Comprehensive GI Surgery — Medical Student Learning Guide

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TOPIC 1: INVESTIGATION OF THE GIT (Gastrointestinal Tract)

Overview

1.1 History & Examination Essentials

• Pain: character, location, radiation, onset (sudden vs. gradual), precipitating/relieving factors
• Bleeding: hematemesis, melena, hematochezia — colour and amount help localise the source
• Altered bowel habits: constipation, diarrhoea, ribbon stools
• Weight loss, anorexia, dysphagia: red flag symptoms for malignancy
• Nausea/vomiting: bilious vs. non-bilious (bilious = obstruction beyond pylorus)
• Jaundice, abdominal distension

1.2 Laboratory Investigations

1.3 Endoscopic Investigations

Key point for exams: Colonoscopy is the preferred modality for LGIB — it identifies the source in >70% of cases and allows therapy. Sleisenger and Fordtran's Gastrointestinal and Liver Disease

1.4 Imaging Investigations

MRI in the acute abdomen: MRI achieves 95–97% sensitivity and specificity for acute appendicitis, comparable to CT. It is now recommended as second-line (after US/CT) especially in pregnant patients, children, and those with radiation concerns. Grainger & Allison's Diagnostic Radiology

1.5 Functional/Physiological Tests

• Gastric emptying scintigraphy — gastroparesis
• Oesophageal manometry/pH study — GORD, achalasia
• Hydrogen breath test — SIBO, lactose intolerance
• Anorectal manometry — sphincter dysfunction, Hirschsprung's

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TOPIC 2: INTESTINAL OBSTRUCTION

2.1 Definition & Classification

2.2 Causes (Remember "HIVA")

1. Adhesions (most common in adults — post-surgical)
2. Hernias (inguinal, femoral, incisional — most common in non-operative patients globally)
3. Volvulus
4. Intussusception (most common cause in children <2 years)
5. Tumour
6. Crohn's disease

1. Carcinoma (most common cause of large bowel obstruction)
2. Sigmoid volvulus (elderly, constipated patients; common in Africa)
3. Diverticular disease
4. Hirschsprung's disease (neonates)

The four major mechanical causes: herniation, adhesions, volvulus, intussusception. Robbins & Kumar Basic Pathology

2.3 Pathophysiology

• Early: hyperactive bowel sounds (attempts to overcome obstruction)
• Late: absent bowel sounds (ileus)
• Fluid/electrolyte losses: hypovolaemia, hypokalaemia, metabolic alkalosis (vomiting), acidosis (ischaemia)

2.4 Clinical Features

2.5 Investigations

• AXR:
  • SBO: dilated small bowel loops (>3 cm), central, "ladder pattern," valvulae conniventes cross entire width
  • LBO: dilated large bowel (>6 cm colon, >9 cm caecum = caecal cut-off sign), peripheral
  • Perforation: free air under diaphragm on erect CXR
• CT abdomen (gold standard): identifies site, cause, presence of strangulation (wall thickening, mesenteric stranding, free fluid)
• Gastrografin enema: for suspected LBO (also therapeutic in some cases)
• Bloods: FBC, U&E, LFTs, amylase, ABG (lactate if strangulation suspected), group & save

2.6 Management

1. IV fluid resuscitation (N/S or Hartmann's)
2. Nasogastric (NG) tube decompression
3. Urinary catheter (monitor urine output)
4. Analgesia, antiemetics
5. Correct electrolyte imbalances
6. IV antibiotics if strangulation/perforation suspected

Surgical intervention is usually required in cases of mechanical obstruction or severe infarction. Robbins & Kumar Basic Pathology

2.7 Intussusception (High-Yield)

• Telescoping of proximal bowel into distal bowel
• Children: usually idiopathic or following viral infection/Peyer's patch hyperplasia; ileocolic most common
• Adults: always investigate for a lead point (polyp, tumour, Meckel's)
• Classic triad: colicky abdominal pain, red "currant jelly" stools, palpable sausage-shaped mass (right hypochondrium/epigastrium)
• Treatment: hydrostatic/pneumatic enema in children; surgery in adults or failures

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TOPIC 3: PERITONITIS AND INTRA-ABDOMINAL ABSCESS

3.1 Peritonitis

3.2 Pathophysiology

• Peritoneal macrophages release cytokines (IL-1, IL-6, TNF-α) → SIRS
• Exudate rich in fibrin → localisation of infection OR generalised peritonitis
• Fluid shifts into peritoneal cavity → hypovolaemia → shock → MOF if untreated

3.3 Common Organisms

• Gram-negative: E. coli, Klebsiella, Enterobacter
• Anaerobes: Bacteroides fragilis
• Gram-positive: Streptococcus, Staphylococcus
• SBP: typically monomicrobial (E. coli, Klebsiella, Streptococcus pneumoniae)

3.4 Clinical Features

3.5 Investigations

• FBC: raised WBC, neutrophilia
• CRP/ESR: elevated
• Serum lactate: if sepsis/shock suspected
• Blood cultures: x2 sets
• Urine R&M, pregnancy test (exclude other causes)
• AXR: ileus pattern, free gas
• Erect CXR: free air under diaphragm (>75% of perforations)
• CT abdomen (CECT): site of perforation, abscess, free fluid, free air — gold standard
• Diagnostic peritoneal lavage: rarely used; may aid if imaging inconclusive
• Ascitic fluid analysis (if SBP suspected): PMN >250 cells/mm³ = diagnostic of SBP

3.6 Management

• IV large-bore access, aggressive fluid resuscitation
• Oxygen, urinary catheter
• NG tube decompression
• IV broad-spectrum antibiotics immediately (piperacillin-tazobactam ± metronidazole; or cefuroxime + metronidazole)
• Sepsis Six bundle if septic shock

• Emergency laparotomy/laparoscopy
• Source control: repair perforation, resect necrotic bowel, drain abscess
• Peritoneal lavage with warm saline
• Consider leaving abdomen open (damage-control surgery) if severe contamination

Medical management is initiated immediately with NG decompression, heparin infusion (if vascular cause), fluid resuscitation, and broad-spectrum antibiotics. Peritonitis requires emergent laparotomy, and delays (such as to obtain imaging) should be minimised. — Current Surgical Therapy

• IV cefotaxime 2g q8h (first-line) or co-amoxiclav
• IV albumin 1.5 g/kg on day 1, then 1 g/kg on day 3 (reduces hepatorenal syndrome risk)
• Prophylaxis: ciprofloxacin/norfloxacin (primary prophylaxis if ascitic protein <1.5 g/dL; secondary prophylaxis after first episode)

3.7 Intra-abdominal Abscess

1. IV antibiotics
2. Percutaneous CT/USS-guided drainage — first-line for most abscesses
3. Surgical drainage — if inaccessible, multiloculated, or not responding

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TOPIC 4: ACUTE ABDOMEN

4.1 Definition

4.2 Causes (Systematic Approach by Location)

Extra-abdominal causes: MI, lower lobe pneumonia, DKA, sickle cell crisis, Herpes Zoster, Addisonian crisis — always consider!

4.3 History-Taking Mnemonic: SOCRATES

• Site, Onset, Character, Radiation, Associations, Time course, Exacerbating/relieving factors, Severity

4.4 Types of Abdominal Pain

4.5 Investigations in Acute Abdomen

• FBC, U&E, LFTs, amylase/lipase, CRP, glucose
• Blood cultures if septic
• Group & save / crossmatch if bleeding suspected
• ABG: lactate (mesenteric ischaemia), metabolic acidosis

• Erect CXR: free air (perforation), pneumonia (referred pain)
• Supine AXR: obstruction, calcification, volvulus
• USS: hepatobiliary, gynaecological, renal pathology (first-line)
• CT abdomen/pelvis with contrast: most informative for all causes of acute abdomen

4.6 Specific High-Yield Conditions

Acute Appendicitis

• Most common surgical emergency globally
• Central colicky pain → migrates to RIF (McBurney's point)
• Signs: McBurney's tenderness, Rovsing's sign (LIF pressure → RIF pain), psoas sign, obturator sign
• Alvarado score: used to risk-stratify (score 7–10 = high probability; proceed to surgery)
• USS first-line (sensitivity 75–90%); CT if USS equivocal
• Treatment: appendicectomy (laparoscopic preferred); antibiotics for uncomplicated appendicitis (select cases)

Perforated Peptic Ulcer

• Sudden onset severe epigastric pain ("like a knife") → generalises
• Board-like rigidity, absent bowel sounds
• Air under diaphragm on erect CXR (~75%)
• Initial: IV fluids, NG tube, IV antibiotics, PPI
• Definitive: laparoscopic/open repair (omental patch); H. pylori eradication post-op

Acute Cholecystitis

• RUQ pain, positive Murphy's sign (arrest of inspiration on RUQ palpation)
• Fever, leukocytosis; USS shows stones, thickened gallbladder wall
• Management: IV fluids, antibiotics, analgesia; laparoscopic cholecystectomy (ideally within 72 hours of presentation or 6 weeks)

Ruptured Ectopic Pregnancy

• Always exclude in any woman of reproductive age with acute abdomen!
• Positive βhCG, haemodynamic instability, free fluid on USS
• Emergency surgical management

Mesenteric Ischaemia

• Severe pain out of proportion to signs (classic early finding)
• Risk factors: AF (emboli), atherosclerosis (thrombosis), hypoperfusion
• CT angiography is diagnostic
• Requires emergency laparotomy with resection of necrotic bowel

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TOPIC 5: UPPER GI BLEEDING (UGIB)

5.1 Definition

5.2 Clinical Presentation

5.3 Causes (by frequency)

5.4 Risk Stratification Scores

• Variables: BUN, Hb, SBP, heart rate, melena, syncope, liver disease, cardiac failure
• Score 0 = low risk (can be managed outpatient)
• Score ≥6 = needs urgent endoscopy

• Variables: age, shock, comorbidity, diagnosis, signs of recent haemorrhage at endoscopy
• Predicts rebleeding and mortality

• Albumin <3 g/dL, INR >1.5, altered mental status, SBP <90, age >65
• Score ≥2 = higher mortality risk

5.5 Investigations

• FBC, U&E (BUN:creatinine ratio >36 suggests UGI bleeding), LFTs, clotting, group & crossmatch
• OGD (upper endoscopy): first-line — diagnoses AND treats
• CT angiography: if haemodynamically stable but endoscopy fails to find source
• Conventional angiography with embolisation: active bleeding not controlled by endoscopy
• Tagged RBC scan: slow bleeds not visible on angiography

5.6 Management

• Large-bore IV access (x2), aggressive IV crystalloid resuscitation
• Transfuse pRBCs if Hb <7 g/dL (or <8 g/dL in cardiovascular disease)
• Correct coagulopathy (FFP, platelets, vitamin K)
• Urinary catheter, NG tube if needed
• Terlipressin/octreotide if variceal bleeding suspected (start before endoscopy)
• IV PPI (pantoprazole/esomeprazole infusion) for non-variceal bleeding (before and after endoscopy)
• Antibiotics (ceftriaxone) for variceal bleeding + cirrhosis (reduces infection risk and improves survival)

• Identifies source in ~95% of cases
• Endoscopic haemostasis techniques:
  • Adrenaline injection (1:10,000)
  • Thermal coagulation (heater probe, APC)
  • Haemoclip application
  • Band ligation (varices)
  • Cyanoacrylate injection (gastric varices)

1. Vasoactive drugs: terlipressin (drug of choice) or octreotide/somatostatin
2. IV antibiotics (prophylactic — reduces mortality)
3. Endoscopic variceal ligation (EVL) — first-line endoscopic therapy
4. TIPS (Transjugular Intrahepatic Portosystemic Shunt) — if EVL fails or high-risk patient (HVPG >20 mmHg); early TIPS shown to reduce mortality
5. Sengstaken-Blakemore tube — balloon tamponade, temporising measure only
6. Secondary prophylaxis: non-selective beta-blocker (propranolol/carvedilol) + EVL

Overall mortality for UGIB: 2–10%. Patients who rebleed or continue to bleed have 30–40% mortality. Sleisenger & Fordtran's

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TOPIC 6: PEPTIC ULCER DISEASE (PUD)

6.1 Definition

6.2 Aetiology & Pathogenesis

• Gram-negative spiral bacterium; colonises gastric antrum
• Produces urease → ammonia → disrupts mucus layer
• Increases gastrin secretion → increased acid production

• 70% of PUD cases associated with H. pylori; only 5–10% of infected individuals develop ulcers

• More commonly causes duodenal ulcers

• Inhibit COX-1 → reduced prostaglandin synthesis → impaired mucosal defence
• More commonly cause gastric ulcers
• Risk increased with age >65, prior PUD history, high-dose/combined NSAID+aspirin

• Gastrin-secreting tumour (gastrinoma) in pancreas or duodenum
• Massive acid hypersecretion → multiple ulcers in stomach, duodenum, even jejunum
• Suspect if: recurrent/multiple/atypical ulcers, diarrhoea, ulcers not responding to treatment
• Diagnosis: fasting serum gastrin >1000 pg/mL + secretin stimulation test
• Treatment: PPI (high dose) + tumour resection

6.3 Clinical Features

6.4 Complications (Mnemonic: BOPS)

6.5 Diagnosis

• Endoscopy (OGD): gold standard; allows biopsy (all gastric ulcers must be biopsied to exclude malignancy)
• H. pylori testing:
  • Non-invasive: ¹³C-urea breath test (best for post-treatment test), stool antigen test, serology
  • Invasive (at endoscopy): rapid urease test (CLO test — fast, cheap), histology, culture
• Barium meal: outlines ulcer crater (filling defect); less commonly used today

6.6 Treatment

• PPI + Amoxicillin + Clarithromycin (avoid if clarithromycin resistance >15%)
• OR PPI + Metronidazole + Clarithromycin

• PPI + Bismuth + Metronidazole + Tetracycline (14 days)

• PPI (omeprazole, pantoprazole, esomeprazole) — mainstay
• H₂ receptor antagonists (ranitidine/famotidine) — second-line
• Sucralfate, misoprostol — mucosal protection

• Stop NSAID if possible; switch to COX-2 inhibitor
• Add PPI prophylaxis if NSAID cannot be stopped
• Misoprostol (PGE₁ analogue) protects against NSAID-induced ulcers

• Perforated ulcer: Graham patch repair (omental patch)
• Bleeding ulcer: endoscopic haemostasis; if fails → under-running the vessel (surgery)
• Gastric outlet obstruction: endoscopic balloon dilation; pyloroplasty/gastrojejunostomy
• Rarely: vagotomy (reduces acid) — truncal vagotomy + pyloroplasty; or highly selective vagotomy

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TOPIC 7: LOWER GI BLEEDING (LGIB)

7.1 Definition

7.2 Causes

In most cases of severe haematochezia: 75% from colon, 17% from UGI source (brisk UGI bleed), 5% from small bowel. Sleisenger & Fordtran's

7.3 Clinical Approach

Rule out UGI source first! If haematochezia + haemodynamic instability → perform UGI endoscopy first (15% of apparent LGIB is actually UGI source).

• Heart rate >100, systolic BP <115 mmHg
• Aspirin or NSAID use
• Active bleeding per rectum on initial examination
• No abdominal tenderness (= diverticular or angiodysplasia, not colitis)

7.4 Investigations

1. Bloods: FBC, U&E, coagulation, crossmatch, iron studies
2. Digital rectal exam: haemorrhoids, rectal mass, melena vs. bright red blood
3. Rigid sigmoidoscopy/proctoscopy: anorectal causes
4. Colonoscopy: preferred modality — identifies source in >70%, allows therapy; perform after bowel prep (PEG purge)
5. CT angiography: if haemodynamically unstable or colonoscopy fails; needs active bleeding rate ≥0.5 mL/min
6. Conventional angiography: active bleeding; allows embolisation
7. Radionuclide scan (Tc-99m RBC): detects bleeding rates ≥0.1 mL/min; helps localise for angiography/surgery
8. Capsule endoscopy / enteroscopy: small bowel source

7.5 Management

• IV access, fluids, transfusion, correct coagulopathy

• Most acute LGIB (80%) stops spontaneously
• Colonoscopic therapy (injection, APC, clips, band ligation) — for diverticular bleeds, angiodysplasia
• Angiographic embolisation — for persistent bleeding; risk of colonic ischaemia
• Surgery (segmental colectomy) — for refractory/recurrent bleeding (24% of severe LGIB ultimately need surgery)

• Originates from right colon (vasa recta rupture at diverticular neck) despite left-sided diverticulosis predominance
• 75–80% stop spontaneously; recurrence rate ~25%
• Colonoscopic treatment if bleeding site identified; embolisation; surgery for failed interventions

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TOPIC 8: PANCREATITIS AND PANCREATIC TUMOURS

8.1 Acute Pancreatitis

• Idiopathic
• Gallstones (most common cause — 40–50%)
• Ethanol/alcohol (second most common — 30%)
• Trauma
• Steroids
• Mumps (viral)
• Autoimmune
• Scorpion venom
• Hyperlipidaemia/Hypercalcaemia
• ERCP (post-ERCP pancreatitis)
• Drugs (azathioprine, thiazides, valproate)

1. Abdominal pain characteristic of pancreatitis (acute onset, severe epigastric, radiating to back)
2. Serum amylase or lipase ≥3× upper limit of normal
3. Characteristic imaging findings (CT/MRI/USS)

• Severe epigastric pain radiating to the back ("boring"), relieved by leaning forward
• Nausea, vomiting
• Fever, tachycardia
• Grey Turner's sign: bruising in flanks (retroperitoneal haemorrhage — rare, severe)
• Cullen's sign: periumbilical bruising (rare, severe)
• Jaundice (gallstone-induced)

• Serum lipase (more specific than amylase; stays elevated longer)
• FBC (leukocytosis), CRP (>150 mg/L at 48h = severe), U&E, LFTs (ALT elevation = gallstone aetiology)
• Serum calcium (hypocalcaemia = saponification; poor prognostic sign)
• USS abdomen: gallstones, biliary dilation, peripancreatic fluid; often limited by bowel gas
• CECT abdomen (CT severity index — best at 72–96 hrs): confirms diagnosis, grades severity, identifies necrosis, guides management
• MRCP: if biliary cause suspected (non-invasive); better for duct anatomy

• Mild: no organ failure, no local/systemic complications → resolves in first week
• Moderately Severe: transient organ failure (<48h), or local complications (APFC, ANC)
• Severe: persistent organ failure (>48h)

Key distinction: pseudocyst (clear fluid, amylase-rich) vs. WON (solid debris) — they look different on CT/MRI and are managed differently. Revised Atlanta Classification 2012

1. Resuscitation: Aggressive IV crystalloid hydration (Lactated Ringer's preferred over N/S; 250–500 mL/hr initially), urinary catheter (target UO >0.5 mL/kg/hr)
2. Analgesia: adequate pain control (opioids not contraindicated); avoid NSAIDs (nephrotoxic)
3. Nutrition: oral/enteral feeding as tolerated — start early oral feeding (within 24–48h) in mild pancreatitis; nasojejunal tube feeding in severe pancreatitis; avoid TPN unless enteral route impossible (ACG Guidelines 2024)
4. Antibiotics: only if infected necrosis confirmed or strongly suspected (do NOT give prophylactic antibiotics)
5. ERCP within 24–48 hrs: if biliary obstruction/cholangitis (gallstone pancreatitis + cholangitis)
6. Cholecystectomy: definitive treatment for gallstone pancreatitis; ideally during same admission for mild pancreatitis
7. Infected pancreatic necrosis:
   • Step-up approach (current standard): percutaneous drainage first → minimally invasive necrosectomy (VARD, endoscopic transgastric necrosectomy) → open necrosectomy as last resort (ACS 2024)
8. Pseudocyst drainage: only if symptomatic — endoscopic (EUS-guided transmural drainage preferred), percutaneous, or surgical

8.2 Chronic Pancreatitis

• Chronic episodic epigastric pain radiating to back
• Steatorrhoea (exocrine insufficiency — occurs when >90% function lost)
• Diabetes mellitus (endocrine insufficiency — pancreatic DM = type 3c)
• Weight loss, malnutrition

• AXR/CT: pancreatic calcification (pathognomonic "chain of lakes"), ductal dilation
• MRCP: ductal changes ("chain of lakes")
• Faecal elastase-1: <200 mcg/g = exocrine insufficiency

• Pain: analgesia (avoid opioids if possible), coeliac plexus block
• Enzyme replacement therapy (PERT): pancreatin with meals
• Diabetes management
• Endoscopic therapy: ductal stenting for strictures, stone removal (ESWL)
• Surgery (Puestow/Frey/Beger procedures): indicated for chronic pain refractory to medical/endoscopic therapy, suspected malignancy

8.3 Pancreatic Tumours

8.3.1 Pancreatic Ductal Adenocarcinoma (PDAC)

• Head tumour (most common — 60–70%): obstructive jaundice (painless), Courvoisier's sign (palpable non-tender gallbladder + jaundice = unlikely stones → likely cancer), weight loss, epigastric pain radiating to back
• Body/tail tumours: epigastric pain, weight loss, late-onset diabetes (no jaundice until advanced)
• Virchow's node (left supraclavicular): distant nodal metastasis
• Sister Mary Joseph nodule: umbilical metastasis
• Trousseau's sign: migratory thrombophlebitis (hypercoagulability)

• Serum CA 19-9 (sensitivity ~80%, but not diagnostic alone; used for monitoring)
• CEA (less sensitive)
• CT pancreas protocol (triple phase): best for staging and resectability
• EUS: best for small tumours (<2 cm), FNA for tissue
• ERCP: biliary decompression/stenting + cytology (if jaundice)
• PET-CT: distant metastases

• Resectable: tumour confined to pancreas, no involvement of major vessels
• Borderline resectable: abutment of major vessels (SMA, PV)
• Locally advanced: encasement of major vessels (unresectable)
• Metastatic: liver, peritoneum, lung

• Surgical (only potentially curative):
  • Head/uncinate: Whipple's operation (pancreaticoduodenectomy) — removes head of pancreas, duodenum, distal stomach, gallbladder, common bile duct; reconstruction with pancreatojejunostomy, hepaticojejunostomy, gastrojejunostomy
  • Body/tail: distal pancreatectomy ± splenectomy
  • Only ~15–20% are resectable at presentation
• Chemotherapy (adjuvant): FOLFIRINOX (5-FU + leucovorin + irinotecan + oxaliplatin) for fit patients; or gemcitabine + capecitabine
• Neoadjuvant chemotherapy: for borderline resectable disease
• Palliative care: biliary stenting (ERCP or percutaneous) for jaundice, duodenal stenting/gastrojejunostomy for obstruction, coeliac plexus block for pain

8.3.2 Other Pancreatic Tumours

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TOPIC 9: NEOPLASMS OF THE COLON AND RECTUM

9.1 Colorectal Cancer (CRC) — Epidemiology

• 3rd most common cancer worldwide; 2nd leading cause of cancer death
• Higher in developed countries; increasing incidence in Africa and Asia
• Peak age: 60–70 years; can occur in younger patients with hereditary syndromes

• Age >50, male sex
• Family history, hereditary syndromes
• Diet: high red/processed meat, low fibre, obesity
• IBD (Crohn's, UC — especially with long-standing pancolitis)
• Adenomatous polyps
• Alcohol, smoking
• Diabetes, insulin resistance

9.2 Adenoma-Carcinoma Sequence

1. APC gene mutation (tumour suppressor) — gatekeeper of colorectal carcinogenesis
2. KRAS oncogene activation
3. DCC/SMAD4 loss
4. TP53 mutation (late event)

• Tubular adenoma: most common (80%); stalk present; lowest malignant potential
• Tubulovillous adenoma: intermediate risk
• Villous adenoma: least common (5–10%); sessile; highest malignant potential (~40%); also produces watery diarrhoea, hypokalaemia

9.3 Hereditary Colorectal Cancer Syndromes

9.4 Clinical Features of CRC

• Rectal bleeding + change in bowel habit (especially in >40 years)
• Iron deficiency anaemia (unexplained)
• PR mass on examination
• Weight loss + lower GI symptoms

9.5 Investigations

• DRE: palpates up to 8 cm from anal verge; detects ~25% of rectal cancers
• Colonoscopy + biopsy: gold standard for diagnosis and tissue sampling; also removes synchronous polyps
• CT colonography (virtual colonoscopy): if colonoscopy contraindicated/incomplete
• Rigid sigmoidoscopy: rectal cancers
• Bloods: FBC (anaemia), CEA (tumour marker — useful for monitoring, not diagnosis), LFTs (liver metastases)
• CT chest/abdomen/pelvis: staging (M stage)
• MRI pelvis: rectal cancer staging (T and N stage, circumferential resection margin — CRM)
• PET-CT: suspected metastatic disease
• EUS: rectal cancer T and N staging

9.6 Staging — TNM (Dukes' equivalent)

9.7 Management

Surgical

• Colon cancer: partial colectomy with en bloc lymph node dissection (minimum 12 nodes examined)
  • Right hemicolectomy (caecum/ascending colon)
  • Extended right hemicolectomy (transverse colon)
  • Left hemicolectomy (descending colon)
  • Sigmoid colectomy
  • Total mesorectal excision (TME): critical for rectal cancer — complete excision of mesorectum within visceral fascia (reduces local recurrence to <10%)
• Rectal cancer:
  • Anterior resection (AR): upper/mid rectal cancer; bowel continuity restored
  • Abdominoperineal resection (APR): low rectal cancer with sphincter involvement; permanent end colostomy
  • TEMS/TAMIS (transanal endoscopic microsurgery): early T1 rectal tumours
• Emergency surgery (obstruction/perforation): Hartmann's procedure (resection + end colostomy ± mucous fistula) or primary resection + anastomosis; stenting as bridge to elective surgery

Chemotherapy

Radiotherapy

• Rectal cancer (not colon cancer): preoperative (neoadjuvant) chemoradiation for T3/T4 or node-positive disease to reduce local recurrence and enable sphincter preservation

9.8 Colorectal Cancer Screening

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TOPIC 10: INVESTIGATION OF THE GUT (Lower Gut — Colon, Rectum, Anal Canal)

10.1 Clinical Assessment

• Change in bowel habit (frequency, consistency — Bristol Stool Chart)
• Rectal bleeding: fresh vs. altered; on paper vs. mixed with stool
• Mucus in stool (colorectal cancer, colitis, villous adenoma)
• Tenesmus, incomplete evacuation (rectal pathology)
• Perianal symptoms: pain, discharge, swelling, pruritus ani
• Systemic features: weight loss, anaemia, fatigue

• Abdominal exam: masses, tenderness, distension
• Perianal inspection: fistulae, external haemorrhoids, skin tags, fissures
• Digital rectal exam (DRE): palpate for rectal mass, assess sphincter tone, check for blood on glove

10.2 Endoscopic Investigations (Lower GI)

10.3 Imaging for Lower GIT

• AXR: obstruction, toxic megacolon
• CT colonography (virtual colonoscopy): non-invasive; sensitivity 90–95% for polyps >6 mm; requires bowel prep; cannot biopsy
• MRI pelvis: rectal cancer staging (CRM assessment), pelvic floor disorders, fistulae
• Endoanal USS: sphincter integrity, depth of rectal lesion
• Defaecating proctogram (defaecography): pelvic floor disorders, rectal prolapse
• Transit studies (radiopaque markers): slow-transit constipation

10.4 Physiological (Anorectal) Tests

10.5 Histopathological Investigations

• Endoscopic biopsy: diagnosis of colorectal cancer, IBD (crypt architectural distortion, goblet cell depletion), infectious colitis
• Full-thickness rectal biopsy: Hirschsprung's disease (absence of ganglion cells in Auerbach's and Meissner's plexuses)
• Staining techniques: H&E (routine), PAS (mucin), special stains for organisms (AFB for TB, periodic acid-Schiff for fungi)
• Immunohistochemistry: tumour markers, MLH1/MSH2 for Lynch syndrome

10.6 Summary Table: Choosing the Right Investigation

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RAPID-REVISION SUMMARY TABLE

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KEY CLINICAL ALGORITHMS

Algorithm 1: Approach to Acute Abdomen

Acute onset severe abdominal pain
         ↓
ABC stabilisation + IV access + bloods
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History (SOCRATES) + Examination
         ↓
Erect CXR + AXR → Free air? → Perforated viscus → Emergency surgery
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Pregnancy test (women of childbearing age)
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USS (hepatobiliary/gynaecological pathology)
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CT abdomen/pelvis (if USS inconclusive or surgical cause suspected)
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Diagnosis + Definitive management

Algorithm 2: UGIB Management

Haematemesis / Melena / Coffee-ground vomiting
         ↓
ABC + IV access (x2) + Bloods + Crossmatch
         ↓
Risk score (GBS/Rockall) → GBS 0 = discharge; GBS ≥1 = admit
         ↓
IV PPI + terlipressin (if varices suspected) + antibiotics (cirrhosis)
         ↓
OGD within 24h (urgent = within 12h if haemodynamically unstable)
         ↓
Identify source → Endoscopic haemostasis (injection + clip/coagulation)
         ↓
Failure of endoscopy → Angiographic embolisation → Surgery

Algorithm 3: Acute Pancreatitis Management

Epigastric pain + ↑amylase/lipase (≥3×)
         ↓
Diagnose (Revised Atlanta) + Severity assessment (APACHE II / Ranson's / BISAP / CRP)
         ↓
Aggressive IV crystalloid resuscitation (Lactated Ringer's preferred)
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Early oral/enteral feeding (within 24–48h)
         ↓
Gallstone aetiology + cholangitis → ERCP within 24–48h
         ↓
Mild → Supportive; Severe → ICU + monitor for complications
         ↓
Infected necrosis suspected → CT-guided FNA → Step-up drainage approach
         ↓
Cholecystectomy (gallstone aetiology) → Same admission (mild) or 6-week interval (severe)

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