Abstract
Introduction. The spectrum of gastric injury due to corrosives can vary. This paper presents a single center experience of over 30 years of corrosive gastric injuries of 39 patients with acute gastric injuries from 1977 till 2006. Patients and Methods. Two thirds of the patients in the acute injury group had a concomitant esophageal injury. The age of the patients ranged from 4 years to 65 years with a slight preponderance of males. (M : F ratio 22 : 17). Results. 36 out of 39 acute gastric injuries were due to ingestion of acids. Three patients had history of caustic soda ingestion. Oral hyperemia or ulcers of varying extent were seen in all patients. The stomach showed hyperemia in 10, extensive ulcers in 13, and mucosal necrosis in 10 patients. Fifteen patients (15/39, 38.5%) were managed conservatively. Twenty four patients (24/39, 61.5%) underwent laparotomy: one for frank peritonitis, 10 for gastric mucosal necrosis, and 13 others for extensive gastric ulcerations. Overall the mortality rate was 29.6 %. Conclusion. Although the mortality and morbidity of acute corrosive gastric injuries is high, the key to improve the survival is early identification of perforation, maintenance of nutrition and control of sepsis.
Highlights
The spectrum of gastric injury due to corrosives can vary
In children, due to careless storing of chemicals and ingestion with suicidal intent and due to free availability of the caustic agents contribute to their occurrence
All patients with acute corrosive injury presented in a critical condition with abdominal pain, vomiting, and hematemesis
Summary
Corrosive injuries of the stomach are not uncommon in developing countries In these countries, accidental or suicidal ingestion of acids is encountered more often than in developed countries where lye or alkaline corrosives are more frequent [1]. The relative extent of esophageal and gastric involvement largely depends on the nature of the corrosive ingested. Acids affect the stomach more commonly than alkalis [2], cause mucosal damage by coagulation necrosis, and require a longer duration of contact [3]. Alkalis cause liquefaction necrosis [3], are more viscous, and tend to adhere to the esophageal mucosa with only a relatively small amount reaching the stomach. The extent of esophageal damage is greater with alkalis than acids. This article presents a single center experience of over 30 years of corrosive gastric injuries of 39 patients with acute gastric injuries emphasizing the spectrum of injuries and the extent of involvement and highlighting the possible modes of management
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