Acute gastritis generally refers to acute inflammation of the gastric mucosa caused by various factors. Histologically, neutrophil infiltration is typically observed. It includes acute erosive hemorrhagic gastritis, acute Helicobacter pylori gastritis, and other acute infectious gastritis unrelated to H. pylori. This section focuses primarily on acute erosive hemorrhagic gastritis.
Etiology and Pathophysiology
Stress
Severe trauma, surgery, multiple organ failure, sepsis, or psychological stress can lead to microcirculatory disturbances and hypoxia in the gastric mucosa. These conditions reduce mucus secretion, impair local prostaglandin synthesis, and damage the mucosal barrier. Increased gastric acid secretion and back-diffusion of hydrogen ions can damage blood vessels and the mucosa, resulting in erosion, bleeding, or even ulcers.
Medications
This is commonly seen with non-steroidal anti-inflammatory drugs (NSAIDs), particularly aspirin (one of the most classic NSAIDs), which are non-selective cyclooxygenase (COX) inhibitors. While enteric-coated NSAIDs can reduce local damage to the gastric mucosa, they can still inhibit COX-1 in mucosal cells after absorption in the small intestine via systemic circulation, leading to acute gastritis.
Antineoplastic chemotherapy drugs, while inhibiting tumor growth, often exert cytotoxic effects on the gastrointestinal mucosa, causing severe mucosal damage and increasing the risk of bacterial and viral infections. In addition, oral iron supplements and potassium chloride can also cause gastric mucosal erosion.
Ethanol
Ethanol's lipophilic and lipid-dissolving properties can lead to gastric mucosal erosion and bleeding. However, neutrophilic infiltration is often minimal.
Trauma and Physical Factors
High-dose radiation exposure and other physical insults can cause gastric mucosal erosion or even ulcers.
Clinical Manifestations
Common symptoms include epigastric pain, fullness, nausea, vomiting, and loss of appetite. Severe cases may present with hematemesis, melena, dehydration, acidosis, or shock. NSAID-induced gastritis (e.g., aspirin) is often asymptomatic or only detected during endoscopic examination. In symptomatic cases, mild epigastric discomfort or vague pain is the predominant presentation.
Diagnosis
A suspected diagnosis is based on the presence of the aforementioned clinical symptoms along with relevant etiological factors or triggers. Definitive diagnosis relies on endoscopic findings of erosions and bleeding lesions, with histopathological examination performed when necessary. Since gastric mucosa repairs rapidly, early endoscopic examination is crucial when clinical suspicion arises.
Treatment
Treatment involves addressing the underlying cause, actively managing primary diseases or injuries, and correcting the associated pathophysiological disturbances. Commonly used medications include acid-suppressing drugs such as proton pump inhibitors (PPIs), potassium-competitive acid blockers (P-CABs), or H2 receptor antagonists (H2RAs). Gastric mucosal protectants can promote mucosal healing and hemostasis.
Prognosis
In most cases, gastric mucosal erosions and bleeding resolve spontaneously with healing and cessation of bleeding. However, in some patients, mucosal erosion may progress to ulcers, increasing the risk of complications. Nevertheless, these conditions generally respond well to medical treatment.
Prevention
Unnecessary use of NSAIDs should be avoided. Patients with severe trauma, burns, major surgeries, organ failure, or those requiring long-term use of aspirin or clopidogrel may benefit from prophylactic administration of PPIs or H2RAs. For individuals with osteoarthritic conditions, selective COX-2 inhibitors, such as celecoxib, can be used to reduce COX-1 inhibition and minimize gastric mucosal damage. Promoting healthy dietary habits and avoiding excessive alcohol consumption are recommended. For portal hypertensive gastropathy, PPIs can be considered, and severe cases may require management of portal hypertension.