Practice Essentials
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 physiologic stress, resulting in minimal-to-severe gastrointestinal (GI) blood loss and leading to blood transfusion if not addressed in time.
Signs and symptoms
Stress-induced gastritis has a variable clinical presentation, but the following clues should raise the level of clinical suspicion for this entity:
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Coffee ground vomitus
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Melena
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Hematemesis (in extreme cases)
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Orthostasis (unusual)
See Presentation for more detail.
Diagnosis
A high degree of clinical awareness is the key to early diagnosis. 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.
Laboratory testing
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Hematocrit
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Coagulation profile
Procedures
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Nasogastric tube and lavage: Useful test to confirm the presence of blood in the upper GI tract and to quantify the amount of blood if found (roughly assessed by the amount of normal saline needed before the aspirate becomes clear)
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Endoscopy: Useful only in the diagnosis of stress-induced gastritis
See Workup for more detail.
Management
Prophylaxis of stress gastritis is the goal of management. Monitor the pH of the gastric contents (target: pH >4.0). If the pH level is below the target pH, consider doubling the dose of the agent used to reduce gastric acid levels if the patient was previously on prophylaxis therapy.
Pharmacotherapy
The following medications are used in the management of stress-induced gastritis:
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Sucralfate: Primary agent for prophylaxis
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Histamine 2 (H2) receptor blockers (eg, ranitidine, famotidine, cimetidine, nizatidine)
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Proton pump inhibitors (eg, esomeprazole, pantoprazole)
See Treatment and Medication for more detail.
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 physiologic stress, resulting in minimal-to-severe gastrointestinal blood loss and leading to blood transfusion if not addressed expeditiously. [1]
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
Common sites for stress ulceration include the gastric body and fundus, antrum, and duodenum. [2]
Acid is secreted by the parietal cells of the gastric mucosa, which is under the influence of several biologic agents or activities (eg, histamine, gastrin, vagal nerve stimulation). [1] The mucosa is protected by the mucous gel layer, which is under the influence of prostaglandins, nitric oxide, [3] 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. [2]
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 etiologic 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. [4] Stress causes decreased blood flow to the mucosa, leading to ischemia with subsequent destruction of the mucosal lining.
Epidemiology
United States data
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 intensive care unit within 24 hours of the onset of the stressor. [5]
Race-, sex-, and age-related demographics
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, may lead to decreased mucous production and, hence, greater susceptibility to erosions and ulcerations.
Etiology
Prolonged mechanical ventilation and coagulopathy increase the predisposition to stress gastritis. Causative factors include the following conditions:
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Severe trauma (stress ulcers in the setting of acute traumatic brain injury are known as Cushing ulcers [2] )
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Massive burns (stress ulcers due to systemic burns are known as Curling ulcers [2] )
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Hypotension
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Sepsis with positive blood culture results
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Central nervous system injury with raised intracranial pressure
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Mechanical ventilation [6]
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Multiorgan failure
Prognosis
In general, the prognosis depends on the severity of the etiologic condition and timely recognition and management of stress-induced gastritis. [1] Gastrointestinal bleeding due to stress ulcerations range from 1.5% to 15%, depending on whether stress ulcer prophylaxis has been provided. [2] If stress gastritis is left untreated, life-threatening intestinal hemorrhage may occur, followed by perforation, with ensuing septic shock and, potentially, death. [1]
Morbidity/mortality
Gastrointestinal bleeding due to stress-related mucosal disease is itself an independent risk factor for greater morbidity/mortality.
Morbidity/mortality 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 gastrointestinal tract, thereby resulting in a 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.
