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SURGICAL INFECTIONS - Complete Study Guide

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1. TETANUS ⭐⭐⭐⭐

Etiology

• Caused by Clostridium tetani - a Gram-positive, anaerobic, spore-forming bacillus
• Spores found in soil, road dirt, house dust, human and animal faeces
• Spores resist prolonged boiling and are extremely hardy
• Produces two exotoxins: Tetanospasmin (neurotoxin - causes clinical disease) and Tetanolysin (haemolysin)

Mechanism of Injury (MOI) / Pathogenesis

• Spores germinate into vegetative forms under anaerobic conditions (devitalized tissue, ischaemia, foreign bodies, or co-infection with other organisms)
• Deep puncture wounds involving muscle are most prone - wounds on farms, gardens, playing fields, roads, garages, sewers
• Tetanospasmin is absorbed by motor nerve endings and travels retrograde along axons to anterior horn cells
• At anterior horn: toxin blocks release of inhibitory neurotransmitters (GABA, glycine) from Renshaw cells
• Loss of inhibition → uncontrolled motor neuron firing → sustained muscle contraction (spasm)
• Toxin also affects the sympathetic nervous system → autonomic dysfunction

Clinical Features

1. Trismus (lockjaw) - tonic spasm of masseter muscles; earliest sign
2. Risus sardonicus - characteristic grinning expression due to facial muscle spasm
3. Opisthotonus - severe arching of back due to spasm of paraspinal muscles

• Dysphagia (pharyngeal spasm)
• Neck stiffness
• Abdominal rigidity ("board-like abdomen")
• Reflex spasms - triggered by any stimulus (touch, sound, light) - can cause laryngospasm and asphyxia
• Autonomic instability: sweating, hyperthermia, labile BP, tachycardia
• Neonatal tetanus (tetanus neonatorum) - inability to suck, trismus

• Grade I: Mild - trismus only, no spasms
• Grade II: Moderate - trismus, dysphagia, mild spasms
• Grade III: Severe - reflex spasms, autonomic disturbance
• Grade IV: Very severe - autonomic storms

Management

• Proper wound care: thorough cleansing, debridement of all devitalized tissue, removal of foreign material, wound closure without tension
• Active immunity: Tetanus Toxoid (TT) 0.5 ml IM - 3 doses (0, 6-8 weeks, 6-12 months); booster every 10 years
• Passive immunity: Human Tetanus Immunoglobulin (HTIG) 250 units IM - for non-immunized patients post-wound

Complications

• Laryngospasm → asphyxia and death
• Aspiration pneumonia
• Urinary retention, constipation
• Vertebral fractures (due to severe spasms)
• Autonomic cardiovascular crises
• Respiratory failure (most common cause of death)
• DVT, pressure sores
• Rhabdomyolysis

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2. CELLULITIS ⭐⭐

• Definition: Acute spreading infection of the dermis and subcutaneous tissue
• Organisms: Most common - Streptococcus pyogenes (Group A), Staphylococcus aureus
• Predisposing factors: Skin breach (wound, tinea pedis), lymphoedema, diabetes, obesity, venous insufficiency
• C/F: Spreading erythema, warmth, oedema, tenderness; no sharp margin (distinguishes from erysipelas); fever, lymphangitis, lymphadenopathy may be present
• Investigations: Blood culture (often negative), raised WBC, CRP
• Treatment:
  • Elevation of limb
  • Oral flucloxacillin/amoxiclav for mild cases
  • IV benzylpenicillin + flucloxacillin for severe cases
  • MRSA: IV vancomycin
  • Mark the border with a skin marker to monitor progression
  • Treat underlying cause (e.g., tinea pedis)

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3. ABSCESS

A) Pyogenic Abscess ⭐⭐⭐

• Definition: A localized collection of pus in a cavity formed by the disintegration of tissue
• Organisms: Staphylococcus aureus (most common), streptococci, coliforms, anaerobes
• Pathogenesis:
  • Bacteria enter → acute inflammation → PMN infiltration → tissue necrosis → pus forms
  • Surrounding wall of granulation/fibrous tissue = pyogenic membrane
• C/F:
  • Cardinal signs of inflammation: rubor, calor, dolor, tumor
  • Fluctuation (pathognomonic) - pus movement felt between two fingers
  • Pointing - skin becomes thin, shiny, and tense at the site of impending rupture
  • Fever, rigors
• Treatment:
  • "Ubi pus, ibi evacua" - Where there is pus, drain it
  • Incision and drainage (I&D)
  • Send pus for C&S
  • Antibiotics for surrounding cellulitis or systemic sepsis
  • Daily wound dressings

B) Cold Abscess ⭐⭐⭐⭐

• Definition: An abscess without the usual signs of acute inflammation (no heat, no redness) - hence "cold"
• Etiology: Mycobacterium tuberculosis (most common); also atypical mycobacteria
• Pathogenesis: Caseous necrosis in a TB focus liquefies → pus tracks along fascial planes → presents at a site distant from the primary focus (hence also called "wandering abscess")
• Common sites:
  • Cervical lymph node TB → collar-stud abscess
  • Spinal TB (Pott's disease) → psoas abscess pointing to inner thigh/groin
  • Rib TB → intercostal cold abscess
• C/F:
  • Soft, fluctuant swelling
  • No heat, no redness, no tenderness (hence "cold")
  • Transillumination positive (clear fluid - unlike pyogenic)
  • Collar-stud abscess: Deep abscess communicates through a defect in deep fascia → superficial component, with dumbbell/collar-stud shape
• Investigations: Aspirate for AFB, ZN staining, Lowenstein-Jensen culture; Mantoux test; CXR; FNAC
• Treatment:
  • Aspiration (not incision - avoid sinus formation)
  • Full course of anti-tubercular therapy (ATT)
  • Surgical excision in selected cases
  • Do NOT incise - leads to chronic discharging sinus

C) Antibioma ⭐⭐⭐⭐⭐

• Definition: A chronic indurated abscess that results from inadequate or incomplete antibiotic treatment of a pyogenic abscess
• Pathogenesis:
  • Antibiotics given for an abscess that has already formed → bacteria killed but pus not drained
  • Pus becomes inspissated (thickened), surrounded by dense fibrosis
  • Results in a hard, firm, non-fluctuant lump - clinically mimics a tumour/carcinoma
• C/F:
  • Hard, indurated, non-tender mass
  • No fluctuation, no heat
  • History of previous pain/swelling treated with antibiotics without drainage
  • May be mistaken for malignancy (especially breast antibioma)
• Investigations: FNAC/biopsy to exclude malignancy; USS shows echogenic material
• Treatment:
  • Surgical excision of the entire mass including the fibrous wall
  • Send specimen for histopathology

D) Hilton's Method of Opening an Abscess

1. Give local/general anaesthesia
2. Make a small stab incision through the skin and superficial fascia only with a pointed scalpel (no. 11 blade)
3. Insert closed sinus forceps (haemostat) through the incision
4. Open the forceps widely in the direction of the important structure (blunt dissection) - this avoids cutting nerves and blood vessels
5. Allow pus to escape; insert gloved finger to break all loculi
6. Insert a corrugated rubber drain or pack with gauze
7. Leave wound open for secondary healing

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4. CARBUNCLE ⭐⭐⭐⭐⭐⭐

Etiopathology

• Definition: A carbuncle is an infective gangrene of the skin and subcutaneous tissue involving multiple adjacent hair follicles and their sebaceous glands
• Compared to a furuncle (involves one follicle), a carbuncle involves multiple follicles
• Organism: Staphylococcus aureus (usually MRSA in serious cases)
• Predisposing factors: Diabetes mellitus (most common), malnutrition, immunosuppression, obesity, poor hygiene, steroid use
• Pathogenesis:
  • Staphylococci infect multiple adjacent hair follicles
  • Infection spreads laterally through the deep dermis and subcutaneous fat
  • Multiple pockets of pus with septa form the characteristic "riddled with holes" appearance
  • Central area undergoes necrosis → sloughing → crater-like ulcer
  • Intense fibrosis surrounds the lesion

Clinical Features

• Typically on the back of neck (nape), back, buttocks, thighs
• Begins as a hard, red, painful, indurated plaque
• Multiple pustules/follicular openings visible on surface - "sieve-like" or "watering can" appearance
• Central area becomes necrotic and sloughs, leaving a deep, ragged, undermined ulcer
• Significant surrounding cellulitis and oedema
• Marked systemic toxicity: high fever, rigors, malaise (more than furuncle)
• Regional lymphadenopathy
• Complications: Septicaemia, metastatic abscesses, cavernous sinus thrombosis (if on face)

Treatment

1. Treat underlying diabetes - blood sugar control is essential
2. Antibiotics: Flucloxacillin IV; clindamycin if MRSA; guided by culture and sensitivity
3. Surgical treatment:
   • Cruciate incision (cross-shaped) through the entire carbuncle
   • All necrotic tissue and septa excised
   • Wound packed with gauze (heals by secondary intention)
   • Alternatively: wide excision with split-thickness skin grafting
4. Nutritional support and correction of immunodeficiency
5. Topical honey/povidone-iodine dressings post-op

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5. ERYSIPELAS ⭐⭐ (3 Marks)

• Definition: Acute superficial infection of the upper dermis and superficial lymphatics with a sharply demarcated edge
• Organism: Almost exclusively Group A beta-haemolytic Streptococcus (Streptococcus pyogenes)
• Entry point: Skin fissures, ulcers, minor abrasions, tinea pedis
• Common sites: Face (butterfly distribution), lower limbs

Clinical Features

• Fiery red, shiny, oedematous plaque with a sharply raised, well-defined advancing border - the hallmark that distinguishes it from cellulitis
• Warm, tender, tense skin
• "Peau d'orange" appearance (orange peel skin) in some cases
• High fever, rigors, malaise preceding the rash
• Lymphangitis and lymphadenopathy
• Vesicles and bullae may develop in severe cases
• Facial erysipelas: "Butterfly" distribution across cheeks and nose

Treatment

• Penicillin V oral (mild) or IV benzylpenicillin (severe) - drug of choice
• Erythromycin if penicillin-allergic
• Elevation of affected part
• Cool saline compresses
• Recurrent erysipelas: monthly penicillin prophylaxis

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6. NECROTISING FASCIITIS ⭐⭐⭐ (6/3 Marks)

Definition

Etiology

• Type I (Polymicrobial): Most common. Mixed aerobic + anaerobic organisms: Streptococcus, Staphylococcus aureus, E. coli, Pseudomonas, Clostridium, Bacteroides, Klebsiella
• Type II (Monomicrobial): Group A Streptococcus pyogenes (flesh-eating bacteria) - most virulent; younger patients
• Type III: Marine organisms (Vibrio vulnificus) - after seafood exposure

Predisposing Factors

Pathogenesis

Clinical Features (Summary Box)

• Unusual, disproportionate pain (pain out of proportion to appearance - early sign)
• Erythema, oedema, warmth
• Crepitus (gas in tissues)
• Blisters, bullae
• Grey/black discolouration - skin turns dusky blue-black
• "Dishwater pus" (grey, thin fluid) from wound
• Cutaneous anaesthesia (necrosis of nerves)
• Fixed skin staining

• High fever, tachycardia, tachypnoea
• Septic shock
• Coagulopathy (DIC)
• Multiorgan failure
• Renal failure (hypovolaemia + septic shock)

Specific Variants

• Fournier's gangrene: NF involving perineum, scrotum, and perianal region
• Meleney's gangrene: NF of abdominal wall

Diagnosis

• Primarily clinical - do not delay treatment for investigations
• Elevated creatine kinase (enormous elevation)
• CT scan: gas tracking along fascial planes (confirmatory when positive)
• Biopsy of fascia: fascial necrosis + acute inflammatory infiltrate
• LRINEC score (Laboratory Risk Indicator for Necrotising Fasciitis): uses CRP, WBC, Hb, Na, creatinine, glucose - score ≥6 is high risk

Treatment

1. ICU admission - fluid resuscitation, haemodynamic monitoring
2. IV antibiotics: High-dose Penicillin G + 3rd generation cephalosporin + metronidazole (empiric broad-spectrum cover); adjust per culture
   • Add clindamycin (anti-toxin effect against Streptococcus)
   • MRSA: add vancomycin
3. Urgent radical surgical debridement - cornerstone of management
   • Wide excision of ALL necrotic tissue going beyond the zone of induration
   • Wound packed and dressed
   • Second-look operation in 24-48 hours - multiple debridements often required
4. Hyperbaric oxygen - adjunct (where available)
5. Reconstructive surgery after infection controlled (skin grafting)

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7. SURGICAL SITE INFECTION (SSI) ⭐⭐ - PIRO Classification

Definition (CDC/NHSN)

Classification of SSI

1. Superficial incisional SSI: Involves only skin and subcutaneous tissue
2. Deep incisional SSI: Involves deep soft tissue (fascia, muscle)
3. Organ/space SSI: Involves any organ or space opened during the procedure (e.g., anastomotic leak, intra-abdominal abscess)

PIRO Classification (Predisposition, Insult/Injury, Response, Organ dysfunction)

Prevention of SSI

• Pre-op: Treat remote infections, glycaemic control, smoking cessation, MRSA screening and decolonisation (mupirocin nasal + chlorhexidine baths), hair clipping (not shaving)
• Intra-op: Antibiotic prophylaxis (within 60 min of incision), maintain normothermia, maintain normovolaemia, minimise dead space, minimize operative time
• Post-op: Proper wound dressings, early removal of drains, glucose control

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8. GAS GANGRENE ⭐⭐⭐

Definition

Etiology

• Primary organism: Clostridium perfringens (welchii) - 80-90% of cases
• Others: Clostridium oedematiens (novyi), Clostridium septicum, Clostridium histolyticum
• Gram-positive, anaerobic, spore-forming rods
• Found in soil, road dirt, human and animal faeces

Types

1. Clostridial myonecrosis (true gas gangrene) - involves muscle
2. Clostridial cellulitis - involves subcutaneous tissue, not muscle (less severe)
3. Anaerobic streptococcal myositis - caused by anaerobic streptococci

Pathogenesis

• Spores enter devitalized tissue (trauma, ischaemia, surgery)
• Germinate under anaerobic conditions → vegetative organisms proliferate
• Produce exotoxins:
  • Alpha toxin (lecithinase) - most important - lyses cell membranes, destroys muscle, causes haemolysis
  • Hyaluronidase, collagenase, protease, DNase - spread infection through tissue planes
• Gas (CO2, H2) produced by fermentation → crepitus in tissues
• Toxins enter bloodstream → systemic toxaemia → cardiovascular collapse
• Alpha toxin produces intravascular haemolysis → haemoglobinuria → renal failure

Clinical Features

• Bursting/throbbing pain at wound site - out of proportion, often the first sign
• Wound appears tense, indurated; skin is red, shiny, tense
• Sero-sanguinous, thin, watery discharge with characteristic sickly sweet smell ("mousy" odour)
• Crepitus on palpation (late sign) - gas crackling in tissues

• High fever, rapid thready pulse (rising pulse rate with falling BP)
• Bronze discolouration of overlying skin → blue-black gangrenous change
• Profound toxaemia, restlessness, confusion
• Haemolytic jaundice (haemoglobinuria - "port wine" urine)
• Septic shock, multiorgan failure, death (if untreated)

Diagnosis

• Clinical - characteristic smell, crepitus, wound appearance
• X-ray: Gas shadows in muscle planes (feathery pattern)
• Gram stain of wound discharge: Large Gram-positive rods, absence of PMNs (toxin kills WBCs)
• Wound swab for C&S
• Blood culture
• CT scan: Gas in muscle compartments

Treatment

1. Surgical - the cornerstone:
   • Wide, radical opening of wound
   • Excision of all necrotic/doubtful muscle (muscle that does not bleed or contract when cut is dead)
   • Wound left open, lightly packed with fluffed gauze
   • Amputation may be necessary to save life (sacrificial surgery)
2. Antibiotics:
   • IV Penicillin G (high dose) - all Clostridia sensitive
   • Add metronidazole and clindamycin (anti-toxin)
   • Clindamycin preferred adjunct - inhibits toxin production
3. Supportive: IV fluids, blood transfusion for haemolysis, vasopressors
4. Hyperbaric oxygen (HBO): Valuable adjunct - raises tissue O2 tension, inhibits Clostridial growth; available in limited centres
5. Antitoxin: Of doubtful value - not routinely used

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9. PARONYCHIA ⭐⭐⭐ (3 Marks)

Acute Paronychia

• Definition: Acute infection of the nail fold (paronychium) - the skin fold surrounding the nail
• Organism: Staphylococcus aureus (most common)
• Causes: Hangnail, manicure injury, nail biting, splinter
• C/F: Throbbing pain, redness, swelling of nail fold; fluctuation; pus visible under nail fold
• Treatment:
  • Early: warm soaks + oral antibiotics (flucloxacillin)
  • Pus present: Incision and drainage - longitudinal incision along nail fold under ring block anaesthesia; if pus under nail - remove portion of nail; Hilton's method not suitable here
  • Severe: Remove entire nail if subungual abscess

Chronic Paronychia

• Definition: Chronic infection/inflammation of the nail fold lasting >6 weeks
• Organism: Candida albicans most common (+ bacteria e.g. Pseudomonas)
• Causes: Repeated wet work, chemical exposure, diabetes, immunosuppression
• C/F: Boggy, swollen, tender nail fold; nail becomes discoloured, ridged, thickened; pus present intermittently; loss of cuticle (earliest sign)
• Treatment:
  • Keep hands dry, avoid wet work
  • Topical antifungals (clotrimazole, miconazole)
  • Systemic antifungals (itraconazole, fluconazole) for persistent cases
  • Surgical: Eponychial marsupialisation (Keystone flap) for refractory cases

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10. FELON ⭐⭐⭐⭐ (3 Marks)

• Definition: An abscess of the pulp space (distal closed fibrous compartment) of the fingertip
• Most common digit: Index finger and thumb
• Organism: Staphylococcus aureus
• Cause: Penetrating injury (needle prick, thorn, splinter), diabetic finger prick

Anatomy (Crucial to understand)

Clinical Features

• Intense throbbing pain - severe, worsens at night
• Tense, shiny, red swelling of the volar (palmar) aspect of the fingertip
• Dorsum of fingertip is NOT involved (distinguishes from herpetic whitlow initially)
• Tenderness on deep palpation of pulp
• Complications if untreated:
  • Osteomyelitis of distal phalanx (bone is adherent to the septa - pus strips periosteum)
  • Septic arthritis of DIP joint
  • Flexor tenosynovitis
  • Ischaemic necrosis of distal phalanx (septa compress digital vessels)

Treatment

1. Early (cellulitis only): Antibiotics + splint + elevation
2. Pus present - Surgical drainage (mandatory):
   • Preferred: Longitudinal volar incision (midline/unilateral longitudinal) - avoids scar on gripping surface
   • Alternatively: "Fish mouth" incision (no longer recommended - causes unstable fingertip)
   • Break all septa inside the pulp space
   • Pack wound open, leave to heal by secondary intention
   • X-ray to exclude osteomyelitis
3. Antibiotics: Flucloxacillin IV post-op

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11. MYCETOMA FOOT (Madura Foot) ⭐⭐⭐⭐

Definition

Etiology

• Madurella mycetomatis (most common worldwide, black grains)
• Scedosporium apiospermum (white grains)

• Nocardia brasiliensis (pale yellow grains)
• Actinomadura madurae (white/yellow grains)
• Streptomyces somaliensis (yellow grains)

Epidemiology

• Endemic in tropical and subtropical regions - India (Tamil Nadu, Gujarat), Africa, Latin America
• "Madura foot" - named after Madurai, South India
• Predominantly affects males, agricultural workers (barefoot)

Pathogenesis

• Inoculation of organism via penetrating trauma (thorn, splinter) in barefoot walkers
• Chronic granulomatous inflammation
• Spread through fascial planes → invades muscle and bone
• Sulfur granules = compact masses of fungal hyphae/actinomycetes in a polysaccharide matrix, surrounded by PMNs

Clinical Features

• Classic triad:
  1. Swelling - painless, progressively enlarging
  2. Sinuses - multiple discharging sinuses on the surface
  3. Grains - coloured granules discharged from sinuses (colour varies by organism - diagnostic)
• Foot most commonly affected (dorsum); also hand, leg, back
• Overlying skin: indurated, violaceous, peppered with sinuses
• Bone involvement: moth-eaten appearance on X-ray, pathological fractures
• No lymph node involvement (distinguishes from other infections)
• No systemic symptoms (chronic, indolent)

Investigations

• Discharge for KOH mount: hyphae in granules
• Gram stain, ZN stain (for actinomycetes)
• Culture: Sabouraud's medium (fungi); blood agar (actinomycetes)
• X-ray foot: Bone destruction, periosteal reaction, "soap bubble" appearance, new bone formation
• MRI: Most sensitive for extent of tissue involvement; shows "dot in circle" sign
• FNAC/biopsy for histology

Treatment

• Co-trimoxazole + amikacin (Domingos-Abreu regimen) - first-line
• Add rifampicin for resistant cases
• Long treatment (6-12 months)

• Itraconazole (most effective) or voriconazole
• Very prolonged treatment (1-2 years)
• Surgical debulking to reduce fungal load

• Wide excision for localised disease
• Amputation for extensive bone involvement - last resort

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12. ONYCHOCRYPTOSIS (Ingrowing Toenail)

• Definition: Ingrowth of the nail edge into the adjacent lateral nail fold (paronychium)
• Most common site: Great toe (hallux), lateral edge

Etiology

• Incorrect nail cutting (cutting too short at sides, curved cut)
• Tight/ill-fitting footwear
• Excessive sweating
• Trauma
• Genetic predisposition (curved nail plate)

Stages (Heifetz Classification)

1. Stage I: Pain, erythema, swelling of nail fold - no discharge
2. Stage II: Infected with discharge (pus/granulation tissue)
3. Stage III: Chronic granulation tissue, recurrent episodes

Treatment

• Conservative (Stage I): Warm soaks, antibiotics, proper nail cutting, cotton wool under nail edge, wider footwear
• Surgical (Stage II/III):
  • Wedge resection (Partial nail avulsion): Under ring block; tourniquet; remove the offending 1/4 of nail plate + germinal matrix ablation (phenol 80% applied for 3 min = chemical matricectomy - gold standard) or surgical excision of matrix
  • Zadik's procedure (Total nail ablation): Complete removal of nail + entire germinal matrix - reserved for severe/recurrent cases or onychogryphosis
  • Winograd procedure: Excision of the nail edge, nail fold, and underlying nail bed in a wedge

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13. UNIVERSAL PRECAUTIONS DURING SURGERY IN HIV PATIENTS (3 Marks)

Standard Universal Precautions:

• Double gloving - reduces needlestick injury risk by 87%
• Waterproof gown/apron
• Face shield or goggles (eye protection)
• N95 mask (for aerosol-generating procedures)
• Shoe covers

• No hand-to-hand passing of sharps - use a neutral zone/kidney dish
• Never recap needles by hand
• Blunt-tip suture needles wherever possible
• Announce before passing sharp instruments ("sharp coming")
• Use stapler/harmonic scalpel/electrocautery to reduce sharp use
• Dispose in puncture-proof sharps containers immediately

• Minimise number of staff in OT
• One-person rule - only one sharp instrument at a time
• Avoid finger-guided suturing (use retractors/instruments, not fingers)
• Use closed-system transfers for blood/fluids
• Instruments-first technique for locking blades
• Electrocautery preferred over sharp dissection

1. Immediately wash with soap and water for 5 minutes; squeeze out blood
2. Report to occupational health immediately
3. Test donor patient (HIV status, Hep B, Hep C) with consent
4. Test exposed worker (baseline)
5. Start Post-Exposure Prophylaxis (PEP) within 2 hours (max 72 hours): TDF + FTC + raltegravir for 28 days
6. Follow-up testing at 6 weeks, 3 months, 6 months

• All blood-soaked materials in yellow biohazard bags
• Sharps in puncture-proof containers
• Incineration of waste

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14. FOURNIER'S GANGRENE ⭐⭐⭐⭐

Definition

Etiology / Risk Factors

• Diabetes mellitus (most common - 40-60%)
• Perirectal/perianal abscess (most common source)
• Perineal trauma
• Urinary tract infection, urethral stricture, phimosis
• Colorectal pathology (Crohn's, colorectal carcinoma)
• Obesity, alcoholism, immunosuppression, malignancy

Organisms

Pathogenesis

• Source of infection: perineal skin, anal canal, urethra, or haematogenous
• Bacteria spread along Colles' fascia (superficial perineal fascia), Dartos fascia (scrotum), Scarpa's fascia (anterior abdominal wall)
• Endarteritis obliterans → thrombosis of subcutaneous vessels → ischaemia → necrosis
• Deep scrotal/penile fascia (Buck's fascia) and testes are usually spared (independent blood supply - internal spermatic artery)

Clinical Features

• Severe perineal pain, swelling
• Crepitus in scrotum/perineum (pathognomonic)
• Skin erythema → dusky/black discolouration → gangrene
• Odour - foul-smelling discharge
• Systemic sepsis: fever, tachycardia, hypotension
• Testes preserved (unlike scrotal skin)
• Mortality: 20-40% (up to 67% in some series)

Fournier's Gangrene Severity Index (FGSI)

Treatment

1. ICU resuscitation - aggressive fluid replacement
2. Broad-spectrum IV antibiotics:
   • Piperacillin-tazobactam + metronidazole + gentamicin
   • MRSA: add vancomycin
3. Urgent surgical debridement - wide excision of ALL necrotic tissue
   • Testes/penis usually preserved (not involved)
   • Wound left open; daily dressings
   • Faecal diversion (colostomy) if perianal source or extensive contamination
   • Urinary diversion (suprapubic catheter) if urethral involvement
4. Second-look surgery at 24-48 hours; multiple debridements common
5. Hyperbaric oxygen - adjunct
6. Reconstruction after infection control: skin grafting, orchiectomy if testicular necrosis

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15. DIRECT AND INDIRECT TRAUMATIC GANGRENE

Traumatic Gangrene

Direct Traumatic Gangrene

• Definition: Gangrene resulting from direct, immediate vascular injury at the site of trauma
• Mechanism:
  • Crush injuries - direct destruction of blood vessels + tissue
  • Avulsion injuries - tearing of vessels
  • Gunshot wounds - primary cavitation destroys vessels
  • Severe burns - direct thermal destruction of vessels and tissue
• Ischaemia is immediate at the site of trauma
• Gangrenous tissue is at the zone of injury
• Examples: Degloving injury, traumatic amputation, blast injury

Indirect Traumatic Gangrene

• Definition: Gangrene occurring at a site remote from or consequent to the primary trauma, due to indirect disruption of blood supply
• Mechanisms:
  • Arterial injury/thrombosis from blunt trauma (intimal tear, spasm) → distal gangrene
  • Compartment syndrome → increased compartment pressure → venous then arterial obstruction → distal ischaemia
  • Prolonged tourniquet application → distal limb gangrene
  • Thromboembolism following trauma → distal gangrene
  • Fractures causing arterial compression/laceration → distal limb gangrene
• Gangrenous tissue is distal to the site of injury
• Classic example: Supracondylar fracture of humerus in children → brachial artery injury → forearm/hand gangrene (Volkmann's ischaemia progressing to gangrene)

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16. HIDRADENITIS SUPPURATIVA (Hydradenitis Suppurativa)

Definition

Pathogenesis

• Not a primary infection - primarily a follicular occlusion disease
• Follicular hyperkeratosis → follicular plugging → follicular rupture → secondary inflammation and infection
• Apocrine glands secondarily involved
• Organisms: Mixed flora - S. aureus, coagulase-negative staphylococci, anaerobes (secondary)
• Chronic suppuration leads to fistulae and scar formation

Risk Factors

• Obesity, smoking (strongest modifiable risk factors)
• Family history (autosomal dominant)
• Female gender (3:1 ratio), onset post-puberty
• Diabetes, hyperandrogenism

Sites (Apocrine-bearing areas)

Clinical Features

• Stage I: Solitary/multiple abscesses, no sinus tracts, no scarring
• Stage II: Recurrent abscesses, single/multiple widely separated sinus tracts and scars
• Stage III: Multiple interconnected sinus tracts and abscesses over an entire region; diffuse involvement

Treatment

• Topical clindamycin 1% (mild, Stage I)
• Oral tetracycline/doxycycline - first-line systemic
• Oral clindamycin + rifampicin (300 mg each BD x 10 weeks) - most effective medical regimen
• Biological therapy: Adalimumab (anti-TNF-alpha) - only FDA-approved biologic; for Stage II/III
• Weight loss, smoking cessation
• Intralesional triamcinolone for acute flares

• I&D: Temporary relief only - high recurrence
• Deroofing/unroofing: Sinus tracts laid open - good local control
• Wide local excision (Stage III) - definitive; wound heals by secondary intention or skin grafting
• Laser hair removal: Nd:YAG laser - adjunct

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17. MRSA (Methicillin-Resistant Staphylococcus Aureus)

Definition

Mechanism of Resistance

• mecA gene on a mobile genetic element (SCCmec - Staphylococcal Cassette Chromosome mec)
• mecA encodes PBP2a (Penicillin-Binding Protein 2a) - modified PBP with low affinity for all beta-lactams
• Beta-lactams cannot inhibit PBP2a → bacteria continue cell wall synthesis → resistance

Types

1. HA-MRSA (Healthcare-Associated MRSA): Hospitals, nursing homes; typically multi-drug resistant
2. CA-MRSA (Community-Associated MRSA): Community setting, no healthcare contact; Panton-Valentine Leucocidin (PVL) toxin positive - causes severe skin/soft tissue infections and necrotising pneumonia; usually more susceptible to non-beta-lactam antibiotics
3. LA-MRSA (Livestock-Associated MRSA): Animal contact (ST398)

Clinical Significance

• SSI, wound infections, bacteraemia, pneumonia, osteomyelitis, septic arthritis, endocarditis

Screening and Decolonisation (Pre-op)

• Nasal swab (most common colonisation site) + groin/perineum/axilla swab
• Decolonisation: Mupirocin 2% nasal ointment TDS x 5 days + Chlorhexidine 4% full-body washes x 5 days
• Repeat swab after decolonisation

Treatment of MRSA Infection

Prevention

• Contact precautions: Gloves, apron; cohort nursing; single rooms
• Hand hygiene (alcohol gel between patients)
• Antibiotic stewardship
• Pre-op MRSA screening and decolonisation
• Environmental cleaning with chlorhexidine/hydrogen peroxide vapour

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SURGICAL PROCEDURES & INSTRUMENTS - Complete Study Guide

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1. SUTURE MATERIALS

Definition

Classification

A. Based on Absorption

B. Based on Number of Strands

• Monofilament: Single strand - less drag, less infection harbour (Prolene, PDS, Monocryl, Nylon)
• Multifilament (Braided/Twisted): Multiple strands twisted together - better handling, knot security, but more friction and infection risk (Silk, Vicryl, Ethibond)

C. Based on Origin

• Natural: Catgut (collagen), Silk (silkworm protein), Linen (flax fibres), Steel
• Synthetic: Nylon, Polypropylene, PDS, Vicryl, Monocryl, Polyester

Suture Sizes

• Measured in the USP system (United States Pharmacopeia): 0, 1, 2 (thicker) → 2-0, 3-0, 4-0... 10-0 (thinner, finest)
• Also metric gauge system (diameter in mm x 10)

Suture Needles

• Cutting needle: Triangular cross-section; 3 cutting edges; for tough tissues (skin, fascia)
• Reverse cutting: Cutting edge on the outside of the curve; stronger; less risk of tearing
• Round/Taper needle: Splits tissue without cutting; for bowel, blood vessels, peritoneum
• Blunt needle: Reduced needlestick injury risk; for fascial closure

Properties of an Ideal Suture

• High tensile strength
• Secure knot holding
• Minimal tissue reaction
• No electrolytic or carcinogenic potential
• Sterile, easily handled, inexpensive
• Predictable absorption

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2. INCISION & DRAINAGE OF ABSCESS ⭐⭐⭐

Principle

General Technique of I&D

• Confirm fluctuation (pus present)
• Mark site of maximum fluctuation
• Consent; anaesthesia (local ring block / general)
• Skin preparation

1. Incision: Make a bold, single incision through the centre of the abscess at the point of maximum fluctuation - large enough for adequate drainage
   • Direction: Langer's lines (tension lines of skin) when possible for cosmesis
   • Hilton's method near neurovascular structures: stab incision + blunt sinus forceps opening
2. Drain pus: Allow pus to flow; send sample for C&S
3. Finger exploration: Break all loculi with a gloved finger
4. Wash out: Irrigate cavity with saline/hydrogen peroxide
5. Do NOT close primarily - leave open for secondary healing
6. Pack/drain: Insert corrugated rubber drain or pack lightly with ribbon gauze
7. Dressings: Change daily; allow granulation from base upwards

• Oral antibiotics for surrounding cellulitis
• Daily dressings
• Review culture result and adjust antibiotics

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BREAST ABSCESS ⭐⭐

Types

1. Lactational (Puerperal) Breast Abscess - During breastfeeding
2. Non-lactational Breast Abscess - Periareolar (young women, smokers) or peripheral

Etiology

• Lactational: Staphylococcus aureus (most common); also streptococci, coliforms
• Non-lactational/periareolar: Mixed anaerobes, Bacteroides, enterococci (associated with duct ectasia)

C/F

• Painful, tender, fluctuant swelling in breast
• Overlying skin: red, oedematous, shiny
• Fever, malaise
• Nipple discharge (sometimes)

Management

• Aspiration under USS guidance (preferred for <3 cm) - can be repeated; preserves cosmesis; allows continued breastfeeding
• Incision and Drainage (I&D): For larger/multilocular abscesses
  • Incision placement:
    • Circumareolar (periareolar) incision for central/subareolar abscesses (best cosmetic result)
    • Radial incision (along Langer's lines, from areola outward) for peripheral abscesses - avoids cutting lactiferous ducts
    • Inframammary incision for large/lower pole abscesses
  • Make generous incision; break loculi; irrigate; pack or drain
  • Breastfeeding can continue from the contralateral breast; discourage or pump from affected side
• Antibiotics: Flucloxacillin (anti-staphylococcal); clindamycin if MRSA

• Often recurrent
• I&D + antibiotics (metronidazole for anaerobes)
• Hadfield's operation (duct excision) for recurrent cases
• Advise smoking cessation

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3. CIRCUMCISION ⭐⭐⭐

Definition

Indications

1. Phimosis - tight prepuce that cannot be retracted over the glans (congenital or acquired/scarring BXO)
2. Paraphimosis - retracted prepuce trapped behind glans causing venous engorgement/gangrene (after acute reduction)
3. Recurrent balanoposthitis (repeated infection of glans + prepuce)
4. Balanitis xerotica obliterans (BXO/Lichen sclerosus) - chronic inflammatory condition causing phimosis
5. Penile carcinoma (partial or total as part of treatment)
6. Religious/ritual (Judaism, Islam) - most common worldwide indication

• Prevention of UTI in infants with recurrent UTI
• Prevention of STIs (HIV, HPV) - evidence supports modest protection
• Hygiene

Pre-operative preparation

• Consent; anaesthesia (local penile block or GA in children)
• Dorsal penile nerve block or caudal block

Technique (Sleeve Resection / Dorsal Slit method)

1. Retract prepuce (if possible); mark circumferential lines on inner and outer prepuce
2. Mark inner incision line: 5-8 mm proximal to coronal sulcus (preserves enough inner prepuce)
3. Mark outer incision line: corresponding mark on outer prepuce
4. Incise along both marks; excise the sleeve of skin
5. Achieve haemostasis (diathermy/ligatures for frenular artery)
6. Approximate inner and outer skin edges with interrupted absorbable sutures (Vicryl 3-0)
7. Dressing: Vaseline gauze wrap

• Single incision through dorsal prepuce to relieve constriction; formal circumcision later

Complications

• Early: Bleeding (most common), haematoma, infection, urinary retention, meatal injury
• Late: Meatal stenosis, inadequate skin removal (recurrence of phimosis), excess skin removal, buried penis, unsatisfactory cosmesis, loss of sensation, inclusion dermoid cyst

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4. VASECTOMY ⭐⭐

Definition

Pre-operative Counselling

• Permanent procedure; reversal (vasovasostomy) possible but success not guaranteed
• Not immediately effective - residual sperm persist for ~20 ejaculations or 3 months
• Does NOT affect testosterone, libido, or erectile function
• Written informed consent

Technique

1. Anaesthesia: Local (1% lignocaine bilaterally into scrotal skin + perivasal tissue)
2. Palpate and isolate vas deferens at the neck of the scrotum
3. Skin incision: Two separate small (1 cm) lateral scrotal incisions or single midline incision
4. Deliver vas through incision; strip perivasal tissue (bare a 2-3 cm segment)
5. Apply two haemostats 2-3 cm apart
6. Excise a 1-2 cm segment of vas between haemostats
7. Ligate both cut ends with non-absorbable sutures (Prolene 2-0)
8. Fascial interposition (Uchida/modified): fold back the fascial sheath to separate the two cut ends (reduces failure rate)
9. Send excised segment for histopathology (confirm vas)
10. Skin closure with absorbable suture (Vicryl 3-0)

• Uses a vas ring clamp + sharp dissecting forceps (Li forceps)
• Punctures scrotal skin instead of incision; stretches the puncture hole
• Lower complication rates than conventional method
• Faster; less haematoma, less infection

Post-operative

• Scrotal support for 48 hours
• Ice pack to reduce swelling
• Abstain from sexual intercourse for 1 week
• Use alternative contraception until semen analysis at 12 weeks confirms azoospermia (or after 20 ejaculations)
• Semen analysis: two consecutive samples showing zero sperm = confirmed sterility

Complications

• Early: Haematoma (most common - 1-3%), wound infection, pain
• Late: Sperm granuloma (tender nodule at cut end), recanalization (failure ~1:2000), post-vasectomy pain syndrome, epididymo-orchitis
• Failure: Recanalization; operation on the wrong structure (lipoma of cord, artery)

Reversal (Vasovasostomy)

• Success (pregnancy) rates: 75% if reversed within 3 years; falls to 30% if >15 years
• Microscopic technique

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5. TRACHEOSTOMY - INDICATIONS (3 Marks)

Definition

Indications

• Laryngeal carcinoma
• Foreign body in larynx/upper trachea (cannot be removed)
• Severe oropharyngeal/laryngeal oedema (trauma, anaphylaxis, Ludwig's angina)
• Bilateral vocal cord paralysis
• Tracheal/subglottic stenosis
• Severe head and neck burns

• Long-term mechanical ventilation (avoids complications of prolonged endotracheal intubation - subglottic stenosis, sinusitis)
• Severe neurological injuries (TBI, GBS, high spinal cord injuries)
• Post-operative head/neck surgery

• Copious secretions the patient cannot clear
• Unconscious patients with retained secretions
• Post-thoracic/cardiac surgery

• Maxillofacial trauma making oral/nasal intubation impossible
• Laryngotracheal trauma
• Base of skull fractures (contraindicate nasal intubation)

• Before major head and neck operations where post-op airway swelling is anticipated

Types

• Surgical tracheostomy: Standard open procedure
• Percutaneous dilatational tracheostomy (PDT): Seldinger technique; bedside ICU procedure
• Mini-tracheostomy: For secretion clearance only (4 mm tube)

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6. INDICATIONS FOR AMPUTATION ⭐⭐⭐ (3 Marks)

Mnemonic: "DIVT CAMP"

Indications:

• Critical limb ischaemia not amenable to revascularization
• Diabetic gangrene with extensive tissue loss

• Traumatic amputation (mangled extremity - MESS score >7)
• Crush injury with non-viable limb
• Blast/gunshot injury - irreparable vascular/skeletal injury
• Degloving with loss of vital structures

• Gas gangrene threatening life
• Necrotising fasciitis not responding to debridement
• Chronic osteomyelitis with non-functional limb
• Fournier's gangrene with extensive penile/scrotal involvement

• Bone tumours (osteosarcoma, Ewing's sarcoma) - when limb salvage is not possible
• Soft tissue sarcomas - inadequate margins otherwise
• Fungating recurrent tumours

• Non-functional congenital limb anomalies where prosthetics would be superior

• Severe post-injury paralysis with non-functional, insensate limb prone to pressure sores

• Full-thickness circumferential burns with established gangrene

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7. APPENDICECTOMY ⭐⭐⭐⭐

Definition

Indications

• Acute appendicitis (principal indication)
• Perforated appendicitis with peritonitis
• Appendicular mass/abscess (interval appendicectomy after 6-8 weeks)
• Appendicular tumours (carcinoid, mucocele)
• Incidentally during other surgeries (controversial)

Pre-operative Preparation

• IV fluids, IV antibiotics (cefuroxime + metronidazole before incision)
• Consent; NPO; catheterization
• Mark the site (RIF)

OPEN APPENDICECTOMY

• Gridiron (McBurney's) incision: Most common - oblique, centered over McBurney's point (junction of lateral 1/3 and medial 2/3 of line joining ASIS to umbilicus), perpendicular to this line
• Lanz incision: Transverse incision at McBurney's point - better cosmesis, preferred
• Rutherford Morrison incision: If appendix or perforation extends further (lateral extension)
• Lower midline/Pfannenstiel: If diagnosis uncertain (gynaecological pathology possible)

1. Incision through skin and subcutaneous fat
2. Grid-iron dissection: External oblique split in direction of fibres → internal oblique + transversus split perpendicular → peritoneum opened
3. Deliver caecum and follow taenia coli to base of appendix
4. Mesoappendix divided: Between haemostats; appendicular artery ligated with 2-0 Vicryl
5. Appendix base: Crush the base with a haemostat; reapply haemostat 5 mm distal; tie a Vicryl 1 ligature at crush mark; divide between ligature and haemostat
6. Stump: Cauterise mucosa; (invaginate into caecum with purse-string suture is optional/historical)
7. Peritoneal lavage with warm saline if peritonitis/perforation
8. Close in layers: Peritoneum (Vicryl 1), muscle layers (Vicryl 1), fascia, subcutaneous, skin
9. In perforation: Drain may be left; skin may be left open for delayed primary closure

• 10 mm umbilical port (camera)
• 5 mm suprapubic port
• 5 mm left iliac fossa (LIF) port

1. Pneumoperitoneum with CO2 (12-14 mmHg)
2. 30-degree laparoscope; identify appendix
3. Mesoappendix divided with Harmonic scalpel/LigaSure/endoloop
4. Appendix base: apply 2 endoloops (Roeder loops) proximally, 1 distally; divide
5. Retrieve appendix in endobag through umbilical port (avoids contamination)
6. Irrigate; deflate; close ports

• Better visualisation of entire abdomen (diagnostic advantage - especially in women)
• Less post-operative pain
• Shorter hospital stay
• Faster return to activity
• Lower wound infection rate
• Better cosmesis

Complications of Appendicectomy

• Early: Wound infection (most common), haematoma, ileus, intra-abdominal abscess (pelvic, subphrenic), urinary retention
• Late: Adhesive intestinal obstruction, stump appendicitis (if stump too long), incisional hernia, faecal fistula (stump blowout)
• Specific: Injury to ileum, right ureter, or right spermatic cord

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8. BASSINI'S HERNIORRHAPHY

History

Principle

Anatomy Revised

• Inguinal canal: 4 cm long; runs from deep ring (midpoint of inguinal ligament) to superficial ring (above pubic tubercle)
• Posterior wall (inguinal floor): Transversalis fascia (weak area in hernia)
• Conjoint tendon: Fusion of transversus abdominis + internal oblique aponeuroses

Steps of Bassini's Operation

1. Incision: Oblique incision in the skin crease above and parallel to the medial 2/3 of inguinal ligament
2. External oblique aponeurosis divided in the direction of its fibres, from the superficial ring outward
3. Spermatic cord is isolated and held on a sling; ilioinguinal nerve protected
4. Hernial sac identified, dissected free, transfixed at neck, and ligated → redundant sac excised
5. Triple layer reconstruction (the key step):
   • The transversus abdominis aponeurosis + transversalis fascia (conjoined together = "triple layer") are sutured to the shelving edge (undersurface) of the inguinal ligament using interrupted non-absorbable sutures (Prolene 1-0 or nylon)
   • Sutures placed from pubic tubercle medially to the deep inguinal ring laterally
   • At the deep ring, the repair is made snug around the cord ("new deep ring")
6. External oblique aponeurosis closed over the cord to reconstruct the inguinal canal
7. Skin closure

Limitations of Bassini's Repair

• Tension repair - suturing structures not naturally in apposition
• Recurrence rate: 10-15% (higher than mesh repairs)
• Shouldice repair (modification with 4 rows of running sutures) has lower recurrence (~1-2%)
• Now largely replaced by tension-free mesh repairs (Lichtenstein, TEP, TAPP)

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9. STAPLERS IN SURGERY

Principle

Types of Surgical Staplers

• Applies 2 or 4 parallel rows of staples WITHOUT cutting
• Used to close (not divide) structures: bronchus, bowel stumps
• Available in lengths: 30, 45, 60, 90 mm

• Applies 4 rows of staples AND cuts between the middle two rows simultaneously
• Creates a side-to-side (functional end-to-end) anastomosis
• Used in: small bowel anastomosis, bowel resection, gastric bypass, lung resection
• Available in lengths: 60, 80, 100 mm; with multiple staple heights (for different tissue thickness)

• Circular array of staples; anvil placed in proximal bowel + cartridge in distal
• Creates an end-to-end circular anastomosis by firing and simultaneously cutting a circular "donut" of tissue
• Used for: colorectal anastomosis (especially low anterior resection), oesophago-gastric, gastrojejunostomy
• Available in diameters: 21, 25, 28, 31, 33 mm
• Donuts (two rings of tissue cut out) must be checked for completeness after firing

• Applies stainless steel staples to approximate skin edges
• Rapid; particularly for long incisions

• Articulating linear cutting staplers for endoscopic use
• Used in: laparoscopic appendicectomy (base of appendix), sleeve gastrectomy, VATS lung resection

Advantages

• Faster than hand-sewn anastomosis
• Consistent, reproducible anastomosis
• Reduced ischaemia (faster)
• Particularly useful in difficult-to-access areas (low pelvis, thorax)
• Reduced risk of contamination

Disadvantages

• Expensive
• Anastomotic leak still possible (≥3%)
• Staple line bleeding
• Require specific tissue thickness for proper firing
• Learning curve

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10. LAPAROSCOPIC SURGERY ⭐⭐⭐⭐

Definition

Basic Principles and Equipment

1. Laparoscope - 0° (straight) or 30° angled telescope; rod-lens system
2. Camera + monitor - high-definition/4K display
3. CO2 insufflator - maintains pneumoperitoneum at 12-14 mmHg
4. Light source - xenon or LED
5. Trocars/ports - 5 mm, 10 mm, 12 mm
6. Instruments: Graspers, dissectors, scissors, clip appliers, suction-irrigation
7. Energy devices: Monopolar, bipolar, harmonic scalpel, LigaSure

Creating Pneumoperitoneum

• Veress needle technique (closed): Blind puncture (usually umbilicus); safer in virgin abdomen
• Hasson (open) technique (preferred): Mini-laparotomy at umbilicus; direct port insertion; safest; used in re-do cases, pregnant patients, obese patients

Advantages Over Open Surgery

Disadvantages / Limitations

• 2D vision (loss of depth perception - 3D cameras/robotic systems address this)
• Reduced tactile feedback (haptics)
• Long learning curve
• Equipment-dependent; expensive
• Difficult in previous abdominal surgery (adhesions)
• CO2 pneumoperitoneum effects: diaphragm elevation, CO2 absorption (hypercarbia), port-site hernias
• Not suitable for all procedures (e.g., complex vascular)

Complications Specific to Laparoscopy

• Pneumoperitoneum-related: Gas embolism (rare), subcutaneous emphysema, pneumothorax, diaphragmatic injury
• Port insertion: Injury to bowel, major vessels (iliac vessels), bladder
• Trocar-site hernia (esp. 10 mm+ ports - fascial closure mandatory)
• Port-site metastasis (in oncological surgery)
• Conversion to open: Not a complication - a decision

Common Laparoscopic Procedures

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11. MESH REPAIR ⭐⭐⭐

Rationale

Types of Mesh

• Polypropylene (Prolene mesh): Most commonly used; permanent, monofilament; promotes good fibroblast ingrowth
• Polyester (Mersilene): Multifilament; good tensile strength
• PTFE (Gore-Tex): Expanded polytetrafluoroethylene; smooth surface; less adhesion (used for intra-peritoneal placement)
• Composite mesh: Polypropylene on parietal side + anti-adhesion coating on visceral side (for intraperitoneal use - IPOM)
• Biological mesh: Derived from human/porcine/bovine dermis or intestinal submucosa; absorbable; for contaminated fields

• Lightweight mesh (large pore, >1 mm): Less foreign body reaction; better patient comfort; preferred now
• Heavyweight mesh (small pore, <1 mm): Stronger; more reaction/pain; older generation

Open Mesh Repair - Lichtenstein Tension-Free Repair (Gold Standard for Open Inguinal Hernia)

1. Standard inguinal incision; open external oblique; isolate spermatic cord
2. Sac reduced/ligated
3. Polypropylene mesh (approx 8x16 cm) tailored to cover the posterior inguinal wall
4. Mesh sutured medially to pubic tubercle; inferiorly to inguinal ligament (continuous Prolene suture)
5. Superiorly to conjoint tendon/internal oblique
6. Keyhole created at the lateral edge to accommodate the cord (creating a new deep ring)
7. Tails of mesh overlapped and sutured; excess trimmed
8. External oblique closed over the mesh

Laparoscopic Mesh Repairs

• Mesh placed in the preperitoneal space without entering the peritoneal cavity
• Approach via umbilical port, balloon dissection of preperitoneal space
• Mesh covers entire myopectineal orifice (inguinal + femoral spaces)
• Advantage: No intraperitoneal entry; less adhesion risk; earlier recovery

• Peritoneal cavity entered; peritoneum flap raised; mesh placed in preperitoneal space; peritoneum closed over mesh
• Allows visualisation of entire abdomen

Complications of Mesh Repair

• Short-term: Seroma (most common), haematoma, wound infection, urinary retention
• Long-term: Chronic groin pain (most significant), mesh migration, mesh erosion (rare), mesh infection (requires mesh removal), testicular atrophy (spermatic cord compression), recurrence

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12. BIPOLAR ELECTROCAUTERY

Principle

Mechanism

Key Difference from Monopolar

Indications for Bipolar

• Neurosurgery (coagulating small vessels near brain/nerve tissue)
• Laparoscopy (fallopian tube sterilization, bleeding control)
• Ophthalmic surgery
• Patients with cardiac pacemakers/implantable defibrillators (ICD)
• Microsurgery
• Coagulating vessels near vital structures (ureter, vas deferens)

Limitations

• Cannot cut tissue
• Cannot be used in saline irrigation (disperses current)
• Requires dry field for effective coagulation

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13. HARMONIC SCALPEL

Principle

Mechanism

• Ultrasonic vibration → hydrogen bond disruption in protein molecules → protein coagulum forms → seals vessels
• Simultaneously: mechanical cutting action from blade movement

Key Features

Advantages

• Precise dissection with minimal thermal spread - safe near nerves, ureters, bowel
• Cuts and coagulates simultaneously - faster surgery
• Seals vessels up to 7 mm
• No electrical current through patient - safe for pacemaker patients
• Minimal smoke - better laparoscopic view
• Less dessication, less tissue sticking to instrument

Common Uses

• Laparoscopic cholecystectomy (dissection in Calot's triangle)
• Laparoscopic colectomy, thyroid surgery, bariatric surgery
• Open oncological resections requiring precise dissection near nerve structures
• Liver resection

Trade names: Harmonic Ace® (Ethicon), SonoSurg® (Olympus)

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14. ROBOTIC SURGERY

Definition

The da Vinci Robotic System (Intuitive Surgical)

• Market leader - over 11 million robotic surgeries performed worldwide as of 2022
• Components:
  1. Surgeon's Console: Where surgeon sits, views 3D image, controls instruments via finger controls and foot pedals
  2. Patient-side Cart (Robotic unit): 3-4 robotic arms attached to ports in the patient; holds camera + instruments
  3. Vision Cart: High-definition 3D camera system, image processing

Advantages over Conventional Laparoscopy

Disadvantages

• No haptic/tactile feedback (surgeon cannot feel tissue resistance)
• Very expensive (system costs $2-3 million; maintenance + disposable instruments costly)
• Bulky: Takes up significant operating room space; difficult to reposition
• Setup time: Docking the robot takes additional time
• Only one patient-side operator possible; no assistant at table
• Proprietary system (Intuitive Surgical monopoly historically)

Common Applications

• Urology: Robotic-assisted radical prostatectomy (RARP) - most common robotic procedure worldwide; radical cystectomy; nephrectomy; pyeloplasty
• Colorectal: Low anterior resection (narrow pelvis), rectopexy
• Gynaecology: Hysterectomy, myomectomy
• Cardiac: Mitral valve repair
• General: Nissen fundoplication, Heller myotomy, Whipple's procedure
• Head & Neck: TORS (transoral robotic surgery) for oropharyngeal tumours

Newer Robotic Systems

• Hugo RAS (Medtronic)
• Versius (CMR Surgical)
• SPORT Surgical System (Titan Medical)
• Single-port robotic systems

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FLUID & ELECTROLYTES + SURGICAL MISCELLANEOUS - Complete Study Guide

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PART A: FLUID & ELECTROLYTE BALANCE

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1. HYPONATRAEMIA ⭐⭐⭐

Definition

Pathophysiology

Classification & Causes (by Volume Status)

A. Hypovolaemic Hyponatraemia (Low TBNa, Low TBW - but Na loss > water loss)

B. Euvolaemic Hyponatraemia (Normal TBNa, slightly increased TBW)

• SIADH (Syndrome of Inappropriate ADH secretion) - most common cause of euvolaemic hyponatraemia
  • CNS: meningitis, SAH, stroke, head injury
  • Pulmonary: pneumonia, TB, SARS
  • Drugs: SSRIs, carbamazepine, chlorpropamide, cyclophosphamide, opioids
  • Malignancies: small cell lung carcinoma (ectopic ADH)
  • Post-operative state
• Hypothyroidism
• Glucocorticoid deficiency
• Psychogenic polydipsia (excess water intake)

C. Hypervolaemic Hyponatraemia (High TBNa, even higher TBW)

• Congestive cardiac failure (CCF)
• Liver cirrhosis (ascites)
• Nephrotic syndrome
• Acute and chronic renal failure

D. Pseudohyponatraemia (measured Na low, actual Na normal)

• Severe hyperlipidaemia, severe hyperproteinaemia (displaces water in lab sample)
• Severe hyperglycaemia (osmotic shift of water into ECF diluting Na)

Clinical Features

• Nausea, vomiting
• Headache, lethargy
• Muscle cramps, weakness
• Altered cognition

• Confusion, disorientation
• Drowsiness progressing to stupor and coma
• Seizures (major risk)
• Respiratory arrest
• Cerebral oedema → cerebral herniation → death

Management

Step 1: Identify the cause and type

• Clinical assessment of volume status
• Urine sodium, urine osmolality, serum osmolality
• TFTs, cortisol, blood glucose

Step 2: Correct based on type

• Faster correction → Osmotic Demyelination Syndrome (ODS) / Central Pontine Myelinolysis (CPM) - irreversible neurological damage

• Correct volume deficit first with isotonic saline (0.9% NaCl)
• Treat the underlying cause

• Fluid restriction (800-1000 mL/day) - cornerstone
• Demeclocycline (tetracycline that causes nephrogenic DI) - for chronic SIADH
• Vaptans (Tolvaptan, Conivaptan): V2-receptor antagonists; block ADH at collecting duct → free water excretion without Na loss ("aquaretics"); for euvolaemic/hypervolaemic hyponatraemia
• Treat underlying cause

• Fluid restriction + salt restriction
• Treat underlying cause (diuretics for CCF, but use cautiously)
• Vaptans

• Hypertonic saline (3% NaCl) - IV infusion
• Raise Na by 1-2 mEq/L/hour until symptoms resolve or Na reaches 125 mEq/L
• Then switch to slower correction
• Do NOT exceed 10-12 mEq/L in 24 hours total
• ICU monitoring; neurological observation

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2. POTASSIUM DISORDERS

A) Hypokaalaemia ⭐⭐⭐

Causes

1. Inadequate intake: Starvation, prolonged IV therapy with K+-free fluids
2. Excessive GI loss:
   • Vomiting (loss of HCl → metabolic alkalosis → renal K+ loss)
   • Diarrhoea, fistulas, ileostomy
   • High nasogastric output
3. Excessive renal loss:
   • Diuretics (loop + thiazide most common)
   • Hyperaldosteronism (Conn's syndrome)
   • Cushing's syndrome (cortisol has mineralocorticoid effect)
   • Renal tubular acidosis (RTA)
   • Drugs: amphotericin B, aminoglycosides, cisplatin (cause Mg2+ depletion → renal K+ wasting)
4. Intracellular shift:
   • Metabolic alkalosis (K+ shifts into cells; K falls 0.3 mEq/L per 0.1 rise in pH)
   • Insulin therapy (especially in DKA correction)
   • Beta-2 agonists (salbutamol)
   • Refeeding syndrome

Clinical Features

• ECG: U waves (characteristic), T-wave flattening, ST depression, prolonged QU interval, arrhythmias
• Increased sensitivity to digoxin toxicity
• Ventricular fibrillation (severe) Renal: Polyuria, polydipsia (K+ depletion impairs tubular concentrating ability)

Management

• Mild (K 3.0-3.5): Oral K+ replacement (KCl tablets/syrup); correct underlying cause
• Moderate-severe (K < 3.0 or symptomatic):
  • IV potassium chloride (KCl) - max 10-20 mEq/hour (never rapid bolus - cardiac arrest)
  • Max concentration peripherally: 40 mEq/L (via central line: up to 80 mEq/L)
  • Monitor ECG and serum K+ during infusion
  • Correct hypomagnesaemia first (if Mg2+ low, K+ repletion is very difficult)
• Identify and treat the underlying cause

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B) Hyperkalaemia

Causes

1. Excess intake: Excess oral/IV K+ supplementation; massive blood transfusion (old blood releases K+)
2. Decreased excretion:
   • Acute/Chronic Renal Failure (most common cause)
   • Addison's disease (aldosterone deficiency)
   • Drugs: K+-sparing diuretics (spironolactone), ACE inhibitors, ARBs, NSAIDs
3. Shift from ICF to ECF:
   • Acidosis (H+ moves into cells, K+ moves out - opposite of alkalosis)
   • Crush injury, rhabdomyolysis, haemolysis (massive)
   • Rapid rise in extracellular osmolality (hyperglycaemia, mannitol)
   • Burns, extensive tissue necrosis

Clinical Features

1. Tall, peaked (tented) T waves - earliest ECG change
2. Prolonged PR interval
3. Flattened/absent P waves
4. Widened QRS complex
5. Sine wave pattern
6. Ventricular fibrillation → cardiac arrest

Management (Emergency if K+ > 6.5 or ECG changes)

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3. TOTAL PARENTERAL NUTRITION (TPN) ⭐⭐⭐⭐

Definition

Indications

• "If the gut works, use it" - TPN only when enteral feeding is not possible

1. Prolonged intestinal failure: Short bowel syndrome, entero-cutaneous fistula (high output)
2. Severe acute pancreatitis (when enteral route not tolerated)
3. Prolonged ileus post major abdominal surgery
4. Inflammatory bowel disease with severe acute flare
5. Major trauma/burns with inaccessible gut
6. Pre-operative nutritional support in severely malnourished patients (>7-10 days)
7. Malabsorption syndromes
8. Radiation enteritis

Contraindications

• Functioning GI tract (always prefer enteral)
• Short-term illness (< 7 days) in well-nourished patients
• Aggressive treatment not consistent with patient's wishes

Components of TPN

Administration

• Central venous catheter (CVC) - mandatory for standard TPN (high osmolarity 1500-2000 mOsm/L causes peripheral vein thrombophlebitis)
  • Subclavian vein, internal jugular, PICC line
• "All-in-one" (3-in-1 or AIO bags): all components premixed in single bag under aseptic conditions (pharmacy prepared)
• Infusion over 24 hours via infusion pump; or cyclic TPN (12-16 hours overnight) for long-term patients

Monitoring

• Daily: Blood glucose (6-hourly initially), fluid balance, weight, electrolytes
• Weekly: LFTs, TFTs, albumin, phosphate, Mg, Zn, CRP
• Catheter site inspection daily

Complications

• Pneumothorax, haemothorax, subclavian artery puncture (insertion)
• Catheter-related bloodstream infection (CRBSI) - most serious complication
• Catheter thrombosis, air embolism

• Hyperglycaemia (most common) - needs insulin
• Refeeding syndrome - sudden drop in phosphate, K+, Mg2+ when feeding starts after starvation; can cause cardiac arrhythmias, respiratory failure, neurological problems
  • Prevent by starting TPN slowly and supplementing phosphate
• Hypoglycaemia (if TPN suddenly stopped)
• Electrolyte disturbances (hypo/hypernatraemia, hypokaalaemia)
• Hypertriglyceridaemia (excess fat)
• Metabolic acidosis (excess chloride in amino acid solutions)

• TPN-associated liver disease (fatty liver, cholestasis, hepatic steatosis)
• Biliary sludge and gallstones (biliary stasis from no enteral stimulation)

• Gut mucosal atrophy (no enteral stimulation → bacterial translocation)
• Increased infection risk

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4. ACID-BASE DISORDERS

Normal Values

• pH: 7.35-7.45
• PaCO2: 35-45 mmHg
• HCO3-: 22-26 mEq/L
• Base Excess (BE): -2 to +2

A) Metabolic Acidosis ⭐⭐⭐⭐

Expected PaCO2 = (1.5 × HCO3-) + 8 ± 2

Causes - Using ANION GAP

• Diarrhoea (loss of HCO3-)
• Renal Tubular Acidosis (RTA)
• Ureterosigmoidostomy (colonic Cl-/HCO3- exchange)
• Pancreatic fistula, small bowel fistula
• Acetazolamide (carbonic anhydrase inhibitor)

Clinical Features

• Kussmaul breathing (deep, rapid breathing) - compensatory
• Fatigue, weakness, nausea, vomiting
• Confusion, drowsiness, coma (severe)
• Cardiac: dysrhythmias, decreased contractility, vasodilation → hypotension
• Peripheral vasodilation with warm peripheries (paradoxically)

Management

1. Treat the underlying cause - primary treatment
   • DKA: insulin + fluids
   • Lactic acidosis: treat shock/sepsis
   • Renal failure: dialysis
2. Sodium bicarbonate (NaHCO3): Only for severe acidosis (pH < 7.1 or HCO3- < 10)
   • Formula: HCO3- deficit (mEq) = 0.5 × body weight (kg) × (desired HCO3- - measured HCO3-)
   • Give half the calculated dose; reassess
   • Risks of NaHCO3: paradoxical CNS acidosis, fluid overload, hypokalaemia, overshoot alkalosis
3. Haemofiltration/dialysis for renal failure or refractory cases

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B) Metabolic Alkalosis

Causes

• Vomiting / NG aspiration (most common surgical cause - loss of HCl)
• Diuretics (thiazide/loop) - loss of Cl- and H+
• Hyperaldosteronism (Conn's/Cushing's) - renal H+ loss
• Bartter's/Gitelman's syndrome

• Volume depletion (avid Na+ reabsorption coupled with H+ secretion)
• Chloride depletion (urine Cl- < 15 mEq/L = "saline-responsive")
• Hypokaalaemia (drives H+ into cells, K+ out)

Classification

• Saline-responsive (Urine Cl- < 15 mEq/L): Vomiting, diuretics, post-hypercapnia - treat with IV normal saline + KCl
• Saline-resistant (Urine Cl- > 25 mEq/L): Hyperaldosteronism, severe K+ depletion - treat underlying cause + potassium

Clinical Features

• Nausea, vomiting
• Paraesthesias, muscle cramps, tetany (low ionised Ca2+)
• Hypoventilation (compensatory)
• Confusion, cardiac arrhythmias

Management

1. Saline-responsive (most cases): Isotonic saline (0.9% NaCl) IV + KCl replacement
2. Treat underlying cause: Stop diuretics; treat hyperaldosteronism
3. Acetazolamide: Causes renal HCO3- excretion (for severe/resistant cases)
4. Dilute HCl infusion (0.1 N HCl via central line) - only for severe, refractory, life-threatening cases

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5. FEEDING GASTROSTOMY vs JEJUNOSTOMY

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6. ROLE OF ELECTROLYTE BALANCE IN SURGICAL PRACTICE ⭐⭐⭐⭐

• Hyponatraemia can cause cerebral oedema, seizures, and cardiovascular instability during anaesthesia induction
• Hypokalaemia (< 3.0 mEq/L) increases the risk of intraoperative cardiac arrhythmias (especially in patients on digoxin) and should be corrected before elective surgery
• Hyperkalaemia (> 5.5 mEq/L) can cause fatal arrhythmias; surgery best deferred until corrected
• Hypocalcaemia and hypomagnesaemia impair neuromuscular function

• Fluid shifts during major surgery (third spacing, blood loss) cause acute electrolyte disturbances
• Massive transfusion causes hyperkalaemia, hypocalcaemia (citrate binds Ca2+), acidosis
• Prolonged surgery with incorrect IV fluids (excess 0.9% saline) causes hyperchloraemic metabolic acidosis
• Balanced crystalloids (Hartmann's/Plasmalyte) are preferred to 0.9% saline for this reason

• SIADH is common post-operatively (pain, opioids, stress all stimulate ADH) → hyponatraemia
• Intestinal losses from NG tubes, drains, fistulas → hypokaalaemia, hyponatraemia
• Refeeding syndrome after prolonged starvation and TPN initiation
• Monitoring post-thyroidectomy for hypocalcaemia (hypoparathyroidism)
• Post-adrenalectomy: Addisonian crisis (hyponatraemia, hyperkalaemia)

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PART B: MISCELLANEOUS SAQS

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1. SURGICAL AUDIT ⭐⭐⭐

Definition

Types of Audit

• Structure audit: Evaluates the setting (equipment, facilities, staffing)
• Process audit: Evaluates what is done (adherence to guidelines, waiting times)
• Outcome audit: Evaluates results (mortality, morbidity, complication rates, readmission)

THE AUDIT CYCLE (Most important concept)

1. Identify a problem/set a standard
        ↓
2. Observe current practice (data collection)
        ↓
3. Compare against the standard
        ↓
4. Implement change
        ↓
5. Re-audit (close the loop)
        ↓ (back to Step 1)

Steps of a Surgical Audit

• Areas with known problems, high volume procedures, or high-risk outcomes
• Examples: SSI rates, anastomotic leak rates, 30-day mortality, time to surgery for hip fracture

• Based on evidence-based guidelines (NICE, SIGN, Royal College of Surgeons)
• Example standard: "100% of patients undergoing elective colectomy should receive pre-operative antibiotic prophylaxis within 60 minutes of incision"

• Retrospective (case notes review) or prospective
• Tools: Operative registers, discharge summaries, complications register, patient surveys
• Databases: CEPOD, NCEPOD, NSQIP (National Surgical Quality Improvement Program)

• Calculate compliance rate
• Identify outliers and areas of non-compliance
• Statistical analysis

• Feedback results to team (mortality & morbidity - M&M meetings)
• Change protocol/guidelines
• Education and training
• Procurement of resources/equipment

• Confirm change has occurred
• Assess whether standard is now being met
• If not: further investigation and action needed

Importance in Surgical Practice

• Identifies variation in care and substandard practice
• Drives continuous quality improvement
• Medico-legal protection (documented standards)
• Peer accountability (M&M meetings)
• Required for surgical training (FRCS/MCh programmes)

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2. PRE-OPERATIVE, INTRA-OPERATIVE & POST-OPERATIVE CARE ⭐⭐⭐⭐

A) Pre-operative Care

• Full surgical, medical, drug, allergy, family, social history
• Systems examination; airway assessment (Mallampati classification)
• Assessment of fitness for anaesthesia: ASA (American Society of Anaesthesiologists) grading

• Routine: FBC, U&E, coagulation, blood group & save; ECG (>40 yrs or cardiac risk); CXR (if indicated)
• Specific to procedure

• Correct anaemia, electrolyte imbalances, coagulopathy
• Glycaemic control (HbA1c < 8.5% for elective surgery)
• Stop anticoagulants/antiplatelets (warfarin - stop 5 days; DOACs - 24-48 hours; aspirin - as per guidelines)
• Treat respiratory infections; optimise COPD/asthma
• Nutritional optimization (malnourished patients)
• MRSA screening and decolonisation

• Written informed consent: nature of procedure, intended benefit, material risks, alternatives
• Never obtained under duress

• Pre-anaesthetic assessment with anaesthetist
• DVT prophylaxis: LMWH (low molecular weight heparin) + TED stockings
• Antibiotic prophylaxis: Given within 60 min of incision

• Fasting: Solids 6 hours, clear fluids 2 hours pre-operatively (ERAS guidelines)
• Pre-medication if indicated (anxiolytics, antacids)
• Mark the operative site
• Shave vs clip: Electric clipping preferred over razor shaving (less SSI)
• Bowel preparation (if indicated for colorectal surgery)
• Urinary catheterisation as needed

B) Intra-operative Care

• General / regional / local anaesthesia as appropriate
• Continuous monitoring: ECG, SpO2, ETCO2, BP, temperature, urine output

• Appropriate for procedure; padding of pressure points; protect nerves (brachial plexus, ulnar, lateral popliteal)
• Prevent DVT: calf compressors (IPC - intermittent pneumatic compression)

• Strict aseptic technique: sterile gowns, gloves, drapes
• Gentle tissue handling (Halsted's principles)
• Careful haemostasis
• Avoid dead space; minimal use of diathermy
• Temperature maintenance: warming blanket/warm IV fluids (hypothermia increases infection, coagulopathy)
• Maintain normovolaemia; goal-directed fluid therapy
• Antibiotic redosing if procedure > 3 hours

• Operation note, anaesthetic record, swab and instrument counts (count in/count out - sign off by scrub nurse)

C) Post-operative Care

• ABC monitoring: airway, breathing, circulation
• SpO2, ECG, BP every 15 min
• Pain assessment and analgesia (WHO ladder)
• Nausea management (anti-emetics)
• Monitor surgical site for bleeding
• Reversal of anaesthesia; assess consciousness

• IV fluids until oral intake established
• DVT prophylaxis: LMWH + TED stockings (restart after haemostasis secured)
• Early mobilisation (reduces DVT, pneumonia, ileus)
• Incentive spirometry; physiotherapy
• Wound care; drain management
• Regular vital signs; urine output monitoring
• Oral intake: ERAS protocols allow early oral feeding

• Stable vital signs, adequate pain control on oral analgesia
• Tolerating oral fluids/diet
• Passing flatus/stool (if bowel surgery)
• Wound satisfactory, no signs of infection
• Patient understands follow-up and warning signs

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3. ANALGESICS IN PAIN MANAGEMENT

WHO Analgesic Ladder (originally for cancer pain; applied to all surgical pain)

Step 3: Severe pain
Strong opioids (Morphine, Oxycodone, Fentanyl) ± adjuvants

Step 2: Moderate pain
Weak opioids (Codeine, Tramadol) ± non-opioids ± adjuvants

Step 1: Mild pain
Non-opioids (Paracetamol, NSAIDs) ± adjuvants

Classes of Analgesics

• Gabapentin/Pregabalin: Neuropathic pain; reduces opioid requirements post-op
• Amitriptyline: Chronic neuropathic pain
• Ketamine (low dose): NMDA receptor antagonist; reduces opioid tolerance; useful for procedural pain and opioid-resistant pain
• Dexamethasone: Reduces post-op pain and nausea

• Local anaesthetics (Lignocaine, Bupivacaine, Ropivacaine)
• Epidural analgesia (gold standard for major abdominal/thoracic surgery)
• Spinal analgesia
• Nerve blocks (femoral, brachial plexus, TAP block)
• Local anaesthetic wound infiltration

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4. SEGREGATION OF BIOMEDICAL WASTE

Legal Basis (India)

Colour-Coded Segregation System

Key Principles

• Waste must be segregated at the point of generation (bedside, OT, lab)
• No mixing of categories
• All bags/containers labelled with biohazard symbol + name of hospital + date
• Bags tied/sealed when 3/4 full
• Transport in sealed containers to central waste area
• Records maintained for all biomedical waste generated and disposed
• Sharp needles: never recap - straight into white sharps container

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5. ASEPSIS, ANTISEPSIS, STERILIZATION & DISINFECTION

A) Asepsis vs Antisepsis

B) Sterilization vs Disinfection

Methods of Sterilization

1. Autoclave (Steam under pressure) - Gold standard
   • 121°C at 15 psi for 15 min (gravity cycle) OR 134°C at 30 psi for 3 min (pre-vacuum cycle)
   • Kills all organisms including spores (latent heat of vaporisation)
   • Used for: metals, glassware, textiles, rubber goods
   • Not for: heat-sensitive materials
2. Dry Heat (Hot air oven)
   • 160°C for 2 hours OR 180°C for 30 min
   • Less efficient than steam (requires higher temp)
   • For: oils, powders, glass syringes, metal instruments that rust in steam
3. Radiation:
   • Gamma radiation (Co-60): Industrial sterilisation of single-use items (syringes, catheters, sutures, implants); penetrates sealed packaging; cold sterilization
   • UV radiation: Air and surface sterilisation in OTs; limited penetration

• 37-63°C, 40-60% humidity; 2-6 hours + aeration time
• For heat-sensitive items: plastic, rubber, endoscopes, electronics
• Toxic/carcinogenic; requires dedicated equipment and aeration

1. Formaldehyde gas (formaldehyde cabinets)
2. Hydrogen peroxide plasma (Sterrad):
   • Low temperature; rapid cycle (45-75 min)
   • Ideal for heat/moisture-sensitive items; OR-compatible
   • Not for liquids or long lumened instruments

• Bowie-Dick test (autoclave function)
• Autoclave tape (chemical indicator strips change colour)
• Biological indicators: Spore tests (Bacillus stearothermophilus for autoclave; Bacillus subtilis for ETO) - gold standard confirmation

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6. ROUTES OF ADMINISTRATION OF NUTRITION

A) Enteral Nutrition

• Ryle's tube: Large bore (14-16 Fr); for gastric decompression AND feeding; short-term (< 4 weeks)
• Fine bore nasogastric tube (6-8 Fr): Dedicated feeding; more comfortable for longer use
• Insertion: Through nostril → nasopharynx → oesophagus → stomach
• Confirm position: Aspirate pH (< 5.5 confirms gastric); CXR (gold standard if doubt)
• Indications: Dysphagia, unconsciousness, post-head/neck surgery, neurological conditions
• Complications: Aspiration (head elevation 30° mandatory), tube displacement/migration, sinusitis, oesophageal erosion

• Direct feeding into stomach via abdominal wall
• PEG (Percutaneous Endoscopic Gastrostomy): Inserted endoscopically under sedation; does NOT require GA or surgery; preferred method
  • Contraindications to PEG: Cannot transilluminate abdominal wall, ascites, previous upper GI surgery, peritoneal dialysis
• Surgical gastrostomy (Stamm's technique): Open or laparoscopic; used when PEG not feasible
• Indications: Long-term feeding (> 4 weeks) for oropharyngeal/oesophageal pathology
• Allows bolus feeding
• Complications: Tube leakage, infection at stoma site, buried bumper syndrome, aspiration

• Direct feeding into proximal jejunum via abdominal wall
• Needle Catheter Jejunostomy: Fine needle (14 G) through abdominal wall at laparotomy; placed at time of major upper GI surgery (oesophagectomy, gastrectomy, Whipple's)
• PEJ: Percutaneous endoscopic jejunostomy
• Indications: Post major upper GI surgery; gastroparesis; pancreatitis; aspiration risk
• Must use continuous pump infusion - no bolus feeding
• Advantages: Allows early post-op feeding (within 6-12 hours); bypasses stomach; lower aspiration risk
• Complications: Tube kinking, diarrhoea (if too fast), rare jejunal necrosis

B) Parenteral Nutrition

• Via peripheral vein (forearm/hand)
• Only for low-osmolarity solutions (< 900 mOsm/L) - partial supplementation
• Short-term (< 7-10 days); limited caloric delivery; thrombophlebitis risk
• Not suitable for full nutritional replacement

• All nutrition via central venous catheter (subclavian, internal jugular, PICC)
• Full nutritional replacement possible
• Long-term (weeks to months)
• See TPN section above for full details

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7. DAY CARE SURGERY

Definition

Indications

• ASA I, II, or stable ASA III
• BMI < 40 (ideally)
• Responsible adult to accompany and care post-op
• Lives within 1 hour of the facility
• Has access to a telephone

• Inguinal hernia repair (mesh)
• Laparoscopic cholecystectomy (selected)
• Varicose vein surgery
• Circumcision, vasectomy
• Cystoscopy, prostatectomy (TURP short stay)
• Laparoscopic appendicectomy (uncomplicated)
• Breast lump excision, sentinel node biopsy
• Dental surgery
• ENT: Tonsillectomy, grommet insertion
• Arthroscopy (knee, shoulder)
• Cataracts, squint correction
• Skin lesion excision, skin graft

Types

1. True day surgery: Admission and discharge same day (< 12 hours)
2. 23-hour surgery (Extended day surgery): Overnight stay up to 23 hours; for slightly complex procedures

Pre-operative Assessment Criteria (Aldrete Criteria - used for suitability)

• Social suitability: responsible carer, transport, home environment
• Medical stability: no uncontrolled systemic disease
• Procedure suitability: not requiring prolonged post-op monitoring

Discharge Criteria (Post-Anaesthetic Discharge Scoring System - PADSS / Modified Aldrete)

Advantages

• Cost-effective (bed resources)
• Reduced hospital-acquired infection risk
• Psychological benefit (home environment)
• Faster recovery
• Reduced patient anxiety

Disadvantages / Complications

• Inadequate pain control at home
• Post-op nausea/vomiting (PONV) requiring admission
• Surgical complications (bleeding) detected later
• Not suitable for all patients or complex procedures

Discharge Instructions

• Written instructions: diet, activity restrictions, wound care
• Warning signs requiring emergency attendance (bleeding, severe pain, fever)
• Responsible adult supervision for 24 hours
• No driving for 24 hours post GA/sedation
• Follow-up appointment

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8. TRIAGE ⭐⭐⭐⭐

Definition

Principles

• Not based on first-come-first-served
• Based on clinical need and likelihood of survival
• Dynamic - patient condition changes, re-triage frequently

Types

1. Can patient walk? → Yes = GREEN
2. Respirations? → Absent after repositioning = BLACK; > 30/min = RED; < 30/min → next step
3. Perfusion (radial pulse / capillary refill > 2s)? → Absent = RED; present → next step
4. Mental status (obey commands)? → Can't = RED; Can = YELLOW

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9. MINIMALLY INVASIVE GENERAL SURGERY ⭐⭐⭐

Definition

Components / Approaches

• Camera + instruments through 5-12 mm ports (3-5 ports typically)
• CO2 pneumoperitoneum (12-14 mmHg)
• 2D or 3D vision via monitor
• Applications: cholecystectomy, appendicectomy, hernia repair (TEP/TAPP), colectomy, fundoplication, bariatric surgery
• (Detailed in previous session)

• Da Vinci system (7 degrees of freedom, 3D HD vision, tremor filtration)
• Surgeon at console, robot arms at patient
• Applications: Prostatectomy (RARP), colorectal, gynaecological, thoracic
• (Detailed in previous session)

• All instruments and camera through a single umbilical incision
• Better cosmesis (nearly invisible scar)
• Technically more challenging (instrument clashing)
• Used for: cholecystectomy, appendicectomy

• Access through natural orifices (mouth, vagina, rectum) into peritoneal cavity
• No external incisions
• Still largely experimental; most developed: POET (per-oral endoscopic myotomy) for achalasia

• Laparoscopy applied to thoracic cavity
• Applications: lobectomy, pneumothorax repair, pleural biopsy/drainage, oesophageal surgery, thymectomy

• Intravascular access via catheters; guidance by fluoroscopy/USS
• EVAR (Endovascular Aneurysm Repair), TEVAR, balloon angioplasty, stenting, embolization

• ERCP: Bile duct stone removal, stenting, sphincterotomy
• EUS (Endoscopic Ultrasound): Tissue sampling, drainage of pseudocysts
• Endoscopic Submucosal Dissection (ESD): En-bloc resection of superficial GI neoplasms
• Transanal minimally invasive surgery (TAMIS/TEM): For rectal polyps and early rectal cancers

Advantages of MIS vs Open Surgery

• Less pain → less analgesia
• Shorter hospital stay → faster return to work
• Less blood loss
• Reduced infection (smaller wounds)
• Reduced ileus
• Better cosmesis
• Lower incisional hernia rate

Limitations

• Expensive equipment
• Long learning curve
• Not suitable for all pathologies (e.g., advanced malignancy, complex anatomy, previous multiple surgeries)
• Risk of conversion to open
• CO2 pneumoperitoneum physiological effects
• Equipment failure dependency

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10. TISSUE TYPING / HLA (Human Leukocyte Antigen) ⭐⭐⭐⭐

Definition

MHC and HLA System

• MHC (Major Histocompatibility Complex): A cluster of genes on chromosome 6p21 encoding highly polymorphic cell surface glycoproteins
• In humans, MHC is called the HLA system
• HLA antigens are expressed on virtually all nucleated cells
• Function: Present peptide antigens to T lymphocytes → direct immune response

HLA Classes

Why HLA Matters in Transplantation

• Mismatched HLA antigens on donor cells are recognised as "foreign" by recipient T cells → allograft rejection
• Better HLA matching → lower rejection risk → better graft survival

Tissue Typing Methods

• Lymphocytes from donor/recipient + specific HLA antisera + complement
• Cell lysis = antigen present
• Historical method; now largely replaced

• PCR-SSP (Sequence-Specific Primers): Quick, low-resolution
• PCR-SSO (Sequence-Specific Oligonucleotides): Intermediate resolution; Luminex-based
• NGS (Next Generation Sequencing): High resolution, most accurate; identifies even subtle differences
• Uses blood (buccal swab) sample

Crossmatch Testing

• Recipient serum + donor lymphocytes + complement
• Cell death = positive crossmatch = absolute contraindication to transplant (hyperacute rejection)

• More sensitive than CDC; detects low-level antibodies
• Positive = significant risk; further evaluation required

• Compare recipient's Panel Reactive Antibody (PRA) profile against donor's HLA typing
• No donor cells needed; used for deceased donor transplants

Panel Reactive Antibody (PRA)

• Percentage of HLA antigens in the population to which the patient has antibodies
• High PRA (> 80%): Highly sensitised patient; difficult to find compatible donor; higher risk of rejection
• Sensitisation from: previous transplant, blood transfusion, pregnancy

HLA Matching Priority

Rejection Types

ABO Blood Group Compatibility

• Always required before solid organ transplant
• Incompatible ABO → hyperacute rejection (anti-A/anti-B antibodies)
• Exception: ABO-incompatible transplantation possible with pre-treatment (plasmapheresis + rituximab) in some centres

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SHOCK, HAEMORRHAGE & BLOOD TRANSFUSION - Complete Study Guide

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PART A: SHOCK

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1A. DEFINITION & CLASSIFICATION OF SHOCK

Definition

Pathophysiology (Common Pathway)

Classification of Shock

• Haemorrhagic: trauma, GI bleed, ruptured AAA, obstetric
• Non-haemorrhagic: vomiting, diarrhoea, burns, pancreatitis, bowel obstruction (third spacing)

• Myocardial infarction, arrhythmias, valvular disease, blunt myocardial injury, cardiomyopathy

• Cardiac tamponade, tension pneumothorax, massive pulmonary embolism, air embolism

• Septic shock (most common distributive)
• Anaphylactic shock (histamine-mediated vasodilatation)
• Neurogenic shock (spinal injury - loss of sympathetic tone)

• Addison's disease/adrenal insufficiency, hypothyroidism

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1B. HYPOVOLAEMIC / HAEMORRHAGIC SHOCK ⭐⭐⭐⭐

Definition

Pathophysiology

• Catecholamine release (adrenaline + noradrenaline) from adrenal medulla
• ↑ Heart rate (tachycardia) - tries to maintain CO (CO = HR × SV)
• Peripheral vasoconstriction (↑SVR) - maintains BP, redistributes blood to heart/brain
• Venoconstriction - increases venous return (autotransfusion from venous capacitance)
• RAAS activation → aldosterone → Na+ + water retention → ↑blood volume
• ADH release → free water retention by kidneys → ↑ blood volume
• Cortisol release → mobilises glucose, supports catecholamines
• Capillary refill from interstitium (transcapillary refill)

• Blood redirected from skin, muscle, GI tract, kidney → to heart and brain
• "Centralization of circulation"
• Anaerobic metabolism in under-perfused tissues → lactic acid + metabolic acidosis

• Blood pressure falls (after 30-40% volume loss)
• Progressive acidosis impairs cardiac contractility
• Coagulation factors diluted/consumed → coagulopathy
• Hypothermia worsens coagulopathy
• "Lethal triad": Hypothermia + Acidosis + Coagulopathy → further bleeding → death

• Ischaemic cells release inflammatory mediators, reactive oxygen species, potassium, acids on reperfusion
• Complement + neutrophil activation → damage to distant organs (lung, kidney)
• SIRS → MODS (systemic inflammatory response → multiorgan dysfunction)

ATLS Classification of Haemorrhagic Shock

Clinical Features

• Tachycardia (earliest reliable sign)
• Hypotension (late sign - appears after 30% loss)
• Narrowed pulse pressure (systolic - diastolic gap) - early sign (vasoconstriction raises diastolic before systolic falls)
• Weak, thready, rapid pulse
• Raised JVP (cardiogenic/obstructive) vs low JVP (hypovolaemic)

• Cool, pale, clammy skin (vasoconstriction + sweating)
• Prolonged capillary refill > 2 seconds
• Collapsed peripheral veins

• Tachypnoea (compensatory, driven by metabolic acidosis)

• Oliguria < 0.5 mL/kg/hour (early = renal compensation; late = renal hypoperfusion)

• Anxiety → confusion → drowsiness → coma (parallel to haemodynamic deterioration)

Investigations

• BP, HR, SpO2, RR, temperature
• Urine output (most sensitive continuous indicator of resuscitation)
• ECG
• Blood glucose (capillary)

• FBC: Hb/Haematocrit (may be normal initially - dilution occurs later); WBC
• U&E, Creatinine: Renal function, electrolytes
• Coagulation (PT, APTT, fibrinogen, platelets): Especially if massive haemorrhage
• ABG: pH, PaO2, PaCO2, lactate (most important marker of shock severity and resuscitation), base excess/deficit
  • Lactate > 4 mmol/L = severe shock; lactate clearance tracks resuscitation success
• Blood Group & Cross-match (4-6 units pRBC urgently)
• Liver function tests
• D-dimer (if PE or DIC suspected)

• E-FAST (Extended Focused Assessment with Sonography in Trauma): Bedside USS for free fluid in abdomen, pericardium, pneumothorax
• CXR, pelvic X-ray (in trauma)
• CT (Trauma survey) - only when haemodynamically stable
• CECT abdomen (for intra-abdominal haemorrhage)

Management

• Direct pressure on external wounds
• Tourniquets (limb haemorrhage) - TCCC/MARCH protocol
• Pelvic binder (pelvic fractures)
• Haemostatic dressings (Combat gauze - kaolin-impregnated)
• FAST call surgeon for internal haemorrhage → emergency surgery

• High-flow oxygen 15 L/min (non-rebreather mask)
• Treat tension pneumothorax (needle decompression + chest drain)

1. IV access: Two large-bore cannulae (14-16G) in antecubital fossae; alternatively intraosseous (IO) access if IV fails
2. Blood samples taken simultaneously (FBC, crossmatch, coagulation, ABG, U&E)
3. Fluid resuscitation:

1. Damage Control Resuscitation:
   • pRBC : FFP : Platelets = 1:1:1 (whole blood equivalent)
   • Avoid excessive crystalloids (dilutional coagulopathy, hypothermia, oedema)
   • Tranexamic acid (TXA) 1g IV over 10 min within 3 hours of injury (CRASH-2 trial) - antifibrinolytic; reduces mortality
   • Maintain normothermia (warm fluids, warm blankets)
   • Correct coagulopathy with cryoprecipitate (fibrinogen) + platelets
2. Vasopressors (if needed):
   • Noradrenaline (norepinephrine) - first choice vasopressor while volume is being restored
   • Note: vasopressors do NOT replace volume; they temporise

• Neurological assessment: GCS, pupils
• Capillary glucose

• Full exposure + log roll; keep warm (prevent hypothermia)

• MAP ≥ 65 mmHg (or SBP > 90 mmHg)
• Urine output ≥ 0.5 mL/kg/hour
• Lactate clearance (fall > 10% per hour)
• Base excess normalising (> -6)
• CVP 8-12 mmHg
• ScvO2 > 70%
• Temperature > 36°C

• Surgery (damage control laparotomy/thoracotomy for internal bleeding)
• Interventional radiology (angioembolization for pelvic, hepatic, splenic bleeding)

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2. SEPTIC SHOCK ⭐⭐⭐⭐

Definitions (Sepsis-3, 2016)

• Infection: Microbial invasion with host inflammatory response
• Sepsis: Life-threatening organ dysfunction caused by a dysregulated host response to infection (organ dysfunction = SOFA score rise ≥ 2)
• Septic shock: Sepsis + vasopressor requirement to maintain MAP ≥ 65 mmHg + serum lactate > 2 mmol/L despite adequate fluid resuscitation
• qSOFA (quick SOFA - bedside screening): 2 of 3: RR ≥ 22/min, altered mentation, SBP ≤ 100 mmHg

Common Causative Organisms

• Gram-negative rods: E. coli, Klebsiella, Pseudomonas, Enterobacter (release endotoxin/LPS)
• Gram-positive cocci: Staphylococcus aureus, Streptococcus (release exotoxins)
• Fungi: Candida (in immunocompromised)
• Source: GI (peritonitis, anastomotic leak), urinary tract, lung, biliary, wound, CVC

Pathophysiology

• LPS (gram-negative endotoxin) or peptidoglycan/teichoic acid (gram-positive) binds Toll-like receptors (TLRs) on macrophages and monocytes
• Triggers massive release of pro-inflammatory cytokines: TNF-α, IL-1, IL-6, IL-8

• Cytokines activate complement, coagulation cascade, neutrophils, endothelium
• Massive endothelial activation → vasodilation (NO synthase induction → ↑ nitric oxide (NO))
• ↓ SVR (vasodilation) → ↓ MAP despite initially ↑ cardiac output

• Endothelial damage → capillary leak → third spacing of fluid → hypovolaemia
• Microthrombi form in capillaries (DIC - disseminated intravascular coagulation)
• Arteriovenous shunting → cells cannot extract oxygen despite adequate delivery

• Mitochondrial dysfunction - cells unable to utilise oxygen (cytopathic hypoxia)
• Anaerobic metabolism → hyperlactataemia even without low cardiac output
• Lactic acidosis

• Initial: hyperdynamic state (high CO, bounding pulse, warm peripheries) - "warm shock"
• Later: myocardial depression from TNF-α, IL-1, NO → falls CO → "cold shock"
• Relative adrenal insufficiency (cortisol resistance)

Clinical Features

• High fever (> 38°C) or hypothermia (< 36°C) - both possible
• Bounding pulse, tachycardia
• Warm, flushed peripheries (vasodilation - different from hypovolaemic shock)
• Wide pulse pressure
• Tachypnoea
• Confusion/agitation

• Becomes cold, clammy (like hypovolaemic shock - myocardial depression + hypovolaemia)
• Severe hypotension (refractory to fluids)
• Oliguria → anuria
• Jaundice (liver involvement)
• ARDS (acute respiratory distress syndrome) - lung failure
• DIC → bleeding from multiple sites, petechiae
• Multiorgan failure: AKI, hepatic failure, encephalopathy, ileus

Investigations

• Blood cultures (2 sets before antibiotics) + cultures from all potential sources
• FBC: WBC ↑↑ (or ↓ in severe sepsis - leucopenia), Left shift (immature neutrophils), Thrombocytopaenia (DIC)
• Lactate: Most important prognostic marker; > 2 = sepsis; > 4 = worse prognosis
• Procalcitonin (PCT): Elevated in bacterial sepsis; useful for monitoring
• CRP (elevated)
• ABG: metabolic acidosis, hypoxaemia
• U&E: AKI (↑creatinine)
• LFTs: hepatic dysfunction
• Coagulation: prolonged PT/APTT, ↑D-dimer, ↓fibrinogen (DIC)
• SOFA score calculation (respiratory, coagulation, liver, cardiovascular, CNS, renal)
• Imaging: CXR, USS, CT to identify source

Management - Surviving Sepsis Campaign Bundles (SSC 2018)

1. Measure lactate; re-measure if initial > 2 mmol/L
2. Blood cultures x2 before antibiotics (but do NOT delay antibiotics > 45 min)
3. IV broad-spectrum antibiotics (within 1 hour of recognition)
4. Crystalloid resuscitation: 30 mL/kg IV if MAP < 65 or lactate ≥ 4 mmol/L
5. Vasopressors if MAP < 65 despite fluids: Noradrenaline first choice

• Balanced crystalloids (Plasmalyte/Hartmann's) preferred over 0.9% saline
• 30 mL/kg initial bolus (Sepsis-3 guideline); reassess with dynamic measures (pulse pressure variation, PLR - passive leg raise test)
• Avoid excessive fluids (ARDS risk, AKI)

• Noradrenaline (Norepinephrine) - first-line vasopressor; target MAP ≥ 65 mmHg
• Vasopressin 0.03 units/min add-on (spares noradrenaline dose)
• Dopamine (now less preferred - more arrhythmias)
• Adrenaline - add-on for refractory septic shock

• Broad-spectrum empiric: (depending on source)
  • Unknown source: Piperacillin-tazobactam + gentamicin (or meropenem if severe)
  • Add metronidazole if GI/abdominal source
  • Add vancomycin if MRSA suspected
  • Antifungals (fluconazole/caspofungin) if fungal sepsis suspected
• De-escalate at 48-72 hours based on culture results
• Duration: typically 7-10 days

• Drain abscesses, remove infected devices (CVCs, drains, prostheses)
• Surgical debridement if necrotising fasciitis
• Biliary drainage for cholangitis
• Source control within 12 hours of diagnosis

• ARDS → Lung-protective ventilation: Tidal volume 6 mL/kg IBW; PEEP; prone positioning
• AKI → CRRT (Continuous Renal Replacement Therapy) or HD if oliguria persists
• Glucose control: Target 7.8-10 mmol/L with insulin infusion
• Stress ulcer prophylaxis: PPI or H2 blocker
• DVT prophylaxis: LMWH + IPC
• Steroids (Hydrocortisone 200 mg/day): Only if refractory septic shock (vasopressor-dependent) - "vasopressor-dependent septic shock"; not routine

• MAP ≥ 65 mmHg
• Lactate clearance ≥ 10%/hour or normalisation
• Urine output ≥ 0.5 mL/kg/hr
• ScvO2 ≥ 70% (central venous O2 saturation)
• CVP 8-12 mmHg

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3A. CLASSIFICATION OF HAEMORRHAGE

By Timing (Surgical)

1. Primary haemorrhage: Occurs at the time of injury/surgery
2. Reactionary haemorrhage: Within 24 hours of surgery - due to dislodgement of clot by resuscitation, rise in BP, vasodilatation, or slipping of a ligature
3. Secondary haemorrhage: 7-14 days post-injury - due to sloughing of vessel wall from infection, pressure necrosis (drain), or malignancy

By Visibility

• Revealed (external): Visible bleeding (wound, haematemesis, haematuria)
• Concealed (internal): Within body cavities (haemothorax, haemoperitoneum, retroperitoneal, limb fractures); must be suspected and actively sought

By Origin

• Arterial: Bright red, pulsatile, rapid
• Venous: Dark red, steady flow
• Capillary: Ooze from small vessels; usually self-limiting

By Volume (ATLS Classification) - See table above (Class I-IV)

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4. MEASUREMENT OF CENTRAL VENOUS PRESSURE (CVP)

Definition

Significance

• Low CVP (< 5 cmH2O): Hypovolaemia, vasodilation
• High CVP (> 12 cmH2O): Fluid overload, right heart failure, cardiac tamponade, tension pneumothorax, PE
• CVP trend over time (response to fluid challenge) is more useful than a single reading

Technique

• Central venous catheter (CVC)
• Manometer/electronic pressure transducer + monitor
• 3-way stopcock
• IV saline + IV administration set

1. Internal jugular vein (IJV) - right side preferred; less risk of pneumothorax
2. Subclavian vein - higher pneumothorax risk but easier nursing care
3. Femoral vein - avoid if possible (infection risk, inaccurate for CVP)

1. Patient positioned supine (or 30° head-up if respiratory compromise)
2. Strict aseptic technique; skin prep, drape, gown, gloves, mask
3. Local anaesthesia; ultrasound guidance strongly recommended (reduces complications)
4. Seldinger technique: Needle → aspiration of dark venous blood → guidewire → dilator → CVC inserted → guidewire removed
5. Confirm position: CXR (tip should be at SVC-RA junction, not in RA - arrhythmia risk)
6. Zero the transducer at the phlebostatic axis (mid-axillary line, 4th intercostal space) - represents level of right atrium
7. Read CVP at end-expiration (respiratory variation is normal)

• Pressure transducer connected to monitor
• Shows characteristic a, c, v waves on CVP waveform:
  • a wave: Atrial contraction
  • c wave: Tricuspid valve closure
  • v wave: Venous return during isovolumetric contraction

Complications of CVC insertion

• Pneumothorax (most feared with subclavian access)
• Arterial puncture (carotid with IJV access)
• Air embolism
• Haematoma
• Line infection/CRBSI
• Arrhythmias (guidewire in right ventricle)
• Thoracic duct injury (left IJV/subclavian)

Limitations

• Does not reliably predict fluid responsiveness
• Affected by venous compliance, PEEP (ventilation), tricuspid valve disease, cardiac tamponade
• Preferred: Dynamic measures (pulse pressure variation, stroke volume variation, passive leg raise test) for fluid responsiveness assessment in ICU

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5A. SIRS (Systemic Inflammatory Response Syndrome) ⭐⭐⭐

Definition

SIRS Criteria (Bone et al., 1992)

Causes of SIRS

• Infectious: Sepsis (bacterial, viral, fungal)
• Non-infectious: Major trauma/surgery, burns, pancreatitis, ischaemia-reperfusion injury, multiple transfusions, autoimmune conditions

Pathophysiology

Clinical Significance

• SIRS + confirmed infection = Sepsis (old definition; superseded by Sepsis-3 but still widely used)
• SIRS is a spectrum - severity correlates with outcome
• Monitoring SIRS criteria guides clinical decision-making

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5B. MULTIPLE ORGAN DYSFUNCTION SYNDROME (MODS)

Definition

Causes / Precipitants

• Prolonged shock (hypovolaemic, septic) - most common
• Major trauma/burns
• Pancreatitis
• Ischaemia-reperfusion injury
• SIRS from any cause

Pathogenesis

Organs Affected (in order of typical involvement)

Mortality

• 2 organs failed: ~40-50%
• 3 organs failed: ~60-70%
• 4+ organs failed: > 80% (often unsurvivable)

Management

• No specific treatment - supportive care of each failing organ
• Remove/treat the underlying trigger (source control)
• Nutritional support (early enteral nutrition)
• Prevention is key - aggressive early resuscitation of shock to limit the duration of hypoperfusion

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6A. REACTIONARY HAEMORRHAGE ⭐⭐⭐

Definition

Causes

1. Rise in blood pressure during recovery from anaesthesia/shock → dislodges a clot that had temporarily sealed a vessel
2. Vasodilatation as patient warms up post-operatively
3. Ligature slippage from a tied vessel
4. Technical failure of haemostasis during surgery (inadequate diathermy/ligation)
5. Inadequate wound closure under tension

Clinical Features

• Fresh bleeding from the wound, drain, stoma, or natural orifice within first 24 hours post-op
• Increasing drain output (bright red)
• Haematoma formation
• Tachycardia, falling BP
• Wound expanding with haematoma

Management

1. Resuscitate: IV access, fluids, blood transfusion
2. Identify source - check wound, drain output
3. Surgical re-exploration - often necessary to identify and control the bleeding point (ligate vessel, re-apply clips, re-suture anastomosis)
4. Never just "wait and see" with significant reactionary haemorrhage

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6B. SECONDARY HAEMORRHAGE ⭐⭐⭐

Definition

Causes

1. Infection/sepsis (most common) - bacterial enzymes digest the vessel wall
2. Pressure necrosis - from a drain lying against a vessel
3. Malignancy - tumour eroding into a vessel
4. Radiotherapy - radiation endarteritis weakens vessel wall
5. Anastomotic dehiscence - breakdown of bowel anastomosis erodes adjacent vessel
6. Aortoenteric fistula - classically presents as "herald bleed" then massive haemorrhage

Clinical Features

• Sudden or insidious fresh bleeding from wound, drain, or natural orifice 7-14 days post-op
• Often preceded by signs of infection (fever, wound discharge, erythema)
• Can be catastrophic (profuse arterial haemorrhage - rare but life-threatening)
• Typically darker blood (from wound infection bed) unless major vessel involved

Management

1. Immediate resuscitation (IV access, crossmatch, blood transfusion)
2. Control active bleeding: Direct pressure; if arterial - immediate surgical exploration
3. Treat the underlying infection aggressively (antibiotics, drainage)
4. Surgical ligation of the bleeding vessel ± bypass grafting if major vessel
5. Angioembolization (interventional radiology) for non-surgically accessible sites
6. Remove/replace the drain (if it caused the pressure necrosis)
7. Pack the wound if infection is the cause; allow healing by secondary intention

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PART B: BLOOD TRANSFUSION

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1. BLOOD TRANSFUSION

A) Principles of Blood Transfusion

1. "First, do no harm" - transfuse only when benefit outweighs risk
2. Correct indication - use restrictive transfusion strategy (transfuse when Hb < 7 g/dL in stable patients; Hb < 8-9 in cardiac/symptomatic patients)
3. ABO and Rh compatibility - mandatory
4. Full cross-match before elective transfusion
5. Patient identification verification before hanging blood (fatal ABO reactions are mostly due to patient ID errors)
6. Informed consent where possible
7. Warm blood for massive transfusion (cold blood exacerbates coagulopathy)
8. Monitoring during transfusion (first 15 min most important for acute reactions)
9. Single unit policy (stable patients) - transfuse one unit, reassess Hb before next unit

B) Indications for Blood Transfusion ⭐⭐⭐⭐

• Active haemorrhage with haemodynamic compromise
• Target Hb ≥ 7-8 g/dL during resuscitation

• Restrictive triggers: Hb < 7 g/dL (in stable, not bleeding patients) - TRICC trial evidence
• Liberal triggers: Hb < 8-9 g/dL in:
  • Acute coronary syndrome / cardiac disease
  • Post-cardiac surgery
  • Symptomatic patients (angina, dyspnoea at rest, tachycardia, hypotension)

• Hb < 8 g/dL before major surgery where blood loss expected
• Or when surgery cannot be delayed

• When Hb < 7 g/dL or symptomatic AND not responding to haematinic/erythropoietin therapy
• Thalassaemia, aplastic anaemia, MDS (maintain Hb 9-10)

• Active bleeding requiring > 10 units pRBC in 24 hours

C) Complications of Blood Transfusion ⭐⭐⭐ (Acute Transfusion Reactions)

ACUTE REACTIONS (within 24 hours):

• Cause: ABO incompatibility (most commonly due to clerical/identification error)
• Mechanism: Pre-formed antibodies (IgM) in recipient → complement-mediated intravascular haemolysis
• C/F: Sudden onset during infusion - fever, chills, loin/back pain, haemoglobinuria (red-brown urine), hypotension, tachycardia, flushing, burning at IV site, DIC, renal failure
• In anaesthetised patients: Unexplained hypotension, haemoglobinuria, oozing from wound (DIC)
• Management:
  1. STOP transfusion immediately
  2. Maintain IV access; change giving set
  3. IV fluids - 0.9% saline; maintain urine output ≥ 1 mL/kg/hr
  4. Furosemide if anuric (force diuresis)
  5. Send remaining blood + fresh blood sample to blood bank; recheck ID
  6. DAT (Direct Antiglobulin Test / Coombs test)
  7. FBC, coagulation, renal function, LFTs
  8. Treat DIC if develops (FFP, platelets, cryoprecipitate)
  9. Dialysis if AKI
  10. Document; incident reporting

• Cause: Leukocyte antibodies in recipient reacting to donor leukocytes; cytokines in stored blood
• C/F: Fever, chills, rigors (usually mild; no haemolysis); temperature rise ≥ 1°C during transfusion
• Now rare with leucodepletion of all blood components in the UK
• Management: Stop transfusion temporarily; paracetamol; restart slowly if no evidence of haemolysis

• Cause: Antibodies to plasma proteins in transfused product
• Range: Mild urticaria (IgE-mediated) → anaphylaxis
• C/F (mild): Urticaria, pruritus, flushing
• C/F (severe - anaphylaxis): Bronchospasm, stridor, hypotension, collapse
• Management:
  • Mild: slow/stop transfusion + antihistamine (chlorphenamine 10 mg IV)
  • Severe anaphylaxis: STOP transfusion; adrenaline 0.5 mg IM; IV fluids; steroids; antihistamines; O2

• Cause: Donor antibodies (anti-HLA, anti-neutrophil) react with recipient leukocytes → neutrophil activation → capillary leak in pulmonary microvasculature
• Particularly associated with FFP (multiple donor exposure)
• C/F: Acute onset (within 6 hours of transfusion) of bilateral pulmonary infiltrates, hypoxaemia, non-cardiogenic pulmonary oedema (resembles ARDS); fever, hypotension
• Management: Stop transfusion; supportive (oxygen, mechanical ventilation); usually resolves in 48-96 hours; no specific treatment; NOT diuretics (not cardiogenic)

• Cause: Rapid infusion of blood products → volume overload → left heart failure
• Risk: elderly, cardiac disease, renal failure, small body weight
• C/F: Dyspnoea, hypertension (unlike TRALI), pulmonary oedema, raised JVP, cardiogenic features
• Management: Stop transfusion; furosemide IV; O2; sit upright
• Distinguish from TRALI: TACO = hypertensive + respond to diuretics; TRALI = hypotensive + diuretics harmful

• Due to bacterial contamination of blood (usually during platelet storage - stored at room temperature)
• Organisms: Pseudomonas, Staphylococcus, Yersinia
• C/F: Rigors, high fever, hypotension shortly after transfusion
• Management: Stop; blood cultures from patient and bag; broad-spectrum antibiotics; resuscitation

• Bradykinin accumulation with bedside leucofiltration in patients on ACE inhibitors → hypotension

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2. BLOOD PRODUCTS

A) Fresh Frozen Plasma (FFP) ⭐⭐⭐

1. Massive haemorrhage (1:1:1 with pRBC and platelets)
2. Documented coagulation factor deficiency with active bleeding (PT or APTT > 1.5x normal)
3. Reversal of warfarin in active bleeding (with Vitamin K)
4. DIC with active bleeding
5. Liver disease with coagulopathy + active bleeding or before invasive procedures
6. TRALI-like reactions from FFP (common source of HLA antibodies)
7. Thrombotic Thrombocytopaenic Purpura (TTP) - plasmapheresis with FFP (provides ADAMTS13)

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B) Cryoprecipitate

• Factor VIII (major component)
• Von Willebrand Factor (vWF)
• Fibrinogen (most important surgical use)
• Factor XIII
• Fibronectin

1. Low fibrinogen (most important indication - fibrinogen < 1.5 g/L with bleeding) - especially massive transfusion
2. Haemophilia A (Factor VIII deficiency) - when DDAVP or specific concentrates unavailable
3. Von Willebrand disease - when specific vWF concentrates unavailable
4. DIC (fibrinogen replacement)
5. Uraemic bleeding (fibronectin helps)

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3. MASSIVE BLOOD TRANSFUSION & COMPLICATIONS ⭐⭐⭐⭐

Definition

Indications

• Major trauma with haemorrhagic shock (Class III/IV)
• Ruptured AAA, ruptured ectopic pregnancy
• Massive upper GI haemorrhage
• Perioperative catastrophic haemorrhage
• Obstetric haemorrhage (PPH)

Massive Transfusion Protocol (MTP)

• 1:1:1 ratio of pRBC : FFP : Platelets (simulates whole blood)
• Tranexamic acid (TXA) 1g IV ASAP (then 1g over 8 hours) - antifibrinolytic
• Cryoprecipitate if fibrinogen < 1.5 g/L
• Warm all blood products (blood warmer)
• Avoid crystalloids
• Calcium (10 mL 10% calcium chloride) - citrate in blood binds Ca2+

"Lethal Triad" of Massive Transfusion

1. Hypothermia (< 35°C)
2. Coagulopathy (dilutional + consumption of clotting factors)
3. Acidosis (metabolic, from shock + anaerobic metabolism) These three are mutually reinforcing and together predict very high mortality.

Complications of Massive Transfusion

• Dilutional coagulopathy - dilution of clotting factors and platelets with each unit of pRBC
• DIC (consumptive coagulopathy)
• Thrombocytopaenia (dilution + consumption; platelet nadir at 1.5x blood volume replaced)

• Hypothermia - stored blood at 4°C + large volumes
• Hypocalcaemia - citrate (anticoagulant in stored blood) chelates ionised Ca2+; corrected with IV calcium
• Hyperkalaemia - stored blood leaks K+ (K+ rises during storage); risk of arrhythmias
• Hypokalaemia - delayed (as cells recover after transfusion; K+ moves back in)
• Metabolic acidosis - stored blood pH is low (CO2 accumulation during storage); resolves as metabolism clears citrate
• Citrate toxicity (in hepatic failure - cannot metabolise citrate)
• Iron overload (chronic repeated transfusion - each unit contains ~250 mg elemental iron; treat with desferrioxamine)

• TRALI (Transfusion-Related Acute Lung Injury)
• TACO (Transfusion-Associated Circulatory Overload)

• Immunosuppression (transfusion-related immunomodulation - TRIM)
• Increased infection risk

• Air embolism (via pressure bags)
• Hypothermia (addresses systemic heat loss)

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4. BLOOD GROUP TYPING & CROSS-MATCHING

ABO Blood Group System

Rhesus (Rh) System

• Rh positive (Rh+): D antigen present on RBCs (85% of population)
• Rh negative (Rh-): D antigen absent
• Anti-D antibodies are NOT naturally occurring (require prior sensitisation)
• Clinical importance: Rh- women sensitised by Rh+ pregnancy/transfusion → anti-D antibodies → haemolytic disease of the newborn (HDN) in subsequent Rh+ pregnancies

Blood Group Typing (BGT)

Cross-Matching

1. Major cross-match: Recipient serum + donor red cells + incubation + anti-human globulin (AHG/Coombs test)
   • Positive (agglutination) = incompatible; transfusion contraindicated
   • This is the critical step
2. Minor cross-match: Donor serum + recipient red cells (now rarely performed in blood banks)
3. Takes 45 minutes

• ABO + Rh type determined
• Serum screened for unexpected antibodies against a panel of RBCs
• If screen negative: electronic cross-match can be done in 2-5 minutes
• If screen positive: full serological cross-match required

• Type-specific blood (ABO + Rh typed only, no full X-match): Available in 10-15 min; acceptable safety
• O-negative (universal donor): For immediate, life-threatening emergency before any typing done
  • O-negative pRBC to females of childbearing age
  • O-positive pRBC to males and post-menopausal females

DAT (Direct Antiglobulin Test / Direct Coombs Test)

• Detects antibodies/complement already bound to patient's red cells
• Positive in: AIHA, haemolytic transfusion reactions, HDN, drug-induced haemolysis

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5. HYPERBARIC OXYGEN (3 Marks)

Definition

Mechanism

• At 3 ATA with 100% O2: dissolved O2 in plasma rises from 0.3 mL/dL to ~6 mL/dL (sufficient for tissue requirements without haemoglobin)
• Markedly increases tissue partial pressure of O2 → reverses hypoxia
• Bactericidal: High PO2 directly kills anaerobic organisms (no tolerance of O2)
• Bacteriostatic: Impairs toxin production
• Enhances leukocyte killing (oxidative burst requires O2)
• Promotes angiogenesis and fibroblast proliferation → wound healing
• Reduces oedema (vasoconstriction at high PO2)
• Displaces CO from haemoglobin (CO poisoning)

Indications

1. Gas gangrene (Clostridial myonecrosis) - inhibits Clostridial growth; adjunct to surgery and penicillin
2. Necrotising fasciitis - adjunct to surgical debridement
3. Chronic non-healing wounds (diabetic foot ulcers, radiation wounds) - promotes angiogenesis
4. Compromised skin flaps and grafts - rescues borderline flaps

Contraindications

• Untreated pneumothorax (absolute)
• Uncontrolled high fever
• Certain medications (bleomycin, cisplatin, disulfiram)

Complications

• Oxygen toxicity seizures (rare at standard pressures)
• Barotrauma (ear, sinus pain)
• Claustrophobia
• Reversible myopia
• Fire risk (100% O2 environment)

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