General surgery notes

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General Surgery Notes - Acute Abdomen & Emergency Surgery

MBBS Level | Sources: Bailey & Love 28th Ed, Schwartz's Surgery 11th Ed, Tintinalli's Emergency Medicine, Rosen's Emergency Medicine, Pye's Surgical Handicraft

1. THE ACUTE ABDOMEN - Overview

The acute abdomen is defined as a sudden onset of severe abdominal pain requiring urgent assessment and often emergency surgery.

Approach (History + Examination)

History - key questions:
  • Site of pain at onset vs. now (migration is key - e.g., appendicitis migrates from peri-umbilical to RIF)
  • Character: colicky (obstruction, ureteric) vs. constant (peritonitis, ischemia)
  • Onset: sudden ("like a thunderclap") suggests perforation or ruptured AAA
  • Associated symptoms: nausea, vomiting, fever, altered bowel habit, last menstrual period (always in women of reproductive age), urinary symptoms
Examination sequence:
  1. General: Vitals, posture (peritonitis patient lies still; renal colic patient is restless)
  2. Inspection: distension, scars, hernias, visible peristalsis
  3. Palpation: tenderness, guarding, rigidity, rebound
  4. Percussion: resonance (gas) vs dullness (fluid)
  5. Auscultation: bowel sounds (high-pitched tinkling = obstruction; absent = paralytic ileus/peritonitis)
  6. Always examine hernial orifices and do PR examination

Peritonism Signs

SignDescription
GuardingInvoluntary reflex abdominal wall contraction
RigidityBoard-like abdomen - diffuse peritonitis
Rebound tendernessPain worsens on lifting hand off abdomen
Referred shoulder tip painDiaphragmatic irritation - C5 dermatome
"If inflammation arises under the diaphragm, shoulder tip ('phrenic') pain may be felt. This is referred pain to the C5 dermatome." - Bailey and Love's Surgery, p. 1109

Categories of Peritonitis (Bailey & Love)

  • Localised - e.g., appendicitis, diverticulitis (contained)
  • Diffuse/generalised - e.g., perforated viscus, faecal peritonitis
Causes of peritoneal inflammation:
  • Bacterial (GI perforation, transmural translocation)
  • Chemical (bile, barium, gastric acid)
  • Ischaemic (strangulated bowel, vascular occlusion)
  • Traumatic
  • Miscellaneous (familial Mediterranean fever, starch peritonitis)
Paths to peritoneal infection:
  • GI perforation (ulcer, appendix, diverticulum)
  • Transmural translocation without perforation (pancreatitis, ischaemic bowel)
  • Exogenous contamination (open trauma, peritoneal dialysis)
  • Female genital tract (PID)
  • Haematogenous spread (rare)

2. ACUTE APPENDICITIS

The most common surgical emergency worldwide.

Pathophysiology

Luminal obstruction (faecalith, lymphoid hyperplasia, tumour) → bacterial overgrowth → wall distension → ischaemia → transmural inflammation → perforation if untreated.

Clinical Features

FeatureDetails
PainStarts peri-umbilical (visceral, T10), migrates to RIF (McBurney's point) within 4-6 hours
AnorexiaAlmost invariable
Nausea/vomitingAfter pain onset (important - vomiting before pain suggests gastroenteritis)
Low-grade fever37.5 - 38.5°C; high fever suggests perforation
ConstipationCommon; diarrhoea in pelvic appendix
Examination signs:
  • McBurney's point tenderness - 1/3 of the way from ASIS to umbilicus
  • Rovsing's sign - pressure in LIF causes pain in RIF (cross-referred pain)
  • Psoas sign - pain on extension of right hip (retrocaecal appendix)
  • Obturator sign - pain on internal rotation of flexed right hip (pelvic appendix)
  • Cutaneous hyperaesthesia at T10-T12 dermatomes
Special situations:
  • Pregnancy: most common surgical emergency; appendix may be displaced upward after 3rd month (though in <25% of cases even in 3rd trimester); peritoneal signs may be diminished. Fetal mortality rises with perforation.
  • Elderly: atypical presentation, higher perforation rate
  • Children: perforation rate higher due to thin-walled appendix and delayed diagnosis

Investigations

Bloods:
  • WBC raised (>10,000/mm³) - earliest marker; but normal WBC does not exclude appendicitis
  • CRP >10 mg/L (useful especially in children <6 years)
  • WBC + CRP combined sensitivity up to 98%; normal values of both make appendicitis unlikely in low pre-test probability
  • Urinalysis: sterile pyuria or microscopic haematuria can occur in appendicitis (don't be misled)
  • Urine pregnancy test in all women of reproductive age (rule out ectopic)
Imaging:
  • Plain X-ray: not helpful; may show appendicolith (up to 50% in children)
  • Ultrasound (US): first-line in children and pregnant women (graded compression technique - non-compressible appendix >6mm diameter)
  • CT abdomen/pelvis: most accurate in adults (sensitivity ~94%, specificity ~95%); identifies perforation, abscess, alternate diagnoses
  • MRI: preferred in pregnant women when US is inconclusive (avoids radiation)

Scoring Systems (MBBS Exam Favourite)

Modified Alvarado Score (MANTRELS):
FeaturePoints
Migration of pain to RIF1
Anorexia1
Nausea/vomiting1
Tenderness in RIF2
Rebound tenderness1
Elevated temperature (>37.3°C)1
Leukocytosis (WBC >10,000)2
Total9
  • Score 1-4: Low risk (observation)
  • Score 5-6: Possible appendicitis (imaging/observation)
  • Score 7-9: Probable appendicitis (surgical referral)
Note: Modified Alvarado has only 72% sensitivity; clinical judgment by an experienced surgeon remains more accurate. - Tintinalli's Emergency Medicine

Management

Conservative (selected cases):
  • Interval appendicectomy after abscess/phlegmon drainage (controversial)
  • Antibiotics alone for uncomplicated appendicitis (growing evidence, but surgery remains standard in most centres)
Surgical:
  • Appendicectomy - laparoscopic (preferred) or open (grid-iron/Lanz incision)
  • Laparoscopic: better visualisation, fewer wound infections, faster recovery
  • Open: grid-iron incision (oblique at McBurney's point); Lanz (transverse, better cosmesis)
  • Drains used if perforation with soiling
Post-op antibiotics: IV metronidazole + cephalosporin for perforated appendicitis

3. INTESTINAL OBSTRUCTION

Classification

TypeDescription
MechanicalPhysical block in lumen
Functional/Paralytic ileusNeuromuscular failure - no mechanical block
VascularMesenteric ischaemia - obstruction due to loss of blood supply
Mechanical subtypes by mechanism:
  • Intraluminal: gallstone ileus, meconium, foreign body, bezoar
  • Intramural: tumour, Crohn's stricture, intussusception
  • Extramural: adhesions (most common), hernias (2nd most common), volvulus, external compression
"It is essential that the hernial orifices should be carefully examined as incarceration in a hernia is one of the commonest causes of obstruction." - Pye's Surgical Handicraft, p. 9038

Small vs Large Bowel Obstruction

FeatureSmall Bowel (SBO)Large Bowel (LBO)
Common causesAdhesions, herniasCarcinoma, diverticular disease, volvulus
PainColicky, central/peri-umbilicalColicky, lower abdominal
VomitingEarly, profuse (bilious proximal; faeculent distal)Late or absent
DistensionModerate (central)Marked (peripheral/flanks)
ConstipationLate featureEarly absolute constipation
X-rayValvulae conniventes (complete bands)Haustral folds (incomplete)
Fluid lossUp to 6 litres/dayLess

Strangulation - RED FLAGS

Suspect strangulation when there is:
  • Continuous pain (not just colicky)
  • Localised tenderness
  • Pyrexia
  • Tachycardia
  • Signs of peritonism
  • Rapid deterioration
Pathophysiology of strangulation: Obstruction to arterial supply or venous drainage → loss of viability → necrosis → gangrene → perforation

Investigations

  • Erect AXR: multiple air-fluid levels
  • Supine AXR: dilated bowel loops; valvulae conniventes (SBO) vs haustra (LBO); pneumoperitoneum (perforation)
  • CT scan: investigation of choice; identifies level, cause, strangulation, perforation
  • Bloods: FBC, U&E (dehydration), LFT, amylase, lactate (ischaemia), group & save

Management

Resuscitation ("drip & suck"):
  • IV fluid resuscitation (crystalloid)
  • NG tube (nasogastric decompression)
  • Urinary catheter (monitor output)
  • Analgesia (does NOT mask signs)
  • Correct electrolyte imbalances (hyponatraemia, hypokalaemia)
Conservative: SBO without strangulation - trial of nasogastric decompression for 24-48 hours (water-soluble contrast study can be diagnostic and therapeutic in adhesional SBO)
Surgery: Emergency laparotomy/laparoscopy for:
  • Strangulation
  • Complete obstruction
  • Failed conservative management
  • LBO with caecal dilatation >9 cm (risk of perforation)

4. PERFORATED PEPTIC ULCER

Overview

Second most common complication of peptic ulcer (after bleeding). Strong association with NSAIDs/aspirin use, especially in the elderly. H. pylori also implicated.

Clinical Features

  • Sudden, severe epigastric pain (knife-like) - classically described as "like being shot"
  • Pain spreads to whole abdomen rapidly
  • Board-like rigidity - classic sign
  • Patient lies still (any movement worsens peritonism)
  • Referred shoulder tip pain (subphrenic gas)
  • Tachycardia, hypotension (if late, septic shock)

Investigations

  • Erect CXR: free gas under diaphragm (pneumoperitoneum) - present in ~70-80%
  • CT abdomen: more sensitive for free gas; also identifies site of perforation, extent of peritoneal soiling
  • Bloods: FBC, U&E, LFT, amylase (raised but usually <3x normal - distinguishes from pancreatitis), coagulation, group & save

Management

Resuscitation first: IV access, fluids, catheter, NG tube, analgesia, IV PPI, broad-spectrum antibiotics
Non-operative (selected stable patients):
  • Only if: haemodynamically stable, perforation radiologically sealed, no peritonitis
  • Strict monitoring; if worsening → immediate surgery
Operative (standard treatment):
Patient typeProcedure
Unstable / exudative peritonitis (>24h perforation)Simple patch closure (Graham's patch / omental patch)
Stable, <24h, chronic symptoms / failed medical RxPatch closure + Highly Selective Vagotomy (HSV)
Perforated gastric ulcer (stable)Distal gastric resection (biopsy all gastric ulcers)
Unstable with perforated gastric ulcerPatch closure + biopsy
"Surgery is almost always indicated for ulcer perforation, although occasionally nonsurgical treatment can be used in the stable patient without peritonitis in whom radiologic studies document a sealed perforation." - Schwartz's Surgery 11th Ed
Post-operative: H. pylori testing and eradication, long-term PPI, stop NSAIDs

5. ACUTE MESENTERIC ISCHAEMIA (AMI)

A surgical emergency with mortality ~50-80% if untreated.

Causes

Type%Details
Superior mesenteric artery (SMA) embolus~50%Cardiac source (AF, MI, valvular)
SMA thrombosis~25%Pre-existing atherosclerosis
Non-occlusive mesenteric ischaemia (NOMI)~20%Low-flow states, vasopressors
Mesenteric venous thrombosis~5-10%Hypercoagulable states, portal hypertension

Clinical Features

  • Classic triad: severe central abdominal pain out of proportion to examination findings (early), vomiting, diarrhoea (may be bloody)
  • Early: soft abdomen despite severe pain (visceral pain phase)
  • Late: peritonism, rigidity, septic shock (transmural infarction + perforation)
  • Risk factors: AF, recent MI, atherosclerosis, hypercoagulable state

Investigations

  • CT angiography: investigation of choice - shows occlusion, bowel wall thickening, pneumatosis intestinalis (gas in bowel wall), portal venous gas (late ominous sign)
  • Bloods: leukocytosis, raised lactate, metabolic acidosis (late)
  • Plain AXR: often normal early; "thumb-printing" (mucosal oedema) late

Management

  • Resuscitation + anticoagulation (heparin)
  • CT angiography to confirm and plan
  • Embolectomy / thrombolysis (endovascular or open)
  • Laparotomy: bowel resection if necrotic; "second look" laparotomy at 24-48 hours to assess bowel viability
  • Antibiotics (broad spectrum, including anaerobic cover)

6. ACUTE PANCREATITIS (Emergency Context)

Aetiology - "GET SMASHED"

LetterCause
GGallstones (most common - 40%)
EEthanol/alcohol (35%)
TTrauma
SSteroids
MMumps / viral
AAutoimmune (IgG4)
SScorpion sting
HHyperlipidaemia / Hypercalcaemia / Hypothermia
EERCP
DDrugs (azathioprine, thiazides, tetracycline)

Severity Scoring - Revised Atlanta / Glasgow Criteria (MBBS Favourite)

Glasgow (Imrie) Score (>3 = severe, assess at 48 hours):
  • PaO₂ < 8 kPa
  • Age > 55
  • Neutrophils (WBC) > 15 × 10⁹/L
  • Calcium < 2 mmol/L
  • Raise in urea > 16 mmol/L
  • Enzymes: LDH > 600 IU/L; AST > 200 IU/L
  • Albumin < 32 g/L
  • Sugar (glucose) > 10 mmol/L (Mnemonic: PANCREAS)
CT Severity Index (Balthazar): CT grading + necrosis score

Management

  • No oral intake (keep nil by mouth if severe/vomiting)
  • Aggressive IV fluid resuscitation (Hartmann's/Ringer's lactate preferred over normal saline)
  • Analgesia (IV opioids)
  • Urinary catheter + fluid balance
  • Blood sugar monitoring + insulin sliding scale
  • ERCP within 24-72h if gallstone pancreatitis with cholangitis / biliary obstruction
  • Antibiotics: not routine (no benefit in sterile necrosis); use only if infected necrosis suspected
  • Surgery: step-up approach for infected necrotising pancreatitis (percutaneous drain → minimally invasive necrosectomy → open)

7. CAUSES OF ACUTE ABDOMEN BY QUADRANT (Quick Reference)

QuadrantCommon Causes
RUQAcute cholecystitis, biliary colic, hepatitis, peptic ulcer, right lower lobe pneumonia
LUQSplenomegaly/rupture, left lower lobe pneumonia, pancreatitis, perforated gastric ulcer
RIFAppendicitis, Meckel's diverticulitis, Crohn's, ovarian torsion/cyst, ectopic pregnancy, mesenteric adenitis, psoas abscess, ureteric calculus
LIFDiverticulitis, sigmoid volvulus, colorectal carcinoma, ovarian pathology, ectopic
EpigastriumPeptic ulcer/perforation, acute pancreatitis, MI (inferior)
GeneralisedDiffuse peritonitis, early appendicitis, mesenteric ischaemia

8. EMERGENCY LAPAROTOMY - GENERAL PRINCIPLES

Indications (operate now):
  • Peritonitis (generalised)
  • Perforated viscus
  • Strangulated bowel
  • Unstable haemorrhage (e.g. ruptured AAA)
  • Failed conservative management
Pre-operative checklist:
  • Resuscitate first (but do not delay surgery if unstable due to intra-abdominal bleeding)
  • IV antibiotics (broad spectrum - cover gram-negative aerobes + anaerobes)
  • Urinary catheter, NG tube
  • Cross-match blood
  • Consent
  • Anaesthetic assessment
The Damage Control Surgery (DCS) concept - applicable in trauma or severe sepsis:
  1. Control contamination and haemorrhage
  2. Temporary abdominal closure
  3. ICU resuscitation
  4. Definitive repair at 24-48h

Key Exam Points - Quick Summary

TopicHigh-Yield Fact
AppendicitisPain migrates peri-umbilical → RIF; Alvarado score max = 9
PeritonitisPatient lies still; vomiting before pain = gastroenteritis
SBO causesAdhesions > hernias > tumour
LBO causesCarcinoma > diverticular disease > volvulus
StrangulationSuspect with tachycardia, fever, constant pain, tenderness
Perforated ulcerFree gas under diaphragm on erect CXR; Graham's patch repair
Mesenteric ischaemiaPain out of proportion to signs; CT angiography; mortality ~50-80%
PancreatitisGallstones + alcohol = 75%; Glasgow score >3 = severe
Shoulder tip painDiaphragmatic irritation - C5 dermatome
Always doPR exam + examine hernial orifices in all acute abdomen

Sources: Bailey and Love's Short Practice of Surgery 28th Ed | Schwartz's Principles of Surgery 11th Ed | Tintinalli's Emergency Medicine | Rosen's Emergency Medicine | Pye's Surgical Handicraft 22nd Ed

Basics of surgery for 2nd year

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Basics of Surgery - 2nd Year MBBS Notes

Sources: Bailey & Love's Surgery 28th Ed | Sabiston Textbook of Surgery | Schwartz's Surgery 11th Ed | Scott-Brown's Otorhinolaryngology | Mulholland & Greenfield's Surgery

UNIT 1: WOUND HEALING

Definition

A wound is a disruption of the normal continuity of body structures. Wound healing is the complex biological process of restoring tissue integrity.

Types of Wound Healing

TypeAlso CalledWhen It Occurs
Primary intentionFirst intentionClean wound, edges approximated within 12-24h (surgical incision, clean laceration)
Secondary intentionSecond intentionLarge/infected wound left open; heals by granulation tissue from base upward
Tertiary intentionDelayed primary closureWound left open initially (contaminated), then closed after 4-5 days once clean
"Healing by first intention is characterized by closure of a wound within 12-24 hours of its formation. These wounds are clean and well perfused... Wound edges are approximated using sutures, skin glue, steri-strips or other mechanical devices." - Scott-Brown's Otorhinolaryngology

Four Phases of Wound Healing (KEY EXAM TOPIC)

Phase 1: Haemostasis (Immediate - minutes)

  • Vascular spasm (immediate response)
  • Platelet plug formation: platelets adhere to exposed collagen via von Willebrand factor → platelet activation → aggregation (primary haemostasis)
  • Coagulation cascade activated → fibrin clot formation (secondary haemostasis)
  • Clot acts as scaffold for subsequent healing

Phase 2: Inflammation (Days 1-4)

  • Vasodilation and increased vascular permeability
  • Neutrophils arrive first (day 1-2): phagocytose bacteria and debris
  • Macrophages arrive day 2-3: debridement + release of growth factors (PDGF, TGF-β, VEGF) - the "master cells" of wound healing
  • Signs: rubor (redness), calor (heat), dolor (pain), tumour (swelling), functio laesa (loss of function) - Celsus's pentad
  • Lymphocytes arrive later - coordinate immune response

Phase 3: Proliferation (Days 4-21)

  • Fibroblasts migrate in (attracted by macrophage-derived growth factors) and synthesise collagen (initially Type III - immature)
  • Angiogenesis (new blood vessel formation) - driven by VEGF; gives granulation tissue its red granular appearance
  • Epithelialisation - keratinocytes migrate across wound surface
  • Wound contraction - myofibroblasts (fibroblasts with smooth muscle features) contract wound edges; major in secondary healing

Phase 4: Remodelling / Maturation (Day 21 - 2 years)

  • Type III collagen replaced by stronger Type I collagen
  • Collagen fibres reorganise along tension lines
  • Vascularity decreases (scar becomes pale)
  • Maximum tensile strength: ~80% of original skin (never reaches 100%)
  • Scar matures over 12-24 months

Wound Strength Timeline

TimeTensile Strength
Day 0-3Nil (fibrin clot only)
Week 1-2~5-10%
3 weeks~20%
6 weeks~50%
3-6 months~80% (maximum)

Factors Affecting Wound Healing

Local factors:
  • Infection (most important local factor)
  • Blood supply (ischaemia delays healing)
  • Foreign body / dead tissue (slows healing)
  • Haematoma / seroma (acts as culture medium)
  • Wound closure tension
  • Radiation damage
Systemic factors:
  • Nutrition: Protein deficiency impairs collagen synthesis; Vitamin C needed for hydroxylation of proline/lysine in collagen; Zinc cofactor for collagen synthesis
  • Diabetes mellitus (poor perfusion, neuropathy, impaired neutrophil function)
  • Steroids / immunosuppressives (inhibit inflammation and collagen synthesis)
  • Anaemia, hypoxia
  • Age (decreased healing in elderly)
  • Jaundice, uraemia
  • Malignancy

Abnormal Wound Healing

ConditionDescription
Hypertrophic scarRaised scar, stays within wound boundaries; regresses over time; treat with silicone, compression, steroids
KeloidGrows beyond wound boundaries; does NOT regress; more common in darker skin, presternal/deltoid/earlobe; treat with excision + adjuvant radiotherapy (high recurrence)
Wound dehiscenceReopening of wound; risk factors: infection, poor nutrition, obesity, steroids
Incisional herniaLate complication of wound; abdominal wall defect under intact skin
Chronic woundFails to progress through normal healing phases; e.g., venous ulcer, diabetic foot ulcer, pressure sore

UNIT 2: SHOCK

Definition

"Shock is a systemic state of low tissue perfusion that is inadequate for normal cellular respiration." - Bailey & Love's Surgery, p. 634

Pathophysiology at Cellular Level

  • Reduced O₂ delivery → cells switch from aerobic → anaerobic metabolism
  • Anaerobic metabolism produces lactic acid → systemic metabolic acidosis
  • Na⁺/K⁺ pump failure → lysosomal enzyme release → cell lysis
  • Potassium released → hyperkalaemia
  • Microvascular injury → capillary leak → tissue oedema → worsens hypoxia

Systemic Compensatory Responses

SystemResponse
CardiovascularBaroreceptor activation → ↑sympathetic tone → tachycardia + vasoconstriction
Respiratory↑ Respiratory rate → compensatory respiratory alkalosis
Renal↓ GFR → ↓ urine output; RAAS activated → Na + water retention, further vasoconstriction
EndocrineADH release → water retention; cortisol + glucagon → hyperglycaemia

Classification of Shock (4 Types - CHOD)

1. Hypovolaemic Shock (most common surgical type)

  • Loss of circulating volume: haemorrhage, burns, GI losses, third-space losses
  • Haemorrhagic shock classes (ATLS):
ClassBlood LossHRBPRRUrine OutputConsciousness
I<750 mL (<15%)<100Normal14-20>30 mL/hNormal
II750-1500 mL (15-30%)100-120Normal20-3020-30 mL/hAnxious
III1500-2000 mL (30-40%)120-140Decreased30-405-15 mL/hConfused
IV>2000 mL (>40%)>140Very low>35NegligibleLethargic/unconscious

2. Cardiogenic Shock

  • Primary pump failure: MI (most common), arrhythmia, valvular disease, myocarditis, blunt cardiac injury
  • Features: low CO, raised JVP, pulmonary oedema
  • Treatment: Inotropes (dobutamine), treat cause

3. Obstructive Shock

  • Mechanical obstruction to cardiac filling/output
  • Causes: Cardiac tamponade, Tension pneumothorax, massive PE, air embolus
  • Each causes reduced ventricular filling → low CO
  • Treatment: Remove obstruction immediately (needle decompression for tension pneumothorax; pericardiocentesis for tamponade)

4. Distributive Shock

  • Maldistribution of blood flow - peripheral vasodilation with low SVR
  • Subtypes:
    • Septic shock (most common distributive): endotoxin → cytokine storm → vasodilation + capillary leak + myocardial depression
    • Anaphylactic shock: histamine-mediated vasodilation; treat with IM adrenaline 0.5 mg
    • Neurogenic shock: loss of sympathetic tone (high spinal cord injury)
Septic shock: Warm peripheries early (high CO, low SVR) → Cold, clammy late (myocardial depression + hypovolaemia)

Summary Table: Cardiovascular Features

TypeHRBPCOSVRJVP
Hypovolaemic
Cardiogenic
Obstructive
Distributive (septic)↑ (early)

Management Principles (Surgical Shock)

  1. Airway + O₂ (100% via non-rebreather mask)
  2. 2 large-bore IV cannulae (antecubital fossa, 14-16G)
  3. Bloods: FBC, U&E, LFT, coagulation, G&S / crossmatch, blood cultures (sepsis), lactate
  4. IV fluid resuscitation: crystalloid bolus (500 mL Hartmann's) - reassess after each bolus
  5. Urinary catheter - monitor urine output (target >0.5 mL/kg/h)
  6. Identify and treat the cause
  7. Blood products if haemorrhagic shock (1:1:1 ratio of PRBC : FFP : platelets in massive haemorrhage)
  8. Vasopressors (noradrenaline) if distributive shock unresponsive to fluids

UNIT 3: FLUID THERAPY & ELECTROLYTES

Body Fluid Compartments

Compartment% Body WeightVolume (70 kg adult)
Total Body Water (TBW)60%~42 L
Intracellular fluid (ICF)40%~28 L
Extracellular fluid (ECF)20%~14 L
- Interstitial15%~10.5 L
- Intravascular (plasma)5%~3.5 L

Maintenance Fluid Requirements (Adults)

  • Water: 25-30 mL/kg/day (~2000 mL/day)
  • Sodium: 1 mmol/kg/day (~70 mmol/day)
  • Potassium: 1 mmol/kg/day (~70 mmol/day)
  • Glucose: ~50-100g/day (prevents protein catabolism)
Standard maintenance regime: 1 L normal saline (0.9% NaCl) + 20 mmol KCl over 8h; followed by 1 L 5% dextrose + 20 mmol KCl over 8h; repeat cycle

Types of IV Fluids

FluidContentsOsmolalityDistributionUse
0.9% NaCl (Normal saline)Na⁺ 154, Cl⁻ 154 mmol/L308 mOsm/LECF onlyResuscitation, hyponatraemia
Hartmann's / Ringer's lactateNa 131, K 5, Ca 2, Cl 111, lactate 29 mmol/L278 mOsm/LECF onlyPreferred resuscitation fluid (more physiological)
5% Dextrose50g/L glucose278 mOsm/LDistributes to all compartmentsMaintenance, hypoglycaemia
Colloids (e.g., Gelatin)Large molecules-Stays intravascularTemporary volume expansion
Blood (PRBC)--IntravascularHaemorrhage, severe anaemia

Electrolyte Disturbances (Surgical Context)

Hyponatraemia (Na⁺ <135 mmol/L):
  • Causes: excess hypotonic fluids, SIADH (post-op), GI losses
  • Symptoms: confusion, seizures (if severe)
  • Treat: fluid restriction; slow correction (max 10 mmol/24h to avoid central pontine myelinolysis)
Hypokalaemia (K⁺ <3.5 mmol/L):
  • Causes: vomiting/NG drainage (with alkalosis), diuretics, diarrhoea
  • Risks: cardiac arrhythmias, ileus
  • Treat: IV KCl (max 20 mmol/h via central line); oral KCl supplements
Hyperkalaemia (K⁺ >5.5 mmol/L):
  • Causes: renal failure, cell lysis, Addison's, massive transfusion
  • Risks: cardiac arrest (sine-wave ECG pattern)
  • Emergency treatment: IV calcium gluconate (membrane stabilisation) → insulin + dextrose → salbutamol → dialysis

UNIT 4: SURGICAL INFECTIONS

Classification of Wounds (Surgical)

ClassDescriptionInfection Risk
CleanElective, no hollow organ entered (e.g., thyroidectomy, hernia repair)1-2%
Clean-contaminatedHollow organ entered under controlled conditions (e.g., cholecystectomy, colonic resection with bowel prep)3-5%
ContaminatedAcute inflammation without pus; major breach of asepsis (e.g., fresh GI spillage, traumatic wound <4h)10-15%
Dirty/InfectedEstablished infection, faecal soiling, perforated viscus (e.g., perforated appendix, faecal peritonitis)>30%

Surgical Site Infection (SSI)

Definition (CDC): Infection occurring within 30 days of operation (or 1 year if implant placed) at the operative site.
Classification:
  • Superficial incisional SSI: skin and subcutaneous tissue
  • Deep incisional SSI: deep soft tissue (fascia, muscle)
  • Organ/space SSI: any part of the anatomy opened during surgery (e.g., anastomotic leak, intraabdominal abscess)
Risk factors:
  • Patient factors: diabetes, obesity (BMI >35), smoking, malnutrition, immunosuppression, ASA grade
  • Operative factors: duration >2 hours, dirty/contaminated wound, inadequate prophylaxis, haematoma, dead space
Prevention:
  • Antibiotic prophylaxis: single dose IV antibiotics 30-60 min before incision (e.g., co-amoxiclav or cefazolin); NOT extended beyond 24h
  • Hair removal: clippers (not razors) on day of surgery
  • Skin preparation: chlorhexidine-alcohol > povidone iodine
  • Maintain normothermia and normoglycaemia intra-operatively
  • Good surgical technique (minimise dead space, avoid haematoma)

Common Surgical Infections

Cellulitis: Spreading infection of dermis/subcutaneous tissue; Strep pyogenes / Staph aureus. Treatment: IV amoxicillin/clavulanate or flucloxacillin
Abscess: Localised collection of pus. Principle: "ubi pus, ibi evacua" (where there is pus, drain it). Treat by incision and drainage (I&D); antibiotics alone insufficient
Necrotising fasciitis:
  • Rapidly spreading infection of fascia and subcutaneous fat; surgical emergency
  • Type I: polymicrobial (Fournier's gangrene)
  • Type II: monomicrobial (Group A Strep)
  • Features: severe pain out of proportion to appearance, dusky skin, crepitus (gas-forming organisms), systemic toxicity
  • Treatment: URGENT surgical debridement (often multiple washouts) + broad-spectrum antibiotics + ICU
Gas gangrene (Clostridial myonecrosis):
  • Clostridium perfringens - gas in tissues, brown exudate, "dishwater" fluid
  • Treatment: surgical debridement + penicillin G + hyperbaric oxygen

Tetanus

  • Clostridium tetani - exotoxin (tetanospasmin) blocks inhibitory interneurons → spastic paralysis
  • Features: trismus (lockjaw), opisthotonus, risus sardonicus
  • Prophylaxis: wound toilet + tetanus toxoid (if >5 years since last booster); add tetanus immunoglobulin (TIG) if dirty wound + unimmunised
  • Treatment: TIG + metronidazole + benzodiazepines (muscle relaxation) + ICU

UNIT 5: HAEMOSTASIS & BLOOD TRANSFUSION

Haemostasis - Overview

Primary haemostasis: Platelet plug (fast, within seconds)
  1. Vascular spasm
  2. Platelet adhesion: vWF bridges platelet GPIb receptor to exposed collagen
  3. Platelet activation: release of ADP, TXA₂ → more platelet recruitment
  4. Platelet aggregation: GPIIb/IIIa receptors bind fibrinogen
Secondary haemostasis (Coagulation cascade): Fibrin clot (minutes)
  • Intrinsic pathway (XII → XI → IX → X): activated by contact with subendothelial collagen; measured by APTT
  • Extrinsic pathway (VII + Tissue Factor → X): activated by tissue injury; measured by PT/INR
  • Common pathway (X → Xa + Va → Prothrombin → Thrombin → Fibrinogen → Fibrin)
Fibrinolysis: Plasmin dissolves clot (tPA activates plasminogen → plasmin)

Tests of Coagulation

TestPathway TestedNormal Value
PT (Prothrombin Time)Extrinsic + common11-13 seconds
INRStandardised PT ratio0.8-1.2
APTTIntrinsic + common25-35 seconds
Thrombin Time (TT)Final common10-15 seconds
Platelet countPrimary haemostasis150-400 × 10⁹/L
Bleeding timePlatelet function2-7 minutes

Anticoagulants in Surgery

DrugMechanismMonitoringReversal
Heparin (UFH)Activates antithrombin III (↑ AT-III activity)APTTProtamine sulphate
LMWH (enoxaparin, dalteparin)Anti-Xa >> anti-IIaAnti-Xa levelPartial reversal with protamine
WarfarinInhibits Vit K-dependent factors (II, VII, IX, X, Protein C&S)INRVit K; FFP (emergency); 4-factor PCC (urgent)
DOACs (rivaroxaban, apixaban)Direct factor Xa inhibitionNo routine testAndexanet alfa (specific) / PCC
DabigatranDirect thrombin (IIa) inhibitorTT, ECTIdarucizumab (specific)

Blood Products & Transfusion

ProductContents1 Unit raises...Indication
Packed Red Blood Cells (PRBC)Red cells, Hb ~270 g/unitHb by ~1 g/dLAnaemia, acute blood loss
Fresh Frozen Plasma (FFP)All clotting factors-Coagulopathy, warfarin reversal
PlateletsPlatelet concentratePlatelets by ~30 × 10⁹/LThrombocytopenia, platelet dysfunction
CryoprecipitateFibrinogen, vWF, Factor VIII, XIIIFibrinogen by ~1 g/LDIC, haemophilia A, vWD
Transfusion trigger: Generally Hb <7-8 g/dL in stable patients (Hb <10 g/dL in cardiac patients or active ischaemia)
Complications of blood transfusion:
ComplicationNotes
Febrile non-haemolytic reactionMost common; leukocyte antibodies; treat with paracetamol, slow transfusion
Acute haemolytic reactionABO incompatibility; STOP transfusion, IV fluids, check sample; life-threatening
Allergic/anaphylacticPlasma protein antibodies; antihistamine/adrenaline
TRALI (Transfusion-Related Acute Lung Injury)Non-cardiogenic pulmonary oedema within 6h; supportive
TACO (Transfusion-Associated Circulatory Overload)Pulmonary oedema in fluid-sensitive patients; treat with diuretics
Infection (viral/bacterial)Rare with modern screening
Massive transfusion complicationsHypocalcaemia (citrate chelates Ca²⁺), hypothermia, dilutional coagulopathy, hyperkalaemia

UNIT 6: PRE-OPERATIVE & POST-OPERATIVE CARE

Pre-operative Assessment

History:
  • Current illness + planned surgery
  • Past medical/surgical history
  • Medications (especially anticoagulants, antiplatelets, antihypertensives, steroids, insulin)
  • Allergies
  • Anaesthetic history (family history of malignant hyperthermia)
  • Smoking, alcohol, substance use
  • Last oral intake (fasting status: 6h for solids, 2h for clear fluids - "6-4-2 rule")
Examination: Cardiovascular, respiratory, airway (Mallampati classification)
Investigations:
TestIndication
FBCAll major surgery
U&EMajor surgery, renal disease, diuretics
LFTLiver disease, jaundice, alcohol history
Coagulation (PT, APTT)Bleeding disorder, anticoagulants, liver disease
Blood glucose/HbA1cDiabetes
ECGAge >40, cardiac history
CXRCardiac/respiratory disease, major surgery
Group & Save / CrossmatchExpected blood loss
Echo, stress testSignificant cardiac history
ASA Physical Status Classification:
GradeDescriptionExample
IHealthy patientYoung fit adult
IIMild systemic diseaseControlled DM, mild HTN
IIISevere systemic diseasePoorly controlled DM, COPD, stable angina
IVSevere, constant threat to lifeRecent MI, severe COPD, liver failure
VMoribund, not expected to survive 24hRuptured AAA
VIBrain-dead organ donor-
E suffixEmergency surgerye.g., IIE, IIIE
Consent: Informed, voluntary, patient must have capacity; must discuss benefits, risks (common + serious), alternatives including no treatment

Pre-operative Preparation

  • Fasting: 6h solids, 2h clear fluids
  • Stop anticoagulants appropriately (warfarin 5 days; DOACs 24-48h; aspirin continue for most surgery)
  • Diabetic management: omit morning oral hypoglycaemics on day of surgery; start insulin sliding scale if prolonged fasting
  • Prophylactic LMWH for DVT prevention (start evening before or post-op)
  • TED stockings / intermittent pneumatic compression
  • Antibiotic prophylaxis: single dose 30-60 min before incision
  • Bowel prep (selected colorectal cases only)
  • Consent and marking the site (especially for laterality)

Post-operative Monitoring

  • Observations every 15-30 min initially: HR, BP, RR, SpO₂, temperature, GCS
  • Urine output: target >0.5 mL/kg/h (30 mL/h in 70 kg adult)
  • NEWS2 score (National Early Warning Score): triggered escalation for deteriorating patients

Post-operative Complications - Timeline

TimeComplication
Immediate (0-24h)Primary haemorrhage, airway obstruction, anaphylaxis, MI, arrhythmia
Early (1-3 days)Reactionary haemorrhage (vasodilation), atelectasis, aspiration pneumonia, UTI, paralytic ileus, hypotension
Delayed (>3 days)DVT/PE, secondary haemorrhage (infection eroding vessel), wound infection, anastomotic leak (day 5-7), SIADH, chest infection
Late (weeks-months)Incisional hernia, adhesional obstruction, keloid, port-site hernia
Common post-op complications by system:
Respiratory:
  • Atelectasis (most common, days 1-2): microcollapses → fever, ↓O₂; treat with physiotherapy, incentive spirometry
  • Pneumonia: cough, fever, consolidation; treat with antibiotics
  • PE (day 5-10 peak): pleuritic chest pain, haemoptysis, tachycardia; CTPA to confirm; treat with anticoagulation
Cardiovascular:
  • DVT: calf pain, swelling; duplex USS; treat with LMWH then DOAC for 3 months
  • MI: ECG + troponin; highest risk day 1-3 post-op
Wound:
  • Haematoma: collection of blood; usually resolves; aspirate/drain if large
  • Seroma: serous fluid collection; common post-mastectomy/hernia; aspirate if symptomatic
  • Wound infection (SSI): days 4-7; erythema, pus, fever; open wound + antibiotics
Urinary:
  • Retention: common post-pelvic surgery and in elderly men; catheterise
  • UTI: very common; MSSU + antibiotics

UNIT 7: SURGICAL NUTRITION

Importance

Surgery is a catabolic state. Stress response (cortisol, glucagon, adrenaline) → protein breakdown, glucose intolerance, negative nitrogen balance. Malnutrition delays wound healing, impairs immunity, prolongs hospital stay.

Nutritional Assessment

  • History: weight loss (>10% in 6 months = significant), reduced intake
  • BMI: <18.5 kg/m² = underweight
  • MUST score (Malnutrition Universal Screening Tool): BMI + weight loss + acute disease effect → low/medium/high risk
  • Serum albumin (<35 g/L = hypoalbuminaemia; marker of chronic malnutrition)
  • Serum prealbumin (half-life 2-3 days, better acute marker)

Nutritional Requirements (Surgical Patient)

  • Calories: 25-30 kcal/kg/day (higher if sepsis/burns/major trauma: up to 35-40)
  • Protein: 1-2 g/kg/day (nitrogen balance)
  • Key micronutrients for healing: Vitamin C, Zinc, Vitamin A

Routes of Nutritional Support

RouteIndicationNotes
OralFirst choice if gut functioningEncourage early post-op eating
Enteral (NGT/NJT)Gut functioning but unable to eat"If the gut works, use it"
Total Parenteral Nutrition (TPN)Non-functional gut: ileus, short bowel, high-output fistula, severe IBDVia central venous catheter; expensive; high complication rate
Advantages of enteral over parenteral:
  • Maintains gut mucosal integrity (prevents bacterial translocation)
  • Lower cost
  • Lower infection risk (TPN associated with line infections, metabolic complications)
  • Preserves gut immune function
TPN complications: Line sepsis, hyperglycaemia, electrolyte imbalance (especially hypophosphataemia = refeeding syndrome), hepatic steatosis, metabolic acidosis
Refeeding syndrome: Rapid reintroduction of carbohydrates in malnourished patients → intracellular shift of phosphate, potassium, magnesium → severe hypophosphataemia → cardiac arrhythmia, respiratory failure, death. Prevent: start feeds slowly, supplement phosphate/K/Mg

UNIT 8: SURGICAL ONCOLOGY BASICS

Tumour Classification

TypeOriginFeatures
BenignAny tissueWell-differentiated, encapsulated, no metastasis, local pressure effects
MalignantAny tissuePoorly differentiated, invasive, metastasises, anaplastic features
CarcinomaEpitheliumMost common in adults
SarcomaConnective tissue / mesenchymeBone, muscle, fat, vessels
LymphomaLymphoid tissue
TeratomaGerm cells

Staging (TNM System)

  • T - Primary tumour (T0-T4)
  • N - Regional lymph nodes (N0-N3)
  • M - Distant metastasis (M0-M1)

Routes of Tumour Spread

  1. Direct / local invasion - into adjacent structures
  2. Lymphatic spread - most common route for carcinomas
  3. Haematogenous spread - common for sarcomas; via portal vein → liver; systemic veins → lungs
  4. Transcoelomic spread - across body cavities (peritoneum, pleura); e.g., gastric cancer → "Sister Mary Joseph nodule" (umbilical), Krukenberg tumour (ovary)
  5. Perineural spread - along nerve sheaths (e.g., prostate cancer)
  6. Implantation - port site metastasis after laparoscopy, surgical seeding

Tumour Markers (Surgical Context)

MarkerTumour
CEAColorectal cancer (monitoring recurrence)
CA 19-9Pancreatic cancer
CA 125Ovarian cancer
AFPHepatocellular carcinoma, testicular (non-seminoma)
PSAProstate cancer
β-hCGChoriocarcinoma, testicular (seminoma + non-seminoma)

QUICK REVISION TABLE - High Yield Points

TopicKey Fact
Wound healing phasesHaemostasis → Inflammation → Proliferation → Remodelling
"Master cell" of wound healingMacrophage
Max tensile strength of healed wound~80% of original skin
Keloid vs hypertrophic scarKeloid extends beyond wound borders; does not regress
Shock definitionInadequate tissue perfusion for cellular respiration
Class III haemorrhagic shock30-40% blood loss; BP drops; confused patient
Most common cause of surgical shockHypovolaemia
Distributive shock featuresWarm, vasodilated (early); high CO; low SVR
Surgical wound classesClean → Clean-contaminated → Contaminated → Dirty
Antibiotic prophylaxis timing30-60 min before incision; single dose
TPN complication to knowRefeeding syndrome (hypophosphataemia)
Enteral over parenteral advantageMaintains gut mucosa, prevents bacterial translocation
Most common post-op complicationAtelectasis (day 1-2)
PE peak timing post-opDay 5-10
DVT prophylaxisLMWH + TED stockings + early mobilisation
Malignant tumour spread (carcinoma)Lymphatic most common
Von Willebrand factor roleBridges platelet GPIb to subendothelial collagen

Sources: Bailey and Love's Short Practice of Surgery 28th Ed | Sabiston Textbook of Surgery | Schwartz's Principles of Surgery 11th Ed | Scott-Brown's Otorhinolaryngology Head & Neck Surgery | Mulholland & Greenfield's Surgery 7th Ed
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