What is Acute Gastritis?
Acute gastritis is an inflammatory condition of the gastric mucosa characterized by sudden onset of mucosal inflammation, typically caused by infectious agents (particularly Helicobacter pylori), NSAIDs, alcohol, or physiologic stress, and manifesting as acute vomiting and/or diarrhea lasting less than 7 days. 1
Pathophysiological Definition
Acute gastritis represents a histologically-defined condition marked by significant inflammatory cell infiltration, particularly neutrophils, distinguishing it from reactive gastropathy which lacks substantial inflammation 2. The condition involves:
- Acute inflammatory infiltrate: Predominantly neutrophils with some eosinophils in the lamina propria, mucus layer, and inside the glands 3
- Mucosal edema and hyperemia: Visible on endoscopic examination 3
- Absence of glandular loss: Unlike chronic atrophic gastritis, acute gastritis does not feature loss of gastric glands or metaplasia 2
Clinical Presentation
The clinical manifestations of acute gastritis include:
- Gastrointestinal symptoms: Epigastric pain or discomfort, nausea, vomiting, and acute diarrhea 1, 4
- Acute gastroenteritis syndrome: Often presents as acute vomiting and/or diarrhea lasting <7 days 1
- Hemorrhagic variant: Acute hemorrhagic gastritis accounts for approximately one-fourth of upper gastrointestinal bleeding cases 5
Etiologic Categories
Infectious Acute Gastritis
- Helicobacter pylori is the primary infectious cause, presenting with intense polymorphonuclear leukocyte infiltration that can endoscopically mimic gastric carcinoma or lymphoma 3
- Other infectious agents can cause acute gastritis as part of infectious diarrhea syndromes 1
Acute Hemorrhagic Gastritis
This important subtype has specific predisposing conditions 5:
- Alcohol abuse: Direct mucosal toxicity
- NSAID use: Both short-term and long-term exposure
- Portal hypertension: Underlying liver disease
- Physiologic stress: ICU patients with severe life-threatening disease or trauma
Acute Phlegmonous Gastritis
- A rare but potentially fatal bacterial infection of the gastric wall characterized by severe infection with gas formation and necrosis 6
- Requires immediate recognition and often surgical intervention 6
Diagnostic Approach
The diagnosis requires:
- Endoscopic visualization: Look for mucosal edema, hyperemia, erosions, or hemorrhagic changes 3
- Histological confirmation: Biopsy showing neutrophilic infiltration without glandular atrophy 2, 3
- Pathogen detection: Testing for H. pylori on both antral and oxyntic mucosa when infectious etiology suspected 3
- CT imaging: For suspected phlegmonous gastritis showing gastric wall thickening, edema, and gas 6
Critical Distinction from Chronic Gastritis
Acute gastritis differs fundamentally from chronic gastritis 2, 7:
- Inflammatory pattern: Neutrophils (acute) versus lymphocytes and plasma cells (chronic)
- Glandular architecture: Preserved in acute gastritis versus atrophic changes in chronic gastritis
- Duration: Days to weeks versus months to years
- Cancer risk: Not established for acute gastritis versus well-documented increased risk (0.1-0.3% per year) for chronic atrophic gastritis 8
Treatment Principles
Management depends on the underlying etiology:
- Infectious gastritis: Antimicrobial therapy—for H. pylori, combination therapy with amoxicillin (2 g/day for 2 months) plus metronidazole (750 mg/day for 15 days) achieves dramatic symptom reduction and pathogen clearance 3
- Hemorrhagic gastritis: Supportive measures plus therapy directed at mucosal healing, similar to peptic ulcer disease management 5
- Prevention: Key strategy for at-risk patients, particularly those with predisposing conditions 5
- Phlegmonous gastritis: Immediate broad-spectrum antibiotics; surgical intervention (total gastrectomy) if conservative treatment fails 6
Common Pitfalls
- Misdiagnosis as malignancy: H. pylori acute gastritis can endoscopically mimic gastric carcinoma or lymphoma, making histology and pathogen detection essential 3
- Delayed recognition of phlegmonous gastritis: Fast disease progression requires immediate action; conservative antibiotic therapy alone may be insufficient 6
- Confusion with gastropathy: Reactive gastropathy lacks significant inflammatory infiltrate and requires different management (removal of offending agent rather than antimicrobial therapy) 2