Matthew C. Gratton
EPIDEMIOLOGY
Peptic ulcer disease (PUD) is a chronic illness manifested by recurrent ulcerations in the stomach and proximal duodenum. The great majority of peptic ulcers are directly related to infection with Helicobacter pylori or NSAID use.
Gastritis is acute or chronic inflammation of the gastric mucosa.
Dyspepsia is continuous or recurrent upper abdominal pain or discomfort with or without associated symptoms.
PATHOPHYSIOLOGY
Hydrochloric acid and pepsin destroy gastric and duodenal mucosa while mucus and bicarbonate ion secretions protect mucosa. Prostaglandins protect mucosa by enhancing mucus and bicarbonate production. The balance between these protective and destructive forces determines whether ulceration occurs.
Helicobacter pylori is a spiral, gram-negative, flagellated bacterium that produces urease, cytotoxins, proteases, and other compounds that disturb the mucous gel and cause tissue injury and ulceration.
Helicobacter pylori infection is present in about 95% of patients who develop duodenal ulcer and about 70% of those who develop gastric ulcer.
Traditional ulcer treatment heals most ulcers, but eradication of H. pylori reduces recurrence rates from 35% to 2% for duodenal ulcers and from 39% to 3% for gastric ulcers.
NSAIDs inhibit prostaglandin synthesis, thereby decreasing mucus and bicarbonate production and mucosal blood flow, which allows ulcer formation.
Acute gastritis is generally caused by ischemia due to severe illness (burns, trauma, shock, etc.), direct toxic effects (NSAIDs, alcohol, etc.), or H. pylori infection.
Dyspepsia has multiple causes including esophagitis, endoscopically negative reflux disease, and PUD, but about 50% of dyspepsia patients have no cause found and are said to have “functional dyspepsia.”
CLINICAL FEATURES
Burning epigastric pain that is relieved with food, milk, or antacids and recurs at night as the stomach empties is the most classic presentation of PUD. Pain tends to occur daily for weeks and then resolve and then recur in weeks to months.
Atypical presentations are common, especially in the elderly.
A change in the character of the pain may indicate a complication: abrupt onset of severe pain in perforation with peritonitis; rapid onset of back pain associated with posterior perforation and pancreatitis; nausea and vomiting from gastric outlet obstruction; and vomiting blood or passing blood per rectum from a GI bleed.
The only physical sign of PUD may be epigastric tenderness, and this is neither sensitive nor specific. Physical examination findings of complications include rigid abdomen (perforation), abdominal distention and vomiting (gastric outlet obstruction), or GI bleeding.
Acute gastritis may present with epigastric pain and nausea and vomiting, although the most common presentation is GI bleeding (microscopic to gross blood).
DIAGNOSIS AND DIFFERENTIAL
The classic history with epigastric tenderness may suggest PUD, but definitive diagnosis cannot be made clinically.
The differential diagnosis of PUD includes gastritis, functional dyspepsia, gastroesophageal reflux disease (GERD), pancreatitis, hepatitis, cholelithiasis, cardiac ischemia, abdominal aortic aneurysm (AAA), gas-troparesis, and gastric cancer.
The “gold standard” for diagnosis is the visualization of an ulcer via upper GI endoscopy. The sensitivity and specificity are both >95%, and this test also allows visualization of other potential abnormalities and biopsy of appropriate lesions.
Although not all patients with epigastric pain require endoscopy, those with “alarm” features suggestive of esophageal or gastric cancer or other serious diseases do (see Table 43-1).
Ancillary tests to consider include complete blood cell count (CBC) to look for anemia in chronic GI blood loss, abdominal ultrasound for cholelithiasis and AAA, electrocardiogram and cardiac enzymes for cardiac ischemia, liver function tests to look for hepatitis and cholelithiasis, lipase to look for pancreatitis, and acute abdominal series to look for perforation.
Helicobacter pylori infection could be investigated in the ED via serologic tests or stool antigen tests, but there is no evidence from the literature describing this in an ED setting and it is probably best deferred to the primary care provider follow-up visit.
TABLE 43-1 “Alarm Features” Suggesting Need for Endoscopy Referral
Age >55 y
Unexplained weight loss
Early satiety
Persistent vomiting
Dysphagia
Anemia or GI bleeding
Abdominal mass
Persistent anorexia
Jaundice
EMERGENCY DEPARTMENT CARE AND DISPOSITION
After PUD is diagnosed, the goal of treatment is to heal the ulcer while relieving pain and preventing complications and recurrence. H2 receptor antagonists (H2RAs) and proton pump inhibitors (PPIs) are the mainstay of treatment, while a variety of antibiotic regimens can be used to eradicate H. pylori.
PPIs (such as omeprazole, 20–40 milligrams PO daily, or lansoprazole, 15–30 milligrams PO daily) will generally heal ulcers faster than H2RAs and have an inhibitory effect against H. pylori.
H2RAs (such as cimetidine, 300 milligrams IV or 800 milligrams PO at bedtime, or ranitidine, 50 milligrams IV or 300 milligrams PO at bedtime) can be instituted for ongoing therapy to promote ulcer healing.
If acute infection with H. pylori is found, antimicrobial and antisecretory therapy is instituted with cure rates of 70% to 90%. Such a regimen might include a PPI, clarithromycin, and amoxicillin or metronidazole for 14 days.
Patients with PUD complications always require consultation, and most require admission to an appropriate inpatient unit based on the diagnosis and hemo-dynamic stability.
Most patients with epigastric pain do not receive a definitive diagnosis in the ED, but if a critical diagnosis (ie, abdominal aortic aneurysm or myocardial infarction) is still in the differential, then consultation for admission and further evaluation is indicated.
When uncomplicated PUD, gastritis, or dyspepsia is strongly suspected, the great majority of patients can be discharged with acid-suppressive therapy with a PPI or H2RA and instructions to follow-up with their primary care physician.
All patients should receive discharge instructions that include avoidance of NSAIDs, alcohol, tobacco, caffeine, and non-enteric-coated aspirin. Early follow-up should be sought for patients with “alarm” features.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 81, “Peptic Ulcer Disease and Gastritis,” by Matthew C. Gratton.