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 a fallback procedure if bleeding cannot be controlled endoscopically. Angiography is unlikely to stop severe gastric bleeding because of the many collateral vessels supplying the stomach. Acid-suppressing drugs 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, chronic liver disease, acute kidney injury, hepatic or renal failure, multiorgan dysfunction, and history of peptic ulcer or gastrointestinal bleeding. A 2020 guideline for gastrointestinal bleeding prophylaxis for critically ill patients recommends that in most critically ill patients the benefit of acid suppression must be weighed against the risk of pneumonia. The guideline includes a calculator to help assess the risk of gastrointestinal bleeding. There is a possible increased risk of nosocomial pneumonia in critically ill patients receiving acid suppression. A recent meta-analysis concluded that proton pump inhibitors (PPIs) and histamine-2 receptor antagonists may increase the risk of pneumonia (absolute increases 5% for PPIs and 3.4% for histamine-2 receptor antagonists; 1). However, a previous large clinical study of a PPI for patients at risk of gastrointestinal bleeding in the intensive care unit found no increased incidence of pneumonia (2). The guideline further recommends using a PPI rather than a histamine-2 receptor antagonist (weak recommendation) and recommends against using sucralfate.
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.
1. Wang Y, Ye Z, Ge L, et al: Efficacy and safety of gastrointestinal bleeding prophylaxis in critically ill patients: Systematic review and network meta-analysis. BMJ 368:l6744, 2020. doi: 10.1136/bmj.l6744PMCID
2. Krag M, Marker S, Perner A, et al: Pantoprazole in patients at risk for gastrointestinal bleeding in the ICU. N Engl J Med 379(23):2199–2208, 2018. doi: 10.1056/NEJMoa1714919
The following is an English-language resource that may be useful. Please note that THE MANUAL is not responsible for the content of this resource.