A mechanism for shock following stomach rupture in the newborn

Background: Stomach rupture often leads to shock and death within a shea pe riod, but the mechanism for this is not well-known. Shock may be due, in pa rt, to endotoxin translocation and endotoxemia. Methods: Sterile, endotoxin-free HCl (0.1 moI/L), with or without endotoxin -feeding, was injected intraperitoneally into 10-day-old rats, simulating s tomach rupture in the newborn. The plasma endotoxin concentration was measu red. Plasma glucose and lactate concentrations were monitored to assess phy siologic response to endotoxemia and shook. 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 contro ls was less than 0.04 ng/mL. However, the endotoxemia did not cause disrupt ion of glucose regulation or death. Injection of HCl alone did not increase plasma endotoxin concentrations and did not alter glucose regulation. Howe ver, HCL injection into endotoxin-fed rats induced endotoxemia (211.1 +/- 7 0.5 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.