Peptic ulcer disease (PUD)

Discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin.

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Etiology

Helicobacter pylori infection:

Gram-negative, motile spiral rod found in 90% of duodenal ulcers and 70% to 90% of gastric ulcers

Non-steroidal anti-inflammatory drugs (NSAIDs):

#2 M/C cause of PUD. The secretion of prostaglandin normally protects the gastric mucosa. NSAIDs block prostaglandin synthesis by inhibiting COX-1 enzyme resulting in a decrease in gastric mucus and bicarbonate production and a decrease in mucosal blood flow.

Hypersecretory environments:

Multiple gastroduodenal, jejunal, or esophageal ulcers

• Zollinger Ellison syndrome
• Systemic mastocytosis
• Cystic fibrosis
• Hyperparathyroidism
• Antral G cell hyperplasia

Social factors:

• Smoking
• Alcohol (irritate gastric mucosa and induce acidity)

Malignancy:

• Gastric cancer
• Lymphomas
• Lung cancers

Stress:

• After acute illness
• Multiorgan failure
• Ventilator support
• Extensive burns (Curling’s ulcer)
• Head injury (Cushing’s ulcer)

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Pathophysiology

Mucosal break of the upper gastrointestinal tract due to acid peptic digestion resulting in ulcer formation which extends beyond the muscularis mucosae into the submucosa.

Modified Johnson Classification system:

Based on location of the ulcer

• Type I (M/C): Lesser curvature; Associated with acid hypersecretion:
  • Type II: Prepyloric + duodenal
  • Type III: Prepyloric only
• Type IV: Proximal gastroesophageal ulcer
  • M/C bleeds, usually from left gastric artery
• Type V: Diffuse occurrence. Associated with the chronic use of NSAIDs (such as ibuprofen)

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Presentation

Signs and symptoms of peptic ulcer disease may vary depending upon the location of the disease and age.

Epigastric pain:

Usually occurs within 15-30 minutes following a meal in patients with a gastric ulcer; on the other hand, the pain with a duodenal ulcer tends to occur 2-3 hours after a meal.

Duodenal ulcers:

Duodenal ulcers are more common than gastric ulcers.

• M/C site: 1st part of duodenum
• Anterior duodenal ulcer presentation: Perforation
• Posterior duodenal ulcer presentation: Bleeding (M/C presentation)
  • Usually due to gastroduodenal artery

Associated features:

• Loss of appetite
• Weight loss

Alarming features:

• Evidence of overt or occult gastrointestinal bleeding: Hematemesis, melena, anaemia, heme-positive stool
• Symptom of impending perforation: Severe persistent epigastric pain
• Symptom of obstruction: Persistent vomiting
• Malignancy: anorexia, unintended weight loss

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Complicatoins

• Upper GI bleeding (15–20%): Manifests as bloody or coffee-ground emesis and/or bloody or tarry stools
• Perforated peptic ulcer (PPU) (2–10%): Manifests as a sudden, severe, piercing epigastric pain followed by rapidly developing symptoms of diffuse peritonitis
• Gastric outlet obstruction (GOO): Results from permanent scarring/edema and inflammation associated with an ulcer located in the pylorus or duodenal bulb manifesting as gastric retention, nausea, and profuse vomiting; some patients develop hypokalemia and alkalosis.

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Diagnosis

Non-invasive Helicobacter pylori testing:

• Urea breath test: A solution containing portions of 13C-labeled or 14C-labeled urea are consumed by the patient. The urea is hydrolyzed by bacterial urease to labeled CO2, which is measured in the expired air after 30 minutes.
• Stool antigen test

Esophagogastroduodenoscopy (EGD):

Gold standard

• Sharply demarcated circular mucosal defect or an irregular cavity with infiltrated edges
  • Gastric ulcers: Lesser curvature or in prepyloric region
  • Duodenal ulcers: Anterior wall of bulb

Differential diagnosis:

Other causes of dyspepsia, nausea and vomiting, and epigastric pain

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Management

Medical management:

• Triple therapy: Proton pump inhibitor (PPI) + clarithromycin + amoxicillin/metronidazole (7-14 days)
  • PPIs work synergistically with antibiotics to eradicate H. pylori
  • Due to increasing antibiotic resistance, the efficacy of triple therapy has fallen below 70% in many countries.
• Bismuth-containing quadruple therapy (for clarithromycin resistance):
  • PPI + bismuth + tetracycline + nitroimidazole (metronidazole/tinidazole) for 14 days
    or
    PPI + clarithromycin + amoxicillin + nitroimidazole

Surgical management:

Indicated if the patient is unresponsive to medical treatment, noncompliant, or at high risk of complications

• Duodenal ulcers:
  • Highly selective vagotomy or truncal vagotomy with antrectomy
• Pyloric stenosis:
  • Truncal vagotomy + pyloroplasty or vagotomy + antrectomy
• Gastric ulcers:
  • Gastric body: Partial gastrectomy + gastroduodenal anastomosis without vagotomy
  • Prepyloric region or gastric + duodenal ulcers: Vagotomy + antrectomy
  • Subcardial region: Partial gastrectomy including pyloric region

Complications of vagotomy & gastric reconstruction:

Highly selective vagotomy has least amount of complications but the highest recurrence rate, whereas truncal vagotomy + antrectomy has the highest reduction in acid secretion with the most vagal complications

• Nutritional complications: Iron deficiency (M/C complication overall), vitamin B12, calcium deficiency
• Internal hernia: Stemmer’s hernia, Peterson’s hernia
• Dumping syndrome (postgastric surgery syndrome)

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Summary: