Complications

• Definition: the bleeding and/or hemorrhage of a peptic ulcer (either duodenal or gastric)

  • The most common complication of PUD

  • Can be a chronic, slow bleed or an overt, rapid, life-threatening hemorrhage

• Etiology

  • Posterior duodenal ulcers are more likely to bleed than anterior duodenal ulcers.

  • Gastric ulcers of the lesser curvature may cause bleeding from the left gastric artery.

  • Duodenal ulcers of the posterior wall may cause bleeding from the gastroduodenal artery.

• Clinical features

  • Hematemesis (coffee-grounds emesis)

  • Melena

  • Anemia

  • Hematochezia (less common; only seen in massive bleeding)

  • Orthostatic hypotension

• Treatment [31]

  • NPO, volume resuscitation, transfusion, endoscopy

• Definition: full-thickness injury and loss of bowel wall integrity that results in leakage of gastrointestinal contents

  • The second most common complication of PUD

  • PUD is the most common cause of GI perforation.

• Etiology

  • Prepyloric gastric ulcers are the most common cause of perforation.

  • Duodenal ulcers of the anterior wall are more likely to perforate than ulcers of the posterior wall.

• Clinical features

  • Sudden, diffuse abdominal pain and rigidity

  • Fever, tachycardia, tachypnea, hypotension

  • Pneumoperitoneum

  • Shoulder pain (irritation of the phrenic nerve)

• Treatment

  • NPO, volume resuscitation, supportive care

  • Graham patch: surgical repair of a small, (generally < 5 mm) perforated duodenal ulcer using a piece of omentum to close the perforation

• Definition: Penetration of a peptic ulcer through the gastric/duodenal wall into adjacent organs (e.g., pancreas, biliary tree, colon) without leaking of gastric contents into the peritoneal cavity

• Etiology: Duodenal ulcers are the most common cause of penetration.

• Clinical features: a change in clinical symptoms that are related to the affected neighboring organs

  • Colon: Gastrocolic or duodenocolic fistulas may manifest with copremesis and postprandial diarrhea.

  • Liver, spleen, or diaphragm: Penetration may result in visceral abscesses (fever, abdominal tenderness, and sepsis).

  • Gastroduodenal artery or aorta: Vascular fistulas may result in severe hemorrhage.

  • Biliary tree: Choledochoduodenal fistulas may manifest with biliary tract obstruction (fever, jaundice, RUQ pain).

  • Pancreas: increased epigastric pain and peritonitis

• Treatment

  • Conservative management: indicated in all patients, as most fistulas close spontaneously

  • Surgical resection: in patients unresponsive to conservative management

GOO is more commonly due to malignancy in regions where the treatment of PUD and H. Pylori is prevalent (see “Gastric cancer” for details).

• Pathophysiology

  • Acute PUD → inflammation and edema

  • Chronic PUD → scarring and fibrosis

• Clinical features

  • Postprandial, nonbilious vomiting

  • Succussion splash

  • Early satiety

  • Progressive gastric dilation

  • Weight loss

• Diagnostics

  • Imaging (e.g., barium swallow, CT abdomen)

  • EGD (confirmatory test)

  • Laboratory studies may show hypokalemic hypochloremic metabolic alkalosis.

• Management

  • Symptomatic: nasogastric suction, electrolyte and fluid replacement, and parenteral nutrition

  • Definitive: surgery or endoscopic dilation

• Gastric ulcers

  • High malignant potential (progression to cancer in 5–10% of cases)

  • Malignancy should be ruled out with biopsy.

• Duodenal ulcers

  • Usually benign

  • Routine biopsy is not required.