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📚 EXAM NOTES: SURGERY — STOMACH & DUODENUM

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PART 1: CONGENITAL PYLORIC STENOSIS

Key Facts (One-liners)

• Incidence: 1 in 350 live births
• Sex: Males : Females = 4:1
• Classic presentation: First-born male baby
• Familial incidence: 6-10%

Aetiology

• Failure of pylorus to relax = Achalasia (most accepted cause)
• Also called "hypertrophic pyloric stenosis"
• Ganglion cell dysfunction (similar to Hirschsprung's disease)

Pathology

• Circular muscle fibres hypertrophied
• Lumen so narrow → only fine probe admitted
• Hypertrophy starts at pyloric antrum, maximal at pylorus
• Duodenum is NORMAL (hypertrophy stops abruptly at pyloro-duodenal junction)

Clinical Features

⚠️ Exam Tip: No bile in vomitus = pre-ampullary obstruction. Bilious vomiting = distal obstruction.

Physical Examination

• Visible peristalsis from left to right across upper abdomen (after feed)
• Palpable mass: Mobile, smooth, olive-shaped in epigastrium = hypertrophied pylorus ("cartilaginous feel")
• Decompress stomach with NG tube to feel the lump

Investigations

• Mainly clinical diagnosis
• Barium meal X-ray: Persistent narrowing + elongation of pyloric canal ("String sign")
• Ultrasound: occasionally used to confirm

Treatment

• Correct dehydration and electrolyte imbalance
• 5% Dextrose in half-normal saline + 30 mEq KCl/L until corrected

• Eumydrin (atropine methylnitrate) 1:1000 — 1-2 ml, 30 min before feed

• Ramstedt's Pyloromyotomy
• Incision: Grid-iron (upper right quadrant)
• Blunt dissection through pyloric musculature, mucosa preserved
• Koop's modification: blunt dissection with scalpel handle
• Check for mucosal leak → push air into stomach, watch for bubbles
• If mucosal perforation → close with 3-4 interrupted chromic catgut + omental patch

• Small feeds (≤5 ml) start after few hours
• Normal feeds by 3-4 days
• Result: ~100% cure, no mortality, no morbidity, no recurrent obstruction

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PART 2: PEPTIC ULCER

Sites

• Common: Gastric, Duodenal
• Rare: Cardiac end of oesophagus, Meckel's diverticulum, anastomotic ulcer

Types

• Acute peptic ulcer: Shallow, multiple
• Chronic peptic ulcer: Single, deep, scirrhous

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AETIOLOGY

Acute Peptic Ulcer Causes (Mnemonic: SSACHI)

1. Stress (hypotension, haemorrhage, endotoxic shock, MI) = "stress ulcers"
2. Sepsis
3. ACIDS/steroids
4. Cushing's ulcer (after cerebral trauma / neurosurgical ops) - increased vagal activity + gastrin
5. Head injury
6. Infarction / burns (Curling's ulcer - within 48 hrs)

Curling's ulcer = Burns | Cushing's ulcer = CNS/neurosurgical

Chronic Gastric Ulcer - Causes

1. Diminished mucosal resistance (pepsin digestion)
2. Pyloroduodenal reflux (bile + duodenal juice)
3. Deficient mucous barrier
4. Mucosal trauma (85% occur along lesser curve / Magenstrasse)
5. Local ischaemia
6. Antral stasis → increased acid secretion
7. NSAIDs (disrupt prostaglandin-driven mucosal protection)
8. H. pylori ⭐

H. pylori - High Yield Facts

• Gram-negative, microaerophilic, spiral rod with 4-6 polar flagellae
• Lives in deep mucous layer of antrum
• Key enzyme: Urease → splits urea → ammonia (strong alkali)
• Ammonia effect on G-cells → gastrin release → hypergastrinaemia → hypersecretion
• Found in 100% of duodenal ulcer patients
• Eradication speeds healing within 6 weeks
• Prevalence in gastric ulcer: >70%
• Virulence factors: urease, catalase, mucinase, lipase, phospholipase A2, haemolysins

Chronic Duodenal Ulcer - Causes

1. Acid hypersecretion (mean acid output 2x normal; twice the parietal cells)
2. Genetic factors (blood group 'O' - no AB antigen)
3. Endocrine organ dysfunction (Zollinger-Ellison, Cushing's, MEN)
4. Liver disease (cirrhosis)
5. Emotional factors (anxiety, stress)
6. Diet and smoking (NSAIDs similar mechanism)
7. H. pylori (isolated in 100% cases)
8. Decreased bicarbonate production

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CLINICAL FEATURES — Gastric vs Duodenal Ulcer

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SPECIAL INVESTIGATIONS

1. Blood: Hb low (melaena/haematemesis), raised ESR → suggests gastric malignancy
2. Stool: Occult blood positive in both
3. Gastric function tests: Basal secretion + stimulation (insulin, histamine, pentagastrin)
4. Barium meal X-ray: First-line imaging
5. Endoscopy: Biopsy essential for gastric ulcer (exclude malignancy)
6. H. pylori testing: CLO test (campylobacter-like organism test)

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TREATMENT

Conservative (Medical) Treatment

• Rest, avoid stress
• Regulated diet, small meals, bland food
• Avoid alcohol, smoking, NSAIDs
• Antacids, H₂-blockers, PPIs

• Endoscopy + biopsy mandatory (to exclude malignancy)
• Check for NSAIDs/corticosteroids use
• H₂-blockers first → PPI if refractory
• Heal within 6-8 weeks
• Follow-up barium meal at 6 weeks

• Aim: keep intragastric pH ~5.5 (pepsinogen not activated)
• Antacids: Aluminium hydroxide (constipating), Magnesium hydroxide (laxative)
• H₂-blockers: Cimetidine (200mg TDS + 400mg at night), Ranitidine (1 tablet BD)
• PPIs: Most effective → heal most ulcers within 2 weeks

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COMPLICATIONS OF PEPTIC ULCER

1. Perforation
2. Haemorrhage (haematemesis / melaena)
3. Stenosis
4. Penetration into neighbouring viscera
5. Residual abscess
6. Carcinoma

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PERFORATED PEPTIC ULCER — High Yield

Epidemiology

• Duodenal perforation >> Gastric perforation
• Male : Female = 12:1 to 20:1
• Age group: 30-50 years
• 80% have previous history of peptic ulcer
• 20% = Silent perforation (no prior history) - often on steroids

Pathology - 3 Stages of Peritonism

⚠️ Exam Tip: Stage II is the "stage of illusion/delusion" - patient feels better but is actually getting worse. Most dangerous time for misdiagnosis.

Clinical Features - Stage I (Primary Stage)

• Acute agonising pain: epigastrium or right hypochondrium
• Pain can radiate to right iliac fossa (acid flows down right paracolic gutter) → mimics appendicitis
• Patient: pale, anxious, dry tongue
• Temp: slightly subnormal (95-96°F)
• Pulse: 90/min
• Respiration: thoracic (abdomen held still)
• Abdomen: board-like rigidity (highest at epigastric + right hypochondriac region)
• Rebound tenderness present
• Liver dullness: obliterated (gas under diaphragm)
• Bowel sounds: absent

Investigations

• Erect X-ray chest/abdomen: Gas under right cupula of diaphragm in 75% of cases ← most important
• If patient cannot stand: Lateral decubitus X-ray
• Note: Negative X-ray does NOT exclude perforation
• Peritoneal aspiration: bile-stained alkaline fluid = duodenal ulcer perforation
• Gastrografin via NG tube: dye escapes through perforation (identifies site)

Types of Perforation

1. Acute: Full thickness, into free peritoneal cavity
2. Subacute ("leaking peptic ulcer"): Circumscribed area contaminated; due to small size, empty stomach, adhesions, or omental plugging
3. Chronic: Walled off by adhesions/viscera; may form chronic abscess or subphrenic abscess

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QUICK REVISION TABLES

Curling vs Cushing Ulcer

H. pylori Treatment Duration

• Classic triple: 2 weeks
• Omeprazole + Amoxicillin: 14 days
• Clarithromycin-based: 7 days (shortest)

Pyloric Stenosis vs Hirschsprung's

• Both involve ganglion cell dysfunction
• Pyloric stenosis: circular muscle hypertrophy
• Hirschsprung's: aganglionic segment of colon

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Source: A Concise Textbook of Surgery (Das) - Chapter 44: The Stomach and Duodenum