Gastritis, stress induced
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.
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.
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)
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
Differential Diagnosis
Nonsteroidal anti-inflammatory drug (NSAID)–induced gastritis
Alcoholic gastropathy
Uremic gastropathy
Lab Studies
- A high degree of clinical awareness is the key to early diagnosis. The presence of any of the previously discussed clinical features should alert the clinician to the presence of stress gastritis.
- Useful investigations and diagnostic tools include the following:
- Hematocrit
- Coagulation profile
- Nasogastric tube and lavage: Gastric lavage is a useful test to confirm whether blood is present in the upper GI tract and to quantify the amount of blood if found. This is roughly assessed by how much normal saline it takes before the aspirate becomes clear.
- Endoscopy is useful only in the diagnosis of stress-induced gastritis.
Medical Care
The goal of management is prophylaxis. This has been shown to reduce the incidence by 50% when started on 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.
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
PPIs have not been fully evaluated in the role of prophylaxis for this disease.
Drug Category: Gastrointestinal agents
Shown to be effective in the prevention of stress-induced gastritis.
| Drug Name | Sucralfate (Carafate) |
| Description | Binds with positively charged proteins in exudates and forms a viscous adhesive substance that protects the GI lining against pepsin, peptic acid, and bile salts. Primary agent for prophylaxis of stress gastritis. |
| Adult Dose | 1g PO q6h |
| Pediatric Dose | 10-20 mg/kg PO q6h |
| Contraindications | Documented hypersensitivity; dysphagia/GI obstruction |
| Interactions | May decrease effects of penicillamine, ketoconazole, ciprofloxacin, tetracycline, phenytoin, warfarin, quinidine, theophylline, and norfloxacin |
| Pregnancy | B - Usually safe but benefits must outweigh the risks. |
| Precautions | Caution in renal failure and conditions that impair excretion of absorbed aluminum |
Drug Category: Histamine H2 antagonists
These agents block H2 receptor binding. The primary indication is to reduce symptoms and to accelerate healing of gastric ulcers. In the acutely bleeding patient, they are of limited benefit. Some have also been used for prophylaxis (eg, famotidine).
| Drug Name | Famotidine (Pepcid) |
| Description | Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations. |
| Adult Dose | 20 mg PO/IV q12h |
| Pediatric Dose | 0.5-1 mg/kg/d PO/IV divided q6h; not to exceed 40 mg/dose |
| Contraindications | Documented hypersensitivity |
| Interactions | May decrease effects of ketoconazole and itraconazole |
| Pregnancy | B - Usually safe but benefits must outweigh the risks. |
| Precautions | If changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment |
| Drug Name | Nizatidine (Axid) |
| Description | Competitively inhibits histamine at H2 receptors of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations. |
| Adult Dose | 300 mg PO hs or 150 mg PO bid |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity |
| Interactions | None reported |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Caution in renal or liver impairment; if changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment |
| Drug Name | Cimetidine (Tagamet) |
| Description | Inhibits histamine at H2 receptors of gastric parietal cells, which results in reduced gastric acid secretion, gastric volume, and hydrogen concentrations. |
| Adult Dose | 150 mg PO qid; not to exceed 600 mg/d
|
| Pediatric Dose | <16 years: 25-30 mg/kg/d PO/IV in 6 divided doses (only if benefits outweigh risk)
|
| Contraindications | Documented hypersensitivity |
| Interactions | Can increase blood levels of theophylline, warfarin, tricyclic antidepressants, triamterene, phenytoin, quinidine, propranolol, metronidazole, procainamide, and lidocaine |
| Pregnancy | B - Usually safe but benefits must outweigh the risks. |
| Precautions | Elderly individuals may experience confusional states; may cause impotence and gynecomastia in young males; may increase levels of many drugs; adjust dose or discontinue treatment if changes in renal function occur |
| Drug Name | Ranitidine (Zantac) |
| Description | Inhibits histamine stimulation of the H2 receptor in gastric parietal cells, which, in turn, reduces gastric acid secretion, gastric volume, and hydrogen ion concentrations. |
| Adult Dose | 150 mg PO bid; not to exceed 600 mg/d; alternatively, 50 mg/dose IV/IM q6-8h |
| Pediatric Dose | <12 years: Not established
|
| Contraindications | Documented hypersensitivity |
| Interactions | May decrease effects of ketoconazole, itraconazole, diazepam, nondepolarizing muscle relaxants, and oxaprozin; may alter serum levels of ferrous sulfate and procainamide |
| Pregnancy | B - Usually safe but benefits must outweigh the risks. |
| Precautions | Caution in renal or liver impairment; if changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment |
Medical/Legal Pitfalls
- Timely prophylaxis with H2 blockers can lead to a significant reduction in the development of stress-induced gastritis and, hence, the avoidance of upper gastrointestinal hemorrhage.
- Possibility of blood product transfusions, dependent on the severity of hemorrhage. This may expose the patient to the unnecessary risk of blood-borne infections.
- The possible resultant hypotension could worsen any vasculature compromise that is present, leading to cerebrovasculature accidents, myocardial infarction, and renal failure.
- This could potentially leave the physician liable for lawsuits, if the patient is not prophylaxed earlier or in a timely manner.
- The geriatric population may be more susceptible to the loss of blood, leading to a worsening of any underlying chronic vascular disease.
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