eMedicine Specialties > Gastroenterology > Stomach

Gastritis, Stress-Induced

Author: Rohan C Clarke, MD, Consulting Staff, Department of Gastroenterology, JPS Health Systems Hospital
Coauthor(s): Rachael M Ferraro, DO, Consulting Staff, Department of Internal Medicine, Regency Hospital and Kindred Hospital; Emmanuel Gbadehan, MD, Instructor in Clinical Medicine, Columbia University College of Physicians and Surgeons; Consulting Staff, Department of Gastroenterology, Harlem Hospital Center, North General Hospital; Uzodinma R Dim, MD, Clinical Cardiac Electrophysiology Fellow, Division of Cardiovascular Medicine, University of Iowa Hospital and Clinics
Contributor Information and Disclosures

Updated: Jan 2, 2010

Introduction

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.1

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

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

More on Gastritis, Stress-Induced

Overview: Gastritis, Stress-Induced
Differential Diagnoses & Workup: Gastritis, Stress-Induced
Treatment & Medication: Gastritis, Stress-Induced
Follow-up: Gastritis, Stress-Induced
References
Further Reading
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References

  1. Feldman M. Friedman LS, Sleisenger MH, eds. Sleisenger & Fordtran's Gastrointestinal and Liver Disease. 7th ed. Philadelphia, Pa: WB Saunders Co; 2002:587-603.

  2. Constantin VD, Paun S, Ciofoaia VV, Budu V, Socea B. Multimodal management of upper gastrointestinal bleeding caused by stress gastropathy. J Gastrointestin Liver Dis. Sep 2009;18(3):279-84. [Medline].

  3. Reveiz L, Guerrero-Lozano R, Camacho A, Yara L, Mosquera PA. Stress ulcer, gastritis, and gastrointestinal bleeding prophylaxis in critically ill pediatric patients: A systematic review*. Pediatr Crit Care Med. Sep 15 2009;epub ahead of print. [Medline].

  4. 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.

  5. Irwin R, Rippe J. Manual of Intensive Care Medicine. Philadelphia, Pa: JB Lippincott Co; 2001.

  6. 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.

  7. Laine L. Sleisenger & Fordtran's Gastrointestinal and Liver Disease. 6th ed. Philadelphia: WB Saunders;. 2000:198-219.

  8. 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].

  9. Petronilho F, Araujo JH, Steckert AV, et al. Effect of a gastrin-releasing peptide receptor antagonist and a proton pump inhibitor association in an animal model of gastritis. Peptides. Aug 2009;30(8):1460-5. [Medline].

  10. van Mark A, Spallek M, Groneberg DA, Kessel R, Weiler SW. Correlates shift work with increased risk of gastrointestinal complaints or frequency of gastritis or peptic ulcer in H. pylori-infected shift workers?. Int Arch Occup Environ Health. Dec 11 2009;epub ahead of print. [Medline].

  11. Wolfe M. Stress-related erosive syndrome. In: Bayless T, ed. Current Therapy in Gastroenterology and Liver Disease. 4th ed. St Louis, Mo: Mosby; 1994:139-43.

  12. 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.

  13. Yardley JH, Hendrix TR. Textbook of Gastroenterology. 2nd ed. Philadelphia, Pa: JB Lippincott Co; 2001:1456-93.

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Further Reading

Related eMedicine Topics

Clinical Trials

Clinical Guidelines

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Keywords

stress-induced gastritis, stress induced gastritis, stress gastritis, mucosal erosions, superficial hemorrhages, gastric acid, parietal cells, gastroesophageal reflux disease, GERD, peptic ulcer disease, PUD, nonsteroidal anti-inflammatory drug–induced gastritis, NSAID–induced gastritis, alcoholic gastropathy, uremic gastropathy, gastric mucosa, gastric acid secretion, physiological stress

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Contributor Information and Disclosures

Author

Rohan C Clarke, MD, Consulting Staff, Department of Gastroenterology, JPS Health Systems Hospital
Rohan C Clarke, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society of Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Coauthor(s)

Rachael M Ferraro, DO, Consulting Staff, Department of Internal Medicine, Regency Hospital and Kindred Hospital
Rachael M Ferraro, DO is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, and American Osteopathic Association
Disclosure: Nothing to disclose.

Emmanuel Gbadehan, MD, Instructor in Clinical Medicine, Columbia University College of Physicians and Surgeons; Consulting Staff, Department of Gastroenterology, Harlem Hospital Center, North General Hospital
Emmanuel Gbadehan, MD is a member of the following medical societies: American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Uzodinma R Dim, MD, Clinical Cardiac Electrophysiology Fellow, Division of Cardiovascular Medicine, University of Iowa Hospital and Clinics
Uzodinma R Dim, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Association of Black Cardiologists
Disclosure: Nothing to disclose.

Medical Editor

Ann Ouyang, MBBS, Professor, Department of Internal Medicine, Pennsylvania State University College of Medicine; Attending Physician, Division of Gastroenterology and Hepatology, Milton S Hershey Medical Center
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Simmy Bank, MD, Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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