AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

Background

Stress-induced gastritis, also referred to as stress-related erosive syndrome, stress ulcer syndrome, and stress-related mucosal disease, can cause mucosal erosions and superficial hemorrhages in patients who are critically ill or in those who are under extreme physiological stress, resulting in minimal-to-severe gastrointestinal blood loss and leading to blood transfusion if not addressed.

Patients who may have an increased risk of stress gastritis are those with massive burn injury, head injury associated with raised intracranial pressure, sepsis and positive blood culture results, severe trauma, and multiple system organ failure.

Pathophysiology

Acid is secreted by the parietal cells of the gastric mucosa, which is under the influence of several biological agents or activities (eg, histamine, gastrin, vagal nerve stimulation). The mucosa is protected by the mucous gel layer, which is under the influence of prostaglandins, nitric oxide, trefoil proteins, and vagal nerve stimulation. This mucous layer forms a barrier between the acidic pH of the stomach and the gastric epithelium. In the presence of noxious agents or conditions, this protective barrier is destroyed. When this occurs, the acid is able to diffuse backward to the epithelium and cause mucosal damage.

Two entities are thought to normally play a role in the breakdown of the mucosal barrier: gastric acid secretion and defense mechanisms. With stress gastritis, gastric acid secretion is invariably either normal or decreased. Thus, acid hypersecretion is not a significant etiological factor; instead, the breakdown of the mucosal defense mechanism is the primary cause. The defense mechanisms, particularly the mucous secretion, tend to have a decrease in bicarbonate concentration and, therefore, are unable to buffer the proton in the stomach (Yardley, 2001). Stress causes decreased blood flow to the mucosa, leading to ischemia with subsequent destruction of the mucosal lining.

Frequency

United States

Of patients who are critically ill, 6% have overt bleeding, while fewer than 2-3% have clinically significant hemorrhage. According to several studies, endoscopy has revealed evidence of intraepithelial hemorrhage in 52-100% of patients in the ICU within 24 hours of the onset of the stressor (Feldman, 2002).

Mortality/Morbidity

Mortality/morbidity figures are high in older patients because of several factors, including atherosclerosis that leads to reduced blood supply and impaired host defenses. The severity of the injury leads to a further reduction in blood flow to the GI tract, thereby resulting in further compromise of the mucosal barrier and an increased risk of gastritis. The presence of Helicobacter pylori may also contribute to the mucosal barrier breakdown and lead to stress gastritis.

Race

No studies have shown any differences among the races with respect to the bleeding rates associated with stress gastritis.

Sex

No differences have been noted between the sexes with respect to stress gastritis.

Age

With increasing age, atherosclerosis may play a role in the decreased blood supply to the gastric mucosa. This, in the setting of a stressor, will lead to decreased mucous production and, hence, greater susceptibility to erosions and ulcerations.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

History

Patients who may have an increased risk of stress gastritis are those with massive burn injury, head injury associated with raised intracranial pressure, sepsis and positive blood culture results, severe trauma, and multiple system organ failure. The clinician should have a high incidence of suspicion for patients in these settings who are noted to have decreased hematocrit values and who are not receiving prophylaxis for stress gastritis.

Physical

Clinical presentation is varied, but the following clues should raise the level of clinical suspicion for this entity:

• Coffee ground vomitus
• Melena
• Hematemesis (in extreme cases)
• Orthostasis (unusual)

Causes

Prolonged mechanical ventilation and coagulopathy increase predisposition to stress gastritis. Causative factors include the following conditions:

• Severe trauma
• Massive burns
• Hypotension
• Sepsis with positive blood culture results
• CNS injury with raised intracranial pressure
• Mechanical ventilation
• Multiorgan failure

DIFFERENTIALS

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

Other Problems to be Considered

Nonsteroidal anti-inflammatory drug (NSAID)–induced gastritis
Alcoholic gastropathy
Uremic gastropathy

WORKUP

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

Lab Studies

• A high degree of clinical awareness is the key to early diagnosis. The presence of any of the previously discussed clinical features should alert the clinician to the presence of stress gastritis.
• Useful investigations and diagnostic tools include the following:
• • Hematocrit
  • Coagulation profile

Procedures

• Nasogastric tube and lavage: Gastric lavage is a useful test to confirm whether blood is present in the upper GI tract and to quantify the amount of blood if found. This is roughly assessed by how much normal saline it takes before the aspirate becomes clear.
• Endoscopy is useful only in the diagnosis of stress-induced gastritis.

TREATMENT

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

Medical Care

The goal of management is prophylaxis. This has been shown to reduce the incidence by 50% when started on admission. Monitor the pH of the gastric contents. The target pH value should be greater than 4.0. Anything less should prompt the clinician to double the dose of the agent used if the patient was previously on prophylaxis.

Sucralfate is the primary agent for prophylaxis of stress gastritis. It has long been used as a means of decreasing the incidence of gastritis. This drug is readily available, easy to administer, and inexpensive. Sucralfate (complex salt of sucrose aluminum hydroxide and sulfate) has a positive charge and binds to the negative charge of the ulcer base to form a gel, which acts to effectively plug the ulcer base and to prevent worsening of the gastritis. For patients on mechanical ventilation, this action has been shown to decrease the risk of nosocomial pneumonias by aspiration.

Histamine 2 (H2) receptor blockers (eg, ranitidine, famotidine) have also been used for prophylaxis. Their action selectively blocks H2 receptors on the parietal cells, thereby reducing the production of hydrogen ions. The H2 blockers are readily affordable and can be administered intravenously. For active hemorrhage, a continuous infusion of H2 blockers over a 24-hour period can be used because this delivers a constant concentration to the gastric mucosa, thus promoting healing. The major adverse effect of this class of drugs is the risk of nosocomial pneumonia, which is thought to result from the suppression of gastric acid and which leads to colonization by secondary organisms and subsequent aspiration pneumonia.

The role of proton pump inhibitors (PPIs) in prophylaxis has not been fully evaluated. The usefulness has been demonstrated in a few small studies, but no large randomized, clinical studies have been done to date. PPIs are prodrugs and usually require an acidic medium to be activated. Hence, in the fasting stressed patient, this may not be the case. PPIs block the final common pathway of acid secretion by blocking the H-K-ATPase enzyme.

PPIs are available in various forms (eg, tablets, microspheres, liquid [IV]). In patients who are critically ill and intubated for nasogastric tube or percutaneous endoscopic gastrostomy (PEG) feeding, the administration of microspheres or intravenous preparations can be useful if the patients are thought to be bleeding from stress gastritis, especially if they have not responded to any of the previously discussed measures.

Small studies have shown the efficacy of PPIs in mechanically ventilated patients to reduce stress gastritis and also to be safe and cost effective. A comparison of PPIs and placebo was performed and demonstrated the superiority of PPIs over placebo in cases of bleeding peptic ulcer. PPIs were also shown to be more effective for rebleed prophylaxis versus H2 blockers.

MEDICATION

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

PPIs have not been fully evaluated in the role of prophylaxis for this disease.

Drug Category: Gastrointestinal agents

Shown to be effective in the prevention of stress-induced gastritis.

Drug Category: Histamine H2 antagonists

These agents block H2 receptor binding. The primary indication is to reduce symptoms and to accelerate healing of gastric ulcers. In the acutely bleeding patient, they are of limited benefit. Some have also been used for prophylaxis (eg, famotidine).

MISCELLANEOUS

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

Medical/Legal Pitfalls

• Timely prophylaxis with H2 blockers can lead to a significant reduction in the development of stress-induced gastritis and, hence, the avoidance of upper gastrointestinal hemorrhage.
• Possibility of blood product transfusions, dependent on the severity of hemorrhage. This may expose the patient to the unnecessary risk of blood-borne infections.
• • The possible resultant hypotension could worsen any vasculature compromise that is present, leading to cerebrovasculature accidents, myocardial infarction, and renal failure.
  • This could potentially leave the physician liable for lawsuits, if the patient is not prophylaxed earlier or in a timely manner.

Special Concerns

• The geriatric population may be more susceptible to the loss of blood, leading to a worsening of any underlying chronic vascular disease.

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Miscellaneous
• References

• Feldman M. Sleisenger & Fordtran's Gastrointestinal and Liver Disease. 7th ed. Philadelphia: WB Saunders Co;. 2002:587-603.
• Fiddian-Green RG, McGough E, Pittenger G. Predictive value of intramural pH and other risk factors for massive bleeding from stress ulceration. Gastroenterology. Sep 1983;85(3):613-20.
• Irwin R, Rippe J. Manual of Intensive Care Medicine. Philadelphia: JB Lippincott Co;. 2001.
• Khuroo MS, Yattoo GN, Javid G. A comparison of omeprazole and placebo for bleeding peptic ulcer. N Engl J Med. Apr 10 1997;336(15):1054-8.
• Laine L. Sleisenger & Fordtran's Gastrointestinal and Liver Disease. 6th ed. Philadelphia: WB Saunders;. 2000:198-219.
• Lin HJ, Lo WC, Lee FY. A prospective randomized comparative trial showing that omeprazole prevents rebleeding in patients with bleeding peptic ulcer after successful endoscopic therapy. Arch Intern Med. Jan 12 1998;158(1):54-8. [Medline].
• Wolfe M. Stress-related erosive syndrome. In: Bayless T, ed. Current Therapy in Gastroenterology and Liver Disease. 4th ed. 1994:139-143.
• Wolfe MM, Sachs G. Acid suppression: optimizing therapy for gastroduodenal ulcer healing, gastroesophageal reflux disease, and stress-related erosive syndrome. Gastroenterology. Feb 2000;118(2 Suppl 1):S9-31.
• Yardley JH, Hendrix TR. Textbook of Gastroenterology. 2nd ed. Philadelphia: JB Lippincott Co;. 2001:1456-93.

Article Last Updated: Aug 31, 2006