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.

ERAS pathways are safe and feasible in select patients undergoing emergency simple closure of PDU.

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Eradication of H. pylori after simple closure of a perforated duodenal ulcer should reduce the incidence of residual and recurrent ulcers.

Superficial swab culture may not be accurate in identifying all the organisms causing diabetic foot osteomyelitis. Bone biopsy specimen taken simultaneously would increase the accuracy of detecting the bacterial isolate.