1. Colonoscopy, 2. Sigmoid volvulus, 3. Intussusception (Mx/Recent advances), 4. Inflammatory disease of large bowel, 5. Hirschsprung's disease, 6. Laparoscopic colonic procedures & complications, 7. Ca. Right colon & Rectum, 8. Ileoanal pouch procedure, 9. Peritonitis, 10. Lap hemicolectomy & complications, 11. FAP, 12. Lap colonic procedure & complications, 13. Staplers in GI surgery

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LARGE INTESTINE - Complete Surgical Answers

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1. COLONOSCOPY

Indications

• Rectal bleeding with normal/equivocal barium enema
• Altered bowel habit
• Iron deficiency anaemia
• Abnormal CT colonography needing tissue biopsy
• Surveillance after colorectal cancer resection
• Surveillance in ulcerative colitis (UC)/Crohn's disease
• Evaluation of known/suspected polyps

• Polypectomy (hot/cold snare, biopsy forceps)
• Endoscopic mucosal resection (EMR)
• Endoscopic submucosal dissection (ESD)
• Haemostasis (APC, clips, injection)
• Stenting (colonic obstruction)
• Sigmoid volvulus decompression/detorsion
• Decompression of acute colonic pseudo-obstruction (Ogilvie's syndrome)

Preparation

• Bowel preparation: low-residue diet + polyethylene glycol (PEG) solution or sodium picosulphate
• IV sedation: midazolam ± fentanyl (conscious sedation) or propofol
• Position: left lateral initially, changed as required

Technique

• Scope inserted through anus, advanced to caecum (identified by appendix orifice + ileocaecal valve)
• Full withdrawal inspection during scope withdrawal
• Carbon dioxide insufflation preferred (absorbed faster, less discomfort)
• Chromoendoscopy / NBI (narrow band imaging) for enhanced mucosal visualisation

Complications (Important for Exam)

Contraindications

• Absolute: Suspected perforation, fulminant colitis
• Relative: Recent MI, bowel prep failure, anticoagulation

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2. SIGMOID VOLVULUS (80-mark question - very high yield)

Definition

Epidemiology

• Most common form of colonic volvulus (50-90% of all cases)
• Mortality rate ~10%
• 2:1 male predominance; peak in 7th decade
• Common in Africa, eastern Europe, South America; uncommon in UK/USA
• Rotation is almost always anticlockwise

Predisposing Factors

• Long redundant sigmoid colon + narrow mesenteric base
• High-residue diet, chronic constipation
• Elderly institutionalised patients; psychiatric/neurological disorders
• Psychotropic drug use (causes GI dysmotility)
• Diabetes, pregnancy

Clinical Presentation

1. Fulminant: Sudden onset, severe pain, early vomiting, rapid deterioration
2. Indolent: Insidious, progressive, less pain, late vomiting

• Obstipation (absolute constipation)
• Gross abdominal distension (often asymmetric, right-sided)
• Colicky abdominal pain
• Late vomiting
• Tachycardia, hypotension, oliguria in advanced disease
• Peritonitis + sepsis if bowel ischaemia/gangrene

Investigations

• Plain AXR: "Bent inner tube" / "Omega loop" / "Coffee bean" sign (60-75% sensitivity)
• CT scan: "Mesenteric whirl sign" + paucity of rectal gas - near 100% accuracy
• CT colonography if diagnosis uncertain

Management

• Flexible sigmoidoscopy/colonoscopy = preferred first-line method
  • "Pinwheel" appearance seen at point of torsion
  • Gently advance scope through twisted segment with insufflation
  • Success rate: 55-94%
  • Leave a soft red-rubber catheter in situ for continued decompression and prevention of early recurrence
• Rigid proctoscopy: higher perforation risk, limited visualisation - use only if flexible endoscopy unavailable

• Recurrence rate after detorsion alone: 85-90%
• Mortality with recurrent volvulus: up to 1 in 3
• Gold standard: Sigmoid resection with primary anastomosis (elective, after bowel prep)
• Colonic fixation (sigmoidopexy) not recommended - high recurrence rate

• Hartmann's procedure (sigmoid colectomy + end colostomy + rectal stump closure) - most commonly performed
• Resection with primary anastomosis + defunctioning ileostomy in selected cases
• Colostomy reversal 3-6 months later
• Current Surgical Therapy 14e

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3. INTUSSUSCEPTION - MANAGEMENT & RECENT ADVANCES

Definition

Types

• Ileo-colic (most common in children)
• Ileo-ileal; colo-colic; ileo-ileo-colic

Epidemiology

• Most common cause of intestinal obstruction in children aged 6 months - 3 years
• Peak: 5-9 months; M:F = 2:1
• In adults: usually has a lead point (60-90%): polyp, Meckel's diverticulum, lymphoma, lipoma, carcinoma

Clinical Features (Children)

• Sudden-onset colicky abdominal pain (child draws up legs, screams, then appears well between episodes)
• Vomiting (initially non-bilious, then bilious)
• "Redcurrant jelly" stools = blood + mucus (late feature - bowel ischaemia)
• Sausage-shaped mass in right hypochondrium (Dance's sign - emptiness in RIF)
• Prostration and lethargy

Investigations

• Ultrasound = investigation of choice: "Target sign" / "Doughnut sign" on transverse section; "Pseudo-kidney sign" on longitudinal section
• Plain AXR: paucity of gas in RIF, soft tissue mass
• CT scan: for adults or if ultrasound inconclusive

Management

• Under fluoroscopic control
• Saline/contrast introduced per rectum under hydrostatic pressure
• Contraindications: signs of perforation, peritonitis, haemodynamic instability

• Air insufflated per rectum under fluoroscopic/ultrasound guidance
• Pressure: 80-120 mmHg maximum
• Success rate: 80-95% (higher than hydrostatic)
• Faster, less messy, lower radiation dose
• Risk of tension pneumoperitoneum if perforation occurs
• Ultrasound-guided hydrostatic/pneumatic reduction - emerging as radiation-free alternative

• US-guided saline enema reduction - avoids radiation entirely; 85% success rate
• Laparoscopic-assisted reduction - for failed enema reduction
• Repeated attempts (2-3) if initial reduction fails, with interval of few minutes
• Delayed repeat enema 8-12 hours after partial reduction

• Failed non-operative reduction
• Signs of peritonitis or perforation
• Haemodynamic instability
• Adults with lead point (requires resection)
• Gangrenous bowel

• Open or laparoscopic right hemicolectomy
• Manual "milking" of intussusceptum (gentle retrograde pressure) - do NOT pull the bowel
• Resection if bowel non-viable or lead point found

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4. INFLAMMATORY DISEASE OF THE LARGE BOWEL (PATHOLOGY)

A. Ulcerative Colitis (UC)

• Diffuse continuous mucosal inflammation beginning at rectum, extending proximally
• Mucosa shows: hyperaemia, haemorrhage, ulceration, crypt abscesses (hallmark)
• Never transmural (confined to mucosa/submucosa)
• "Lead pipe" colon on barium enema (loss of haustra)
• Pseudopolyps = oedematous islands of mucosa between ulcers

• Crypt distortion + crypt abscesses
• Goblet cell depletion
• Plasma cell infiltration at base of crypts
• Paneth cell metaplasia

• Toxic megacolon (>6 cm), perforation
• Colorectal carcinoma (risk increases with disease duration and extent)
• Stricture formation
• Haemorrhage

B. Crohn's Disease (Large Bowel Involvement)

• Transmural inflammation (all layers of bowel wall)
• Skip lesions (discontinuous)
• Affects any part of GI tract from mouth to anus
• Cobblestone mucosa - due to deep fissuring ulcers + intact mucosa between
• Non-caseating granulomas (hallmark - 60% of specimens)
• Rose thorn/collar stud ulcers; fistulae; strictures

C. Diverticular Disease (Inflammatory Complications)

• Inflammation/infection of a diverticulum
• Left iliac fossa pain ("left-sided appendicitis"), fever, altered bowel habit
• Hinchey classification for complicated diverticulitis:
  • I: Pericolic abscess
  • II: Pelvic/distant abscess
  • III: Purulent peritonitis
  • IV: Faecal peritonitis

• Uncomplicated: oral antibiotics + liquid diet
• Complicated (Hinchey III/IV): emergency surgery (Hartmann's or primary anastomosis ± defunctioning stoma)

D. Ischaemic Colitis

• Typically affects "watershed areas" - splenic flexure (Griffith's point) and rectosigmoid junction
• Causes: low-flow states, thromboembolic disease, post-aortic surgery
• Presents: bloody diarrhoea + LIF pain

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5. HIRSCHSPRUNG'S DISEASE

Definition

Incidence & Genetics

• 1 in 5000 live births
• Male:Female = 4:1 (short-segment); nearly equal in long-segment
• 3-5% have Down syndrome
• Abnormal locus on chromosome 10 - associated with RET proto-oncogene
• Autosomal dominant with variable penetrance

Pathophysiology

• Failure of migration of neural crest cells to the distal colon during embryogenesis (weeks 5-12)
• Absence of ganglia → failure of relaxation of internal anal sphincter → functional obstruction
• The aganglionic segment (narrow) is DISTAL; the dilated hypertrophied segment is PROXIMAL
• Transition zone between dilated and collapsed colon

Extent of Aganglionosis

• Rectosigmoid (80%) - short segment (most common)
• Splenic/transverse colon (17%)
• Total colonic aganglionosis with small bowel involvement (8%) - long segment

Clinical Features

• Failure to pass meconium within first 24 hours of life
• Abdominal distension
• Bilious vomiting
• On PR examination: explosive release of gas + faeces ("squirt sign")

• Chronic constipation and abdominal distension
• Failure to thrive

• Alternating diarrhoea and obstipation
• Fever, bloody diarrhoea, haematochezia, peritonitis, septic shock

Diagnosis

1. Contrast enema: Narrow distal aganglionic segment + dilated proximal bowel with transition zone; failure to evacuate contrast after 24 hours = strongly diagnostic
2. Anorectal manometry: Failure of internal sphincter to relax on rectal balloon distension (absent RAIR = recto-anal inhibitory reflex)
3. Rectal biopsy (Gold Standard): Absent ganglion cells + hypertrophied nerve trunks + positive acetylcholinesterase staining; calretinin staining now standard adjunct
   • Suction biopsy (neonates, at bedside) - specimens ≥1 cm above dentate line
   • Full-thickness biopsy under GA (older children)

Management

• Laparoscopic-assisted or completely transanal (TEPT = transanal endorectal pull-through) approach now preferred
• Intraoperative frozen sections confirm level of normal ganglionation

• Constipation (most common)
• Soiling/incontinence
• Post-operative enterocolitis
• Anastomotic leak/stricture
• Need for intermittent rectal decompression

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6 & 12. LAPAROSCOPIC COLONIC PROCEDURES & COMPLICATIONS

Various Laparoscopic Colonic Procedures

• Indications: Carcinoma caecum/ascending colon, Crohn's disease, intussusception with lead point
• Medial-to-lateral dissection (preferred) or lateral-to-medial
• Resection of terminal ileum + right colon with ileocolic, right colic, right branch of middle colic vessels
• Extracorporeal or intracorporeal anastomosis

• Indications: Sigmoid Ca, diverticular disease, sigmoid volvulus (elective)
• Splenic flexure mobilisation often required
• Identify and protect left ureter throughout

• For UC, FAP, synchronous bowel cancers, Ogilvie's syndrome

• For upper/mid-rectal Ca
• Total mesorectal excision (TME) - complete sharp dissection of mesorectal envelope
• Stapled colorectal anastomosis

• For low rectal Ca, anal canal Ca
• Permanent end colostomy (left iliac fossa)

• COST, CLASICC, COLOR trials showed equivalent oncological outcomes vs. open with faster recovery

Advantages of Laparoscopic Colectomy

• Less post-operative pain
• Earlier return of bowel function
• Shorter hospital stay
• Better cosmesis
• Reduced wound complications
• Fewer adhesions

Complications (10-mark topic)

• Visceral injury (small bowel, spleen, ureter, bladder)
• Vascular injury (iliac vessels, mesenteric vessels)
• Conversion to open (5-10%) - not a complication but a safety measure

• Anastomotic leak (most feared; 2-5%)
• Bleeding (anastomotic, mesenteric)
• Ileus vs. early obstruction
• Ureteric injury (may present late as urinoma, urinary fistula)
• Wound infection
• Deep vein thrombosis/pulmonary embolism
• Urinary retention

• Port site hernia (especially 10/12mm ports)
• Port site recurrence (rare; 1-2% in cancer cases)
• Anastomotic stricture
• Adhesive bowel obstruction
• Stoma-related complications (if stoma formed)

• Sexual dysfunction (bladder/sexual nerve injury) - due to autonomic nerve damage in pelvis
• Bladder dysfunction
• Anastomotic leakage (higher risk in low rectal anastomosis)
• Pelvic abscess
• Anterior resection syndrome (frequent stools, urgency, clustering, incontinence)

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7. CARCINOMA - RIGHT COLON & RECTUM

COLORECTAL CANCER - Overview

• Greatest cause of cancer mortality in non-smokers in Europe, North America, Australasia
• Risk increases with age; diet high in meat and low in fibre = increased risk
• 10% of cases have hereditary component
• 50% of tumours are in sigmoid colon or rectum

• Vogelstein model: APC mutation → K-ras → DCC → p53 mutations

Carcinoma of Right Colon

• Ascending colon/caecum
• Tend to be polypoid/fungating (exophytic) tumours
• Presents late as large bowel has wide lumen
• Symptoms: Iron deficiency anaemia (chronic occult bleeding), weight loss, palpable RIF mass
• Rarely cause obstruction early (wide lumen + liquid content)
• May present as acute appendicitis if obstructs appendix orifice
• On examination: palpable right-sided mass

• Colonoscopy + biopsy (definitive)
• CT chest/abdomen/pelvis (staging)
• CEA (baseline + follow-up)

• Resection of terminal ileum + ascending colon to hepatic flexure
• Ligation of ileocolic, right colic, and right branch of middle colic arteries at origin
• Ileocolic anastomosis

Carcinoma of Rectum

• Annular (stenosing) pattern more common - causes obstruction
• Rectal bleeding (bright red blood mixed with stool), tenesmus, mucous discharge
• Change in bowel habit
• Rectal mass palpable on PR examination (up to 10-15 cm)
• Late: pelvic pain (sacral nerve invasion), bladder/urinary symptoms, fistulae

1. Pre-operative: MRI pelvis (assesses mesorectal fascia margin), CT C/A/P for staging; CEA
2. Neoadjuvant therapy: Short-course radiotherapy (5x5 Gy) or long-course chemoradiotherapy for locally advanced/T3-T4 disease (to downstage, reduce local recurrence)
3. Surgery - Total Mesorectal Excision (TME): Sharp dissection in mesorectal plane under direct vision - reduces local recurrence from 30% to <5%

• Anterior Resection (AR): Upper/mid rectum; colorectal anastomosis - preserve anal sphincter
• Low Anterior Resection (LAR): Below peritoneal reflection; coloanal anastomosis often with protective loop ileostomy
• Abdominoperineal Resection (APR): Low rectal Ca (within 2-3 cm of anorectal junction) - permanent colostomy
• Hartmann's Procedure: Emergency (obstruction/perforation) - resection + end colostomy

• Distal resection margin: ≥1 cm (rectal Ca)
• Circumferential radial margin (CRM): ≥1 mm (involvement = higher recurrence)
• Adjuvant chemotherapy for node-positive (FOLFOX/CAPOX)

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8. ILEOANAL POUCH PROCEDURE (Restorative Proctocolectomy)

Indications

• Ulcerative Colitis (not responding to medical therapy, or requiring colectomy for dysplasia) - most common indication
• Familial Adenomatous Polyposis (FAP) - prophylactic surgery
• Selected cases of Crohn's colitis (controversial)

Procedure: Total Proctocolectomy + IPAA (Ileal Pouch-Anal Anastomosis)

1. Total proctocolectomy (removal of entire colon + majority of rectum)
2. Construction of ileal reservoir (J-pouch, S-pouch, W-pouch, or H-pouch)
3. Anastomosis to anal canal/lower rectum

Pouch Configurations

Anastomosis Technique

1. Stapled IPAA (preferred): Apex of J-pouch stapled to distal rectum leaving short rectal cuff - superior continence, faster
2. Hand-sewn IPAA (mucosectomy): 2-cm anorectal mucosectomy then hand-sewn anastomosis - indicated in dysplasia/cancer (to remove all at-risk mucosa)

Staging of Surgery

• 2-stage procedure (most common): IPAA + covering loop ileostomy → ileostomy closure 8-12 weeks later
  • Required when patient on immunosuppressives or in poor nutritional state
• 1-stage procedure (no ileostomy): Selected patients not on immunosuppression with good nutrition

Key Technical Points

• Mesenteric mobilisation to level of pancreas to reduce pouch tension
• Preserve ileocolic vessels entirely
• Adequate pouch reach to anus without tension = essential

Complications of IPAA

• Anastomotic leak (2-10%)
• Pelvic sepsis
• Small bowel obstruction
• Haemorrhage

• Pouchitis (most common complication, 20-50%) - non-specific inflammation; treated with metronidazole/ciprofloxacin
• Pouch failure (10-15%) - requiring pouch excision ± permanent ileostomy
• Cuffitis (inflammation of retained rectal cuff)
• Sexual dysfunction
• Fistulae (pouch-vaginal most common in women)
• Stricture at anastomosis
• Infertility (female - due to pelvic adhesions; 2-3x increased rate)

Functional Results

• Average 4-6 stools/day; good continence in >90%
• Avoids permanent stoma
• Quality of life generally excellent

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9. PERITONITIS

Definition

Classification

• Localised peritonitis: confined area; parietal peritoneum involvement → somatic pain, guarding, rebound
• Diffuse/generalised peritonitis: life-threatening surgical emergency

• Primary (spontaneous): No intra-abdominal source; haematogenous/lymphatic; SBP in cirrhosis (E. coli, Klebsiella, pneumococcus); also Tb peritonitis
• Secondary: Most common - intra-abdominal source (perforation, transmural spread, trauma, iatrogenic)
• Tertiary: Recurrent or persistent peritonitis after adequate treatment; resistant organisms; poor host defences

Causes of Peritoneal Inflammation (Bailey & Love)

• Bacterial (GI and non-GI)
• Chemical - bile, barium, urine
• Allergic - starch peritonitis
• Traumatic - operative handling
• Ischaemic - strangulated bowel, vascular occlusion
• Familial Mediterranean fever

Paths to Peritoneal Infection

• GI perforation (peptic ulcer, appendix, diverticulum)
• Transmural translocation (pancreatitis, ischaemic bowel)
• Exogenous contamination (trauma, drains, open surgery, peritoneal dialysis)
• Female genital tract (PID)
• Haematogenous spread (rare)

Clinical Features

• Pain in affected quadrant
• Involuntary guarding (muscle rigidity)
• Rebound tenderness
• Peritonism - tachycardia, pyrexia
• Phrenic pain = diaphragmatic irritation → shoulder tip pain (C5 dermatome)
• Pelvic peritonitis: assessed by PR/PV examination

• Board-like rigidity of entire abdomen
• Patient lies still, shallow breathing
• Systemic: fever, tachycardia, hypotension → septic shock
• Absent bowel sounds
• Nausea, vomiting

Investigations

• CT scan = investigation of choice (identifies cause in majority)
• FBC (leukocytosis), CRP, LFTs, amylase
• AXR: free gas under diaphragm (perforation)
• Erect CXR: gas under diaphragm
• Peritoneal fluid: aspirate for organisms + white cells (Gram stain, culture)
• Laparoscopy if above inconclusive

Management

• IV access, fluid resuscitation
• IV broad-spectrum antibiotics (cover gram-negative + anaerobes)
• NG tube, urinary catheter
• Analgesia (does not mask signs - opiates safe)
• Monitor urine output, ABG

• Aims: Remove underlying cause + lavage/dilute contamination
• Peritoneal lavage with warm saline (no proven benefit of antibiotics in lavage)
• Repair perforation / resect gangrenous bowel
• May require staged surgery ("damage control") in septic shock
• Open abdomen technique in severe contamination

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10 & 6(overlap). LAPAROSCOPIC HEMICOLECTOMY & COMPLICATIONS

Laparoscopic Right Hemicolectomy (for Right Colon Ca)

1. Patient supine, Trendelenburg + right side up
2. Four ports: umbilical camera + 3 working ports
3. Medial-to-lateral approach (preferred): Identify ileocolic vessels first, dissect retroperitoneal plane (Toldt's fascia), then mobilise lateral attachments
4. Division of ileocolic + right colic + right branch of middle colic vessels
5. Specimen delivered through small Pfannenstiel or extended umbilical incision
6. Extracorporeal anastomosis (functional end-to-end or end-to-end ileocolic)

• Ureteric injury (right ureter at risk at level of gonadal vessels/inferior mesenteric artery for left hemicolectomy)
• Duodenal injury (right hemi - retroperitoneal duodenum in medial dissection)
• Bowel injury - especially terminal ileum
• Vascular injury (SMA, SMV branches)
• Splenic injury (left hemi - splenic flexure mobilisation)
• Conversion to open

• Anastomotic leak (most feared; presents day 4-7 with fever, peritonitis, rising CRP)
  • Management: CT-guided drainage if localised; re-operation if diffuse
• Paralytic ileus (common; nasogastric tube, early feeding)
• Haemorrhage (intra-abdominal, anastomotic)
• Wound infection / port site infection
• DVT/PE (prophylaxis: LMWH + TED stockings)
• Urinary retention (especially in elderly males)
• Chest infection

• Adhesive small bowel obstruction
• Incisional/port site hernia (10-12 mm ports - fascial closure needed)
• Anastomotic stricture
• Stoma complications (if stoma formed): prolapse, retraction, parastomal hernia, skin excoriation
• Port site metastasis (rare in colorectal surgery; 1-2%)
• Bladder/sexual dysfunction (left hemi/rectal surgery)

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11. FAMILIAL ADENOMATOUS POLYPOSIS (FAP) (10-mark question)

Definition & Genetics

• Autosomal dominant inherited disease due to germline mutation in APC (adenomatous polyposis coli) tumour suppressor gene on chromosome 5q21
• Clinically defined as: >100 synchronous colorectal adenomas, OR <100 polyps with positive family history
• Lifetime CRC risk = nearly 100% by age 35-40 if untreated
• 25-30% are de novo mutations (no family history)

Key Mutations

• Most mutations between codons 168-1640
• Codon 1309 = most severe disease (earliest onset)
• Mutations 1286-1513 = worse prognosis, earlier onset

Clinical Features

• Polyps visible on sigmoidoscopy by age 15 years; almost always by age 30
• Predominantly in left colon and rectum
• Present in 15% by age 10 years and 75% by age 20 years
• Symptoms: rectal bleeding, diarrhoea, abdominal pain, mucous discharge

• Duodenal adenomas - 95% of FAP patients; most common around ampulla of Vater → risk of duodenal/periampullary cancer (5-10%)
• Duodenal cancer = 2nd leading cause of death in FAP
• Gastric fundic gland polyps (30-90%, low malignant potential)
• Gastric adenomas (10-30%; higher risk in Asian populations)

• CHRPE (Congenital Hypertrophy of Retinal Pigment Epithelium) - 75%; useful for family screening
• Osteomas (benign; 80%) - mandible, skull, long bones
• Epidermoid/sebaceous cysts (50%)
• Desmoid tumours (30%) - locally invasive, non-metastasising, may involve mesentery → can be unresectable; leading surgical cause of death
• Supernumerary teeth
• Cerebellar medulloblastoma (Turcot's syndrome variant)

Surveillance

• Colonoscopy from age 10-12 years annually (or flexible sigmoidoscopy annually if polyps not yet seen on scope)
• EGD from age 20 (for duodenal surveillance) - Spiegelman scoring system guides intervals
• Genetic testing: APC gene mutation analysis

Surgical Treatment (Prophylactic - to prevent CRC)

1. Total proctocolectomy + permanent ileostomy: Removes all risk; no need for surveillance; significant quality of life impact
2. Colectomy + ileorectal anastomosis (IRA): Rectal preservation possible if rectal polyp burden is low; requires regular rectal surveillance for synchronous/metachronous polyps; risk of rectal cancer remains
3. Restorative proctocolectomy + IPAA (J-pouch) (preferred for restoration of intestinal continuity): Removes all at-risk colon and most at-risk rectum; better quality of life than permanent ileostomy

• APC mutation associated with <100 polyps
• Presentation often in 4th decade (later)
• Right-sided predominance

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13. STAPLERS IN GI SURGERY (20-mark question)

Principles of Stapling

• Anastomosis (joining two segments of bowel)
• Resection (cutting and stapling bowel ends simultaneously)
• Haemostasis (vascular stapling)

Types of Surgical Staplers

• Fires a double or triple row of staggered staples WITHOUT cutting
• Closes a bowel lumen or tissue
• Used for: bowel closure after resection, closure of duodenal stump
• Sizes: 30, 60, 90 mm

• Fires two double rows of staggered staples AND cuts between them simultaneously
• Creates a functional side-to-side anastomosis
• Used for: side-to-side bowel anastomosis (functional end-to-end), division of bowel, creation of J-pouch (two firings of 75/100 mm GIA)
• Sizes: 55, 75, 80, 100 mm

• Fires a circular double row of staples + circular blade cuts internally creating a lumen
• Inserted transanally for colorectal/coloanal anastomosis
• Used for: Anterior resection, low anterior resection, coloanal anastomosis
• Sizes: 21, 25, 28, 29, 31, 33 mm (size chosen to match bowel lumen)
• Key features: adjustable gap for tissue compression; anvil placed in proximal bowel and shaft inserted transanally; "doughnuts" checked after firing for complete rings

• Laparoscopic linear cutting stapler with articulating heads
• Used for: laparoscopic bowel resection, vessel division (mesenteric vessels, hepatic pedicle)
• Sizes: 30, 45, 60 mm; colour coded for tissue thickness:
  • White: vascular (0.75mm closed height)
  • Blue: standard tissue (1.0mm)
  • Green: thick tissue (1.5mm)

Use of Staplers in Specific Colonic Operations

Advantages of Staplers over Hand-Sewn Anastomosis

• Faster (reduced operative time)
• Consistent, standardised technique
• Enables anastomosis in difficult locations (low rectum, deep pelvis)
• Reduced contamination
• Reproducible results

Complications of Stapled Anastomosis

• Anastomotic leak (2-5%) - higher with EEA in low rectal anastomosis
• Anastomotic stricture (more common with circular stapler)
• Bleeding from staple line
• Incomplete rings ("doughnuts") on firing EEA = incomplete anastomosis (must check both rings complete)
• Twist/misalignment of bowel ends
• Staple line failure if misfire

Checking Circular Stapler Anastomosis (Integrity Test)

1. Check both "doughnuts" are complete circular rings
2. Fill pelvis with water + inflate per anum = pneumatic/hydrostatic leak test
3. If leak: reinforce with sutures or place defunctioning stoma

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BONUS TOPIC: PRINCIPLE OF ANASTOMOSIS OF INTESTINES

Requirements for a Good Anastomosis (the "5Bs")

1. Blood supply - adequate (no tension on mesentery)
2. Bowel preparation - clean lumen, no faecal loading
3. Broad lumens - matching lumens (if mismatched: Cheatle slit or fish-mouth end-to-side)
4. Both ends tension-free - no traction
5. Bacteria-free field (relative - bowel always has bacteria)

Techniques

• Single-layer interrupted (preferred): Full-thickness/seromuscular; PDS/Vicryl; 3-0 or 4-0
• Two-layer: Inner continuous all-layers + outer interrupted seromuscular (Lembert sutures)
• End-to-end or end-to-side or side-to-side

• Side-to-side functional end-to-end: GIA stapler
• End-to-end in deep pelvis: Circular EEA

Layers of Bowel Wall (from inside out)

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Sources: Bailey & Love's Short Practice of Surgery 28e; Sabiston Textbook of Surgery 21e; Current Surgical Therapy 14e; Pye's Surgical Handicraft 22e; Sleisenger & Fordtran's GI & Liver Disease; Fischer's Mastery of Surgery 8eAll 13 topics covered. Here is a quick exam-strategy summary of what was covered and the weightage indicators from your notes:

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Exam Weightage Summary

1. Sigmoid Volvulus (80 marks) - know the complete algorithm
2. Staplers in GI surgery (20 marks) - know all 4 types with uses
3. Lap hemicolectomy complications (20 marks) - intra-op + early + late, table format

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PANCREAS - Complete Surgical Answers

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EXAM WEIGHTAGE MAP (from your notes)

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1 / 5 / 15. ACUTE PANCREATITIS - CIF, PATHOPHYSIOLOGY, Mx, RECENT Mx (20-mark high-yield)

Definition

Causes (Aetiology) - "I GET SMASHED"

• I - Idiopathic
• G - Gallstones (most common cause; 40-60%)
• E - Ethanol/Alcohol (second most common; 30-40%)
• T - Trauma (blunt abdominal injury)
• S - Steroids
• M - Mumps, Malignancy (pancreatic Ca obstructing duct)
• A - Autoimmune (type 1 & 2 autoimmune pancreatitis)
• S - Scorpion sting / Snake bite
• H - Hyperlipidaemia (triglycerides >1000 mg/dL), Hypercalcaemia, Hypothermia
• E - ERCP (post-ERCP pancreatitis)
• D - Drugs (valproate, azathioprine, 6-MP, tetracyclines, L-asparaginase, thiazides)
• Others: Pancreas divisum, Annular pancreas, Sphincter of Oddi dysfunction, Viral infections (Coxsackievirus, EBV, HIV)

Pathophysiology (Key for 15/20-mark question)

• Inappropriate activation of trypsinogen → trypsin within pancreatic acinar cells (normally activated only in duodenum)
• Gallstones/alcohol/other insults → premature fusion of zymogen granules with lysosomes → cathepsin B activates trypsinogen intracellularly

1. Trypsin activates other zymogens: phospholipase A2, elastase, kallikrein, complement
2. Phospholipase A2: Destroys cell membranes (acinar necrosis + pulmonary surfactant damage → ARDS)
3. Elastase: Dissolves elastic fibres of blood vessels → haemorrhage
4. Kallikrein: Activates bradykinin → vasodilation, oedema, pain
5. Activated enzymes escape into peripancreatic fat → fat necrosis (saponification with calcium) + systemic inflammation

Clinical Features

• Severe epigastric pain: Sudden onset, constant, radiates to back ("boring" through to back)
• Nausea and vomiting (does not relieve pain)
• Fever
• Absolute pain relief on leaning forward (reduces stretch on coeliac plexus)
• Abdominal distension (ileus)

• Epigastric tenderness ± guarding
• Reduced/absent bowel sounds
• Jaundice (biliary obstruction / coexistent gallstones)
• Grey Turner's sign: Flank bruising (haemorrhagic pancreatitis)
• Cullen's sign: Periumbilical bluish discolouration
• Fox's sign: Bruising in inguinal region
• Tetany (hypocalcaemia from saponification)
• In severe cases: shock, ARDS, AKI, DIC

Investigations

• Serum lipase (preferred - more sensitive and specific than amylase; peaks early, stays elevated 1-2 weeks)
• Serum amylase (rises within hours, returns to normal in 3-5 days; >3x upper limit of normal = diagnostic)
• Note: degree of elevation does NOT correlate with severity
• FBC: leukocytosis
• CRP (>150 mg/L at 48h = severe disease)
• LFTs: ALT >3x = gallstone pancreatitis (PPV 95%)
• RFTs: urea, creatinine (AKI)
• Calcium (hypocalcaemia = bad prognostic sign)
• Triglycerides (if >1000 mg/dL - aetiology)
• ABG: pO2 <60 mmHg = ARDS/organ failure
• Blood glucose, Hb

• Abdominal ultrasound: FIRST investigation - looks for gallstones, biliary dilation; poor at visualising pancreas directly due to bowel gas
• CT scan with IV contrast (CECT) = Gold standard for severity assessment:
  • Not routine at presentation
  • Indicated if: (1) diagnostic uncertainty (2) rule out other pathology (3) failure to respond to treatment after 48-72 hours
  • Best performed 3-7 days after onset (necrosis may not be apparent early)
  • CT Severity Index (CTSI/Balthazar score) grades severity A-E
  • Necrosis = areas of no enhancement on contrast CT
  • Normal CT in 15-30% of mild cases
• MRI/MRCP: Superior for gallbladder/biliary imaging; equivalent sensitivity to CT for pancreatitis
• ERCP: NOT routine; reserved for suspected biliary obstruction + cholangitis
• EUS: Useful for idiopathic pancreatitis - detects missed biliary stones/sludge, CP, occult malignancy

Severity Classification

Prognostic Scoring Systems (Topic 5)

• Age >55 years
• WBC >16,000/mm³
• Blood glucose >200 mg/dL (non-diabetic)
• LDH >350 IU/L
• AST >250 IU/L

• Fall in Hct >10%
• Rise in BUN >5 mg/dL
• Serum Ca <8 mg/dL
• PaO2 <60 mmHg
• Base deficit >4 mEq/L
• Fluid sequestration >6L

• 15 variables; can be applied on admission and repeated
• Score ≥8 = severe disease
• Validated for dynamic monitoring in ICU

• BUN >25 mg/dL
• Impaired mental status (Glasgow Coma Scale <15)
• SIRS (≥2 criteria)
• Age >60 years
• Pleural effusion on imaging
• Score ≥3 = high risk for severe disease

• Absence of rebound tenderness/guarding
• Normal haematocrit
• Normal serum creatinine
• All 3 = 97% specific for mild disease

• CRP >150 mg/L at 48 hours = predictor of severe disease
• Widely available, simple

Management of Acute Pancreatitis

1. IV fluid resuscitation - aggressive early (lactated Ringer's preferred over normal saline - reduces acidosis)
   • Rate: 250-500 mL/hr in first 12-24 hours, titrated to urine output (>0.5 mL/kg/hr)
2. Analgesia - IV opiates (morphine/pethidine); NSAIDs
3. Nothing by mouth (NBM) initially; early enteral nutrition preferred (within 48 hours if tolerated)
   • Nasogastric (NG) feeding = as effective as nasojejunal (NJ) feeding
   • Enteral > parenteral (TPN) - lower infection, lower cost
4. Monitor: urine output, vitals, oxygen saturation, blood glucose
5. Antibiotics: NOT routine prophylactically; only if signs of infection (infected necrosis)
6. DVT prophylaxis: LMWH once haemodynamically stable

• Gallstone pancreatitis: Early laparoscopic cholecystectomy (within 3 days in mild disease = standard of care)
  • Reduces recurrence
  • ERCP + sphincterotomy only if coexisting cholangitis or biliary obstruction (elevated bilirubin)
• Hypertriglyceridaemia-induced: Insulin infusion + plasmapheresis
• Hypercalcaemia-induced: Treat underlying cause

Recent/Modern Management (Topic 1 - 2015 question)

1. Step-up approach for necrotising pancreatitis (replaces early open necrosectomy):
   • Percutaneous drainage → minimally invasive retroperitoneal necrosectomy (MIRP) → open surgery only if step-up fails
   • PANTER trial showed step-up reduces organ failure and reduces new-onset diabetes vs. open necrosectomy
2. Endoscopic transmural necrosectomy (ETN/VARD):
   • EUS-guided puncture of walled-off necrosis (WON) → lumen-apposing metal stent (LAMS) placement → direct endoscopic necrosectomy
   • Lower morbidity and cost vs. surgery; preferred for collections apposed to gastric/duodenal wall
3. Lumen-apposing metal stents (LAMS): Hot AXIOS stent - allows direct endoscopic debridement through transmural access
4. Delayed intervention (minimum 4 weeks): Allow demarcation of necrosis → "step-up" is safest after walled-off necrosis (WON) forms
5. Lactated Ringer's (LR) preferred over normal saline - reduces SIRS response
6. Early enteral nutrition via NG/NJ tube - reduces infectious complications; no benefit to very early oral feeding
7. Antibiotics: Carbapenems (imipenem) reserved for proven/suspected infected necrosis; NOT prophylactic

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2 & 3. MRCP (Magnetic Resonance Cholangiopancreatography) & MRCP IN PANCREATIC DUCT DISORDERS

Definition

Principle

Sequences Used

• HASTE/SSFSE (single-shot fast spin echo): Single breath-hold images
• 3D MRCP: Multiple thin slices reconstructed with MIP (Maximum Intensity Projection)
• MRCP now widely replaces diagnostic ERCP as it is non-invasive and has zero risk of post-ERCP pancreatitis

Indications

• Suspected choledocholithiasis (CBD stones)
• Obstructive jaundice - identify level and cause
• Primary Sclerosing Cholangitis (PSC)
• Biliary strictures (benign or malignant)
• Cholangiocarcinoma
• Post-operative biliary complications
• Evaluation before laparoscopic cholecystectomy (suspected CBD stones)

• Pancreas divisum - failure of fusion of dorsal and ventral ducts; Santorini duct drains majority through minor papilla; MRCP shows separate drainage
• Chronic pancreatitis: Ductal dilatation ("chain of lakes" appearance), strictures, calculi within duct
• Pancreatic ductal adenocarcinoma: Abrupt cutoff of main pancreatic duct + CBD dilation = "double duct sign"
• IPMN (Intraductal Papillary Mucinous Neoplasm): Dilation of main duct and/or branch ducts; communication between cysts and main duct
• Pancreatic pseudocyst: Communication between pseudocyst and main duct (guides drainage strategy - transpapillary vs. transmural)
• Annular pancreas: Pancreatic tissue encircling duodenum; MRCP shows ring-like duct
• Post-ERCP leak/stricture assessment
• Sphincter of Oddi dysfunction: MRCP + secretin stimulation (S-MRCP) assesses duct dilation after stimulation

MRCP vs ERCP

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4. CHRONIC PANCREATITIS - ETIOPATHOLOGY, CIF & MANAGEMENT (80 marks - most important topic)

Definition

Aetiology (TIGAR-O System)

Pathology (Histology)

• Irregular fibrosis (perilobular then intralobular)
• Loss of acinar cells (exocrine insufficiency)
• Ductal changes: strictures, dilatation, intraductal calculi (protein plugs calcify → pancreatic stones)
• Preservation of islets of Langerhans until late (endocrine insufficiency = late feature)
• Protein plugs → obstruct small ducts → upstream ductal hypertension → acinar atrophy
• Macroscopic: hard, nodular gland; duct may show "chain of lakes" appearance

Cambridge Classification (Pancreatographic Severity)

• Normal: No changes
• Equivocal: <3 abnormal branch ducts
• Mild: ≥3 abnormal branch ducts
• Moderate: Abnormal main duct + branch ducts
• Severe: Moderate + one or more of: large cavity, obstruction, filling defects, severe duct irregularity

Clinical Features

1. Abdominal pain (most common; epigastric, radiates to back; worse after eating/alcohol; may be continuous in severe disease; "burned out" in late disease when gland is destroyed)
2. Exocrine insufficiency - Steatorrhoea (malabsorption of fat; >90% of exocrine function must be lost before steatorrhoea appears), weight loss, nutritional deficiencies (fat-soluble vitamins A, D, E, K)
3. Endocrine insufficiency - Diabetes mellitus ("Type 3c" pancreatogenic diabetes); occurs late

• Obstructive jaundice (stricture of CBD in head of pancreas)
• Duodenal obstruction (head fibrosis)
• Pancreatic ascites (duct rupture → pancreatic fistula)
• Pleural effusion (pancreatic fistula tracking into chest)
• Pseudocysts
• Splenic vein thrombosis → gastric varices (left-sided/"sinistral" portal hypertension)
• Increased risk of pancreatic ductal adenocarcinoma (x10-20 risk)

Investigations

• Faecal elastase-1 (FE-1): Non-invasive; <200 μg/g = moderate-severe insufficiency; screening test of choice
• 72-hour faecal fat estimation (gold standard for steatorrhoea): >7g/day = abnormal
• Secretin-CCK stimulation test (gold standard for exocrine function): Duodenal aspiration after secretin + CCK injection; reduced bicarbonate and enzyme output; invasive/rarely done
• BT-PABA test, Lundh test meal (indirect tests)

• Amylase/lipase: Often normal in advanced CP
• Blood glucose/HbA1c (diabetes)
• CA 19-9 (if malignancy suspected)

• Plain AXR: Pancreatic calcification (pathognomonic of CP)
• Ultrasound: Dilated pancreatic duct (>3mm in body), calcification, pseudocysts, parenchymal heterogeneity
• CT scan: Best for calcification, parenchymal changes, ductal dilation, complications
• MRCP: Visualises duct anatomy - "chain of lakes" (alternating strictures + dilatation); Santorini duct in pancreas divisum
• EUS: Most sensitive for early/mild CP; Rosemont criteria (major A: hyperechoic foci with shadowing; major B: lobularity with honeycombing; + minor criteria for ductal changes)
• ERCP: Reserved for therapeutic intervention (stenting, stone extraction)

Management

1. Stop alcohol and smoking (most important)
2. Pain management:
   • Analgesic ladder: paracetamol → NSAIDs → weak opioids → strong opioids
   • Antioxidants (selenium, ascorbic acid, β-carotene, methionine, α-tocopherol) - reduce pain in some trials
   • Coeliac plexus block (EUS-guided or CT-guided) - for refractory pain; partial/temporary relief
   • Pregabalin/gabapentin (neuropathic pain component)
3. Exocrine insufficiency:
   • Pancreatic enzyme replacement therapy (PERT): Creon (pancrelipase) capsules with meals + snacks; enteric-coated microspheres; dose titrated to response
   • Fat-soluble vitamin supplementation (A, D, E, K)
   • Medium-chain triglycerides (MCT)
4. Endocrine insufficiency: Insulin therapy; higher hypoglycaemia risk than type 1/2 DM (glucagon also deficient)
5. Nutritional support: Low-fat diet, small frequent meals

• Pancreatic duct stenting: For dominant strictures causing ductal hypertension; temporary relief
• Pancreatic stone extraction: After ESWL (extracorporeal shock wave lithotripsy) to fragment stones; success ~70%
• Pseudocyst drainage: Transmural (EUS-guided) or transpapillary
• Biliary stenting: For CBD stricture causing jaundice

1. Intractable pain not responding to medical/endoscopic treatment
2. Pancreatic ductal dilation + head mass (inflammatory)
3. Biliary/duodenal obstruction not amenable to stenting
4. Suspected malignancy
5. Portal/splenic vein thrombosis with bleeding varices
6. Pseudocyst complications

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6. ACUTE NECROTIZING PANCREATITIS - CIF, ASIS & MANAGEMENT

Definition

Atlanta 2012 - Local Complication Classification

• Infected necrosis occurs in up to 70% of patients with necrosis within 2-3 weeks
• Infected necrosis + sepsis = main cause of late mortality in severe AP

Diagnosis of Necrotizing Pancreatitis

• CT with IV contrast: Areas of non-enhancement = necrosis (sensitivity >90%)
• Best assessed at 72-96 hours after onset (earlier CT may underestimate extent)
• FNA (CT/EUS-guided) with Gram stain + culture if infected necrosis suspected

ASIS (Signs indicating severity/systemic response)

• Fever >38.5°C
• Tachycardia, hypotension (shock)
• Rising WBC, CRP >150mg/L
• Organ failure: PaO2 <60 (ARDS), creatinine rising, oliguria
• Rising blood glucose
• Fall in haematocrit
• Hypocalcaemia (<2 mmol/L)
• Pleural effusion (especially left-sided) - indicates retroperitoneal inflammation tracking

Management

1. ICU admission for severe cases
2. Aggressive IV fluid resuscitation
3. Enteral nutrition (NG/NJ) - maintains gut barrier, reduces bacterial translocation
4. Antibiotics: Only if infected necrosis (Gram stain-positive FNA or clinical deterioration despite conservative care)
   • Carbapenems (imipenem/meropenem) penetrate pancreatic necrosis best
   • NOT prophylactic routine use (no mortality benefit proven)

• CT/US-guided drainage of liquefied necrotic collections
• Can treat up to 35% of infected necrosis without further intervention

• Video-assisted retroperitoneal debridement (VARD) via flank incision
• Through tract established by PCD catheter

• EUS-guided transgastric/transduodenal access to WON
• Lumen-apposing metal stent (LAMS/AXIOS stent) placed
• Direct endoscopic debridement with multiple sessions
• MISER trial: Endoscopic "step-up" reduced fistulae formation vs. surgical step-up

• Laparotomy, manual debridement of necrosis, wide drainage
• Higher morbidity than minimally invasive; reserved for failure of above
• Techniques: open packing, closed continuous lavage, planned re-laparotomy

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7. PANCREATIC STONES & MANAGEMENT

Definition

Composition

• Calcium carbonate (predominantly)
• Calcium phosphate + protein plug matrix
• Forms from calcification of protein plugs obstructing small ducts

Clinical Significance

• Obstruct main pancreatic duct → ductal hypertension → pain
• Distinguish intraductal stones from parenchymal calcifications (different clinical significance)
• Found in 50% of alcoholic CP patients within 10 years

Diagnosis

• Plain AXR: Radio-opaque calcifications in pancreatic distribution (pathognomonic of CP)
• CT scan: Most sensitive for detecting and localising stones
• MRCP: Visualises duct anatomy and stones (filling defects within duct)
• ERCP: Direct visualisation + therapeutic

Management

• ESWL (Extracorporeal Shock Wave Lithotripsy) + ERCP:
  • ESWL fragments stones → ERCP retrieves fragments via sphincterotomy/basket extraction
  • Success rate: ~70% stone clearance
  • First-line for stones >5mm or impacted in head/body
• Pancreatic sphincterotomy + stone extraction (for smaller stones at papilla)
• Pancreatic duct stenting (for strictures causing ductal hypertension)
• Intraductal lithotripsy: Laser or electrohydraulic lithotripsy via pancreatoscope

• Indicated when endoscopic treatment fails or diffuse stones
• Puestow procedure (longitudinal pancreaticojejunostomy): Duct opened longitudinally, stones removed, side-to-side Roux-en-Y drainage
• Frey procedure for combined head mass + stones
• Ductal surgery: ductotomy + manual extraction + Roux drainage

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8. TECHNIQUES OF PANCREATIC DUCT ANASTOMOSIS

Purpose

Key Anastomoses Used in Pancreaticoduodenectomy (Whipple)

• Most technically demanding but lowest leak rate
• Main pancreatic duct individually anastomosed to jejunal mucosa
• Using 5-0 or 6-0 PDS interrupted sutures
• External or internal pancreatic duct stent often used
• Preferred when duct is dilated (>3-4mm)

• Pancreatic stump "telescoped" into the lumen of jejunum
• Mattress sutures anchor pancreatic parenchyma to jejunal wall
• Simpler but higher leak rate; used with soft pancreas/small duct

• Pancreatic stump anastomosed to posterior wall of stomach
• Technically easier; equivalent leak rates compared to PJ in meta-analyses
• Blood supply of stomach absorbs pancreatic juice (less leakage)
• Simpler when pancreas is soft + small duct (high-risk situation)

• Duct opened from head to tail along its entire length (ductal decompression)
• Side-to-side Roux-en-Y anastomosis between opened duct and jejunal loop
• Requires duct >6-7mm (dilated duct); effective for pain in 60-80%
• Single layer, interrupted absorbable sutures

Key Technical Points for Any Pancreatic Anastomosis

• Haemostasis of anastomotic edges
• Tension-free with adequate mesentery length
• Pancreatic duct stent (internal or external transanastomotic): reduces leak risk
• Drain placement near anastomosis to monitor for leak
• Soft gland + small duct = highest-risk for POPF (post-operative pancreatic fistula)
• Drain amylase level on post-op day 3: >3x serum = POPF

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9. PANCREATIC INJURY - ASIS, GRADING & MANAGEMENT

Mechanism

• Blunt trauma most common (road traffic accidents, handlebar injuries, child abuse)
• Pancreas protected by retroperitoneal position but vulnerable when compressed against vertebral column
• Penetrating trauma (stab/gunshot wounds) - more severe

ASIS (Features suggesting pancreatic injury)

• Epigastric pain + mechanism consistent with blunt abdominal trauma
• Elevated serum amylase/lipase (delayed - not reliable in early phase)
• Peritonism
• CT: stranding/oedema around pancreas, duct disruption, fluid between pancreas and splenic vein

AAST (American Association for Surgery of Trauma) Grading

Management

• Non-operative: NPO, IV fluids, analgesia, serial clinical assessment
• Drain placement if fluid collection

• Distal pancreatectomy + splenectomy (operation of choice)
• Oversew transected duct; drain pancreatic bed
• If haemodynamically unstable: damage control → resect + closed drain → reconstruction later

• Pancreaticoduodenectomy (Whipple) - for near-complete destruction of head, combined CBD/duodenal/pancreatic duct injury, uncontrolled bleeding
• In trauma setting: damage control first (haemorrhage + contamination control) → ICU resuscitation → return for Whipple reconstruction
• Whipple in trauma = rare but needed for grade V injury

• Traumatic pancreatitis
• Pancreatic fistula (most common late complication)
• Pseudocyst (2-3 weeks post-injury)
• Abscess
• Haemorrhage (pseudoaneurysm formation)

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10 / 18. PANCREATIC FUNCTION TESTS

A. EXOCRINE FUNCTION TESTS

1. Secretin-CCK Test (Gold Standard for Exocrine Function):
   • IV secretin (2 CU/kg) stimulates bicarbonate-rich ductal secretion
   • IV CCK (cholecystokinin) stimulates enzyme-rich acinar secretion
   • Duodenal aspiration (via Dreiling tube) → measure volume, bicarbonate concentration, enzyme output
   • Normal peak bicarbonate: >80 mEq/L
   • Abnormal in CP, pancreatic Ca, cystic fibrosis
   • Invasive; now replaced largely by indirect tests
2. Secretin-stimulated MRCP (S-MRCP):
   • Secretin given IV → MRI images acquired at intervals
   • Assesses ductal filling and duct dynamics (Sphincter of Oddi dysfunction, pancreas divisum)

1. Faecal Elastase-1 (FE-1) - Most used clinically:
   • Elastase-1 is a pancreas-specific enzyme; stable through gut transit
   • <200 μg/g = moderate-severe exocrine insufficiency
   • 200-500 μg/g = borderline
   • Easy, non-invasive, stool sample
   • Unaffected by enzyme replacement therapy (unlike chymotrypsin)
2. 72-hour Faecal Fat Estimation:
   • Patient consumes 100g fat/day × 3 days; collect all stool
   • >7g fat/day = steatorrhoea (>90% exocrine function lost)
   • Gold standard for steatorrhoea but cumbersome
3. NBT-PABA (BT-PABA) Test:
   • Oral N-benzoyl-L-tyrosyl-PABA (bentiromide) cleaved by chymotrypsin → PABA absorbed → urinary excretion
   • Reduced urinary PABA = reduced chymotrypsin = exocrine insufficiency
4. Pancreolauryl Test:
   • Fluorescein dilaurate cleaved by pancreatic esterase → fluorescein → urinary excretion
   • Used in Europe for diagnosis of excabo CP
5. Faecal Chymotrypsin:
   • Low sensitivity; largely superseded by FE-1
6. ¹³C-Mixed Triglyceride Breath Test:
   • Labelled fat ingested → pancreatic lipase cleaves → ¹³CO₂ exhaled
   • Non-invasive; measures fat digestion

B. ENDOCRINE FUNCTION TESTS

1. Fasting blood glucose, OGTT, HbA1c (for diabetes mellitus)
2. Insulin, C-peptide levels (for insulinoma)
3. Serum glucagon (for glucagonoma)
4. VIP levels (for VIPoma - watery diarrhoea, hypokalaemia, achlorhydria)
5. Serum gastrin (for Zollinger-Ellison syndrome / gastrinoma)
6. Chromogranin A (marker for pancreatic neuroendocrine tumours)

C. TUMOUR MARKERS

1. CA 19-9 (Carbohydrate Antigen 19-9):
   • Most widely used for pancreatic ductal adenocarcinoma
   • Sensitivity 70-80%, specificity 80-85%
   • Can be elevated in obstructive jaundice, cholangiocarcinoma, other GI cancers
   • Role: diagnosis + monitoring treatment response + recurrence
2. CEA (Carcinoembryonic Antigen): Raised in pancreatic Ca; less specific

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11. PSEUDOCYST OF PANCREAS - CIF & MANAGEMENT (20 marks - 2020)

Definition

Aetiology

• Complication of acute pancreatitis (most common): ductal disruption → enzyme-rich fluid leaks + encapsulates
• Chronic pancreatitis: Ductal obstruction → retention pseudocyst
• Pancreatic trauma: direct ductal injury

Locations

• Lesser sac (most common)
• Retroperitoneal (para-renal, pelvic, mediastinal)

Clinical Features

• Persistent/worsening abdominal pain after an episode of pancreatitis
• Nausea, vomiting (gastric outlet/duodenal compression)
• Epigastric fullness/mass (palpable in large cysts)
• Obstructive jaundice (biliary compression)
• Early satiety, weight loss
• Fever (infected pseudocyst)

Investigations

• Ultrasound: Round/oval anechoic fluid collection; follow size; guides drainage
• CT scan: Best for size, position, complications; assess wall, content, communication with duct
• MRCP: Shows communication with pancreatic duct (guides drainage strategy)
• EUS: Assess for solid debris, malignant features; guides aspiration/drainage
• Cyst fluid analysis (EUS-guided FNA):
  • Amylase >250 IU/L = pancreatic communication
  • CEA >192 ng/mL = mucinous cyst (suggests IPMN/MCN - NOT pseudocyst)
  • Cytology (if malignancy suspected)

Natural History

• 40-50% resolve spontaneously within 6 weeks (especially small cysts <4-6 cm)
• Complications: Infection, haemorrhage, rupture, fistula, biliary/duodenal obstruction

Indications for Intervention

• Symptomatic (pain, obstruction, jaundice)
• Infected pseudocyst
• Expanding/not resolving after 6 weeks
• Size >6 cm (relative indication; size alone not sufficient)
• Complication: haemorrhage (pseudoaneurysm), rupture

Drainage Options

• Rest, analgesics, NPO initially
• Octreotide (reduces pancreatic secretion, may help resolve fistula)
• Serial imaging (US/CT) to monitor

1. Transpapillary drainage (ERCP-based):
   • If pseudocyst communicates with main duct (shown on MRCP)
   • Pancreatic sphincterotomy + pancreatic duct stent bridges leak
   • Best for small (<6cm) communicating pseudocysts
   • Avoids risks of transmural approach
2. Transmural drainage (EUS-guided):
   • EUS-guided cystogastrostomy or cystoduodenostomy
   • EUS identifies pseudocyst apposed to gastric/duodenal wall
   • Access needle → guidewire → balloon dilation → double-pigtail plastic stent or LAMS
   • LAMS (Hot AXIOS): Large-bore self-expanding metal stent - allows direct endoscopic entry into cyst for debridement if WON
   • Most effective for large pseudocysts (>6cm) adjacent to stomach/duodenum
   • Success rate >90%
3. Combined transpapillary + transmural approach for complex communications

• Simple, minimally invasive
• For infected pseudocysts (need drainage + antibiotic lavage)
• High recurrence rate if not combined with ductal stenting
• Preferred for collections distant from stomach/duodenum (paracolic, pelvic)

• Indicated: failed endoscopic/percutaneous; pseudocyst not amenable to endoscopic access; suspicion of malignancy; haemorrhage (pseudoaneurysm)

• Cystogastrostomy: Anastomosis between pseudocyst and posterior stomach wall (most common)
• Cystoduodenostomy: For pseudocyst intimately related to duodenum
• Roux-en-Y cystojejunostomy: For pseudocysts not close to stomach/duodenum; most versatile
• Distal pancreatectomy: If pseudocyst + distal duct transection

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12. DISTAL PANCREATECTOMY - INDICATIONS & COMPLICATIONS

Definition

Indications

• Pancreatic ductal adenocarcinoma of body/tail
• Neuroendocrine tumours (insulinoma, non-functioning NET) in body/tail
• Mucinous cystic neoplasm (MCN) of body/tail
• Main-duct IPMN of body/tail
• Distal cholangiocarcinoma (rare)
• Metastases to body/tail

• Chronic pancreatitis confined to body/tail (with failed duct drainage)
• Traumatic transection of pancreatic duct at level of spine (Grade III injury)
• Symptomatic pseudocyst of body/tail with ductal disconnection
• Benign cysts

Types

1. Open distal pancreatectomy + splenectomy (standard, especially for malignancy)
2. Laparoscopic distal pancreatectomy (LDP) + splenectomy (now preferred in many centres)
3. Spleen-preserving distal pancreatectomy (SPDP):
   • Kimura technique: Preserve splenic artery + vein (meticulous dissection)
   • Warshaw technique: Divide splenic vessels; spleen preserved on short gastric vessels
   • Indications: Benign/borderline tumours; younger patients
   • Reduces post-splenectomy sepsis risk; preserves immune function
4. Robotic distal pancreatectomy: High splenic preservation rate; technically superior spleen preservation

Surgical Technique (Open/Laparoscopic)

• Mobilise spleen from retroperitoneal attachments
• Expose posterior pancreas, identify splenic artery and vein
• Individually ligate splenic vessels
• Divide pancreas at defined level (left of SMA/portal vein)
• Transected pancreas: oversew with 3-0 absorbable U-sutures; oversew visible pancreatic duct
• Wide external drainage of pancreatic bed (essential)
• If haemodynamically unstable (trauma): fire linear cutting stapler across splenic vessels + pancreas simultaneously

Complications

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13 / 17. PERIAMPULLARY CARCINOMA - PATHOLOGY, CIF, DIAGNOSIS, TREATMENT & PROGNOSIS (30 marks - highest value)

Definition & Types

Pathology of Pancreatic Ductal Adenocarcinoma (Most common)

• Hard, poorly-defined, grey-white mass; "gritty" texture
• 60-70% in pancreatic head (causes biliary obstruction early)
• 15-20% in body, 5-10% in tail (present late, worse prognosis)
• Invasion of surrounding structures: portal vein, SMA, celiac axis, duodenum, CBD

• Well to moderately differentiated adenocarcinoma of ductal origin
• Desmoplastic stroma (dense fibrous reaction)
• Perineural invasion (common; causes pain)
• Vascular invasion
• Lymphatic invasion

• KRAS mutation (>90%) - initiating mutation; earliest change
• CDKN2A (p16) loss (80-90%)
• TP53 mutation (75%)
• SMAD4/DPC4 loss (55%) - associated with metastatic disease
• Precursor lesions: PanIN (Pancreatic Intraepithelial Neoplasia, Grade 1-3) → adenocarcinoma

• T1: ≤2 cm or confined to pancreas
• T2: 2-4 cm in greatest dimension
• T3: >4 cm
• T4: Involves celiac axis or SMA (unresectable by definition)
• N0: No nodal metastasis; N1: 1-3 nodes; N2: ≥4 nodes
• M0: No distant mets; M1: Distant mets (liver most common, then lung, peritoneum)

Clinical Features

1. Progressive painless obstructive jaundice (most common presenting feature in head Ca)
   • Dark urine (bilirubinuria), pale stools, pruritus
   • Jaundice may be fluctuating in ampullary/CBD Ca
2. Epigastric pain (dull, radiating to back; perineural invasion)
3. Weight loss (marked; cachexia)

• Courvoisier's sign: Palpable, non-tender gallbladder in presence of jaundice (bile duct obstruction below cystic duct by non-calculous cause - carcinoma)
• Trousseau's sign: Migratory thrombophlebitis (pancreatic Ca associated)
• New-onset diabetes mellitus (tumour secretes anti-insulin peptides)
• Depression (common paraneoplastic)
• Acute pancreatitis (duct obstruction)
• Duodenal obstruction (late)
• Hepatomegaly (liver metastases)
• Ascites (peritoneal spread)
• Virchow's node (left supraclavicular LN metastasis)
• Sister Mary Joseph's nodule (periumbilical metastasis)
• Blumer's shelf (perirectal metastasis - PR examination)

Investigations

• LFTs: Obstructive pattern (raised bilirubin, ALP, GGT; mild transaminases)
• CA 19-9: Elevated (>37 U/mL); sensitivity 70-80%; cannot diagnose if jaundiced (false positives)
• CEA: Less specific
• FBC: Anaemia, thrombocytosis
• Clotting: Prolonged PT (vitamin K malabsorption)
• Blood glucose: Elevated (new-onset DM)

• Ultrasound (first-line): Dilated intrahepatic ducts + dilated CBD + "double duct sign" (CBD + pancreatic duct dilated); hypoechoic head mass; gallbladder distension
• CT (triple-phase/pancreatic protocol CECT):
  • Gold standard for staging
  • Hypovascular mass (doesn't enhance like normal pancreas in arterial phase)
  • Assess: SMA, celiac axis, SMV, portal vein involvement (tumour-vessel interface)
  • Liver metastases, lymph nodes, peritoneal deposits
  • Criteria for unresectability: SMA/celiac encasement >180°; SMV/portal vein occlusion without reconstruction option; liver/distant mets; peritoneal disease
• MRCP: Detailed biliary/pancreatic duct imaging; "double duct sign" on MRCP = malignant obstruction until proven otherwise
• EUS (Endoscopic Ultrasound): Best for local staging (T + N); tissue sampling (EUS-FNA) with >90% sensitivity; detects small tumours not seen on CT
• PET-CT: Assess for occult distant metastases before surgery (selected cases)
• Staging laparoscopy: Before Whipple, to detect peritoneal/liver surface metastases not seen on CT (especially if CA 19-9 very high or borderline resectable)
• Diagnostic ERCP: Brush cytology from duct; biliary stenting for jaundice pre-op or palliation; less often used for pure diagnosis

Resectability Assessment

Treatment

• Resection of: pancreatic head, duodenum (D1-D4), distal 5cm of CBD, distal stomach (or pylorus-preserving), cholecystectomy + regional lymphadenectomy
• Standard Whipple: includes antrectomy
• Pylorus-Preserving Pancreaticoduodenectomy (PPPD/Traverso-Longmire): Pylorus + 1st part of duodenum preserved; equivalent oncological outcomes, better GI function
• Reconstruction:
  1. Pancreaticojejunostomy (PJ) or Pancreaticogastrostomy (PG)
  2. Hepaticojejunostomy (biliary)
  3. Gastrojejunostomy (gastric)
• All on a single Roux-en-Y jejunal loop (Child reconstruction) or separate loops
• Operative mortality at high-volume centres: <3-5%

• Post-operative pancreatic fistula (POPF) (most common; 10-20%)
• Delayed gastric emptying (DGE) (nasogastric drainage >10 days; 20-30%)
• Post-pancreatectomy haemorrhage (PPH)
• Bile leak
• Wound infection
• Adhesive obstruction

• Gemcitabine + capecitabine (ESPAC-4 regimen): Standard adjuvant after R0 resection
• Modified FOLFIRINOX (for fit patients): Superior to gemcitabine in adjuvant setting

• ERCP + biliary stenting (self-expanding metal stent preferred; relieve jaundice + pruritus)
• Surgical bypass (palliative open): hepaticojejunostomy + gastrojejunostomy (double bypass) - if endoscopic fails or long-term palliation needed
• Coeliac plexus neurolysis (EUS-guided or CT-guided): Pain relief
• Palliative chemotherapy: FOLFIRINOX (5-FU, leucovorin, irinotecan, oxaliplatin) - first line for fit patients; Gemcitabine + nab-paclitaxel; Gemcitabine alone (for unfit patients)
• Palliative radiotherapy (pain, local control)

Prognosis

• Resection margin status (R0 vs R1) - most important
• Lymph node ratio
• Tumour size
• Grade
• CA 19-9 response to treatment

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14. COMPLICATIONS OF CHRONIC PANCREATITIS (20 marks - 2023)

Local Complications

Systemic/Functional Complications

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16. ANATOMY OF PANCREAS & CYSTIC NEOPLASMS (20 marks - 2022)

Anatomy of Pancreas (Mulholland & Greenfield's Surgery)

• Head/Uncinate/Neck: Gastroduodenal artery (GDA) → superior pancreaticoduodenal artery (ant + post) + inferior pancreaticoduodenal artery from SMA → form anterior and posterior arcades
• Body and Tail: Splenic artery (branches: caudal pancreatic a., great pancreatic a. [arteria pancreatica magna], inferior pancreatic a.)
• Ampulla receives blood from superior + inferior pancreaticoduodenal arteries (3 branches at 11, 1, 6 o'clock positions)
• Aberrant hepatic artery (20-30%): replaced right hepatic artery from SMA runs posterior to head of pancreas (CRITICAL to identify during Whipple)

• Head → superior + inferior venous arcades → portal vein + SMV
• Body + tail → branches directly into splenic vein
• IMV drains into splenic vein (behind pancreatic body) - identify before dividing during left pancreatectomy

• Superior, inferior, anterior, posterior, splenic

• Main duct of Wirsung: From tail → head; joins CBD at ampulla of Vater
• Duct of Santorini (accessory duct): From main duct at neck → minor papilla (1-2 cm proximal to major papilla)
• Pancreas divisum: Failure of dorsal + ventral bud fusion during embryogenesis; Santorini duct drains majority through minor papilla; most common congenital anomaly

Cystic Neoplasms of Pancreas

Key Points for Exam

• Honeycomb/microcystic appearance on CT/MRI; central scar with "sunburst" calcification
• VHL syndrome association (chromosome 3p)
• Essentially benign; surgical resection only if symptomatic or large (>4 cm) or uncertain diagnosis

• Always in body/tail; ovarian-type stroma on histology (hallmark)
• Does NOT communicate with pancreatic duct (unlike IPMN)
• Resection recommended in all fit patients (premalignant)
• Spectrum: cystadenoma → borderline → cystadenocarcinoma

• Mucin-secreting intraductal tumours; "fish-mouth" appearance of ampulla on endoscopy (mucin extruding)
• Branch-duct IPMN: Surveillance acceptable if "worrisome features" absent (cyst <3cm, no mural nodule, main duct not involved)
• Main-duct IPMN: High-grade dysplasia/invasive Ca → resection required
• "High-risk stigmata" → surgery: obstructive jaundice, mural nodule, main duct ≥10mm, positive cytology

• Large, well-encapsulated; CT shows solid + cystic components with haemorrhagic content
• β-catenin mutation
• Surgical resection curative even with local invasion
• Can metastasise (liver) in ~10%

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Sources: Mulholland & Greenfield's Surgery 7e; Sleisenger & Fordtran's GI & Liver Disease; Rosen's Emergency Medicine 9e; Clinical GI Endoscopy Expert Consult 3e; Yamada's Textbook of Gastroenterology 7e; Current Surgical Therapy 14e; Fischer's Mastery of Surgery 8e; Henry's Clinical Diagnosis & Laboratory MethodsAll 18 PANCREASE topics are covered. Here's your priority revision map based on the marks shown in your notes:

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Exam Priority Summary - PANCREAS