Stress-Induced Gastritis Treatment & Management
- Author: Rohan C Clarke, MD; Chief Editor: BS Anand, MD more...
The goal of management is prophylaxis. This 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 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.
Constantin et al compared the results of their study group (n = 36) with those of available international data regarding the prevention of stress-related mucosal disease and bleeding in critical care patients with PPI and H2 receptor antagonist therapy. Despite prophylactic acid suppressive therapy, the investigators found patients admitted to the ICU with various underlying conditions consistently had clinical and endoscopic diagnoses of bleeding from stress-related gastric mucosal disease.
In another study, Reveiz et al performed a systematic review of randomized trials to evaluate the effects prophylactic treatment of stress-related ulcers, gastritis, and upper gastrointestinal bleeding in critically ill children admitted to the pediatric ICU. Their pooled analysis of 2 randomized controlled studies totaling 300 patients found a significant difference among children who received prophylactic therapy for upper gastrointestinal bleeding (macroscopic or important bleeding) relative to those who did not receive such therapy.
Frandah et al conducted a similar study and concluded that the administration of prophylaxis in the ICU is inconsistent and that physician education and implementation of hospital protocols could be improved.
Pilkington et al also studied the stress ulcer prophlyaxis protocol using routine prescriptions of ranitidine and early enteral feeding to determine if the evidence supports their use for treatment of stress-related mucosal disease and gastrointestinal bleeding. They concluded that the evidence did not support the claim for the benefits of such treatment.
In one trial (n =48) of children who were on mechanical ventilation, those who received ranitidine demonstrated significant differences with normal gastric mucosal endoscopic findings by histologic specimens ; however, using different drugs (eg, omeprazole, ranitidine, sucralfate, etc), doses, or regimens for main outcomes (deaths, endoscopic evidence of erosion/ulcers, upper gastrointestinal bleeding, pneumonia) did not result in any significant differences.
Reveiz et al concluded that although their analysis of the pooled data appears to suggest a benefit of providing prophylactic treatment for prevention of upper gastrointestinal bleeding, there is still limited high-quality evidence to guide clinical practice.
Herzig et al found that cases of nosocomial GI bleeding outside of the intensive care unit were rare and that noncritically ill patients should not be given routine prophylactic acid-suppressive medication.
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