain not responding to empirical treatment
• Dysphagia, odynophagia
• Upper GI bleeding (haematemesis, melaena, iron-deficiency anaemia)
• Suspected peptic ulcer disease, GORD, Barrett's oesophagus
• Suspected malignancy (oesophageal, gastric)
• Surveillance: Barrett's oesophagus, post-gastric surgery (partial gastrectomy)
• Nausea, vomiting, unexplained weight loss
• Biopsy for H. pylori (CLO test), coeliac disease (duodenal biopsy)
Therapeutic:
• Haemostasis of upper GI bleeding (injection, thermocoagulation, clips, band ligation)
• Variceal banding (oesophageal varices) or injection sclerotherapy
• Polypectomy (gastric polyps)
• Dilatation of oesophageal strictures
• Stent insertion (malignant oesophageal obstruction)
• PEG (Percutaneous Endoscopic Gastrostomy) tube insertion
• Foreign body removal
• Endoscopic Mucosal Resection (EMR) and Endoscopic Submucosal Dissection (ESD) for early
cancers

Contraindications
Absolute:
• Recent MI or haemodynamic instability
• Perforated viscus (suspected/confirmed)
• Uncooperative patient (without anaesthesia)
Relative:
• Recent cardiac or thoracic surgery
• Large Zenker's diverticulum
• Severe coagulopathy (correct if possible)
• Cervical spine instability

Patient Preparation and Procedure

Preparation:
• Nil by mouth: 6 hours for solids, 2 hours for clear fluids
• Written informed consent
• IV access; pulse oximetry monitoring
• Throat spray (lignocaine) or IV sedation (midazolam ± fentanyl)
• Patient in left lateral decubitus position
• Mouthguard placed
Procedure:
• Scope introduced through oral cavity, oropharynx, past cricopharyngeus (C6) into oesophagus
• Oesophagus examined (cardia at ~40 cm from incisor teeth, GOJ at ~38–40 cm)
 • Retroflexion (J-manoeuvre) to view gastric cardia/fundus
• Duodenum examined to D2 (ampulla of Vater)
• Biopsies, interventions performed as needed
• Scope withdrawn with careful inspection

Endoscopic Assessment of Upper GI Bleeding

Rockall Score (predicts re-bleeding and mortality):
Variables scored: age, shock (HR, BP), comorbidity, diagnosis, endoscopic stigmata of recent
haemorrhage
Score ≤2: low risk; ≥5: high risk
Forrest Classification of Peptic Ulcer Bleeding:
• Ia: Active arterial spurting (highest risk of re-bleeding ~90%)
• Ib: Active oozing
• IIa: Non-bleeding visible vessel (~50% re-bleeding)
• IIb: Adherent clot
• IIc: Flat pigmented spot (~7% re-bleeding)
• III: Clean base (lowest risk ~3%)
Endoscopic therapy for Forrest Ia, Ib, IIa, IIb (dual therapy: injection + mechanical/thermal)

Complications of OGD
• Perforation: oesophageal perforation most serious (0.03–0.1%); higher with stricture dilatation,
therapeutic procedures
• Aspiration pneumonia
• Bleeding: significant only after therapeutic procedures
• Adverse reactions to sedation (respiratory depression, airway compromise)
• Infection: bacteraemia (rare, risk with biopsy)
• Hypoxia/cardiac events in elderly
• Mortality: <0.01% for diagnostic OGD
17. ENDOSCOPIC ULTRASOUND (EUS)
Definition
Endoscopic Ultrasound (EUS) combines upper GI endoscopy with high-frequency ultrasound
transducer at the tip of the endoscope to provide high-resolution images of the GI tract wall and
adjacent structures (pancreas, bile ducts, mediastinum, lymph nodes) from within the GI lumen.

Types
• Radial EUS: 360° circumferential view; primarily diagnostic
• Linear (curvilinear) EUS: sector view; essential for EUS-guided Fine Needle Aspiration (EUS-FNA)
• High-frequency mini-probes: for superficial mucosal/submucosal lesions
• Three-dimensional EUS: for fistula, sphincter assessment

Clinical Applications
• 1. Staging of GI Cancers:
• Oesophageal cancer: T-staging (most accurate for T1–T3), N-staging, FNA of suspicious nodes;
determines resectability
• Gastric cancer: T and N staging
• Rectal cancer: T and N staging (complementary to MRI)
• Pancreatic cancer: tumour visualisation, T and N staging, vascular invasion, FNA for cytology
• 2. Pancreatobiliary Disease:
• Chronic pancreatitis: parenchymal and ductal changes
• Pancreatic cysts: characterisation (serous vs mucinous); FNA for fluid analysis (CEA, amylase,
cytology)
• IPMN (Intraductal Papillary Mucinous Neoplasm): surveillance, risk stratification
• Choledocholithiasis: sensitivity >95% for CBD stones (comparable to MRCP, avoids ERCP in
negative cases)
• Biliary strictures: FNA for tissue diagnosis
• 3. Submucosal Lesions (SMTs):
• GIST (Gastrointestinal Stromal Tumour): hypoechoic mass in 4th layer (muscularis propria)
• Leiomyoma: homogeneous, hypoechoic, 2nd/3rd layer
• Carcinoid: 3rd layer (submucosal)
• Lipoma: hyperechoic, 3rd layer
• EUS helps distinguish layer of origin and echogenicity to characterise SMTs
• 4. EUS-Guided Fine Needle Aspiration (EUS-FNA):
• Pancreatic masses: cytological diagnosis; sensitivity 75–90%
• Lymph nodes (mediastinal, coeliac axis): staging
• Pancreatic cyst fluid analysis
• Liver lesions (left lobe)
• Adrenal lesions
• 5. Therapeutic EUS:
• EUS-guided coeliac plexus block/neurolysis: for pain in chronic pancreatitis/pancreatic cancer
• EUS-guided drainage of pancreatic pseudocysts and walled-off necrosis (WON)
• EUS-guided biliary drainage: when ERCP fails (rendezvous, hepaticogastrostomy,
choledochoduodenostomy)
• EUS-guided gastroenterostomy

Advantages and Limitations

Advantages:
• Superior soft tissue resolution for adjacent structures
• Real-time imaging during FNA/therapeutic procedures
 • No radiation
• Combined diagnostic + therapeutic in single session
Limitations:
• Operator-dependent (high learning curve: >150 cases for competency)
• Limited access: requires specialised endoscopy suite
• Cannot see beyond air/bone
• Interposition of gas/bone limits views
• Higher risk than standard OGD (perforation risk with Zenker's, post-surgical anatomy)
18. TUMOUR MARKERS
Definition
Tumour markers are substances (proteins, hormones, enzymes, receptors, or genetic material)
produced by tumour cells or by normal cells in response to tumour, which can be detected in blood,
urine, or tissue. They are used as an aid in cancer diagnosis, staging, monitoring treatment
response, and surveillance.

Ideal Tumour Marker Properties

• High sensitivity: detect all cases of the cancer (few false negatives)
• High specificity: positive only in cancer (few false positives)
• Correlates with tumour burden (aids monitoring)
• Early detection before clinical symptoms
• Simple, cheap, reproducible assay
• No ideal marker currently exists; used in combination with clinical/imaging findings

Classification and Clinical Surgical Tumour Markers

Marker Type Associated Cancers Uses and Notes
CEA Oncofetal glycoprotein Colorectal cancer Gold standard for CRC
(Carcinoembryonic (CRC), pancreas, monitoring; NOT for
Antigen) gastric, lung, breast screening; elevated in
smokers, cirrhosis,
IBD. Rising CEA post-
CRC surgery →
recurrence
AFP (Alpha- Oncofetal protein Hepatocellular AFP >400 ng/mL +
fetoprotein) carcinoma (HCC), hepatic mass → HCC;
germ cell tumours (yolk monitor treatment; also
sac) elevated in pregnancy,
hepatitis, cirrhosis
PSA (Prostate Specific Kallikrein-related serine Prostate cancer Screening and
Antigen) protease monitoring; elevated in
BPH, prostatitis,
urinary retention;
free:total PSA ratio
helps differentiate
CA 19-9 Sialylated Lewis blood Pancreatic cancer, Not specific; best for
group antigen biliary cancer, gastric monitoring treatment of
known pancreatic
cancer; elevated in
jaundice, pancreatitis
CA 125 Mucin glycoprotein Ovarian cancer Monitoring treatment;
(epithelial) elevated in
endometriosis, fibroids,
pregnancy, PID; ROMA
score with HE4
CA 15-3 MUC-1 antigen Breast cancer Monitoring metastatic
breast cancer; NOT for
screening or diagnosis
CA 72-4 TAG-72 mucin Gastric cancer, Best marker for gastric
colorectal, ovarian cancer (combined with
CEA)
 Marker Type Associated Cancers Uses and Notes
β-hCG (beta-hCG) Glycoprotein hormone Choriocarcinoma, Monitoring and
testicular non- diagnosis; elevated in
seminomatous GCT pregnancy
LDH Enzyme Testicular cancer (non- Staging/prognosis
specific), lymphoma, marker; non-specific
melanoma
Calcitonin Peptide hormone Medullary thyroid Diagnosis and
carcinoma (MTC) monitoring; stimulation
test for occult MTC
Thyroglobulin Protein Differentiated thyroid Post-thyroidectomy
cancer (PTC, FTC) monitoring for
recurrence (should be
undetectable)
Chromogranin A Protein Neuroendocrine Most sensitive NET
tumours (NETs) marker; elevated in PPI
use
5-HIAA (urinary) Serotonin metabolite Carcinoid tumours 24-hour urine
collection; elevated in
carcinoid syndrome
VMA/metanephrines Catecholamine Phaeochromocytoma Plasma metanephrines
(urinary/plasma) metabolites most sensitive
screening test
PLAP Alkaline phosphatase Seminoma Monitoring; elevated in
isoenzyme smokers
S-100, LDH, NSE Various Melanoma, Prognostic in
neuroblastoma melanoma; NSE in
neuroblastoma

Limitations of Tumour Markers

• No marker is 100% sensitive or specific
• Benign conditions elevate most markers
• Cannot be used for population screening (except PSA – controversial)
• Normal levels do not exclude cancer
• Need serial measurements (trend more important than single value)
• Inter-laboratory variation
• Best used in known cancer patients for monitoring
19. MOLECULAR DIAGNOSIS AND FINE NEEDLE ASPIRATION
CYTOLOGY (FNAC)
A. MOLECULAR DIAGNOSIS IN SURGERY
Molecular diagnostic techniques allow analysis of DNA, RNA, and proteins for diagnosis, staging,
prognosis, and treatment selection in surgical oncology and infectious diseases.

Polymerase Chain Reaction (PCR)

• In vitro amplification of specific DNA sequences
• Principle: denaturation → primer annealing → extension (repeated cycles)
• Uses: H. pylori detection, TB diagnosis, genetic mutations in cancer, infectious diseases
• RT-PCR (Real-Time PCR): quantitative; viral load measurement
• qPCR: real-time quantification
• Reverse Transcriptase PCR (RT-PCR): for RNA targets
• Clinical applications in surgery: detection of KRAS/BRAF mutations in colorectal cancer; HER2 gene
amplification in breast/gastric cancer; RET mutations in MEN2/MTC

Immunohistochemistry (IHC)
• Detects proteins in tissue sections using labelled antibodies
• Applications in surgical pathology:
- HER2/neu expression: breast cancer (guide trastuzumab therapy)
- ER/PR receptors: breast cancer (guide endocrine therapy)
- PD-L1: immunotherapy selection
- ALK, ROS1: NSCLC (guide targeted therapy)
- Ki-67: tumour proliferation index
- CD117 (c-kit): GIST (imatinib therapy)
- Calretinin, WT-1: mesothelioma
- Mismatch Repair (MMR) proteins (MLH1, MSH2, MSH6, PMS2): Lynch syndrome screening in
CRC

FISH (Fluorescence In Situ Hybridisation)

• Detects specific DNA sequences within chromosomes
• HER2 gene amplification: gold standard for equivocal IHC results
• BCR-ABL translocation (CML)
• N-myc amplification (neuroblastoma – poor prognosis)

Next Generation Sequencing (NGS)

• Massively parallel sequencing of multiple genes simultaneously
• Clinical applications: comprehensive genomic profiling of tumours; detect actionable mutations
(KRAS, NRAS, BRAF, EGFR, PIK3CA, BRCA1/2)
• Liquid biopsy: cell-free DNA (cfDNA)/circulating tumour DNA (ctDNA) from plasma – early
recurrence detection, monitoring treatment response, minimal residual disease

B. FINE NEEDLE ASPIRATION CYTOLOGY (FNAC)

Definition: FNAC is a minimally invasive diagnostic procedure in which cells are aspirated from a
lesion/mass using a fine needle (21–25 gauge) and syringe, and the aspirated material is examined
cytologically.

Indications
• Palpable or imaging-visible superficial lumps: thyroid, lymph nodes, breast, salivary glands, soft
tissue masses
 • Deep-seated lesions: under USS or CT guidance (liver, pancreas, retroperitoneum, lung)
• Neck swellings, thyroid nodules (TIRADS assessment)
• EUS-FNA for mediastinal, pancreatic, and perigastric lesions
• Bone lesions (under X-ray/CT guidance)

Technique
• No anaesthesia required for superficial lesions (topical EMLA for children)
• 21–23 gauge needle on 10–20 mL syringe
• Aspiration with negative pressure while moving needle back and forth within lesion
• Specimen expressed onto glass slide; smear preparation; immediate fixation (wet fix with alcohol for
Papanicolaou stain) or air-dried (for Giemsa/MGG stain)
• Liquid-based cytology (LBC): increasingly used
• USS-guidance for non-palpable/deep lesions
• Rapid On-Site Evaluation (ROSE): cytopathologist available in room for immediate adequacy
assessment

Reporting Systems
Thyroid (Bethesda System):
• I: Non-diagnostic/unsatisfactory
• II: Benign
• III: Atypia of undetermined significance (AUS/FLUS)
• IV: Follicular neoplasm/suspicious
• V: Suspicious for malignancy
• VI: Malignant
Breast (UK – B categories):
• B1: Inadequate
• B2: Benign
• B3: Uncertain malignant potential
• B4: Suspicious for malignancy
• B5: Malignant (B5a = in situ; B5b = invasive)

Advantages and Limitations of FNAC

Advantages:
• Minimally invasive (outpatient)
• Rapid (results in 24–48 hours with ROSE)
• Cheap, repeatable
• Can guide treatment before definitive surgery
• Wide applicability (superficial + deep)
• High sensitivity (80–95%) and specificity (85–99%) in experienced hands
Limitations:
• Cytology only – cannot assess architecture (architecture needed to distinguish follicular adenoma
from carcinoma in thyroid, or LCIS vs IDC in breast)
• Sampling error
• Requires experienced cytopathologist
• Cannot always distinguish between lymphoma subtypes
• Cannot assess grade of some tumours
20. LOCAL ANAESTHESIA
Definition and Mechanism
Local anaesthetics (LA) are drugs that reversibly block nerve conduction when applied locally, by
blocking voltage-gated sodium channels on nerve fibres, preventing depolarisation and action
potential propagation. They preferentially block smaller fibres first (pain and temperature) before
larger motor fibres.

Chemistry
• Structure: aromatic ring (lipophilic) – intermediate chain – amine group (hydrophilic)
• Two types based on intermediate chain:
- Amides (metabolised in liver): Lidocaine, Bupivacaine, Levobupivacaine, Ropivacaine, Prilocaine,
Mepivacaine
- Esters (hydrolysed by plasma cholinesterase): Cocaine, Procaine, Amethocaine/Tetracaine,
Benzocaine
• Ester allergies (paraaminobenzoic acid – PABA) do NOT cross-react with amides

Types of Local Anaesthesia

• 1. Topical (Surface) anaesthesia:
• EMLA cream (eutectic mixture: 2.5% lignocaine + 2.5% prilocaine): for venepuncture, FNAC in
children; applied 1 hour before
• Lignocaine spray 4–10%: throat (before OGD), urethral application
• Amethocaine gel (Ametop): paediatric venepuncture
• Cocaine 4–10%: nasal mucosa (also vasoconstrictive)
• 2. Infiltration anaesthesia:
• Injection into wound/incision site
• Used for: minor excisions, wound closure, biopsies
• Maximum dose: Lidocaine 3 mg/kg (plain), 7 mg/kg (with adrenaline)
• 3. Field block:
• Ring of LA injected around a surgical site
• Blocks all nerves entering the area
• 4. Nerve block (Regional nerve block):
• Injection adjacent to specific nerve trunk
• Examples: femoral nerve block, sciatic nerve block, brachial plexus block (axillary/supraclavicular
approach), digital nerve block, ankle block, penile block, intercostal nerve block
• 5. Epidural anaesthesia:
• Injection into epidural space; blocks nerve roots as they leave spinal cord
• Used in thoracic and abdominal surgery, labour
• Catheter inserted for continuous infusion
• 6. Spinal anaesthesia (subarachnoid block):
• Heavy bupivacaine 0.5% injected into CSF (subarachnoid space, L3-L4 or L4-L5)
• Dense, rapid onset block for lower abdominal/perineal/lower limb surgery
• Single shot only (cannot repeat)
• 7. Intravenous regional anaesthesia (Bier's block):
• Prilocaine (NOT lignocaine due to cardiac toxicity) into IV of bloodless limb maintained by tourniquet
• Upper limb surgery of ≤90 minutes
• Tourniquet must NOT be released for at least 20 minutes

Commonly Used Local Anaesthetic Agents

 Agent Type Onset Duration Max Max Dose Notes
Dose (+Adrenaline)
(plain)
Lidocaine Amide Rapid 1–2 h 3 7 mg/kg (500 Most commonly used;
(Lignocaine) (2–5 min) mg/kg mg) versatile
(200
mg)
Bupivacaine Amide Slow 4–8 h 2 2.5 mg/kg Most cardiotoxic; DO
(10–20 mg/kg (200 mg) NOT use for Bier's
min) (150 block
mg)
Levobupivacaine Amide Slow 4–8 h 2 – S-enantiomer of
mg/kg bupivacaine; less
(150 cardiotoxic
mg)
Ropivacaine Amide Moderate 3–6 h 3 – Less cardiotoxic;
mg/kg differential
(200 motor/sensory block
mg)
Prilocaine Amide Moderate 1–3 h 6 8 mg/kg (600 Drug of choice for
mg/kg mg) Bier's block; high dose
(400 →
mg) methaemoglobinaemia
Cocaine Ester Rapid 45–60 1.5 – Only LA with intrinsic
min mg/kg vasoconstriction; nasal
(150 use only; CNS
mg) stimulant

Vasoconstrictors (Adrenaline)
• Added to LA solutions (1:200,000 = 5 µg/mL)
• Benefits: reduces systemic absorption → increases duration of action (by 50–100%), reduces
bleeding, allows higher doses
• Contraindications to adrenaline-containing LA:
- End-arterial sites: fingers, toes, penis, nose, ear pinna (risk of ischaemic necrosis)
- Thyrotoxicosis, phaeochromocytoma
- MAO inhibitor use, tricyclic antidepressants
- Caution in cardiac disease (arrhythmias)

Side Effects and Complications

A. Local Complications:
• Haematoma: from vessel puncture
• Nerve damage: intraneural injection, compression
• Infection at injection site
• Tissue damage from ischaemia (adrenaline in end-arteries)
• Failure of block (inadequate spread, wrong technique)
B. Systemic Toxicity (Local Anaesthetic Systemic Toxicity – LAST):
Causes: inadvertent intravascular injection, excessive dose, rapid absorption
CNS toxicity (lower threshold than cardiac):
Early (excitatory): circumoral tingling, tinnitus, metallic taste, dizziness, confusion, visual disturbance
Later: agitation, tremors, convulsions
Severe: CNS depression, coma, respiratory arrest
Cardiovascular toxicity:
• Tachycardia → bradycardia
• Arrhythmias (ventricular fibrillation – especially bupivacaine)
• Hypotension → cardiovascular collapse
• Bupivacaine: most cardiotoxic (binds more tightly to Na-channels)
Management of LAST:
• 1. STOP injecting LA immediately
• 2. Call for help; 100% O₂ ; airway management
• 3. Treat seizures: benzodiazepines (IV midazolam/diazepam), thiopentone; avoid succinylcholine
4. 20% Intralipid (lipid emulsion therapy): 1.5 mL/kg IV bolus, then 15 mL/kg/hr infusion – sequesters
lipid-soluble LA; FIRST-LINE for severe LAST
• 5. CPR if cardiac arrest; standard ALS with modifications
• 6. Avoid vasopressin (ineffective in LA cardiac arrest)
• 7. Avoid beta-blockers, calcium channel blockers, lignocaine (as antiarrhythmic)
C. Allergic Reactions:
• True allergy: rare, mainly to ester agents (PABA)
• Anaphylaxis: urticaria, bronchospasm, anaphylactic shock
• Amide allergy: very rare; may be to preservative (metabisulphite)
• Vasovagal syncope often confused with allergy
D. Methaemoglobinaemia:
• Caused by prilocaine (o-toluidine metabolite) and benzocaine
• Cyanosis unresponsive to O₂
• Treatment: methylene blue 1–2 mg/kg IV
21. TOTAL PARENTERAL NUTRITION (TPN)
Definition
Total Parenteral Nutrition (TPN) is the delivery of all or most of a patient's caloric and nutritional
requirements via the intravenous route, bypassing the gastrointestinal tract. It is used when the
enteral route is unavailable, inadequate, or contraindicated.

Indications
• Non-functioning GI tract: prolonged ileus, short bowel syndrome, enterocutaneous fistula (high
output >500 mL/day), intestinal obstruction, radiation enteritis
• Conditions requiring bowel rest: severe pancreatitis (when EN not tolerated), Crohn's disease with
fistula (adjunct)
• Malabsorption: severe IBD, post-massive bowel resection
• Inability to meet nutritional requirements enterally: severe trauma, burns, cancer with nutritional
failure
• Pre-operative nutritional optimisation in severely malnourished patients (where delay of surgery
acceptable)
• Post-operative: when return of bowel function delayed >7–10 days

Contraindications
• Functioning GI tract (enteral nutrition preferred – "if the gut works, use it")
• Patient not expected to survive
• Short-term starvation (<5–7 days in otherwise well-nourished patient)
• Patient/family refusal
• Metabolically unstable (must be corrected first)

Components of TPN
Macronutrients:
• Carbohydrates (glucose/dextrose): major energy source; 4 kcal/g; 50–60% of total calories; given as
20–50% dextrose solutions
• Lipids (fat emulsion): 9 kcal/g; 30–40% of total calories; prevents essential fatty acid deficiency;
Intralipid (soya bean oil); no more than 1–2 g/kg/day; essential fatty acids (linoleic, linolenic)
• Amino acids (protein): 4 kcal/g; 0.8–1.5 g/kg/day (up to 2 g/kg/day in critically ill/burns); standard
solutions contain essential + non-essential AAs
Micronutrients:
• Electrolytes: Na, K, Cl, Mg, Ca, phosphate (daily requirements individualised)
• Vitamins: fat-soluble (A, D, E, K) and water-soluble (B complex, C); vitamin K must be monitored
(affects warfarin)
• Trace elements: Zn, Cu, Mn, Se, Cr, Mo, I
• Water: approximately 30–35 mL/kg/day
Energy requirements:
• Standard: 25–30 kcal/kg/day (non-protein calories)
• Critically ill: 20–25 kcal/kg/day (permissive underfeeding to avoid complications)
• Harris-Benedict equation or indirect calorimetry to determine needs

Route of Administration
Central Venous Access (required for standard TPN):
• Hyperosmolar solutions (>900 mOsm/L) must be given via central vein
• Routes: subclavian vein (lowest infection risk), internal jugular, femoral (highest infection risk),
peripherally inserted central catheter (PICC)
• Dedicated TPN lumen (not for blood sampling or other drugs)
Peripheral Parenteral Nutrition (PPN):
 • Lower osmolarity solutions (<800 mOsm/L)
• For short-term use only (<7–10 days)
• Risk of thrombophlebitis
• Cannot meet full nutritional requirements

Complications of TPN
A. Access-related:
• Pneumothorax, haemothorax (during CVP insertion)
• Air embolism
• Catheter misplacement, arterial puncture
• Thrombosis
B. Infectious:
• Catheter-related bloodstream infection (CRBSI): most common serious complication
- Coagulase-negative Staphylococci most common
- Management: remove catheter, blood cultures, IV antibiotics
• Line sepsis: fever, rigors, positive blood cultures from line
C. Metabolic:
• Hyperglycaemia: most common metabolic complication (stress response + glucose load); monitor
blood glucose 6-hourly; insulin sliding scale; target 6–10 mmol/L
• Hypoglycaemia: on sudden discontinuation of TPN; always taper
• Electrolyte imbalances: hypokalaemia, hypophosphataemia, hypomagnesaemia
• Refeeding syndrome: dangerous complication in severely malnourished patients (see below)
• Uraemia (excessive amino acids)
• Hyperlipaemia (excessive lipid infusion)
D. Hepatic:
• TPN-associated liver disease: steatosis, cholestasis, steatohepatitis; biliary sludge (lack of enteral
stimulation)
• Abnormal LFTs (raised ALP, GGT): common, usually reversible on cessation
• Severe: hepatic fibrosis, cirrhosis (long-term TPN)
E. Refeeding Syndrome:
• Occurs in severely malnourished patients when nutrition rapidly reintroduced
• Pathophysiology: increased insulin release → cellular uptake of phosphate, potassium, magnesium
→ severe hypophosphataemia, hypokalaemia, hypomagnesaemia
• Effects: cardiac arrhythmias, respiratory failure, haemolytic anaemia, neuromuscular dysfunction,
seizures, death
• Prevention: identify at-risk patients (BMI <18.5, negligible intake >5 days, history of
alcohol/malnutrition); start at 10 kcal/kg/day and increase slowly over 4–7 days; thiamine 200–300
mg before starting feeding; replace electrolytes proactively

Monitoring
Daily: blood glucose, fluid balance, electrolytes (Na, K, Cl, HCO₃ , urea, creatinine, Ca, Mg,
phosphate)
Weekly: LFTs, albumin, TFTs, FBC, coagulation, zinc, selenium, trace elements, weight
Periodic: bone mineral density (long-term TPN), visual inspection of central line
22. DAY CARE SURGERY (DAY SURGERY / AMBULATORY SURGERY)
Definition
Day care surgery (ambulatory surgery) refers to planned surgical procedures performed on patients
who are admitted, operated upon, and discharged on the same calendar day (within 12–23 hours),
without an overnight hospital stay.

Advantages
For patients:
• Less psychological distress (own familiar environment for recovery)
• Lower risk of hospital-acquired infections
• Faster return to normal activities
• Greater patient convenience and satisfaction
For the healthcare system:
• Reduced hospital bed utilisation
• Cost-effective (40–50% cheaper than inpatient)
• Increased surgical throughput
• Reduced waiting lists

Patient Selection Criteria

Surgical criteria:
• Duration: operation <90 minutes to 2 hours
• Blood loss minimal, blood transfusion unlikely
• Procedure allows adequate pain control with oral analgesics
• Post-operative fluid intake must be possible orally
• No major risk of post-operative complications requiring urgent medical intervention
Patient criteria:
• ASA grade I, II, or selected ASA grade III
• Age: no strict age limit (paediatric and elderly with caution)
• BMI: ideally <35 kg/m² (obese patients require careful assessment)
• Social criteria (essential):
- Responsible adult must accompany patient home
- Responsible adult must remain with patient for 24 hours post-op
- Patient must live within reasonable distance of hospital (within 1 hour)
- Telephone access at home
- Patient comprehends aftercare instructions

Contraindications to Day Surgery

• Poorly controlled systemic disease (ASA IV/V)
• Obstructive sleep apnoea with CPAP requirements (relative)
• Morbid obesity (BMI >40) – relative
• Patient lives alone without carer
• Inability to understand post-operative instructions
• No telephone access
• Procedures with high risk of major bleeding, airway complications
• Poorly controlled diabetes, hypertension, COPD
• Prior anaphylaxis to anaesthesia

Common Day Surgery Procedures

General surgery:
 • Inguinal/femoral/umbilical hernia repair
• Laparoscopic cholecystectomy (selected)
• Haemorrhoidectomy, anal fissure surgery, anal fistula (simple)
• Excision of skin lesions, lipomas
• Breast biopsy, wide local excision
• Varicose vein surgery
• Laparoscopic appendicectomy (selected)
• Pilonidal sinus surgery
Urology:
• Cystoscopy, bladder biopsy
• TURBT, circumcision, orchidopexy, vasectomy
Orthopaedic:
• Knee arthroscopy, carpal tunnel release, trigger finger
Ophthalmology:
• Cataract surgery, strabismus correction
ENT:
• Tonsillectomy, adenoidectomy, myringotomy, septoplasty

Pre-operative Assessment
• Detailed history and physical examination at pre-assessment clinic (weeks before surgery)
• Investigations as required: ECG, FBC, U&E, coagulation (based on age and comorbidities, not
routine)
• Anaesthetic assessment: choice of GA, regional, or LA
• Medication review (anticoagulants, diabetic medications)
• Fasting instructions: 6h solid food, 2h clear fluids
• Patient information leaflet: expectations, aftercare instructions

Discharge Criteria (Post-operative)

Must meet all criteria before discharge:
• Stable vital signs for at least 1 hour
• Alert and orientated
• Adequate pain control with oral analgesics
• Nausea/vomiting controlled
• Voided urine (mandatory for urological procedures and spinal anaesthesia)
• Wound dry, no excessive bleeding
• Able to take oral fluids
• Responsible adult present for escort
• Written post-operative instructions given
• Out-of-hours contact number provided
23. LIVER TRAUMA AND SPLENIC INJURY
LIVER TRAUMA
The liver is the most commonly injured abdominal organ in blunt abdominal trauma (20–25% of all
abdominal injuries) and the second most common in penetrating trauma (after small bowel).

Mechanism of Injury
• Blunt trauma: RTA (most common), falls, direct blows, sports injuries (right lobe injured due to its
size and location)
• Penetrating trauma: stab wounds, gunshot wounds
• Iatrogenic: liver biopsy, hepatic artery catheterisation

AAST Liver Injury Scale (Grading)

Grade Injury Description Management
I Haematoma: subcapsular, Non-operative management
<10% surface area OR (NOM) if stable
Laceration: capsular tear, <1 cm
depth
II Haematoma: subcapsular, 10– NOM if stable
50% surface area /
intraparenchymal <10 cm
diameter OR Laceration: 1–3
cm depth, <10 cm length
III Haematoma: subcapsular >50% NOM if haemodynamically
or expanding, ruptured stable; angioembolisation for
subcapsular / intraparenchymal ongoing bleed
>10 cm OR Laceration: >3 cm
depth
IV Laceration: parenchymal Often operative;
disruption 25–75% of a hepatic angioembolisation for selected;
lobe OR Vascular: juxtahepatic damage control
venous injuries
V Laceration: parenchymal Operative; damage control
disruption >75% of hepatic lobe surgery; very high mortality
OR Vascular: hepatic
venous/IVC injury (retrohepatic)
VI Hepatic avulsion Near 100% mortality

Clinical Features of Liver Trauma

• Hypotension, tachycardia (haemodynamic instability)
• Right upper quadrant tenderness, guarding
• Peritonism if haemoperitoneum
• Right shoulder tip pain (referred from diaphragmatic irritation – Kehr's sign, positive when right
shoulder)
• Signs of chest injury (lower right rib fractures)
• FAST: free fluid in hepatorenal space (Morison's pouch)
• CT abdomen with contrast: definitive assessment of grade and active extravasation

Management of Liver Trauma

Non-Operative Management (NOM) – preferred in haemodynamically stable patients:
• Suitable for >90% of blunt liver injuries (Grades I–III, selected IV)
 • Criteria: haemodynamic stability, no peritoneal signs, absence of associated bowel injury, CT
demonstrates injury grade
• Intensive monitoring: ICU/HDU, serial haematocrit
• Bed rest for 24–48 hours
• Angiography ± embolisation: for Grades III–IV with active contrast extravasation on CT ("blush")
Operative Management – for haemodynamically unstable patients:
• Indications: haemodynamic instability despite resuscitation, peritonism, associated injury requiring
surgery, failure of NOM
• Damage control surgery (DCS) principles:
- Control haemorrhage (hepatotomy with direct suture ligation, Pringle manoeuvre – compresses
hepatoduodenal ligament for up to 60 minutes of warm ischaemia)
- Perihepatic packing (most important manoeuvre)
- Control bile duct injury
- Temporary abdominal closure (TAC/laparostomy)
- ICU resuscitation (correct coagulopathy, hypothermia, acidosis)
- Re-look at 24–48 hours for definitive repair and pack removal
• Anatomical resection: rarely performed in emergency; for lobar devascularisation
• Juxtahepatic venous injuries: extremely high mortality; atriocaval shunt or total hepatic vascular
isolation
Complications:
• Bile leak/biloma: CT-guided drainage; ERCP + stenting
• Haemobilia: angioembolisation
• Hepatic artery pseudoaneurysm: angioembolisation
• Liver abscess: drainage
• Haemorrhage: delayed rupture of haematoma
• Post-traumatic hepatic failure

SPLENIC INJURY
The spleen is the most commonly injured solid organ in blunt abdominal trauma. Splenic rupture is
a surgical emergency.

Mechanism
• Blunt trauma: RTA, falls, sports injuries, assault (left lower rib fractures suggest splenic injury)
• Penetrating trauma: knife, gunshot wounds
• Pathological rupture: splenomegaly (malaria, infectious mononucleosis, leukaemia, portal
hypertension) – may rupture with minor trauma

AAST Splenic Injury Scale (Grading)

Grade Injury Description NOM Success Rate
I Haematoma: subcapsular <10% >95%
surface area OR Laceration:
capsular tear <1 cm depth
II Haematoma: subcapsular 10– ~90%
50%, intraparenchymal <5 cm
OR Laceration: 1–3 cm depth,
not involving trabecular vessels
III Haematoma: subcapsular >50% ~75%
or expanding, intraparenchymal
>5 cm or expanding OR
Laceration: >3 cm depth or
involving trabecular vessels
 Grade Injury Description NOM Success Rate
IV Laceration: involving segmental ~50%
or hilar vessels producing major
devascularisation (>25%)
V Completely shattered spleen <25%; usually operative
OR Hilar vascular injury with
devascularised spleen

Clinical Features of Splenic Injury

• Left upper quadrant pain and tenderness
• Left shoulder tip pain – Kehr's sign (referred pain from diaphragmatic irritation of blood –
pathognomonic of haemoperitoneum)
• Signs of haemorrhagic shock
• Ballance's sign: fixed dullness in left flank, shifting dullness in right flank (haemoperitoneum with
blood pooling)
• Left lower rib fractures (10th, 11th, 12th ribs)
• FAST: free fluid in splenorenal recess and Morrison's pouch
• CT abdomen: definitive staging; "blush" = active extravasation

Management of Splenic Injury

Non-Operative Management (NOM) – preferred in all ages:
• Haemodynamically stable patients → NOM (applicable to 80–90% of blunt splenic trauma)
• Grades I–III: NOM with close monitoring; angioembolisation for active blush
• Grade IV–V: selected patients with angioembolisation + intensive monitoring
• Advantages of spleen preservation: avoids overwhelming post-splenectomy infection (OPSI)
• Failure of NOM (~10%): persistent haemodynamic instability, falling Hb requiring >4 units blood in
24h, peritoneal signs → operative management
Angiography and Embolisation:
• Splenic artery embolisation: main splenic artery (proximal) or selective (distal) for active blush on CT
• Increases NOM success rate for Grades III–V
Operative Management:
• Splenorrhaphy (repair): Grades I–III; suture repair, argon beam coagulator, mesh wrap, haemostatic
agents
• Splenectomy: Grades IV–V, failed repair, haemodynamic instability
• Laparoscopic splenectomy: in stable patients with delayed splenic rupture or Grade I–II
Splenectomy Complications:
• Overwhelming Post-Splenectomy Infection (OPSI): Streptococcus pneumoniae (most common),
Neisseria meningitidis, Haemophilus influenzae; presents as fulminant septicaemia; mortality 50–
80%
• Prevention: vaccinations (pneumococcal, meningococcal, H. influenzae type b) – ideally 2 weeks
before elective splenectomy, 14 days after emergency; lifelong penicillin prophylaxis (amoxicillin 250
mg OD); medic alert bracelet; patient education
• Subphrenic abscess
• Pancreatic tail injury (iatrogenic)
24. GLASGOW COMA SCALE (GCS)
Definition and History
The Glasgow Coma Scale (GCS) is a standardised neurological assessment tool developed by
Teasdale and Jennett in 1974 at the University of Glasgow, used to objectively quantify the level of
consciousness in patients with brain injury. It provides a reliable, reproducible measure of conscious
level by assessing three components: eye opening, verbal response, and motor response.

Components of GCS
Component Response Score
Eye Opening (E) Spontaneous 4
To voice/speech 3
To pain 2
None 1
Verbal Response (V) Orientated (time, place, person) 5
Confused (conversational 4
speech, disoriented)
Inappropriate words (random 3
words)
Incomprehensible sounds 2
(moaning, groaning)
None 1
Motor Response (M) Obeys commands 6
Localises to pain 5
Withdraws from pain (normal 4
flexion)
Abnormal flexion (decorticate – 3
wrist/elbow flexion)
Extensor posturing (decerebrate 2
– extension/pronation)
None 1

Scoring Interpretation
• Minimum score: 3 (deeply unconscious/dead)
• Maximum score: 15 (fully conscious)
• Expressed as total (e.g., GCS 9/15) and components (e.g., E3V3M3)
• Always document components individually, not just total score
• Mild head injury: GCS 13–15
• Moderate head injury: GCS 9–12
• Severe head injury: GCS ≤8 (define coma – requires intubation and mechanical ventilation)
• Vegetative state: GCS 3–5 (no command following; may have eye opening cycles)
• Threshold for intubation: GCS ≤8 (unconscious, cannot protect airway)

Assessment Guidelines
Eye opening:
• Assess with eyes closed, speak to patient, if no response apply pain stimulus (sternal rub,
supraorbital pressure, nail bed pressure)
 • Document if eyes closed due to swelling (C for closed) or intubated (T for tube)
Verbal response:
• Orientated = knows name, location, date
• If intubated: record as 'T' (e.g., E4VTM6 = GCS 11T)
• Dysphasic patients: document accordingly
Motor response:
• Best arm response recorded (not leg)
• Pain stimuli: central (sternal rub/supraorbital) for eye and verbal; peripheral (nail bed) for motor
• Localising pain: arm reaches above the clavicle (chin level) in response to supraorbital pressure

Limitations
• Intubation prevents verbal assessment (use E+M with notation)
• Periorbital oedema prevents eye opening assessment
• Sedation and paralytic agents alter responses
• Not validated for children under 5 (paediatric GCS/children's GCS modified)
• Does not assess brainstem reflexes (requires FOUR score or additional neuro assessment)
• Inter-rater variability
• Cannot differentiate different causes of unconsciousness

Paediatric GCS
Modified for children <5 years – verbal component altered:
• 5: smiles, follows/localises, vocalises (age-appropriate)
• 4: cries but consolable, inappropriate interaction
• 3: inconsistently consolable, moaning
• 2: inconsolable, agitated
• 1: no response

Clinical Applications
• Triage of head-injured patients (mild/moderate/severe)
• Indication for airway management (intubation if GCS ≤8)
• Monitoring neurological progress (serial GCS)
• Prognosis prediction (GCS at 6h, 24h post-injury correlates with outcome)
• Scoring systems: GCS used in APACHE II, SOFA, Trauma Score, Revised Trauma Score (RTS)
25. LE FORT'S CLASSIFICATION OF MIDFACE FRACTURES
Historical Background
René Le Fort, a French surgeon, described his classification of midface (midfacial) fractures in 1901,
based on cadaveric experiments using blunt trauma. He identified three horizontal planes of
weakness in the midface. These fractures result from severe blunt trauma to the mid-face (road
traffic accidents, assaults, sports injuries).

Anatomy of Le Fort Fractures

All Le Fort fractures involve the pterygoid plates of the sphenoid bone (a key landmark – if pterygoid
plates are not fractured, it is NOT a Le Fort fracture). The fractures are named in increasing severity
and level.

Le Fort I (Horizontal / Guérin Fracture)

• Level: Transverse fracture at the level of the nasal floor and base of the maxillary sinuses
• The entire lower maxilla (dental alveolus) separates from the face
• Fracture line passes through: anterior nasal spine, lateral nasal walls, maxillary sinuses, pterygoid
plates
• Floating palate: upper dental arch movable independently from facial skeleton
• Clinical features: swelling of upper lip, malocclusion (anterior open bite), step deformity of upper jaw,
floating palate on bimanual examination, epistaxis, subconjunctival haemorrhage absent (below
orbit)
• Management: ORIF, maxillomandibular fixation (MMF)

Le Fort II (Pyramidal Fracture)

• Level: Triangular/pyramidal shaped fracture through midface
• Fracture line: across nasal bones → medial orbital walls → floor of orbit → zygomaticomaxillary
junction → pterygoid plates
• The entire central midface (central pyramid) moves as a unit (nose, maxilla, palate)
• Clinical features: bilateral periorbital ecchymosis ("racoon/panda eyes"), facial swelling and
flattening, gross nasal oedema, epistaxis, CSF rhinorrhoea (if cribriform plate also fractured),
malocclusion, infraorbital nerve paraesthesia, subconjunctival haemorrhage (posterior extent)
• Management: ORIF (titanium plates)

Le Fort III (Craniofacial Dysjunction)

• Level: Complete separation of the entire face from the cranial base
• Fracture line: zygomatic arches → lateral orbital walls → orbital floors → ethmoid sinuses → nasal
root → pterygoid plates → crosses nasofrontal suture
• Entire facial skeleton separates from skull as single unit (craniofacial dysjunction)
• Clinical features: "dishface" deformity (elongated, flat face), gross periorbital ecchymosis, bilateral
subconjunctival haemorrhage, CSF rhinorrhoea, massive facial oedema, total malocclusion,
hypophthalmos, Battle's sign if temporal bone involved, massive haemorrhage (from sphenopalatine
artery)
• Management: ORIF; maxillomandibular fixation; may need combined craniofacial approach

Summary Comparison
Feature Le Fort I Le Fort II Le Fort III
Level Low (alveolus) Mid (pyramidal) High (craniofacial)
What moves Lower maxilla/palate Central midface Entire face
Nose involved No Yes Yes
Orbit involved No Floor/medial wall Entire orbit
Zygomatic arch No No Yes (fractured)
 Feature Le Fort I Le Fort II Le Fort III
CSF rhinorrhoea Rare Possible Common
Periorbital bruising No Yes (panda eyes) Yes (severe)
Pterygoid plates Yes Yes Yes (always)

Management Principles
Emergency:
• ATLS priorities (ABCDE): airway often compromised (blood, oedema, posterior displacement of
palate)
• Awake fibreoptic intubation or surgical airway (tracheostomy) may be needed
• Control haemorrhage: pressure packing, angioembolisation for severe arterial bleeding
• Rule out C-spine injury (force required to cause Le Fort fractures)
• Treat associated injuries: orbital, nasal, mandible, skull base fractures
Definitive:
• Open Reduction and Internal Fixation (ORIF) with titanium miniplate systems
• Maxillomandibular fixation (MMF) to restore occlusion
• Timing: ideally within 5–10 days before oedema subsides and fibrous union begins
• Involve: maxillofacial/plastics surgery, ophthalmology, neurosurgery
26. TRIAGE
Definition and Origin
Triage (from French trier = to sort) is the process of rapidly sorting and prioritising patients according
to the severity of their injuries or illnesses, especially during mass casualty incidents (MCIs) or
emergency situations, to maximise the number of survivors and ensure optimal use of limited
resources. Developed by Dominique Jean Larrey, Napoleon's chief surgeon.

Principles of Triage
• Maximise total number of survivors (not save the most critically injured at expense of many
salvageable)
• Allocate resources to those who will most benefit
• Decisions based on clinical assessment, not social factors
• Reassess dynamically (triage is not static – patient condition changes)
• Delegate triage to experienced personnel

Types of Triage
• 1. Hospital triage (Emergency Department): daily triage for non-MCI situations
• 2. Field triage: at scene of MCI before hospital
• 3. Medical/Military triage: in austere/combat environments
• 4. Reverse triage: in chemical/biological incidents (most contaminated treated first to prevent spread)

Triage Sieve (Field Triage – Primary Triage)

Quick initial sort at scene using simple assessment (<30 seconds per patient):
Step 1: Can patient walk? → Yes → MINOR (Green, T3)
Step 2: Is patient breathing? → No → Reposition airway → If not breathing → EXPECTANT (Black)
[or DEAD]
Step 3: Respiratory rate → <10 or >30 breaths/min → IMMEDIATE (Red, T1)
Step 4: Capillary refill time (CRT) → >2 seconds OR radial pulse absent → IMMEDIATE (Red, T1)
All others → URGENT (Yellow, T2)

Triage Sort (Secondary Triage)

More detailed assessment for prioritisation:
Based on Revised Trauma Score (RTS):
• Respiratory rate
• Systolic blood pressure
• Glasgow Coma Scale (GCS)
Each scored 0–4; combined score 0–12
RTS <12 → further prioritisation

Triage Categories
Priority Colour Category Description Examples
T1 (P1) Red IMMEDIATE Life-threatening Airway
injuries, compromise,
salvageable; treat tension
first pneumothorax,
major
haemorrhage,
haemodynamic
instability
 Priority Colour Category Description Examples
T2 (P2) Yellow URGENT Serious injuries, Open fractures,
stable; can wait moderate burns,
1–2 hours closed abdominal
injury
T3 (P3) Green MINOR / Walking Minor injuries; can Minor lacerations,
Wounded wait 4+ hours; sprains, minor
help themselves burns
T4 / Expectant Blue/Black EXPECTANT / Unsurvivable GCS 3, massive
DELAYED injuries given burns >90%,
available decapitation,
resources OR cardiopulmonary
dead arrest with
asystole

START Triage System (USA)

Simple Triage and Rapid Treatment:
• Step 1: Walking? → Green (Minor)
• Step 2: Breathing? → No → Reposition airway → No = Black (Dead); Yes = Red (Immediate)
• Step 3: RR → >30 = Red (Immediate); <30 → Step 4
• Step 4: Radial pulse/CRT → Absent/>2s = Red; Present → Step 5
• Step 5: Mental status → Follows commands = Yellow (Delayed); Cannot = Red (Immediate)

Hospital Major Incident Declaration – METHANE

Mnemonic for reporting a major incident:
• M – Major incident declared
• E – Exact location
• T – Type of incident (explosion, RTA, flood)
• H – Hazards present or potential
• A – Access routes (to scene)
• N – Number and severity of casualties
• E – Emergency services present and required

Paediatric Triage
• JumpSTART: Modified START for children <8 years
• Children have different physiological parameters (RR, BP, HR)
• Special considerations: difficult IV access, higher hypothermia risk, different drug doses
• SALT Triage (Sort, Assess, Lifesaving interventions, Treatment/Transport): more comprehensive
27. DAMAGE CONTROL SURGERY (DCS)
Definition
Damage Control Surgery (DCS) is an abbreviated, staged surgical approach where the initial
operation is limited to controlling haemorrhage and contamination, with definitive repair deferred to
a second or subsequent operation after physiological resuscitation in the ICU. The term was adapted
from the US Navy's strategy of keeping a damaged ship operational until definitive repairs can be
made.

Rationale – The Lethal Triad

DCS is indicated to break the "lethal triad" or "trauma triad of death":
• 1. Hypothermia (core temperature <35°C): impairs coagulation, cardiac function, drug metabolism
• 2. Acidosis (pH <7.35): impairs coagulation, myocardial contractility; from poor tissue perfusion/lactic
acidosis
• 3. Coagulopathy (dilutional, consumptive, hypothermia-induced): perpetuates haemorrhage
These three form a vicious cycle: haemorrhage → acidosis + hypothermia → coagulopathy → more
haemorrhage

Phases of Damage Control Surgery

Phase 0 – Damage Control Resuscitation (DCR) / Pre-hospital:
• Controlled haemorrhage before surgery
• Tourniquets, wound packing (haemostatic dressings – QuikClot, Combat Gauze)
• Permissive hypotension (target SBP 80–90 mmHg in penetrating; MAP >50 in blunt) until surgical
haemostasis
• Tranexamic acid within 3 hours
• Damage control resuscitation: 1:1:1 pRBC:FFP:Platelets
Phase 1 – Initial Abbreviated Operation:
Performed within "Golden Hour"; limited to 60–90 minutes maximum:
• Haemorrhage control:
- Direct pressure, packing (liver, retroperitoneum, pelvis)
- Vascular shunts for major vascular injuries (allows distal perfusion, definitive repair later)
- Ligation of smaller vessels
- Pringle manoeuvre (hepatoduodenal ligament compression for liver)
• Contamination control:
- Staple or clamp bowel (no anastomosis at this stage)
- Rapid suture of gastric/colon perforations with stapler
- NOT primary bowel anastomosis
• Temporary abdominal closure (TAC):
- Laparostomy – abdomen left open to prevent abdominal compartment syndrome
- Bogota bag, vacuum-assisted closure (VAC/NPWT)
Phase 2 – ICU Resuscitation (6–48 hours):
• Correct physiological derangements:
- Warm the patient (target >36°C): warming blankets, warm IV fluids, warm operating theatre
- Correct acidosis: adequate resuscitation, lactate clearance
- Correct coagulopathy: FFP, cryoprecipitate, platelets, factor concentrates (PCC, rFVIIa in
refractory)
- Correct hypothermia
• Ventilatory support, vasopressors if needed
• Monitor for abdominal compartment syndrome (target bladder pressure <20 mmHg)
 • Serial monitoring: lactate, ABG, coagulation
Phase 3 – Definitive Surgery (24–72 hours when stable):
• Restore physiology confirmed: temperature >36°C, pH >7.35, INR <1.5, lactate <2 mmol/L, urine
output adequate
• Pack removal
• Definitive vascular repair (take down shunts, perform anastomoses)
• Bowel anastomosis or stoma formation
• Abdominal closure (direct closure or planned hernia if too tense)

Indications for DCS

• pH <7.30 at start of operation
• Temperature <35°C
• Estimated blood loss >10 units pRBCs
• Coagulopathy (INR >1.5, PT >16s)
• Lethal associated injuries (traumatic brain injury, multiple long bone fractures)
• Inability to achieve haemostasis with conventional methods
• Complex anatomical injury (juxtahepatic venous, retrohepatic IVC, iliac vessel injury)
• Inaccessible major venous injury
• Anticipated prolonged operative time in unstable patient

DCS in Specific Situations

DCS Abdomen (most common):
• Damage Control Laparotomy as described above
• Abdominal compartment syndrome: monitor bladder pressure; fasciotomy of abdomen
DCS Orthopaedics:
• Temporary external fixation of long bone/pelvic fractures
• Definitive fixation deferred until stable
• Pelvic binder/clamp for pelvic ring injuries
DCS Thoracic:
• Emergency thoracotomy (resuscitative thoracotomy)
• Lung clamping (whipstitch) rather than lobectomy
• Pulmonary tractotomy
• Vascular shunts to major pulmonary vessels
DCS Vascular:
• Temporary intravascular shunts (Argyle, Javid shunts) to restore distal flow
• Definitive vascular repair at re-look surgery

Damage Control Resuscitation (DCR) Principles

• Haemostatic resuscitation: 1:1:1 ratio (pRBC:FFP:Platelets) → MTP (Massive Transfusion Protocol)
• Minimise crystalloid use (crystalloids worsen coagulopathy and acidosis, cause abdominal
compartment syndrome)
• Tranexamic acid (TXA): 1g IV within 3 hours of injury (CRASH-2 trial); repeat 1g over 8 hours
• Permissive hypotension: SBP 80–90 mmHg until surgical haemostasis
• Calcium supplementation with blood products (citrated blood chelates calcium)
• Hypothermia prevention: warm environment, warm fluids, bair hugger
29. ENHANCED RECOVERY AFTER SURGERY (ERAS) / FAST-TRACK
SURGERY
Definition
Enhanced Recovery After Surgery (ERAS) – also known as Fast-Track Surgery or Enhanced
Recovery Programmes (ERP) – is a multimodal, evidence-based perioperative care pathway
designed to reduce surgical stress, maintain physiological function, and accelerate postoperative
recovery, thereby reducing hospital stay and complications. Developed by Professor Henrik Kehlet
(Copenhagen) in the 1990s.

Goals of ERAS
• Reduce the physiological and psychological stress of surgery
• Maintain homeostasis perioperatively
• Reduce post-operative complications
• Shorten hospital length of stay
• Improve patient outcomes and satisfaction
• Reduce costs

ERAS Pathway – Perioperative Components

PREOPERATIVE:
• Pre-assessment clinic: identify and optimise comorbidities, provide education/counselling
• Patient education: written/verbal information about the process and expectations
• Prehabilitation: exercise, smoking cessation, alcohol reduction (4+ weeks before)
• Nutritional optimisation: oral nutritional supplements if malnourished (2 weeks before)
• Carbohydrate loading: clear carbohydrate drink (12.5% CHO) 2 hours before surgery → reduces
insulin resistance, reduces catabolism, improves patient well-being
• Fasting: clear fluids until 2 hours pre-op; solids until 6 hours pre-op (NOT extended fast)
• Avoidance of prolonged fasting (reduces catabolic stress response)
• Bowel preparation: selective use only (no routine bowel prep in colorectal surgery)
• Antibiotic prophylaxis: single dose 30–60 minutes before incision
• DVT prophylaxis: LMWH preoperatively and continued postoperatively
INTRAOPERATIVE:
• Anaesthetic technique:
- Short-acting agents (propofol TIVA or sevoflurane)
- Epidural or spinal anaesthesia (reduces opioid requirement, blunts stress response)
- Spinal anaesthesia ± spinal opioids for colonic surgery
• Multimodal analgesia (opioid-sparing): paracetamol, NSAIDs/COX-2 inhibitors, local anaesthetic
infiltration, wound catheters, TAP block, ketamine
• Minimally invasive surgery: laparoscopic approach reduces surgical stress, pain, ileus
• Avoid hypothermia: warming blanket (Bair Hugger), warm IV fluids, warm theatre
• Goal-directed fluid therapy: balanced crystalloids; avoid fluid overload (causes oedema, ileus); avoid
fluid deficit; use cardiac output monitoring (LiDCO, Flo-Trac) to guide
• Avoid prolonged nasogastric tubes (remove before extubation if used)
• Avoid routine surgical drains (or remove early)
• Avoid excessive opioid use intraoperatively
POSTOPERATIVE:
• Multimodal analgesia: paracetamol + NSAIDs (regular) + LA (wound infiltration, epidural, nerve
blocks) ± gabapentin; minimise opioids (cause ileus, nausea, sedation)
• Early mobilisation: out of bed Day 0 or Day 1; physiotherapy; minimum 2 hours sitting out/day
• Early oral feeding: clear fluids within 2–4 hours of surgery; normal diet Day 1; ileus prevented by
avoiding opioids and excess fluids
 • Anti-emetics: PONV prophylaxis (ondansetron, dexamethasone, metoclopramide)
• Early removal of urinary catheter (Day 1 for colorectal surgery)
• VTE prophylaxis: LMWH + TED stockings + early mobilisation
• Euglycaemia: target blood glucose 6–10 mmol/L
• Discharge planning: set criteria-based discharge (tolerating oral diet, adequate analgesia, mobile);
not based on number of days

Evidence for ERAS

• Systematic reviews and meta-analyses demonstrate:
- 30–50% reduction in hospital length of stay
- Reduction in post-operative complications by 20–30%
- No increase in readmission or mortality
- Faster return to normal activities
- Patient satisfaction maintained or improved
• Best evidence in: colorectal surgery, hip/knee replacement, cardiac surgery, hepatopancreatobiliary
surgery
• ERAS Society guidelines published for multiple surgical specialties

Barriers to Implementation
• Cultural resistance among surgical and anaesthetic teams
• Lack of co-ordinated multidisciplinary teams
• Resource requirements for ERAS nurse coordinators
• Compliance monitoring challenges
• Patient compliance (adherence to early mobility, oral intake)
30. IMMEDIATE AND LATE POSTOPERATIVE COMPLICATIONS
Overview
Postoperative complications can be classified by timing (immediate, early, late) or by type (general
vs specific to a procedure). Understanding and anticipating complications is fundamental to surgical
practice.

Classification by Time
• Immediate (0–24 hours): complications occurring in theatre or in the immediate post-anaesthetic
period
• Early (1–7 days): complications during first week of admission
• Late (>1 week / months–years): delayed complications

Immediate Postoperative Complications (0–24 hours)

Respiratory:
• Airway obstruction: tongue falling back (supine position), laryngeal oedema (intubation trauma),
haematoma (after neck surgery), laryngospasm
• Aspiration pneumonia: aspiration of gastric contents → Mendelson's syndrome (acid pneumonitis);
prevent with RSI, head-up positioning, proper fasting
• Atelectasis: collapse of lung segments; most common respiratory complication; prevented by deep
breathing, physiotherapy
• Bronchospasm: in asthmatics; treat with bronchodilators
Cardiovascular:
• Haemorrhage: primary (during surgery), reactionary (within 24h – as BP rises, clot disturbed),
secondary (7–14 days – usually infective)
• Hypotension: haemorrhage, inadequate fluid replacement, cardiac dysfunction, regional anaesthesia
• Hypertension: pain, anxiety, full bladder, pre-existing hypertension not controlled
• Arrhythmias: hypoxia, hypercapnia, electrolyte imbalances (hypokalaemia)
• Cardiac arrest: haemorrhage, MI, anaphylaxis, PE, tension pneumothorax
Neurological:
• Delayed recovery from anaesthesia: drug overdose, hypothermia, metabolic derangement
(hypoglycaemia), CO₂ retention
• Agitation/delirium: pain, urinary retention, hypoxia, drugs (opioids, ketamine)
Urological:
• Urinary retention: common after pelvic/perineal surgery, spinal anaesthesia; treat with catheterisation
• Oliguria/anuria: hypovolaemia (most common), renal failure, urinary retention, blocked catheter

Early Postoperative Complications (1–7 days)

Fever (common, use "5 Ws" mnemonic):
• Wind (Day 1–2): atelectasis, pneumonia, aspiration
• Water (Day 3–5): urinary tract infection (catheter-associated)
• Wound (Day 3–7): surgical site infection
• Walking (Day 3–5): deep vein thrombosis (DVT)
• Wonder drugs (any time): drug reactions, C. difficile diarrhoea
Respiratory:
• Pneumonia: Gram-positive (community-acquired) or Gram-negative (hospital/ventilator-acquired)
• Pleural effusion, empyema
• ARDS: in critically ill, trauma, major sepsis
• Pulmonary embolism (PE): Days 3–14; tachycardia, hypoxia, pleuritic chest pain; Wells score, D-
dimer, CTPA; treat with LMWH/NOAC or unfractionated heparin
Wound complications:
 • Wound infection (SSI): redness, warmth, purulent discharge; open wound, drainage, antibiotics
• Wound dehiscence/burst abdomen: skin-only (minor) or deep (major/complete – serious); pink
serous fluid from wound suggests deep disruption; treat with immediate return to theatre for re-
suturing
• Haematoma: collection of blood in wound; painful swelling; may require evacuation
GI:
• Ileus: absent bowel sounds, abdominal distension, nausea/vomiting; treat conservatively (NBM, NG
tube, IV fluids, correct electrolytes); distinguish from obstruction
• Anastomotic leak: fever, peritonism, rising CRP/WBC, change in drain output (faeculent); CT
confirms; minor → drain + antibiotics; major → re-operation
• Nausea and vomiting: PONV; treat with ondansetron, metoclopramide, cyclizine
DVT/Thromboembolism:
• DVT: calf swelling, tenderness, warmth; confirm with duplex USS; treat with LMWH/NOAC
• PE: as above
Metabolic:
• Hypoglycaemia/hyperglycaemia (diabetic patients)
• Electrolyte imbalances: hyponatraemia (SIADH, excess hypotonic fluids), hypokalaemia (NG losses,
diuretics)
• Fluid overload: periorbital oedema, pulmonary oedema, weight gain

Late Postoperative Complications (>1 week)

Wound:
• Incisional hernia: most common long-term complication of abdominal surgery; risk factors: obesity,
wound infection, poor technique, corticosteroids; treat with repair (mesh preferred) when
symptomatic
• Keloid/hypertrophic scar: treat with compression, steroid injections, revision
• Sinus/fistula formation: persistent wound discharge; may indicate deep infection, foreign body (non-
absorbable sutures), Crohn's disease, malignancy, TB
Bowel:
• Adhesional intestinal obstruction: most common late complication of abdominal surgery; bands of
fibrous tissue cause obstruction; presents weeks/months/years post-op; treat with nasogastric tube,
IV fluids, observation; surgery if fails to resolve or strangulation suspected
• Anastomotic stricture: progressive dysphagia/change in bowel habit; endoscopic dilatation or re-
operation
• Post-gastrectomy syndromes: dumping syndrome (early/late), bile reflux gastritis, B12 deficiency
Vascular:
• Lymphoedema: after lymph node dissection (axillary, inguinal); treatment: elevation, compression,
lymphatic massage
• Arteriovenous fistula: after vascular surgery
Urological:
• Urinary fistula: vesicovaginal or ureterovaginal after gynaecological or pelvic surgery
• Urethral stricture: after urethral procedures
Neurological:
• Nerve damage: post-surgical paraesthesia, pain (e.g., ilioinguinal nerve after inguinal hernia);
phantom limb pain after amputation; neuropathic pain
• Post-thoracotomy/mastectomy pain syndrome
Psychological:
• Post-operative cognitive dysfunction (POCD): especially in elderly
• Anxiety, depression
• PTSD after ICU stay
Recurrence of disease:
• Cancer recurrence (local, nodal, systemic)
• Hernia recurrence
• Stone recurrence
31. FLUID MANAGEMENT IN TRAUMA AND SHOCK
Overview
Fluid management in trauma and shock has evolved significantly, moving away from aggressive
crystalloid resuscitation toward haemostatic resuscitation and damage control resuscitation
principles. The goals are to restore tissue perfusion, correct coagulopathy, and prevent the lethal
triad.

Types of IV Fluids
Crystalloids:
• Normal Saline (0.9% NaCl): Na 154 mmol/L, Cl 154 mmol/L; isotonic; large volumes cause
hyperchloraemic metabolic acidosis
• Hartmann's Solution (Ringer's Lactate): Na 131, K 5, Ca 2, Cl 111, lactate 29 mmol/L; more
physiological; lactate metabolised to bicarbonate; preferred crystalloid in trauma
• 5% Dextrose: provides free water; NOT for resuscitation (no Na, no osmotic support)
• Hypertonic Saline (3%, 7.5%): high sodium concentration; reduces oedema; used in traumatic brain
injury to reduce ICP; single bolus for haemorrhage control (limited evidence)
Colloids (not routinely recommended in trauma):
• Human Albumin Solution (4.5%, 20%): expensive, natural protein; used in cirrhotic patients, SBP,
after large-volume paracentesis
• Gelofusine, Voluven (gelatins, starches): synthetic colloids; associated with coagulopathy, renal
failure, anaphylaxis; NOT recommended in sepsis/trauma (CRISTAL, 6S trials)
Blood Products (the true resuscitation fluid in haemorrhagic shock):
• Packed Red Blood Cells (pRBCs): carries oxygen; 1 unit raises Hb by ~10 g/L
• Fresh Frozen Plasma (FFP): all coagulation factors; 1 unit raises PT/INR 3–4%
• Platelets: 1 adult dose raises count by 30–50 × 10⁹/L
• Cryoprecipitate: fibrinogen, factor VIII, vWF, XIII; target fibrinogen >2 g/L
• Prothrombin Complex Concentrate (PCC): factors II, VII, IX, X; rapid reversal of anticoagulants

Principles of Fluid Resuscitation in Haemorrhagic Shock

• 1. Haemorrhage control FIRST ("stop the bleeding, then give fluid"):
• External compression, tourniquet, wound packing
• Permissive hypotension until surgical haemostasis achieved
• REBOA (Resuscitative Endovascular Balloon Occlusion of Aorta) in selected cases
• 2. Permissive Hypotension (Hypotensive Resuscitation):
• Target systolic BP 80–90 mmHg (MAP 50–65 mmHg) in penetrating trauma
• Higher target in blunt trauma with TBI: MAP ≥80 mmHg (maintain cerebral perfusion)
• Rationale: aggressive crystalloid resuscitation dilutes clotting factors, increases hydrostatic pressure
(dislodges clot), causes hypothermia, worsens coagulopathy
• Avoid once surgical haemostasis achieved
• 3. Damage Control Resuscitation (DCR):
• 1:1:1 ratio of pRBC : FFP : Platelets (balanced/haemostatic resuscitation) – as per PROPPR trial
• Rationale: mimics whole blood; restores coagulation, oxygenation simultaneously
• Cryoprecipitate/fibrinogen concentrate: if fibrinogen <2 g/L (give early in massive haemorrhage)
• Massive Transfusion Protocol (MTP): activated when >10 units pRBCs in 24h expected; co-
ordinated delivery of 1:1:1 products
• 4. Tranexamic Acid (TXA):
• Anti-fibrinolytic agent (inhibits plasminogen activation)
• CRASH-2 trial: 1g IV over 10 minutes, then 1g over 8 hours; reduces mortality if given within 3 hours
of injury (harm if given >3 hours)
• MaTTERS trial: improved survival in military trauma
• Now part of standard trauma resuscitation
 • 5. Minimise Crystalloid:
• Initial crystalloid bolus: 250–500 mL Hartmann's, then reassess
• Do NOT give 2 L crystalloid blindly (old ATLS guideline abandoned)
• Crystalloid >1.5 L associated with worse outcomes (dilutional coagulopathy, hypothermia, abdominal
compartment syndrome, ARDS)
• Any ongoing fluid needs met with blood products

Fluid Management in Septic Shock

Surviving Sepsis Campaign 2021 / Hour-1 Bundle:
• 30 mL/kg crystalloid IV in first 3 hours for hypotension or lactate ≥4 mmol/L
• Balanced crystalloids (Hartmann's/Ringer's Lactate) preferred over normal saline (SMART trial,
SALT-ED)
• After initial bolus: reassess – use dynamic measures of fluid responsiveness:
- Pulse pressure variation (PPV >13% with controlled ventilation → fluid responsive)
- Straight leg raise (SLR) test: raise legs 45° for 1 min → increase in CO/BP = fluid responsive
- Avoid colloids: starches (VISEP, 6S trials) increase mortality and AKI; gelatin no clear benefit
• Vasopressors (noradrenaline) if not responding to fluids: start when MAP <65 mmHg; do not wait for
fluid loading to be completed if shocked
• Target: MAP ≥65 mmHg, urine output ≥0.5 mL/kg/hr, lactate clearance ≥10%/2h, ScvO₂ ≥70%

Fluid Management in Special Situations

Traumatic Brain Injury (TBI):
• Target CPP (cerebral perfusion pressure) = MAP – ICP ≥60–70 mmHg
• Avoid hypotension (MAP <80 mmHg worsens cerebral ischaemia)
• AVOID hypotonic fluids (5% dextrose, Ringer's lactate debate) → cerebral oedema
• 0.9% Normal Saline or hypertonic saline preferred
• Mannitol 0.25–1 g/kg IV: osmotic diuretic, reduces cerebral oedema, increases CPP (acute use)
Burns:
• Parkland formula: 4 mL × weight (kg) × %TBSA (Hartmann's/Ringer's lactate)
• Half in first 8 hours (from time of burn, not admission); rest over next 16 hours
• Add colloid after 8–12 hours in some protocols
• Monitor urine output: 0.5–1 mL/kg/hr (adults); 1 mL/kg/hr (children)
• Avoid over-resuscitation (abdominal compartment syndrome, pulmonary oedema, compartment
syndrome)
Paediatric Trauma:
• Fluid bolus: 10 mL/kg Hartmann's (not 20 mL/kg)
• Blood transfusion: 10 mL/kg pRBCs if haemodynamic instability
• MTP ratio 1:1:1 applies to paediatric major haemorrhage

Monitoring Adequacy of Resuscitation

Clinical:
• Heart rate, blood pressure, respiratory rate
• Urine output (≥0.5 mL/kg/hr in adults; ≥1 mL/kg/hr in paediatrics)
• Mental status, skin perfusion (capillary refill, temperature)
Biochemical:
• Lactate: target <2 mmol/L (or ≥10% clearance per 2 hours)
• Base deficit: target > -6 mEq/L
• pH: target ≥7.35
• Serial ABGs: evaluate metabolic acidosis, oxygenation
Haemodynamic:
• Central venous pressure (CVP): target 8–12 cmH₂ O (limited utility alone)
• Arterial line: continuous BP monitoring, ABG sampling
• Cardiac output monitoring (PiCCO, PA catheter, TOE)
• Pulse pressure variation (PPV): dynamic fluid responsiveness
• POCUS/FAST: fluid in cavities, cardiac function assessment