Acute gastritis
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"acute gastritis" AND management
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Here is a thorough overview of acute gastritis drawn from Sleisenger & Fordtran, Robbins & Kumar Basic Pathology, Harrison's Principles (22nd Ed, 2025), and Tintinalli's Emergency Medicine.
Acute Gastritis
Definition
Acute gastritis is histologically documented inflammation of the gastric mucosa characterized by a neutrophilic infiltrate. It must be distinguished from "gastropathy," where mucosal injury and regeneration occur without significant inflammation, and from the endoscopic finding of mucosal erythema (which does not equal gastritis). - Harrison's Principles of Internal Medicine 22E, p. 2581
Note: The correlation between histologic findings, endoscopic appearance, and clinical symptoms is poor - there is no "typical" clinical picture.
Etiology and Classification (Harrison's Table 335-10)
I. Acute Gastritis
| Type | Examples |
|---|---|
| Acute H. pylori infection | Most common infectious cause; presents with sudden epigastric pain, nausea, vomiting |
| Bacterial (phlegmonous) | Group A Streptococci, gram-negative bacilli, anaerobes, Clostridium |
| Emphysematous (gas-forming) | C. perfringens, E. coli, S. aureus |
| Viral | CMV, HSV, norovirus |
| Fungal | Mucormycosis (immunocompromised) |
| Chemical/Toxic | NSAIDs, alcohol, corrosives (acids/bases) |
| Stress-related | Shock, trauma, burns, organ failure |
Pathogenesis
The gastric mucosa normally defends itself through:
- A mucus layer with neutral pH (bicarbonate secretion by foveolar cells)
- Rich mucosal blood supply to buffer back-diffusing protons
- Prostaglandin E2 and I2 (stimulated by COX enzymes) promoting mucus and bicarbonate secretion
Acute gastritis occurs when these defenses are overwhelmed:
Mechanisms of gastric injury and protection (Robbins & Kumar Basic Pathology)
Key mechanisms:
- NSAIDs - inhibit COX-dependent prostaglandin synthesis, reducing mucosal blood flow and bicarbonate secretion
- H. pylori - urease generates ammonia, which inhibits gastric bicarbonate transporters and triggers neutrophil chemokine release
- Ischemia/stress - splanchnic vasoconstriction in critical illness reduces bicarbonate secretion; systemic acidosis lowers intracellular pH of mucosal cells
- Alcohol, radiation, chemotherapy - direct epithelial/stromal cell toxicity
- Ingestion of caustics - direct chemical injury
- Robbins & Kumar Basic Pathology, p. 553
Morphology (Histology)
- Mild/Gastropathy: Lamina propria edema, vascular congestion; surface epithelium intact, foveolar cell hyperplasia; neutrophils absent or sparse
- Active inflammation (acute gastritis proper): Neutrophils above the basement membrane in contact with epithelial cells - this is the hallmark
- Severe: Erosions, hemorrhage, or "acute erosive hemorrhagic gastritis" (concurrent erosion + hemorrhage)
Phlegmonous/suppurative gastritis (rare):
- Infection of submucosa and muscularis propria
- Edematous, thickened wall with polymorphonuclear infiltrate, gram-positive/gram-negative bacteria, vascular thrombosis, mucosal necrosis
Emphysematous gastritis (most severe):
- Gas-producing organisms (C. perfringens, E. coli, S. aureus)
- Gas visible in the stomach wall and portal venous system on CT
Stress-Related Mucosal Disease (Specific Type)
Occurs in critically ill patients:
- >75% of ICU patients develop endoscopically visible gastric lesions within 3 days
| Name | Location | Association |
|---|---|---|
| Stress ulcers | Stomach | Shock, sepsis, severe trauma |
| Curling ulcers | Proximal duodenum | Severe burns or trauma |
| Cushing ulcers | Stomach/duodenum/esophagus | CNS injury (stroke) - high perforation risk |
Pathogenesis: ischemia from hypotension/splanchnic vasoconstriction; Cushing ulcers additionally involve vagal stimulation causing acid hypersecretion. - Robbins & Kumar Basic Pathology, p. 553
Clinical Features
- Often asymptomatic
- Epigastric pain, nausea, vomiting, anorexia
- Hematemesis, melena, or massive hemorrhage (in erosive/hemorrhagic forms)
- Phlegmonous/emphysematous gastritis: septic appearance, acute upper abdominal pain, peritonitis, purulent ascitic fluid, fever, hypotension
Diagnosis
- Histology (endoscopic biopsy) is the gold standard - endoscopic appearance alone is insufficient
- H. pylori: urea breath test, stool antigen, or biopsy with urease test/culture
- Phlegmonous/emphysematous gastritis: CT scan (gas in stomach wall, portal vein gas), plain films, US; gastroscopy with biopsy/culture of gastric contents
- Acute H. pylori: histology shows marked neutrophilic infiltrate with edema and hyperemia
- Harrison's Principles of Internal Medicine 22E
Management
| Cause | Treatment |
|---|---|
| H. pylori | Triple or quadruple eradication therapy; if untreated, evolves into chronic active gastritis with lifelong infection |
| NSAIDs/alcohol | Discontinue offending agent; acid suppression (PPIs/H2 blockers) |
| Stress ulcers | PPIs or H2 antagonists for prophylaxis in ICU patients; treat underlying illness |
| Caustic ingestion | Supportive care; avoid emesis; urgent endoscopy within 12-24 hrs |
| Phlegmonous/emphysematous gastritis | Broad-spectrum IV antibiotics; surgical intervention may be required |
| CMV gastritis | Ganciclovir |
Complications and Progression
- Hypochlorhydria lasting up to 1 year after acute H. pylori infection
- Untreated H. pylori: chronic active gastritis → peptic ulcer disease → gastric adenocarcinoma or MALToma
- Phlegmonous gastritis can spread to liver/spleen, cause abscess; emphysematous gastritis can progress to gastric gas gangrene and death
- Sleisenger and Fordtran's Gastrointestinal and Liver Disease, p. 909
Sources: Sleisenger and Fordtran's Gastrointestinal and Liver Disease | Robbins & Kumar Basic Pathology (Robbins Pathology) | Harrison's Principles of Internal Medicine 22E (2025) | Tintinalli's Emergency Medicine
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