Pathogenesis and disease course
Although the stomach normally secretes hydrochloric acid, which can neutralize alkalis, it is defenseless against ingested strong acids such as sodium hypochlorite. Exposure to the aggressive chemical agent causes necrosis of the mucosal and submucosal layers with their subsequent sloughing.
The further course depends on the depth of the lesion:
- In severe cases, necrosis involves the entire thickness of the gastric wall. This is a life-threatening condition that frequently results in organ perforation.
- In less severe cases, granulation tissue begins to form on the exposed areas of the wall. Collagen synthesis is triggered, ultimately leading to pronounced fibrosis and stricture formation.
As an outcome, the stomach becomes shrunken and deformed, and its patency is impaired, making total gastrectomy necessary in many cases.
Diagnostic radiology
The radiologic pattern directly depends on the severity of the chemical burn and the time elapsed since the injury.
- Initial stage. Radiographs show marked edema, irregular mucosal contours, and specific bullae. If mucosal sloughing occurs, the contrast agent (barium) may dissect beneath it. In this case, the detached mucosa appears as a thin radiolucent line running parallel to the contour of the gastric wall.
- Late stage. Characterized by fibrous shrinkage of the stomach. At this stage, the picture may resemble syphilitic gastritis or infiltrative carcinoma (linitis plastica). In the most severe cases, the gastric lumen is so narrowed that its size does not exceed the duodenal bulb.
Differential diagnosis
Cicatricial changes in corrosive gastritis must be differentiated from other conditions causing gastric wall thickening or luminal narrowing:
- Linitis plastica — an infiltrative tumor mimicking fibrous shrinkage of the stomach.
- Syphilitic gastritis — may present a similar picture in late scarring stages.
- Eosinophilic gastroenteritis — manifests as diffuse wall thickening on CT, but occurs without ascites and responds successfully to steroids.
- Amyloidosis — a rare pathology in which the gastric wall and folds thicken and become rigid due to the deposition of a protein-polysaccharide complex. Radiologically, it may simulate linitis plastica; a definitive diagnosis is established only by biopsy.
Briefly: answers to topical questions
How to differentiate corrosive gastritis from linitis plastica on computed tomography?
Available materials lack specific CT criteria for differentiation, although a general radiologic similarity between these pathologies is noted.
Conditions mimicking linitis plastica (linitis plastica):
- Corrosive gastritis (Gastritis corrosiva) — in the late stage, causes fibrous shrinkage of the stomach, narrowing its lumen down to the size of the duodenal bulb.
- Amyloidosis (Amyloidosis) — causes wall thickening and rigidity due to the deposition of a protein-polysaccharide complex; final diagnosis is confirmed only by biopsy.
Class and exam questions
Why is the stomach more vulnerable to acids than to alkalis?
The stomach's own hydrochloric acid is capable of neutralizing ingested alkalis, but cannot neutralize strong acids.
How does mucosal sloughing appear on contrast study?
Barium dissects beneath the sloughed mucosa, causing it to appear as a thin radiolucent strip parallel to the gastric wall.
What is the outcome of corrosive gastritis?
In severe cases, perforation occurs, and upon survival, a shrunken, fibrotic stomach with impaired patency develops, requiring total removal.
What else to study on this topic
- Clinical presentation and endoscopic classification of gastric burns
- Management tactics for suspected gastric perforation
- Classification and diagnostic imaging of gastric polyps
- Association of hyperplastic polyps with H. pylori and atrophic gastritis
- Features of detecting fundic gland polyps during PPI therapy
- Adenomatous polyps as a precancerous condition
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