Duodenal Ulcer

Epidemiology & Aetiology

1. Helicobacter pylori (H. pylori) infection - present in up to 90% of duodenal ulcer patients. The organism colonizes the gastric antrum preferentially, driving antral-predominant gastritis with impaired somatostatin secretion, resulting in hypergastrinemia and excess acid production.
2. NSAID use - prostaglandin inhibition disrupts the mucosal protective barrier.

• Zollinger-Ellison syndrome (gastrinoma)
• Stress (critically ill patients - "Curling's ulcer" after burns)
• Smoking (impairs mucosal defenses and increases acid secretion)
• Idiopathic hypersecretory states
• Mulholland & Greenfield's Surgery, p. 2253
• Current Surgical Therapy 14e, p. 3099

Pathophysiology

• Excess gastric acid and pepsin secretion
• Duodenal ulcer patients, as a group, have maximal acid output (MAO) averaging ~40 mEq/hr versus ~20 mEq/hr in normal subjects - though considerable overlap exists
• Accelerated gastric emptying of liquids after meals, with failure of the normal feedback braking mechanism, prolongs duodenal acidification

• Infects the gastric antrum → suppresses somatostatin (D cells) → unrestrained gastrin release (G cells) → increased acid secretion
• The cagA pathogenicity island encodes the CagA protein, which is injected into host epithelial cells, phosphorylated by cellular kinases, and activates signaling pathways that disrupt cellular polarity, barrier function, and favor apoptosis over restitution - impairing ulcer healing
• Paradoxically, acute H. pylori infection causes transient hypochlorhydria (IL-1β inhibits acid) before transitioning to chronic hyperchlorhydria

• Bicarbonate secretion
• Mucus layer integrity
• Mucosal blood flow
• Epithelial restitution
• Mulholland & Greenfield's Surgery, p. 2253-2254

Clinical Features

• Epigastric pain that is burning, aching, gnawing, or described as "hunger pain"
• Typically occurs in the fasted state - 2-3 hours after meals or at night (follows the circadian peak of acid secretion between 11 PM and 2 AM)
• Relieved by food or antacids (this differentiates it from gastric ulcer where food often worsens pain)
• Patients typically maintain or gain weight
• Pain clusters lasting 1-3 months with asymptomatic intervals of weeks to months

• Constant pain → deeper ulcer penetration
• Radiation to the back → penetration into the pancreas
• Diffuse peritonism → free perforation

• Yamada's Textbook of Gastroenterology, p. 1020
• Sabiston Textbook of Surgery, p. 1779

Red Flag (Alarm) Symptoms Warranting Urgent Endoscopy

• Yamada's Textbook of Gastroenterology, p. 1020

Diagnosis

1. Esophagogastroduodenoscopy (EGD) - the gold standard; allows direct visualization, biopsy for H. pylori (antral biopsy), and therapeutic intervention
   • Biopsy of a duodenal ulcer itself is not required (low malignancy risk), but gastric biopsies should be taken to test for H. pylori
   • Biopsy of gastric ulcers is always needed to exclude malignancy
2. Upper GI barium radiography - demonstrates barium filling the ulcer crater (round or oval niche); less sensitive than endoscopy
3. H. pylori testing:
   • Non-invasive: Urea breath test (UBT), fecal antigen test
   • Invasive (via endoscopy): Rapid urease test, histology, culture, PCR
4. Labs: CBC, liver function, creatinine, amylase, calcium; serum gastrin in refractory or surgically managed cases to exclude gastrinoma

• Sabiston Textbook of Surgery, p. 1780
• Current Surgical Therapy 14e

Medical Management

• Clarithromycin triple therapy: PPI + clarithromycin + amoxicillin (or metronidazole)
• Bismuth quadruple therapy: PPI + bismuth + tetracycline + nitroimidazole (preferred where clarithromycin resistance is high)
• Sequential therapy: PPI + amoxicillin for 5-7 days, then PPI + clarithromycin + nitroimidazole for 5-7 days
• Hybrid therapy: PPI + amoxicillin for 7 days, then PPI + amoxicillin + clarithromycin + nitroimidazole for 7 days

Recent evidence (2024): A network meta-analysis (PMID 39294424) found that vonoprazan (a potassium-competitive acid blocker, P-CAB) is non-inferior or superior to PPIs for treatment and prevention of gastric/duodenal ulcers, representing an emerging therapeutic option.

• Current Surgical Therapy 14e, p. 3099

Complications & Surgical Management

1. Perforation (most common surgical indication)

• Presents as acute abdomen with sudden severe epigastric pain
• Signs: Board-like rigidity, peritonitis, tachycardia; hypotension is a late sign
• Upright CXR: Pneumoperitoneum in 85-90% of cases
• CT abdomen: Extraluminal air +/- free peritoneal fluid (very sensitive)
• Mortality up to 30% in modern series; rises significantly with delayed treatment
• Treatment: Fluid resuscitation + emergency surgery (Graham patch repair or omental patch)

2. Bleeding (most common reason for hospitalization and death)

• Posterior duodenal ulcers can erode the gastroduodenal artery
• Endoscopic hemostasis is the primary treatment; surgery reserved for failures
• "Kissing ulcers" (anterior perforated + posterior bleeding) can occur simultaneously

3. Obstruction (gastric outlet obstruction)

• Caused by edema, spasm, or fibrosis at the pylorus/duodenum
• Presents with projectile vomiting (non-bilious), weight loss, distended stomach
• Treat underlying ulcer medically; endoscopic balloon dilation or surgery if persistent

4. Intractable ulcer

• Failure of appropriate medical therapy (adequate PPI, confirmed H. pylori eradication, NSAID cessation)
• Rare in the modern era; requires reassessment for gastrinoma, malignancy, or poor compliance
• Current Surgical Therapy 14e, p. 3102-3316

Summary Table