AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Gastritis includes a myriad of disorders that involve inflammatory changes in the gastric mucosa, including erosive gastritis caused by Helicobacter pylori bacterial infections, other infectious gastritises, nonsteroidal anti-inflammatory drugs (NSAIDs), noxious irritants, reflux gastritis from exposure to bile and pancreatic fluids, infectious gastritis, and gastric mucosal atrophy.

Peptic ulcer disease (PUD) refers to 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 ED 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.

For more information, see Medscape's Peptic Ulcer Disease Resource Center.

Pathophysiology

The mechanisms of mucosal injury in gastritis and PUD are thought to be mainly caused by H pylori infections, coupled an imbalance of aggressive factors, such as acid production or pepsin, and defensive factors, such as mucus production, bicarbonate, and blood flow.

Erosive gastritis usually is associated with serious illness or with various drugs. Stress, ethanol, bile, and nonsteroidal anti-inflammatory drugs (NSAIDs) disrupt the gastric mucosal barrier, making it vulnerable to normal gastric secretions.

Infection with H pylori, a short, spiral-shaped, microaerophilic gram-negative bacillus, is the leading cause of PUD and is associated with virtually all ulcers not induced by NSAIDs. H pylori colonize the deep layers of the mucosal gel that coats the gastric mucosa and presumably disrupts its protective properties. H pylori is thought to infect virtually all patients with chronic active gastritis. Eradication of H pylori was thought to be the pathway to curing ulcer disease, but that has proven increasingly challenging.

NSAIDs and aspirin also interfere with the protective mucus layer by inhibiting mucosal cyclooxygenase activity, reducing levels of mucosal prostaglandins. Many people with known H pylori colonization or who are taking NSAIDs do not suffer from gastritis or PUD, which indicates other important causative factors must be involved.

Frequency

United States

Approximately 10% of Americans eventually develop 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 PUD is decreasing in the developed world but increasing in developing countries.

Mortality/Morbidity

• Complications of gastritis include PUD and, rarely, extensive bleeding. PUD accounts for more than 50% of all causes of upper gastrointestinal bleeds in the United States.
• Complications of peptic ulcer disease include bleeding, occasionally massive, and perforation leading to peritonitis and sepsis (rare).
• The mortality rate is low.

Sex

• Male-to-female ratio of gastritis is approximately 1:1
• Male-to-female ratio of PUD is approximately 2:1

Age

• An estimated 60% of Americans older than 60 years harbor H pylori.
• Duodenal ulcers usually occur in those aged 25-75 years.
• Gastric ulcer prevalence peaks in those aged 55-65 years.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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
• NSAID-induced gastritis or ulcers are usually 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 normal.
• Signs of peritonitis or GI bleeding may be manifest. Perform a rectal examination and Hemoccult testing.

Causes

• H pylori (most common cause of ulceration)
• NSAIDs, aspirin
• Gastrinoma (Zollinger-Ellison syndrome)
• Severe stress (eg, trauma, burns), Curling ulcers
• Alcohol
• Bile reflux
• Pancreatic enzyme reflux
• Radiation
• Staphylococcus aureus exotoxin
• Bacterial or viral infection

DIFFERENTIALS

Section 4 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Gastric cancer
Esophageal varices
Mallory-Weiss tears
Atrophic gastritis
Nonulcer dyspepsia
Functional gastrointestinal disorder
Atypical appendicitis in the pregnant patient

WORKUP

Section 5 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Complete blood count test is used to evaluate acute or chronic blood loss.
• Electrolytes, BUN, and creatinine are useful tests for critical-appearing patients who require fluid resuscitation.
• Type, crossmatch, and screen are indicated if transfusion in unstable or potentially critical patients is needed.
• While a blood test for H pylori exists, it is of limited value in the acute setting.

Imaging Studies

• A chest x-ray may be useful to detect free abdominal air when perforation is a possibility.
• A CT scan is only useful when other conditions are being considered.

Other Tests

• Relief of symptoms with a GI cocktail is not a diagnostic indicator.
• Serial exams are useful in determining that the patient is improving and not developing hemorrhage or peritonitis.

Procedures

• Placement of a nasogastric (NG) tube is helpful only when an upper GI bleed is suspected.

TREATMENT

Section 6 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Prehospital Care

• Pursue aggressive fluid resuscitation in patients with evidence of massive upper GI bleeding.

Emergency Department Care

• Most patients do not require acute interventions.
• Antacids or a GI cocktail (ie, typically an antacid with an anesthetic such as viscous lidocaine and/or an antispasmodic) may be used therapeutically for symptoms.
• Administer supportive therapy as needed.
• Massive gastric bleeds are the most difficult complication to treat. Mainstays of resuscitation include the following:
• • Begin volume replacement, initially with crystalloid. In the face of continued hypotension after 2 L, consider blood transfusion.
  • NG suction helps to keep the stomach empty and contracted.
  • IV H2 antagonists are recommended but unproven in acute upper GI bleeds.
  • Emergent surgical or endoscopic intervention may be required.
• The ED is not the place to distinguish between gastritis and PUD, which usually requires endoscopy or contrast radiography. Gastric mucosal biopsy culture, 13C-urea breath test, or enzyme-linked immunosorbent assay (ELISA) for H pylori immunoglobulins aid in the diagnosis of H pylori infection. These tests are not performed in the ED.
• H2-receptor blockers and proton pump inhibitors probably have no major effect on the acute management of gastritis and peptic ulcer disease. Effect of treatment takes several weeks.

Consultations

• Consult with a general surgeon for most acute complications, such as perforation, bleeding, and outlet obstruction.
• In some instances, the GI endoscopist may be able to treat bleeding definitively.

MEDICATION

Section 7 of 11  

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Treatment goals are the relief of discomfort and protection of the gastric mucosal barrier to promote healing. Eradication of H pylori infection is a prolonged and complicated process requiring confirmation of the presence of the organism, which is beyond the scope of practice in the ED.
 
Cessation of the causative agent and antacids may be sufficient outpatient therapy in mild cases. Most patients require an H2-receptor antagonist (H2RA) or a proton pump inhibitor (PPI), which has been proven to provide faster and more reliable healing than antacids. Either an H2RA or a PPI can be used as a first-line agent. With continued symptoms, they may be used together. In refractory cases, sucralfate also may be indicated.

PPI are more effective than H2RAs in reducing upper GI bleeds in patients taking NSAIDs, aspirin, or clopidogrel. None of the antisecretory agents have a significant effect in reducing bleeding risk in patients taking other anticoagulants.

Drug Category: Antacids

Aluminum-containing and magnesium-containing antacids can be helpful in relieving symptoms of gastritis by neutralizing gastric acids. These agents are inexpensive and safe.

Drug Category: H2-receptor antagonists

Inhibit the action of histamine on the parietal cell, which inhibits acid secretion. The 4 drugs in this class are all equally effective and are available over the counter in half prescription strength for heartburn treatment. Although the IV administration of H2 blockers may be used to treat acute complications (eg, GI bleeding), the benefits are yet to be proven.

Drug Category: Proton pump inhibitors

Bind to the proton pump of parietal cell, inhibiting secretion of hydrogen ions into gastric lumen. Proton pump inhibitors relieve pain and heal peptic ulcers more rapidly than H2 antagonists do. Drugs in this class are equally effective. They all decrease serum concentrations of drugs that require gastric acidity for absorption, such as ketoconazole or itraconazole. Five drugs are now FDA approved in this category. Omeprazole will soon go off patent and be available as a generic.

Drug Category: Gastrointestinal agents

Are effective in the treatment of peptic ulcers and in preventing relapse. Their mechanism of action is not clear. Multiple doses are required, and they are not as effective as the other options.

Drug Category: Prostaglandins

Can prevent peptic ulcers in patients taking NSAIDs and may be used with NSAIDs in patients at a high risk of complications.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• Patients with significant or potentially significant hemorrhage require admission, usually to the intensive care unit. While in the ED, their care should focus on restoration of intravascular volume by infusion of saline or blood through large bore IV lines as clinically indicated. A central venous catheter to monitor such resuscitation may be considered.
• High-risk patients include those with the following characteristics:
• • Bleeding with hemodynamic instability
  • Repeated hematemesis or any hematochezia
  • Failure to clear with gastric lavage
  • Coagulopathy
  • Comorbid disease (especially cardiac, pulmonary, or renal)
  • Advanced age
• Patients with gastric perforation require operative repair.
• Hospitalization usually is necessary for gastric outlet obstruction to provide gastric rest and IV fluids. Surgical treatment usually is indicated for persistent or recurrent obstruction. Anticholinergic agents are contraindicated.

Further Outpatient Care

• A follow-up visit should be made in 2-6 weeks to evaluate efficacy of treatment.
• Severe or recurrent symptoms indicate prompt referral for endoscopy and testing for H pylori.
• Symptomatic relief with therapy does not preclude malignancy.

Complications

• Malignancy
• Hemorrhage
• Perforation
• Obstruction

Prognosis

• The prognosis is excellent. Most patients are cured when the cause has been identified and treated appropriately.

Patient Education

• Patients should be warned of known or potentially injurious drugs and agents. Some examples are as follows:
• • NSAIDs
  • Aspirin
  • Alcohol
  • Caffeine (eg, coffee, tea, colas)
• For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center, Liver, Gallbladder, and Pancreas Center, and Heartburn/GERD/Reflux Center. Also, see eMedicine's patient education articles Gastritis, Peptic Ulcers, Heartburn, Understanding Heartburn/GERD Medications, and Abdominal Pain in Adults.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Failure to consider other, nongastrointestinal etiologies for epigastric pain, including myocardial infarction and abdominal aortic aneurysm
• Failure to consider gastric hemorrhage in absence of abdominal pain, especially in elderly patients
• Failure to refer patients for follow-up care may result in failure to diagnose H pylori infection or gastric cancer

MULTIMEDIA

Section 10 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Gross pathology of a gastric ulcer
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Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

• Friedman LS, Peterson WL. Peptic ulcer and related disorders. In: Fauci AS, Braunwald E, Isselbacheret KJ, et al, eds. Harrison's Principles of Internal Medicine. 14^th ed. McGraw-Hill; 1998:1596-1616.
• Logan RP, Walker MM. ABC of the upper gastrointestinal tract: Epidemiology and diagnosis of Helicobacter pylori infection. BMJ. Oct 20 2001;323(7318):920-2. [Medline].
• McColl KE. Helicobacter pylori-negative ulcer disease. J Gastroenterol. 2000;35 Supple 12:47-50. [Medline].
• Moss SF, Sood S. Helicobacter pylori. Curr Opin Infect Dis. Oct 2003;16(5):445-51. [Medline].
• Pang SH, Leung WK, Graham DY. Ulcers and gastritis. Endoscopy. Feb 2008;40(2):136-9. [Medline].
• Peek RM, Blaser MJ. Pathophysiology of Helicobacter pylori-induced gastritis and peptic ulcer disease. Am J Med. Feb 1997;102(2):200-7. [Medline].
• Soll AH. Consensus conference. Medical treatment of peptic ulcer disease. Practice guidelines. Practice Parameters Committee of the American College of Gastroenterology. JAMA. Feb 28 1996;275(8):622-9. [Medline].
• Suerbaum S, Michetti P. Helicobacter pylori infection. N Engl J Med. Oct 10 2002;347(15):1175-86. [Medline].
• The Medical Letter. Drugs for treatment of peptic ulcers. Med Lett Drugs Ther. Jan 3 1997;39(991):1-4. [Medline].
• Yeomans ND. Management of peptic ulcer disease not related to Helicobacter. J Gastroenterol Hepatol. Apr 2002;17(4):488-94. [Medline].
• Yuan Y, Padol IT, Hunt RH. Peptic ulcer disease today. Nat Clin Pract Gastroenterol Hepatol. Feb 2006;3(2):80-9. [Medline].

Article Last Updated: Aug 21, 2008