Common causes of erosive gastritis include
Less common causes include
Superficial erosions and punctate mucosal lesions occur. These may develop as soon as 12 hours after the initial insult. Deep erosions, ulcers, and sometimes perforation may occur in severe or untreated cases. Lesions typically occur in the body, but the antrum may also be involved.
Acute stress gastritis, a form of erosive gastritis, occurs in about 5% of critically ill patients. The incidence increases with duration of intensive care unit stay and length of time the patient is not receiving enteral feeding. Pathogenesis likely involves hypoperfusion of the gastrointestinal mucosa, resulting in impaired mucosal defenses. Patients with head injury or burns may also have increased secretion of acid.
Patients with mild erosive gastritis are often asymptomatic, although some complain of dyspepsia, nausea, or vomiting. Often, the first sign is hematemesis, melena, or blood in the nasogastric aspirate, usually within 2 to 5 days of the inciting event. Bleeding is usually mild to moderate, although it can be massive if deep ulceration is present, particularly in acute stress gastritis.
In severe gastritis, bleeding is managed with IV fluids and blood transfusion as needed. Endoscopic hemostasis should be attempted, with surgery (total gastrectomy) a fallback procedure. Angiography is unlikely to stop severe gastric bleeding because of the many collateral vessels supplying the stomach. Acid suppression should be started if the patient is not already receiving it.
For milder gastritis, removing the offending agent and using drugs to reduce gastric acidity (see Drug Treatment of Gastric Acidity) to limit further injury and promote healing may be all that is required.
Prophylaxis with acid-suppressive drugs can reduce the incidence of acute stress gastritis. However, it mainly benefits certain high-risk intensive care unit patients, including those with severe burns, central nervous system trauma, coagulopathy, sepsis, shock, multiple trauma, mechanical ventilation for > 48 hours, hepatic or renal failure, multiorgan dysfunction, and history of peptic ulcer or gastrointestinal bleeding.
Prophylaxis consists of IV H2 blockers, proton pump inhibitors, or oral antacids to raise intragastric pH > 4.0. Repeated pH measurement and titration of therapy are not required. Early enteral feeding also can decrease the incidence of bleeding.
Acid suppression is not recommended for patients simply taking nonsteroidal anti-inflammatory drugs unless they have previously had an ulcer.