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.
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.
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 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.
No studies have shown any differences among the races with respect to the bleeding rates associated with stress gastritis.
No differences have been noted between the sexes with respect to stress gastritis.
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.
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.
Clinical presentation is varied, but the following clues should raise the level of clinical suspicion for this entity:
- Coffee ground vomitus
- Hematemesis (in extreme cases)
- Orthostasis (unusual)
Prolonged mechanical ventilation and coagulopathy increase predisposition to stress gastritis. Causative factors include the following conditions: