Stress-Induced Gastritis Treatment & Management

Updated: Aug 26, 2018
  • Author: Rohan C Clarke, MD; Chief Editor: BS Anand, MD  more...
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Medical Care

The goal of management for stress-induced gastritis is prophylaxis, [1, 2] which has been shown to reduce the incidence by 50% when treatment is started at 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 to reduce gastric acid levels 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.

Although the role of proton pump inhibitors (PPIs) in prophylaxis has not been fully evaluated, these agents have been recommended as first-line agents for prophylaxis. [1, 2] However, PPIs are prodrugs and usually require an acidic medium to be activated. Hence, in the fasting stressed patient, or in a subset of critical care patients who present with overt GI bleeding but without stress ulceration or stress-related mucosal disease (eg, variceal bleeds, vascular anomalies, diverticulosis), [2] this may not be the case. PPIs block the final common pathway of acid secretion by blocking the H-K-ATPase enzyme. In addition, there appears to be a higher risk (38.6%) of hospital-acquired Clostridium difficile infection when PPIs are used for prophylaxis and treatment of stress ulcers than when H2RAs are used. [7, 8]

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 have also found them to be safe and cost effective. In a comparison of PPIs and placebo, the superiority of PPIs over placebo was demonstrated in cases of bleeding peptic ulcer. PPIs were also shown to be more effective for rebleed prophylaxis versus H2 blockers.

In a review of studies from a MEDLINE search through August 2015, Barletta and colleagues found that PPIs appear to be the dominant drug class used worldwide. However, when the researchers evaluated only trials that were at low risk for bias, the evidence failed to clearly support lower bleeding rates with proton pump inhibitors over histamine 2 receptor antagonists. [9]

In a search of the Cochrane library, MEDLINE, EMBASE, ACPJC, clinical trials registries, and conference proceedings through November 2015, Alshamsi et al reviewed randomized controlled trials of PPIs versus H2-receptor antagonists (H2RAs) for stress ulcer prophylaxis in critically ill adults. They found that in 19 trials enrolling 2117 patients, PPIs were more effective than H2RAs in reducing the risk of clinically important gastrointestinal (GI) bleeding and overt GI bleeding, without significantly increasing the risk of pneumonia or mortality. [10]

In a more recent meta-analysis with trial sequential analysis that included 34 randomized controlled trials comprising 3220 critically ill adults who received PPIs or H2RAs versus placebo, control, no therapy, or enteral nutrition, the strategy of stress ulcer prophylaxis was associated with significant reductions in bleeding but did not affect mortality. [11]

In a retrospective study (2008-2013) of data from 200 patients at risk for stress gastropathy due to mechanical ventilation in a surgical trauma intensive care unit (ICU) at a single center, investigators noted that the incidence of clinically significant GI bleeding (CSGB) was low (0.50%) and that of stress gastropathy was rare in this population. [12] Moreover, pharmacologic stress gastropathy prophylaxis provided no benefit once at-risk surgical and trauma patients tolerated enteral nutrition, potentially secondary to sufficient gut blood flow rending the stress gastropathy prophylaxis unnecessary. [12]

A prospective observational study (2010-2015) of 40 ICU patients regarding the effects of 1484 time-dependent doses of epinephrine (average dose per day at time t) on the occurrence of stress ulcer-related CSBG found that an increase in the average daily epinephrine dose raised the time to occurrence of stress ulcer in these critically ill patients, as did enteral feeding. [13] However, renal replacement therapy increased the occurrence of stress ulcers.


Surgical Care

In general, surgical interventions are for life-saving measures—such as refractory bleeding despite endoscopic or angiographic therapy, or in individuals who are hemodynamically unstable to undergo these procedures. [2]

Surgical intervention may also be required in the setting of deep ulcers that lead to perforation of the gastric wall, resulting in acute peritonitis that necessitates urgent laparotomy. [2]