Acute Hemorrhagic/Erosive and Stress-Related Gastropathy

Chapter: Acute Hemorrhagic/Erosive and Stress-Related Gastropathy
McMaster Section Editor(s): John K. Marshall, Paul Moayyedi
Section Editor(s) in Interna Szczeklika: Andrzej Dąbrowski, Marek Hartleb, Ewa Nowakowska-Duława, Małgorzata Szczepanek
McMaster Author(s): Arnav Agarwal, Grigorios I. Leontiadis
Author(s) in Interna Szczeklika: Andrzej Dąbrowski, Krzysztof Marlicz†
† Deceased.
Additional Information

Definition, Etiology, PathogenesisTop

Acute hemorrhagic (erosive) gastropathy is reactive noninflammatory damage to the gastric mucosa caused by various exogenous and/or endogenous irritants or hypoxia. It manifests as bleeding from multiple superficial mucosal erosions. Acute erosive gastropathy may be caused by one of the following:

1) Nonsteroidal anti-inflammatory drugs (NSAIDs): Chronic NSAID use is associated with both acute and chronic reactive gastritis and ulceration due to inhibited prostaglandin production, decreased mucosal blood flow, and degradation of the protective mucosal barrier.

2) Alcohol: Chronic or excessive use is associated with decreased mucosal blood flow, degradation of the protective mucosal barrier, and depletion of mucosal sulfhydryl compounds.

3) Bile exposure: Reflux of biliary salts into the stomach due to pyloric sphincteric incompetence, such as may be seen in the context of gastric surgery.

4) Other: Exposure to oral preparations of iron salts, bisphosphonates, sodium phosphate; exposure to endogenous toxins (eg, in uremia).

Gastritis may also be seen in the setting of critical illness with stress-induced gastrointestinal (GI) bleeding. Mechanical ventilation for ≥2 days, coagulopathy, and likely sepsis are associated with increased risk of clinically significant hemorrhage related to stress-induced gastritis. Other causes of mucosal ischemia that may lead to gastritis—including trauma, burns (Curling ulcers), shock of any origin, severe central nervous system injury (Cushing ulcers), hypovolemia, and cocaine use—may also be associated with similar stress-induced gastritis.

Glucocorticoids likely do not cause gastritis or gastropathy but may worsen NSAID-induced lesions.

Bacterial invasion of the gastric wall (with organisms other than Helicobacter pylori) may also be associated with infection-driven gastritis.

Clinical Features and Natural HistoryTop

Patients may present with dyspepsia, nausea, emesis, or loss of appetite. Some patients may experience upper GI bleeding, which may be associated with no other signs or symptoms or may be accompanied by dyspepsia. Deep ulcers may develop, complicated by hemorrhage or perforation. Patients with gastritis may also be asymptomatic.

DiagnosisTop

A detailed medical history should include:

1) Recent NSAID use (dose, frequency, duration).

2) Concurrent anticoagulant or glucocorticoid use.

3) Recent or history of alcohol misuse.

4) Prior peptic ulcers or GI bleeding.

5) Age (age >60 years is associated with increased risk).

6) Previous gastric or abdominal surgery (including biliary surgery).

7) History of gastroesophageal reflux disease (GERD).

8) Critical illness or mechanical ventilation exposure and associated duration of hospitalization, intensive care unit (ICU) admission, and invasive therapy.

9) History of coagulopathies or thrombocytopenia.

10) Symptoms: Dyspepsia, abdominal pain, fever, nausea, emesis; signs and symptoms of critical illness, infection, sepsis, or other concurrent medical conditions.

Diagnostic Tests

Endoscopy allows to directly evaluate the gastric mucosa for gastritis or other abnormalities. In patients with suspected erosive gastritis mucosal biopsy may not be necessary, although it is often obtained for histopathologic examination and to exclude alternative etiologies, such as H pylori infection.

Endoscopy is recommended for patients aged ≥60 years with dyspepsia and for patients <60 years with alarming symptoms (anemia, weight loss, dysphagia, emesis). Patients with a family history of esophageal or GI cancer, lymphadenopathy, suspected or known abdominal mass, or treatment-refractory symptoms should undergo endoscopy.

Endoscopic evaluation may reveal mucosal edema and erythema, petechiae, hemorrhage, erosions, or ulcerations (in severe cases). Curling ulcers are usually located in the gastric fundus (or may also involve the gastric body). Lesions caused by NSAID or alcohol use most often cover the entire stomach; these erosions are usually smaller and heal more rapidly than those associated with ischemic gastritis and gastropathy.

The diagnosis of bile reflux–related gastritis is based on gross endoscopic examination showing severe erythema of the gastric mucosa (fiercely red discoloration) and incrustation of the mucosa with bile crystals (note that the presence of bile in the stomach does not warrant by itself the diagnosis of bile reflux gastropathy).

NSAID-induced gastritis and alcohol-induced gastritis are primarily diagnosed based on clinical suspicion. Patients with prior ulceration, age >60 years, high NSAID use, or concurrent anticoagulant or glucocorticoid use are at especially high risk of NSAID-related complications.

Differential Diagnosis

Differential diagnosis includes gastric lymphoma or carcinoma, dyspepsia not associated with ulcers, GERD, and peptic ulcer disease (PUD) (although this is often related to gastritis).

TreatmentTop

Treatment of gastritis is focused on discontinuation of the offending agent and therapy aimed at preventing further mucosal injury. The goals of treatment are reduction of gastric inflammation, symptomatic relief, and resolution of the underlying cause.

1. Discontinuation of the offending agent: When NSAID-induced or alcohol-induced erosive gastritis is suspected, reduction or discontinuation of the offending agent is recommended. When the cause of hemorrhagic gastropathy is removed, it generally resolves without further treatment.

2. Acid suppression (dosage: see Gastroesophageal Reflux Disease): Therapy with either H2 antagonists or proton pump inhibitors (PPIs) is effective in the suppression of acid secretion and associated with both symptomatic relief and mucosal healing.

3. Patients with biliary reflux–associated gastritis: Therapy with a PPI or sucralfate may be indicated.Evidence 1Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). Low Quality of Evidence (low confidence that we know true effects of the intervention). Quality of Evidence lowered due to the risk of bias. Santarelli L, Gabrielli M, Candelli M, et al. Post-cholecystectomy alkaline reactive gastritis: a randomized trial comparing sucralfate versus rabeprazole or no treatment. Eur J Gastroenterol Hepatol. 2003 Sep;15(9):975-9. PubMed PMID: 12923369. Antacid drugs may be added.

PreventionTop

1. Prevention of NSAID-induced gastritis and gastropathy: see Peptic Ulcer Disease.

2. Prevention of stress ulcers in seriously ill patients: H2 antagonists or PPIs have traditionally been recommended for stress ulcer prophylaxis in the setting of critical illness. Recently their benefit has been questioned and new clinical studies are being conducted. The strongest risk factors are mechanical ventilation >48 hours and coagulopathy (platelet counts <50,000/microL or international normalized ratio [INR] >1.5).

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