eMedicine Specialties > Emergency Medicine > Gastrointestinal

Gastritis and Peptic Ulcer Disease

Author: Philip Shayne, MD, Associate Professor, Residency Program Director, Vice Chair for Education, Department of Emergency Medicine, Emory University School of Medicine
Coauthor(s): Wendi S Miller, MD, Resident Physician, Department of Emergency Medicine, Emory University School of Medicine
Contributor Information and Disclosures

Updated: Nov 10, 2009

Introduction

Background

Gastritis technically refers to endoscopic or histological findings of inflammatory changes in the gastric mucosa; however, the term is often used clinically to refer to the symptoms of dyspepsia. The most common causes are H elicobacter pylori bacterial infection and the use of nonsteroidal anti-inflammatory drugs (NSAIDs) and aspirin. Other medications that have been associated with gastritis include potassium and iron supplements. Ethanol has been implicated in the development of gastritis in both chronic and binge drinkers. Less common causes include autoimmune disorders; radiation; noxious irritants; reflux of bile and pancreatic fluids; and infections with bacterial, viral, parasitic, and fungal organisms.

Peptic ulcer disease (PUD) refers to the development of a discrete mucosal defect in the portions of the gastrointestinal tract (gastric or duodenal) exposed to acid and pepsin secretion. Presentations of gastritis and PUD usually are indistinguishable in the ED, and thus the management is generally the same. Emergent complications include hemorrhagic shock and peritonitis secondary to a perforated ulcer. The clinician should be concerned about other life-threatening conditions (eg, acute coronary syndromes and aortic aneurysms), which can mimic the presentation of gastritis.

Pathophysiology

The pathogenesis of peptic ulcer disease is multifactorial and results from an imbalance of the aggressive gastric luminal factors, acid and pepsin, and defensive mucosal barrier functions of mucus and bicarbonate. Several environmental and host factors contribute to ulcer formation by increasing gastric acid secretion or weakening the mucosal barrier. Environmental factors include NSAID use, cigarette smoking, excessive alcohol intake, and extreme emotional or physical stress. Host factors include H pylori and other infections as well as hypersecretory states such as Zollinger-Ellison syndrome.¹

NSAID and aspirin use has become the most common cause of gastrointestinal mucosal damage and bleeding in Western countries, and it is estimated that up to 30% of regular NSAID users have one or more ulcers.² NSAID users also have a near 4-fold increase in risk of ulcer complications such as bleeding compared with nonusers. Both NSAIDs and aspirin interfere with the protective mucus layer by inhibiting mucosal cyclooxygenase activity and reducing levels of mucosal prostaglandins. Misoprostol, a prostaglandin E2 analog, has been shown to reduce the risk of ulcer complications. Gastric acid exacerbates NSAID injury, and acid suppression with proton-pump inhibitors (PPIs) has become the mainstay of management of NSAID-associated ulcer disease.

Infection with H pylori, a short, spiral-shaped, microaerophilic gram-negative bacillus, is the leading cause of peptic ulcer disease (PUD) in developing countries and of almost all other ulcers not induced by NSAIDs. H pylori colonize the deep layers of the mucosa and weaken its defense system by reducing the thickness of the mucus gel layer and diminishing mucosal blood flow. Infection is the primary cause of the histologic changes seen in patients with chronic active gastritis.³ Successful eradication of H pylori has lead to decreasing prevalence of peptic ulcer disease; however, the rates of treatment failure are increasing.

Many people with known H pylori colonization or who are taking NSAIDs do not suffer from gastritis or PUD, which indicates that other important causative factors are involved.⁴ Identification of these factors may also lead to understanding of the mechanism underlying the development of idiopathic, or non-H pylori non-NSAID, ulcers which are reportedly found with increasing frequency, especially in the United States.

Frequency

United States

Approximately 10% of Americans eventually develop peptic ulcer disease (PUD), and about 10% of patients presenting to the ED with abdominal pain are diagnosed with PUD. Prevalence has decreased in the United States over the last 30 years.

International

Frequency of peptic ulcer disease (PUD) is decreasing in the developed world but increasing in developing countries.

Mortality/Morbidity

• Complications of gastritis include PUD and, rarely, extensive bleeding.
• PUD remains a major cause of upper gastrointestinal bleeds in the United States.
• Ulcer perforation can lead to peritonitis and sepsis (rare).
• Other complications include gastric outlet obstruction and adenocarcinoma.
• The overall mortality rate is estimated at 1:100,000.

Sex

• In the past, peptic ulcer disease (PUD) was a predominantly male disease, but, today, the male-to-female ratio of both gastritis and PUD is approximately 1:1.

Age

• Age at diagnosis is increasing overall.
• H pylori infection is more common with increasing age.
• Duodenal ulcers usually occur in those aged 30-50 years.
• Gastric ulcer prevalence peaks in those aged 50-70 years.

Clinical

History

• Patients typically present with abdominal pain that has the following characteristics:
  • Epigastric to left upper quadrant
  • Frequently described as burning
  • May radiate to the back
  • Usually occurs 1-5 hours after meals
  • May be relieved by food, antacids (duodenal), or vomiting (gastric)
  • Typically follows a daily pattern specific to patient
• "Alarm features" that warrant prompt gastroenterology referral⁵ include the following:
  • Bleeding or anemia
  • Early satiety
  • Unexplained weight loss
  • Progressive dysphagia or odynophagia
  • Recurrent vomiting
  • Family history of GI cancer
• NSAID-induced gastritis or ulcers may be silent.
• Sudden onset of symptoms may indicate perforation.
• Gastritis may present as bleeding, which is more likely in elderly patients.
• Symptoms consistent with anemia (eg, fatigue, dyspnea) may manifest.

Physical

• Epigastric tenderness is present and usually mild.
• Bowel sounds are typically normal.
• Perform a rectal examination and Hemoccult testing.
• Signs of peritonitis may be present with perforation.
• A succussion splash may be present with gastric outlet obstruction.

Causes

• H pylori
• NSAIDs, aspirin
• Gastrinoma (Zollinger-Ellison syndrome)
• Severe stress (eg, trauma, burns), Curling ulcers
• Alcohol
• Bile reflux
• Pancreatic enzyme reflux
• Radiation
• Crohn's disease
• Bacterial or viral infection

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