Gut failure and translocation following burn and sepsis

Sepsis with multisystem organ failure is a major cause of morbidity and mortality in burns. We studied the anatomic, physiologic, and metabolic changes of gut mucosa as a normal barrier against sepsis and systemic inflammatory response after burn and sepsis in the chronic porcine model. Flow probes were placed on the mesenteric and hepatic arteries and portal vein. Catheters were placed in the pulmonary artery (Swan-Ganz), aorta, superior mesenteric, and hepatic veins. After 5 days, baseline data were collected and studied after a 40%, third degree burn. They were resuscitated with Ringer's lactate solution (Parkland formula). Eighteen hours later, Escherichia coli endotoxin (100 micrograms/kg) was administered. All animals were sacrificed after 30 hr. The data were compared to a group of sham animals. Following thermal injury the cardiovascular status was stable. Endotoxin administration decreased systemic vascular resistance index and mean arterial pressure, but increased cardiac index. Mesenteric blood flow, vascular resistance, and oxygen consumption showed a transient fall after endotoxin infusion with 20, 23, and 40% reduction, respectively. These changes were associated with a rise in plasma levels of conjugated dienes. The intestinal ornithine decarboxylase activity was elevated at the end of the experiment, evidence of gut repair. Gut bacteria translocated into mesenteric lymph nodes, spleen, and burn wounds in 50% of the animals. We concluded that bacterial translocation into mesenteric lymph nodes, spleen, and wound is due to gut mucosal failure after burn trauma and sepsis. These pathophysiologic changes may be the result of mesenteric ischemia and reperfusion injury.