Spontaneous gastric rupture in non-neonatal children: a case report.

This case reports an idiopathic gastric rupture in a 3-year-old girl who had an episode of nausea and vomiting after a large meal. Abdominal ultrasound and CT scan revealed free air and fluid in the abdominal cavity, leading to the diagnosis of gastro-intestinal perforation. During emergency surgery, gastric rupture was detected on the anterior wall of the gastric body near the greater curvature and treated by performing a sleeve gastrectomy. The intra-operative course was complicated by a cardiac arrest. The child survived following intensive postoperative care. All articles on spontaneous idiopathic gastric rupture in pre-school age children have only been reported in Japanese and Chinese literature.

A mechanism for shock following stomach rupture in the newborn.

BACKGROUND: Stomach rupture often leads to shock and death within a short period, but the mechanism for this is not well-known. Shock may be due, in part, to endotoxin translocation and endotoxemia. METHODS: Sterile, endotoxin-free HCl (0.1 mol/L), with or without endotoxin-feeding, was injected intraperitoneally into 10-day-old rats, simulating stomach rupture in the newborn. The plasma endotoxin concentration was measured. Plasma glucose and lactate concentrations were monitored to assess physiologic response to endotoxemia and shock. RESULTS: Endotoxin feeding alone caused endotoxemia (0.49 +/- 0.12 ng/mL; P < 0.05) in 10-day-old rats, while plasma endotoxin concentration in controls was less than 0.04 ng/mL. However, the endotoxemia did not cause disruption of glucose regulation or death. Injection of HCl alone did not increase plasma endotoxin concentrations and did not alter glucose regulation. However, HCl injection into endotoxin-fed rats induced endotoxemia (211.1 +/- 70.5 ng/mL; P < 0.05), hypoglycemia, lactacidemia and mortality (45%; P < 0.05). CONCLUSION: Early development of shock following stomach rupture may be in part due to endotoxin translocation and endotoxemia.