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KembaraXtra -Medicine- Emergency and Acute Medicine – Peptic Ulcer Disease
Peptic ulcer disease (PUD) results from a breakdown in the protective mucosal defenses of the stomach or duodenum, leading to ulceration from acid and pepsin injury. The condition develops when there is an imbalance between gastric acid production and the mucosa’s ability to protect itself. The two most common causes are infection with Helicobacter pylori and nonsteroidal anti-inflammatory drug (NSAID) use.
Helicobacter pylori is a gram-negative spiral bacterium that colonizes the gastric mucous layer. It is responsible for approximately 90–95% of duodenal ulcers and 80% of gastric ulcers. The organism increases antral gastrin production and impairs mucosal integrity. NSAIDs, including aspirin, interfere with prostaglandin synthesis, weakening mucosal defenses and predisposing to ulcer formation. Additional risk factors include cigarette smoking, alcohol use, severe physiologic stress, hypersecretory states (such as Zollinger–Ellison syndrome), and genetic predisposition, with more than 20% of patients reporting a family history.
Patients commonly present with epigastric pain described as burning, gnawing, or aching. The pain is typically midline and may be localized to the xiphoid or umbilical region. Duodenal ulcer pain usually occurs 90 minutes to 3 hours after meals, may awaken the patient at night, and is often relieved by food or antacids. In contrast, gastric ulcer pain typically worsens after meals and may be associated with nausea and anorexia. Clinical differentiation between gastric and duodenal ulcers can be difficult. Relief with antacids is common. Some patients present with heme-positive stools.
Complications are critical to recognize in the emergency setting. Acute perforation presents with sudden severe pain, rigid boardlike abdomen, generalized rebound tenderness, and possible radiation to the back or shoulder. Gastric outlet obstruction manifests with vomiting, abdominal distention, and a succussion splash. Hemorrhage may present with hematemesis, melena, hypotension, tachycardia, pallor, and orthostatic changes. NSAID-induced ulcers may be clinically silent until complications occur.
Initial evaluation includes a careful abdominal examination, Hemoccult testing, and assessment of vital signs including orthostatics. Laboratory findings are often normal in uncomplicated disease. A low hematocrit suggests bleeding, while leukocytosis may indicate perforation or penetration. Amylase and lipase may be elevated with penetration or when pancreatitis is in the differential. Type and cross-match should be performed in significant blood loss. Testing for H. pylori may include urea breath test, serology, or stool antigen testing. Chest or abdominal radiographs are useful when perforation or obstruction is suspected. Endoscopy is the diagnostic procedure of choice, allowing direct visualization, biopsy, and evaluation for malignancy.
Emergency management begins with ABC stabilization. Hypotensive patients require IV fluid resuscitation with large-bore IV access and early type and cross-match. Nasogastric decompression may be indicated in obstruction or significant hemorrhage. Pain may be treated with antacids or IV H2-receptor antagonists. Narcotics should be used cautiously to avoid masking serious pathology.
Ulcer healing is promoted with acid suppression therapy. Proton pump inhibitors (PPIs) such as omeprazole, pantoprazole, or lansoprazole are highly effective. H2-receptor antagonists (e.g., famotidine) may also be used. Sucralfate and misoprostol are additional options. Combined use of sucralfate with H2 blockers or PPIs is generally not recommended due to lack of additional benefit. NSAIDs should be discontinued whenever possible.
Eradication of H. pylori is essential in infected patients. Standard triple therapy includes a PPI plus clarithromycin and amoxicillin for 14 days. In penicillin-allergic patients, clarithromycin and metronidazole are substituted. Quadruple therapy with bismuth, tetracycline, metronidazole, and a PPI is used in resistant cases or as second-line therapy.
Complications require urgent consultation. Active upper GI bleeding necessitates fluid resuscitation, possible transfusion, and gastroenterology consultation for endoscopic therapy. Perforation requires emergency surgical consultation and broad-spectrum antibiotics. Gastric outlet obstruction requires decompression and supportive care.
Patients with uncomplicated disease, stable vital signs, normal hematocrit, and heme-negative stools may be discharged with acid suppression therapy and close outpatient follow-up. Admission is required for obstruction, perforation, active bleeding, significant anemia, or uncontrolled pain. All patients should have follow-up within 2–6 weeks to assess response to therapy. Patients older than 55 years or those with alarm symptoms should undergo endoscopic evaluation to exclude malignancy.
Early recognition and appropriate eradication of H. pylori, along with acid suppression and avoidance of NSAIDs, are the cornerstones of therapy. Failure to ensure follow-up may result in missed complications, including gastric cancer.
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