Introduction
Hemorrhagic and erosive gastropathy are used for multifocal superficial mucosal hemorrhage and mucosal erosions without peptic ulcers. These are characterized by lesions that develop shortly after the gastric mucosa is exposed to an irrational substance or a substantial reduction in the blood flow to the mucosa.
What Is Hemorrhagic and Erosive Gastropathy?
Hemorrhagic and erosive gastropathy are used for multifocal superficial mucosal hemorrhage and mucosal erosions without peptic ulcers. These are characterized by lesions that develop shortly after the gastric mucosa is exposed to an irrational substance or a substantial reduction in the blood flow to the mucosa. It is reactive, non-inflammatory damage to the mucosa. It is seen as bleeding from multiple superficial mucosal erosions. The most frequently observed causes of this condition are non-steroidal anti-inflammatory drugs (NSAIDs) and the use of large amounts of alcohol.
It is one of the reasons for upper gastrointestinal bleeding, accounting for about one-fourth of upper GI bleeding in endoscopic studies. It is typically acute with evidence of bleeding but subacute or chronic with few or no symptoms. The condition can likely have many nutritional, metabolic, and vascular factors contributing to its pathogenesis.
What Are the Causes of Hemorrhagic and Erosive Gastropathy?
It is damage caused to the gastric mucosa due to exogenous or endogenous irritants or hypoxia (inadequate supply of oxygen). Hemorrhagic and erosive gastropathy can also be caused by:
1. Non-steroidal anti-inflammatory drugs (NSAIDs) - Chronic use of NSAIDs can cause acute and chronic reactive gastritis as prostaglandin production is reduced, reducing the flow of mucosa, and the protective mucosal barrier is destroyed.
2. Alcohol - Chronic or excessive alcohol use can reduce mucosal flow, destroy mucosal layers, and cause a scarcity of mucosal sulfhydryl compounds.
3. Bile salts - Reflex of biliary salts in the stomach due to pyloric sphincter incompetence, etc., can be seen in gastric surgery cases.
4. Stress.
5. Radiation.
6. Viral infections like cytomegalovirus.
7. Vascular injury.
8. Direct trauma, like nasogastric tubes.
9. Crohn’s disease (chronic inflammatory disease of the bowel).
10. Other - Exposure to preparations of iron salts, bisphosphonates, sodium phosphate, exposure to endogenous toxins, etc.
Gastritis can also be associated with critical illness and stress-induced GI bleeding. Mechanical ventilation (a therapy that aids in breathing when one cannot breathe on its own) for more than two days, coagulopathy, and sepsis are associated with the increased risk of hemorrhage, which is clinically significant and related to stress-induced gastritis.
The other reasons behind mucosal ischemia (death of cells due to a lack of oxygen supply) that may cause gastritis are trauma, burns (curling ulcer), a shock of any origin (cushing ulcer), any severe injury to the central nervous system, hypovolemia, and the use of cocaine. Glucocorticoids do not cause gastritis directly but can worsen the lesions caused by NSAID overuse. Invasion of the gastric wall (with organisms other than H. pylori) is also associated with gastritis caused by infections.
What Are the Symptoms of Hemorrhagic and Erosive Gastropathy?
When the condition is mild, the patient might be asymptomatic, though a few might complain of dyspepsia (discomfort in the upper abdomen, often described as a burning sensation, bloating, or gas; feeling of fullness when starting to eat), nausea, and vomiting. Usually, the first sign is hematemesis (vomiting blood), melena (dark stool with or without blood that occurs due to GI bleeding), or blood in nasogastric aspiration, usually within two to five days of the provoking event. Generally, bleeding can be mild to moderate, although if the ulceration is deep, bleeding can also be severe.
What Are the Differential Diagnoses of Hemorrhagic and Erosive Gastropathy?
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Hemorrhage induced by radiation.
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Viral gastritis.
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H.pylori infection.
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Gastric lymphoma.
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Gastric carcinoma.
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Dyspepsia is not associated with ulcers.
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GERD (Gastroesophageal reflux syndrome).
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Peptic ulcer.
How Are Hemorrhagic and Erosive Gastropathy Diagnosed?
A detailed medical history should be taken. It should include the following:
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Recent NSAID usage (dosage and frequency should be noted).
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Concurrent anticoagulant or glucocorticoid use.
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History of alcohol intake.
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Previous history of peptic ulcer or GI bleeding.
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Age (risk increases as age goes beyond 60).
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Previous gastric or abdominal surgery.
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History of any serious illness or mechanical ventilation, length of time spent in the hospital, and invasive therapy.
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History of gastroesophageal reflux disease (GERD).
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History of coagulopathies and thrombocytopenia.
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Symptoms present.
Endoscopy is done to diagnose hemorrhagic and erosive gastropathy. Endoscopy provides direct visualization of the gastric mucosa to evaluate conditions and abnormalities. A biopsy might not be mandatory in suspected cases, but it is taken for pathologic studies and to rule out alternative etiologies like H. pylori infection. It is recommended in patients older than sixty with dyspepsia and those younger than sixty with alarming symptoms like anemia, weight loss, emesis, etc. Patients whose primary relatives have a history of esophageal or GI cancer, lymphadenopathy, a suspected abnormal mass, etc., should also undergo endoscopy.
Endoscopic examination may reveal mucosal edema, erythema, petechiae (pin-point spots that appear due to bleeding), hemorrhage, erosions, or ulcerations. Curling's ulcer is usually located in the gastric fundus. Lesions associated with NSAIDs or alcohol are typically seen over the entire stomach; these lesions are minor and heal faster than the ones due to ischemia.
Endoscopic examination of bile-induced gastritis reveals severe erythema of the asterisk mucosa and its encrustation in bile salts.
How Are Hemorrhagic and Erosive Gastropathy Treated?
Treatment is based on stopping or limiting the use of the offending agent, and therapy is aimed at preventing further mucosal damage. The main goals of the treatment are the reduction of gastric inflammation, relief of the symptoms, and resolution of the underlying cause.
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Stopping the offending agent: When NSAID-induced or alcohol-induced gastritis is diagnosed, stopping the causative agent is advised. The condition usually resolves when the offending agent is stopped and might not require further treatment.
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Acid suppression: Therapy with H2 antagonists or proton pump inhibitors is usually effective in acid suppression, relieves the symptoms, and heals the mucosa.
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Biliary reflux-associated gastritis: Therapy with proton pump inhibitors or sucralfate may be given. Antacids can be added to the therapy.
Endoscopic hemostasis can be done to control bleeding. However, severe cases might require IV infusions and blood transfusions.
How Are Hemorrhagic and Erosive Gastropathy Prevented?
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Prevention of NSAID-induced gastritis and gastropathy: Avoid overuse and over-the-counter NSAIDs. If it is necessary, antacids or other gastro-protective drugs should be given.
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Diet: Although patients usually associate certain foods with aggravating or relieving the condition, this has not been proven scientifically. Modifying the diet according to the patient’s comfort can provide symptomatic relief.
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Quit smoking: Tobacco smoking increases the risk of the condition, delays healing, and worsens the existing condition.
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Prevention of stress ulcers in severely ill patients: H2 antagonists or proton pump inhibitors can be given to severely ill patients to reduce stress ulcers.
Conclusion:
Hemorrhagic and erosive gastropathy are used for multifocal superficial mucosal hemorrhage and mucosal erosions without peptic ulcers. These are characterized by lesions that develop shortly after the gastric mucosa is exposed to an irrational substance or a substantial reduction in the blood flow to the mucosa. Treatment of the condition is based on stopping or limiting the use of the offending agent, and therapy is aimed at preventing further mucosal damage. The main goals of the treatment are the reduction of gastric inflammation, relief of the symptoms, and resolution of the underlying cause.
