Peptic Ulcer Disease & Surgical Complications

Peptic ulcer disease (PUD) is a breach in the mucosa of the stomach or duodenum extending through the muscularis mucosae, produced by acid–peptic activity. While medical therapy has made elective ulcer surgery almost obsolete, the complications — perforation, bleeding, gastric outlet obstruction and malignant change — remain heavily tested in NEET PG, straddling both Surgery and Medicine.

Definition & Classification

A peptic ulcer is a mucosal defect ≥5 mm penetrating the muscularis mucosae (smaller breaches are erosions). The two dominant sites are the duodenum (first part, anterior or posterior wall) and the stomach (most often the lesser curve at the incisura angularis).

Modified Johnson classification of gastric ulcers is a recurring favourite:

Type	Location	Acid level	Association
I	Lesser curve / incisura (commonest)	Low / normal	Blood group A
II	Body of stomach + duodenal ulcer	High	Blood group O
III	Prepyloric	High	NSAID-related, blood group O
IV	High lesser curve, near GE junction	Low	Poor prognosis, hard to operate
V	Anywhere (diffuse)	Variable	NSAID/drug-induced

High-yield: Type I and IV gastric ulcers have normal or low acid; Type II and III behave like duodenal ulcers with high acid secretion. Mnemonic for high-acid types: "2 and 3 secrete plenty" (II = ulcer + duodenum, III = prepyloric).

Etiology & Pathophysiology

PUD reflects an imbalance between mucosal aggressive factors (acid, pepsin, H. pylori) and defensive factors (mucus–bicarbonate layer, prostaglandins, mucosal blood flow).

• Helicobacter pylori — the dominant cause. ~90–95% of duodenal ulcers and ~70–80% of gastric ulcers. A gram-negative, microaerophilic, urease-producing spiral bacillus that colonises the antrum, increases gastrin, and reduces somatostatin.
• NSAIDs — second commonest; inhibit COX-1, depleting protective prostaglandins. Classically cause gastric ulcers and are a leading cause of bleeding in the elderly.
• Zollinger–Ellison syndrome (gastrinoma) — suspect with multiple/distal ulcers, ulcers refractory to therapy, ulcers in unusual sites (e.g. jejunum), diarrhoea, or with MEN-1.
• Others: smoking, steroids, physiological stress ulcers (Curling — burns; Cushing — raised ICP/head injury).

Duodenal vs gastric pathophysiology — the duodenal ulcer is a disease of acid hypersecretion with rapid gastric emptying; the gastric ulcer (esp. Type I) is a disease of impaired mucosal defence with normal/low acid.

Feature	Duodenal ulcer	Gastric ulcer
Age	Younger (25–50)	Older (>50)
Acid secretion	High	Normal / low
Pain vs food	Relieved by food; hunger pain, night pain	Worsened by food; weight loss
Blood group	O	A (Type I)
Malignant potential	Virtually never malignant	Can be malignant — always biopsy
Effect on weight	Stable/gains (eats to relieve)	Loses weight (afraid to eat)

High-yield: A duodenal ulcer is almost never malignant; a gastric ulcer may be malignant, so every gastric ulcer needs multiple biopsies (≥6–8 from the rim) and repeat endoscopy at 6–8 weeks to confirm healing.

Clinical Features

• Epigastric burning/gnawing pain — the cardinal symptom. Duodenal ulcer: pain 2–3 h after meals and at night, relieved by food/antacids. Gastric ulcer: pain soon after eating, leading to food fear and weight loss.
• Nausea, bloating, early satiety.
• Posterior duodenal ulcers may erode the gastroduodenal artery → brisk haemorrhage. Posterior penetration can reach the pancreas → back pain and raised amylase.
• Anterior duodenal ulcers tend to perforate into the peritoneum.

Diagnosis & Investigation of Choice

Upper GI endoscopy (OGD) is the investigation of choice — direct visualisation, biopsy of gastric ulcers (rule out malignancy), and therapeutic haemostasis.

H. pylori testing:

• Urea breath test (UBT) and stool antigen test — best non-invasive tests; also used to confirm eradication (≥4 weeks after antibiotics, ≥2 weeks off PPI).
• Rapid urease (CLO) test on biopsy — best during endoscopy.
• Histology / culture — culture for resistant cases.
• Serology — cannot distinguish current from past infection; least useful for confirming cure.

If gastrinoma suspected: fasting serum gastrin (>1000 pg/mL diagnostic) and secretin stimulation test; localise with somatostatin-receptor scintigraphy / DOTANOC PET.

High-yield: Stop PPIs ~2 weeks and antibiotics ~4 weeks before UBT/urease/biopsy testing to avoid false negatives. Serology stays positive after cure — never use it to confirm eradication.

Medical Management & Drug of Choice

• H. pylori eradication is curative for most ulcers. Standard triple therapy: a PPI + clarithromycin + amoxicillin for 14 days. In high clarithromycin-resistance areas, bismuth quadruple therapy (PPI + bismuth + tetracycline + metronidazole) is preferred.
• PPIs (omeprazole, pantoprazole) — drug of choice for acid suppression and ulcer healing.
• Stop NSAIDs; if unavoidable, co-prescribe a PPI ± switch to a COX-2 selective agent.
• Gastric ulcers: re-scope at 6–8 weeks to confirm healing and exclude malignancy.

Surgical Complications

Modern surgery is largely reserved for the four classic complications: Perforation, Penetration, Haemorrhage and Obstruction.

1. Perforation

The most dramatic emergency — anterior duodenal ulcers are the commonest to perforate.

• Sudden, severe, generalised abdominal pain; board-like rigidity (chemical then bacterial peritonitis); silent abdomen; shock.
• Erect chest X-ray shows free gas under the diaphragm (pneumoperitoneum) in ~70–80%. Absence does not exclude perforation.
• CT abdomen is most sensitive for free air and free fluid when X-ray is equivocal.

Stepwise management: Resuscitate (NBM, IV fluids, nasogastric decompression, IV PPI, broad-spectrum antibiotics, analgesia) → confirm with erect CXR/CT → emergency laparotomy/laparoscopy → Graham's omental patch (a pedicled omental plug sutured over the perforation) → peritoneal lavage → later H. pylori eradication and endoscopic follow-up.

High-yield: Graham's patch (omental patch) is the standard repair for a perforated duodenal ulcer. A large gastric perforation may need biopsy/excision or partial gastrectomy because of malignancy risk. The Boey score (preoperative shock, delay >24 h, major comorbidity) predicts mortality — each factor adds risk.

2. Haemorrhage

The commonest cause of death in PUD. Posterior duodenal ulcers erode the gastroduodenal artery; lesser-curve gastric ulcers erode the left gastric artery.

Forrest classification (endoscopic appearance — guides rebleeding risk and need for intervention):

Forrest	Appearance	Rebleed risk
Ia	Active spurting (arterial)	Very high (~90%)
Ib	Active oozing	High (~10–30%)
IIa	Non-bleeding visible vessel	High (~50%)
IIb	Adherent clot	Intermediate (~25–30%)
IIc	Flat pigmented (haematin) spot	Low (~7–10%)
III	Clean ulcer base	Lowest (~3–5%)

Stepwise approach: Resuscitate + transfuse, IV high-dose PPI → risk-stratify with Glasgow-Blatchford / Rockall score → urgent endoscopy within 24 h → endoscopic haemostasis: dual therapy (adrenaline injection 1:10,000 plus a second modality — thermal coagulation or haemoclips) for Forrest Ia–IIb → if rebleeding, repeat endoscopy → failed endoscopy → angiographic embolisation or surgery (under-running the ulcer, e.g. three-point ligation of the gastroduodenal artery).

High-yield: Adrenaline injection alone is inadequate — always combine with a second modality. Forrest Ia, Ib, IIa, IIb warrant endoscopic therapy; IIc and III generally do not.

3. Gastric Outlet Obstruction (Pyloric Stenosis)

Chronic prepyloric/pyloric or duodenal ulcer scarring narrows the outlet.

• Projectile, non-bilious vomiting of stale food, weight loss, visible gastric peristalsis, succussion splash (>4 h after a meal).
• Metabolic derangement: loss of HCl → hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria.
• Diagnosis: endoscopy (after gastric decompression) ± biopsy to exclude malignancy; saline load test historically.

Management: Correct dehydration and alkalosis with normal saline + potassium (this also corrects the alkalosis by allowing renal chloride/bicarbonate handling) → NG decompression → endoscopic balloon dilatation for benign strictures → surgery (gastrojejunostomy ± vagotomy, or pyloroplasty) if refractory or malignant.

High-yield: The classic biochemical picture of GOO is hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria — corrected by 0.9% saline with potassium, not by bicarbonate.

4. Malignant Change

Gastric ulcers (never duodenal) carry malignant potential. Features suggesting malignancy: irregular heaped margins, rolled edges, necrotic base, failure to heal at 6–8 weeks. Every gastric ulcer must be biopsied and followed to confirmed healing.

Elective Ulcer Surgery — Operative Principles

Though rare today, the types of vagotomy and resection are classic MCQ material.

Vagotomy types:

1. Truncal vagotomy — divides both vagal trunks at the oesophageal hiatus. Denervates the whole stomach (and viscera) → causes gastric stasis, so must be combined with a drainage procedure (pyloroplasty or gastrojejunostomy).
2. Selective vagotomy — divides gastric branches but preserves the hepatic and coeliac branches; still needs drainage.
3. Highly selective / proximal gastric / parietal cell vagotomy — denervates only the acid-secreting fundus/body, preserves the antropyloric nerve of Latarjet, so the pylorus stays functional and no drainage is needed. Lowest dumping/diarrhoea but highest recurrence.

Resections:

• Billroth I — distal gastrectomy with gastroduodenal anastomosis (more physiological).
• Billroth II (Polya) — distal gastrectomy with gastrojejunal anastomosis and a duodenal stump; higher complication rate.
• Roux-en-Y — used to divert bile and reduce reflux/dumping.

High-yield: Truncal vagotomy always needs a drainage procedure (pyloroplasty/gastrojejunostomy); highly selective vagotomy does not, because the nerve of Latarjet keeps the pylorus working. Recurrence is lowest with truncal vagotomy + antrectomy but dumping is highest; recurrence is highest with HSV but side effects are least.

Postgastrectomy / Postvagotomy Complications

Complication	Mechanism	Key feature
Early dumping	Rapid osmotic load into jejunum (15–30 min)	Cramps, diarrhoea, tachycardia, sweating
Late dumping	Reactive hypoglycaemia (1–3 h)	Sweating, tremor, faintness; relieved by sugar
Afferent loop syndrome	Obstructed afferent limb after Billroth II	Bilious projectile vomiting that relieves pain
Bile (alkaline) reflux gastritis	Bile entering stomach	Burning pain + bilious vomiting not relieved by it
Dumping nutritional	Loss of intrinsic factor / iron / rapid transit	Iron-deficiency & B12 anaemia, osteomalacia
Gastric remnant cancer	Long-term (>15–20 y)	Increased risk after Billroth II

High-yield: Afferent loop syndrome vomiting is bilious, projectile and relieves the pain. Bile reflux gastritis vomiting is bilious but does not relieve the pain — the differentiating MCQ point.

Key Differentials

• Gastric cancer — weight loss, anorexia, Virchow's node; differentiated by biopsy of a gastric ulcer.
• GORD / functional dyspepsia — retrosternal burning, no ulcer on scope.
• Acute pancreatitis — epigastric pain to back, raised lipase; mimics penetrating posterior ulcer.
• Acute cholecystitis / biliary colic — right upper quadrant, Murphy's sign.
• Myocardial infarction (inferior wall) — epigastric pain; always ECG in older patients.
• Mesenteric ischaemia / ruptured AAA — in elderly with acute abdomen.

Recently asked / exam angle

• Forrest classification matched to rebleeding risk and which grades need endoscopic therapy (Ia–IIb yes; IIc/III no).
• Site of perforation (anterior duodenal) vs site of bleeding (posterior duodenal → gastroduodenal artery).
• Graham's patch as the answer for perforated duodenal ulcer repair.
• Biochemical picture of gastric outlet obstruction — hypochloraemic hypokalaemic metabolic alkalosis, paradoxical aciduria, and saline + KCl correction.
• Which vagotomy needs a drainage procedure (truncal/selective) and which does not (highly selective).
• Modified Johnson classification — which gastric ulcer types are high vs low acid.
• H. pylori test selection — UBT/stool antigen to confirm cure; serology cannot.
• Boey score for perforation mortality and Rockall/Blatchford for upper GI bleed.
• Differentiating afferent loop syndrome from bile reflux gastritis by whether vomiting relieves pain.
• Gastric ulcer = biopsy mandatory; duodenal ulcer = essentially never malignant.

Rapid revision

1. Duodenal ulcer = high acid, blood group O, never malignant, pain relieved by food; gastric ulcer = normal/low acid, blood group A, may be malignant, pain worse with food.
2. H. pylori causes ~90% of duodenal and ~70% of gastric ulcers; eradicate with PPI + clarithromycin + amoxicillin × 14 days (or bismuth quadruple).
3. Investigation of choice = upper GI endoscopy; confirm H. pylori cure with urea breath / stool antigen test, never serology.
4. Anterior duodenal ulcer perforates; posterior duodenal ulcer bleeds (gastroduodenal artery).
5. Perforation → gas under diaphragm on erect CXR → emergency repair with Graham's omental patch; Boey score predicts mortality.
6. Forrest Ia = spurting (highest rebleed); endoscopic dual therapy for Forrest Ia–IIb; adrenaline alone is never enough.
7. Gastric outlet obstruction → hypochloraemic hypokalaemic metabolic alkalosis with paradoxical aciduria; treat with normal saline + KCl.
8. Modified Johnson: Types I & IV = low acid; Types II & III = high acid.
9. Truncal & selective vagotomy need a drainage procedure; highly selective (parietal cell) vagotomy preserves the nerve of Latarjet and does not.
10. Billroth I = gastroduodenal anastomosis; Billroth II (Polya) = gastrojejunal with duodenal stump.
11. Afferent loop syndrome — bilious projectile vomiting that relieves pain; bile reflux gastritis — bilious vomiting that does not relieve pain.
12. Suspect Zollinger–Ellison with multiple/refractory or distal ulcers, diarrhoea or MEN-1; fasting gastrin >1000 pg/mL is diagnostic.